Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Markers expression.
Статті в журналах з теми "Markers expression"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся з топ-50 статей у журналах для дослідження на тему "Markers expression".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Переглядайте статті в журналах для різних дисциплін та оформлюйте правильно вашу бібліографію.
1
Deng, Yongyan, Hongjin Li, and Yujiao Tang. "The Effect of Suppression Taurine on Relocation and Epithelial-Mesenchymal Transition in Mankind Lung Cancer Cells." Journal of Healthcare Engineering 2021 (April 14, 2021): 1–11. http://dx.doi.org/10.1155/2021/6656080.
Повний текст джерелаАнотація:
Aim. Taurine is believed to have antioxidant properties and has been implicated in the treatment of neurodegenerative disease, atherosclerosis, coronary heart disease, and prostate cancer. This research focused on taurine inhibition effects of expression related to migration and epithelial-mesenchymal transition- (EMT-) A549 study on related genes of human being non-small-cell lung cancer. Methods. MTT assays assessed cell viability and a RadiusTM assay showed that taurine also inhibited the lung cancer cell migration. Using RT-PCR and Western blot, the migration and EMT markers were identified and evaluated. Results. We found that taurine significantly decreased the expression of migration markers matrix metallopeptidase 9 (MMP-9) and vascular endothelial growth factor (VEGF). In contrast, TIMP metallopeptidase inhibitor 1 (TIMP-1) and TIMP metallopeptidase inhibitor 2 (TIMP-2) expressions were increased with taurine treatment. In addition, we found an association between taurine treatment and the expression of EMT markers. The expression of epithelial marker E-cadherin and the mesenchymal marker N-cadherin TWIST-1 was decreased, but the expression of zinc finger protein SNAIL-1 and E-zinc finger homeobox 1 (ZEB-1) was increased. Conclusion. Taken together, our study strongly suggests the therapeutic significance of taurine, which possesses antimigration activity and induces EMT markers expression in lung cancer cells.
2
Link, C. D., C. W. Ehrenfels, and W. B. Wood. "Mutant expression of male copulatory bursa surface markers in Caenorhabditis elegans." Development 103, no. 3 (July 1, 1988): 485–95. http://dx.doi.org/10.1242/dev.103.3.485.
Повний текст джерелаАнотація:
In a search for molecular markers of male tail morphogenesis in C. elegans, we have detected two surface markers that are specifically observed in the copulatory bursa of adult males and the vulva of adult hermaphrodites. These markers are defined by binding of a monoclonal antibody (Ab117) and the lectin wheat germ agglutinin (WGA) to live intact animals. Expression of these markers is dependent on sex, stage and anterior-posterior position in the animal. Four of ten mutants with specific defects in bursal development show altered expression of one or both markers. Because the WGA marker can be expressed in intersexual animals with very little bursal development, posterior surface expression of this marker can serve as an indication of subtle masculinization of hermaphrodites. The timing of expression of these markers is not affected by heterochronic mutations that cause larval animals to express adult cuticles or adult animals to express larval cuticles, indicating that marker expression can be uncoupled from general cuticle development. Mutant lin-22 males, which have an anterior-to-posterior transformation of cell fates in the lateral hypodermis, ectopically express both markers in a manner consistent with a ‘posteriorization’ of positional information in these animals. These markers should be useful for the isolation and characterization of mutants defective in bursal and vulval development, sex determination and expression of anterior-posterior positional information.
3
Koren, Ana, Matija Rijavec, Izidor Kern, Eva Sodja, Peter Korosec, and Tanja Cufer. "BMI1,ALDH1A1, andCD133Transcripts Connect Epithelial-Mesenchymal Transition to Cancer Stem Cells in Lung Carcinoma." Stem Cells International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/9714315.
Повний текст джерелаАнотація:
Epithelial-mesenchymal transition (EMT) is the underlying mechanism of tumor invasion and metastasis. Evidences from lung cancer cellular models show EMT can trigger conversion to a cancer stem cell (CSC) phenotype. In this study, we assessed mRNA expression levels of EMT-inducing transcription factors (BMI1,TWIST1), CSC (CD133,ALDH1A1), and epithelial (EpCAM) markers in primary tumor and whole blood samples obtained from 57 patients with operable non-small-cell lung cancer (NSCLC) as well as in circulating tumor cells (CTCs) of 13 patients with metastatic disease; then possible associations between marker expressions were evaluated. In primary tumors as well as in whole blood, correlations betweenBMI1andALDH1A1and betweenBMI1andCD133mRNA expressions were identified. No correlations betweenTWIST1and CSC markers were observed.BMI1mRNA expression in tumors positively correlated withBMI1mRNA expression in blood. The immunohistochemical analysis confirmed coexpression of BMI1 and CSC markers in tumors. Gene expression profiling in CTCs revealed upregulated expression of EMT/CSC markers in CTCs. Our results suggest CSCs are present in both, tumor tissue and blood of NSCLC patients, whereas Bmi1 may play an important role in initiation and maintenance of CSCs and might be involved in the blood-borne dissemination of NSCLC.
4
Naghavi Alhosseini, Mahdieh, Marianna Palazzo, Luigi Cari, Simona Ronchetti, Graziella Migliorati, and Giuseppe Nocentini. "Overexpression of Potential Markers of Regulatory and Exhausted CD8+ T Cells in the Peripheral Blood Mononuclear Cells of Patients with B-Acute Lymphoblastic Leukemia." International Journal of Molecular Sciences 24, no. 5 (February 24, 2023): 4526. http://dx.doi.org/10.3390/ijms24054526.
Повний текст джерелаАнотація:
B-acute lymphoblastic leukemia (B-ALL) is one of the most common pediatric cancers, wherein regulatory T cells (Treg) and exhausted CD8+ T cells may be important in its development and maintenance. In this bioinformatics study, we evaluated the expression of 20 Treg/CD8 exhaustion markers and their possible roles in patients with B-ALL. The mRNA expression values of peripheral blood mononuclear cell samples from 25 patients with B-ALL and 93 healthy subjects (HSs) were downloaded from publicly available datasets. Treg/CD8 exhaustion marker expression was normalized with that of the T cell signature and correlated with the expression of Ki-67, regulatory transcription factors (FoxP3, Helios), cytokines (IL-10, TGF-β), CD8+ markers (CD8α chain, CD8β chain), and CD8+ activation markers (Granzyme B, Granulysin). The mean expression level of 19 Treg/CD8 exhaustion markers was higher in the patients than in the HSs. In patients, the expression of five markers (CD39, CTLA-4, TNFR2, TIGIT, and TIM-3) correlated positively with Ki-67, FoxP3, and IL-10 expression. Moreover, the expression of some of them correlated positively with Helios or TGF-β. Our results suggested that Treg/CD8+ T cells expressing CD39, CTLA-4, TNFR2, TIGIT, and TIM-3 favor B-ALL progression, and targeted immunotherapy against these markers could be a promising approach for treating B-ALL.
5
R, Naveen Kumar, Charanjeet Ahluwalia, Sunita Malik, and Rashmi Arora. "Evaluation of Epithelial Mesenchymal Transition Markers E-Cadherin and Vimentin in Carcinoma Cervix." Annals of Pathology and Laboratory Medicine 7, no. 6 (July 7, 2020): A282–287. http://dx.doi.org/10.21276/apalm.2746.
Повний текст джерелаАнотація:
Background: Cervical cancer is the second most common in developing areas. Epithelial to mesenchymal transformation, one of the critical elements in invasion, progression and metastasis of tumour. This study highlights the expression of epithelial mesenchymal markers E-cadherin and vimentin in carcinoma cervix and whether there is any association of expression of these markers with grade of cervical cancer.
Objectives:
To study the expression of epithelial mesenchymal transition (EMT) markers
E-cadherin and vimentin in cervical cancer.
To correlate the immunohistochemical expression of these markers with grade of cervical cancer.
Methods: 30 cases (n=30) of carcinoma cervix & 30 controls (n=30) of non specific cervicitis diagnosed on H&E were included in this study. H&E stained sections was examined for histological type and grade. Immunohistochemistry for E-Cadherin and Vimentin was performed in all these cases.
Result: Immunohistochemical expression of epithelial marker E-cadherin and of mesenchymal marker vimentin was correlated with the grade of cervical carcinoma. The expression of E-cadherin is reduced and expression of vimentin is increased with increasing grades of carcinoma cervix.
Conclusion: The expression of these EMT markers can be used as a prognostic marker in cervical cancer that are in high risk of progression.
6
Mo, Chia-Kuei, Yige Wu, Terekhanova Nadezhda, Caravan Wagma, Preet Lal, Siqi Chen, Nataly Naser AL Deen, et al. "Abstract 2025: Spatial transcriptomic profiling of progression markers in clear cell renal cell carcinoma." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2025. http://dx.doi.org/10.1158/1538-7445.am2022-2025.
Повний текст джерелаАнотація:
Abstract Next-generation sequencing enabled molecular landscaping and the discovery of novel tumor markers in ccRCC. However, the spatial relationships and histological features of the tumor microenvironment were lost during this process. Combining snRNA-seq, snATAC-seq, Spatial Transcriptomics (ST) technology, and immunofluorescence labeling, we discovered novel ccRCC progression tumor markers, and uncovered their spatial dependent expression pattern in both human ccRCC tumors and patient-derived xenograft (PDX). Using snRNA-seq and snATAC-seq, novel tumor progression markers such as NDRG1, MGST1, ABCC3 and PCSK6 were discovered, and their expressions were validated in ST. We found that one of the key novel tumor markers, CP, exhibited specific spatial expression patterns on tissue slides. The elevation of CP expression region is associated with a higher degree of hyalinization in ccRCC human tumor samples. Similarly, using immunofluorescence labeling, we validated the co-expression of CP and PCSK6 canonical ccRCC marker CA9. Overall, this study revealed novel ccRCC progression markers and linked their spatial expression pattern with histological features. Citation Format: Chia-Kuei Mo, Yige Wu, Terekhanova Nadezhda, Caravan Wagma, Preet Lal, Siqi Chen, Nataly Naser AL Deen, Ruiyang Liu, Yanyan Zhao, Kazuhito Sato, Lijun Yao, Mamatha Serasanambati, Andrew Shinkle, Reyka G. Jayasinghe, Li Ding, Feng Chen. Spatial transcriptomic profiling of progression markers in clear cell renal cell carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2025.
7
Zhyvetska-Denysova, A. A., I. I. Vorobiova, N. Ya Skrypchenko, S. M. Tolkach, S. M. Razdaibedin, and Yu M. Bondarenko. "Placental markers of miscarriage." Pathologia 18, no. 3 (December 1, 2021): 328–39. http://dx.doi.org/10.14739/2310-1237.2021.3.232302.
Повний текст джерелаАнотація:
Successful implantation involves a high degree of development of spiral arteries, combined with high proliferative activity, which ensures the formation of a healthy placenta, full uterine-placental circulation, and the birth of a healthy child. The placenta is the unique organ of the biological monitoring, the mirror of pregnancy. Identification of placental markers of miscarriage is a promising direction for preventing reproductive losses. The aim of the work is to identify the markers of miscarriage and premature labor in the structures of the chorion and placenta. Materials and methods. The main group included tissue samples of the 22 chorions and 64 placentas after termination of current pregnancy from women with a history of reproductive losses. The control group included tissue samples of the 20 chorions after artificial abortion and 20 placentas after physiological pregnancy and birth. The placenta was examined according to the protocol (form No. 013-1/0). The expressions of VEGF, CD31/PECAM1, CD105/Endoglin/TGFβ 1/3 Receptor, Bcl-2α Ab-1, TNF-α, CD45/T200/LCA, CD56/NCAM1 were studied in the structures of chorion and placenta by immunohistochemistry. Results. Based on histological and immuno-histochemical study of chorion and placenta samples in women with reproductive history and termination of the current pregnancy, it was established that embryo-endometrial dysfunction is the cause of miscarriage in the first trimester, and inflammation is the precondition of preterm birth; markers of miscarriage and premature labor in the structures of the chorion and placenta have been identified. Conclusions. The markers of miscarriage are pathomorphological changes in endometrium and chorion combined with high expression of TNF-α and NK-CD56, low expression of CD31/PECAM1, negative expression of VEGF to indicate a violation of cytotrophoblast invasions. The markers of inflammation and premature labor are structural and functional changes of placenta in combination with moderate expression of TNF-α in syncytium, high expression of NK-CD56 in villous stroma, high expression of CD45/T200/LCA in the decidual membrane.
8
Kakiuchi-Kiyota, Satoko, Leslie A. Obert, Danielle M. Crowell, Shuhua Xia, Marc D. Roy, Timothy M. Coskran, John M. Kreeger, et al. "Expression of Hematopoietic Stem and Endothelial Cell Markers in Canine Hemangiosarcoma." Toxicologic Pathology 48, no. 3 (January 10, 2020): 481–93. http://dx.doi.org/10.1177/0192623319897539.
Повний текст джерелаАнотація:
Several chemicals and pharmaceuticals increase the incidence of hemangiosarcomas (HSAs) in mice, but the relevance to humans is uncertain. Recently, canine HSAs were identified as a powerful tool for investigating the pathogenesis of human HSAs. To characterize the cellular phenotype of canine HSAs, we evaluated immunoreactivity and/or messenger RNA (mRNA) expression of markers for hematopoietic stem cells (HSCs), endothelial cells (ECs), a tumor suppressor protein, and a myeloid marker in canine HSAs. Neoplastic canine cells expressed EC markers and a myeloid marker, but expressed HSC markers less consistently. The canine tumor expression results were then compared to previously published immunoreactivity results for these markers in human and mouse HSAs. There are 2 noteworthy differences across species: (1) most human HSAs had HSC marker expression, indicating that they were comprised of tumor cells that were less differentiated than those in canine and mouse tumors; and (2) human and canine HSAs expressed a late-stage EC maturation marker, whereas mouse HSAs were negative, suggesting that human and canine tumors may retain greater differentiation potential than mouse tumors. These results indicate that HSA development is variable across species and that caution is necessary when discussing translation of carcinogenic risk from animal models to humans.
9
Jha, R., G. Grover, and P. Bose. "Lymphoid associated antigen expression in new cases of Acute Myeloid Leukemia." Journal of Pathology of Nepal 3, no. 6 (October 24, 2013): 487–90. http://dx.doi.org/10.3126/jpn.v3i6.8999.
Повний текст джерелаАнотація:
Background: Occurrence of aberrant phenotype has been reported in acute leukemias with varying frequency though its prognostic importance remains controversial. In acute myeloid leukemias, aberrant phenotype, as high as 88 %, has been reported. To evaluate the occurrence of aberrant lymphoid phenotypes and to correlate their presence with various French American British classification, 100 cases of fresh acute myeloid leukemias were analyzed for lymphoid markers CD 4,7,8,10 and 19. Materials and Methods: Whole blood or bone marrow aspirate collected in EDTA were processed by standard method and subjected to immunophenotyping for B Cells marker CD 19 and 10 and T cell marker CD 4, 7 and 8. Results: Aberrant lymphoid markers were seen in 35(35%) cases. All FAB subtypes except M7 showed aberrancy for the markers studied. However it was the most common in M0 (100%), followed by M2 (51.9%). T cell aberrancy was the most common, comprising 62.8% (22/35) of total aberrancy. CD 7 was the most common aberrantly expressed marker, seen in 20% AML, followed by CD 4(14%) and CD 19 (8%). Conclusion: Occurrence of lymphoid phenotypes is frequent in pediatric as well adult AML. Though T cell markers are more common, only B cell as well as both B and T cell markers may be co expressed. DOI: http://dx.doi.org/10.3126/jpn.v3i6.8999 Journal of Pathology of Nepal (2013) Vol. 3, 487-490
10
Limantara, Eunice, Felicia Kartawidjajaputra, and Antonius Suwanto. "Evaluation of potential gene expression as early markers of insulin resistance and non-alcoholic fatty liver disease in the Indonesian population." Indonesian Journal of Biotechnology 23, no. 2 (December 24, 2018): 84. http://dx.doi.org/10.22146/ijbiotech.36975.
Повний текст джерелаАнотація:
Early detection of insulin resistance (IR) or non-alcoholic fatty liver disease (NAFLD) is crucial to preventing future risks of developing chronic diseases. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), Liver Fat Score (LFS), and Fatty Liver Index (FLI) are generally employed to measure severity stages of IR and NAFLD. The study of gene expressions could explain the molecular mechanisms that occur early on in IR and NAFLD; thus providing potential early markers for both diseases. This study was conducted to evaluate the gene expressions that could potentially be early markers of IR and NAFLD. All participants (n = 21) had normal blood glucose and were categorized as without hepatosteatosis (n = 10), at higher risk of hepatosteatosis (n = 6), and hepatosteatosis (n = 5). Gene expression analysis was performed using the 2-∆∆CT relative quantification method. There were significant differences in galnt2 (p < 0.002) and sirt1 (p < 0.010) expression between the first and the third tertiles of HOMA-IR; and in ptpn1 (p < 0.012) expression between the first and the second tertiles of LFS. In conclusion, the expressions of galnt2 and sirt1 could be used as early markers of IR, while the expression of ptpn1 could be employed as an early marker of NAFLD.
11
Yuspa, S. H., A. E. Kilkenny, P. M. Steinert, and D. R. Roop. "Expression of murine epidermal differentiation markers is tightly regulated by restricted extracellular calcium concentrations in vitro." Journal of Cell Biology 109, no. 3 (September 1, 1989): 1207–17. http://dx.doi.org/10.1083/jcb.109.3.1207.
Повний текст джерелаАнотація:
Epidermal differentiation is characterized by a series of coordinated morphological and biochemical changes which result in a highly specialized, highly organized, stratified squamous epithelium. Among the specific markers expressed in differentiating epidermis are (a) two early spinous cell proteins, keratins 1 and 10 (K1 and K10); and (b) two later granular cell proteins, filaggrin and a cornified envelope precursor (CE). In vitro, epidermal basal cells are selectively cultured in 0.05 mM Ca2+ medium, and terminal differentiation is induced when the Ca2+ concentration is increased to 1 mM. However, only a small fraction of the cells express the markers K1, K10, CE, or filaggrin in the higher Ca2+ medium. To explore the factors required for marker expression, cultured epidermal cells were exposed to intermediate Ca2+ concentrations and extracts were analyzed using specific antibody and nucleic acid probes for the four markers of interest. These studies revealed that marker expression was enhanced at a restricted concentration of Ca2+ in the medium of 0.10-0.16 mM. At this Ca2+ concentration, both protein and mRNA levels for each marker were substantially increased, whereas at higher or lower Ca2+ concentrations they were diminished or undetected. The percentage of cells expressing each marker was increased two- to threefold in the permissive Ca2+ medium as determined by immunofluorescence analysis. This optimal level of Ca2+ was required both to initiate and sustain marker expression. At the permissive Ca2+ concentration, expression of the markers was sequential and similar to the order of appearance in vivo. K1 was expressed within 8-12 h and K10 was expressed in the ensuing 12-24-h period. CE and filaggrin were expressed in the subsequent 24 h. Inhibition of K1 expression by cycloheximide suggested that an inducible protein was involved. Other investigators have determined that a shallow Ca2+ gradient exists in epidermis, where the basal cells and spinous cells are in a Ca2+ environment substantially below serum Ca2+ levels. These in vitro results suggest that the Ca2+ environment is a fundamental regulator of expression of epidermal differentiation markers and provide an explanation for the existence of the Ca2+ gradient in vivo.
12
Coni, Pierpaolo, Monica Piras, Marco Piludu, Joanna Izabela Lachowicz, Anna Matteddu, Stefano Coni, Alessandra Reali, et al. "Exploring cell surface markers and cell-cell interactions of human breast milk stem cells." Journal of Public Health Research 12, no. 1 (January 2023): 227990362211503. http://dx.doi.org/10.1177/22799036221150332.
Повний текст джерелаАнотація:
Background: Breakthrough studies have shown that pluripotent stem cells are present in human breast milk. The expression of pluripotency markers by breast milk cells is heterogeneous, relating to cellular hierarchy, from early-stage multi-lineage stem cells to fully differentiated mammary epithelial cells, as well as weeks of gestation and days of lactation. Design and methods: Here, we qualitatively analyze cell marker expression in freshly isolated human breast milk cells, without any manipulation that could influence protein expression. Moreover, we use electron microscopy to investigate cell-cell networks in breast milk for the first time, providing evidence of active intercellular communication between cells expressing different cellular markers. Results: The immunocytochemistry results of human breast milk cells showed positive staining in all samples for CD44, CD45, CD133, and Ki67 markers. Variable positivity was present with P63, Tβ4 and CK14 markers. No immunostaining was detected for Wt1, nestin, Nanog, OCT4, SOX2, CK5, and CD34 markers. Cells isolated from human breast milk form intercellular connections, which together create a cell-to-cell communication network. Conclusions: Cells freshly isolated form human breast milk, without particular manipulations, show heterogeneous expression of stemness markers. The studied milk staminal cells show “pluripotency” at different stages of differentiation, and are present as single cells or grouped cells. The adjacent cell interactions are evidenced by electron microscopy, which showed the formation of intercellular connections, numerous contact regions, and thin pseudopods.
13
Seregni, E., C. Botti, E. Bajetta, L. Ferrari, A. Martinetti, S. Nerini-Molteni, and E. Bombardieri. "Hormonal Regulation of MUC1 Expression." International Journal of Biological Markers 14, no. 1 (January 1999): 29–35. http://dx.doi.org/10.1177/172460089901400106.
Повний текст джерелаАнотація:
Several circulating mucinous markers, including CA 15.3, MCA, CA 459, CASA, and Truquant BR, are secreted products of the polymorphic MUC1 gene, and are used as diagnostic tools in patients with breast cancer. In clinical practice the measurement of the levels of these markers in the blood can give important information on the tumor's response to treatment and its biological behavior during disease monitoring. Since the marker levels reflect the activity of the tumor, it is important to know all factors influencing the production/secretion and the blood concentrations of MUC1 mucin. Recent findings suggest that MUC1 gene expression is regulated by steroid hormones and other substances present in the serum. Such observations are very important not only because of their biological significance but also for their clinical implications, as one approach to breast cancer therapy is based on chemical hormone manipulation. Nevertheless, we have preliminarily demonstrated that endocrine treatment in breast cancer patients does not influence the circulating CA 15.3 serum levels, so changes in marker levels are related only to the clinical evolution of the tumor.
14
Kovaleva, Olga V., Madina A. Rashidova, Daria V. Samoilova, Polina A. Podlesnaya, Rasul M. Tabiev, Valeria V. Mochalnikova, and Alexei Gratchev. "CHID1 Is a Novel Prognostic Marker of Non-Small Cell Lung Cancer." International Journal of Molecular Sciences 22, no. 1 (January 5, 2021): 450. http://dx.doi.org/10.3390/ijms22010450.
Повний текст джерелаАнотація:
There is an urgent need for identification of new prognostic markers and therapeutic targets for non-small cell lung cancer (NSCLC). In this study, we evaluated immune cells markers in 100 NSCLC specimens. Immunohistochemical analysis revealed no prognostic value for the markers studied, except CD163 and CD206. At the same time, macrophage markers iNOS and CHID1 were found to be expressed in tumor cells and associated with prognosis. We showed that high iNOS expression is a marker of favorable prognosis for squamous cell lung carcinoma (SCC), and NSCLC in general. Similarly, high CHID1 expression is a marker of good prognosis in adenocarcinoma and in NSCLC in general. Analysis of prognostic significance of a high CHID1/iNOS expression combination showed favorable prognosis with 20 months overall survival of patients from the low CHID1/iNOS expression group. For the first time, we demonstrated that CHID1 can be expressed by NSCLC cells and its high expression is a marker of good prognosis for adenocarcinoma and NSCLC in general. At the same time, high expression of iNOS in tumor cells is a marker of good prognosis in SCC. When used in combination, CHID1 and iNOS show a very good prognostic capacity for NSCLC. We suggest that in the case of lung cancer, tumor-associated macrophages are likely ineffective as a therapeutic target. At the same time, macrophage markers expressed by tumor cells may be considered as targets for anti-tumor therapy or, as in the case of CHID1, as potential anti-tumor agents.
15
Chen, Haiming, Daocheng Zhu, Richard A. Campbell, Christine Pan James, Cathy S. Wang, Janice Santos, Benjamin Bonavida, and James R. Berenson. "Pleitrophin Alone Induces Transdifferentiation of Human Monocytes and Bone Marrow Stem Cells into Endothelial Cells." Blood 104, no. 11 (November 16, 2004): 1472. http://dx.doi.org/10.1182/blood.v104.11.1472.1472.
Повний текст джерелаАнотація:
Abstract Bone marrow angiogenesis is a hallmark of multiple myeloma (MM). We have recently shown that MM patients express pleitrophin (PTN), a secreted protein that binds syndecan, and it is found at high levels in MM serum. This protein has been shown to stimulate angiogenesis. We have discovered a novel mechanism leading to blood vessel formation by tumor cells. First, we cloned human monocytic THP-1 cells with PTN sense or antisense whole sequencing DNA. We examined expression by RT-PCR of endothelial cell markers (Flk-1), Tie-2, von Willebrand factor (vWf)) and monocyte markers (c-fms and CD68). THP-1 cells infected with PTN sense strand expressed high amounts of Flk-1, Tie-2 and vWf similar to that found in human coronary artery endothelial cells and lost expression of c-fms and CD68. Endothelial cell marker RNA was not detected in either THP-1 cells infected with PTN anti-sense strand or the GFP control vector but these cells showed the continued presence of monocyte markers. Immunohistochemical studies showed THP-1 cells infected with PTN sense strand expressed endothelial markers but not cells treated with antisense or control cells. We have recently found high levels of PTN in MM serum and expression of PTN by MM cell lines including RPMI8226. Next, we cultured THP1 monocytes with RPMI8226 in transwell cultures, serum derived from MM patients with high serum levels of PTN, cell lines lacking PTN expression, and normal controls lacking serum PTN. The THP-1 cells exposed to the MM cell lines or MM serum showed expression of endothelial markers and lost expression of monocyte markers. The expression of endothelial markers was blocked by adding anti-PTN antibody. In contrast, control serum and cell lines lacking PTN expression did not change monocyte marker expression on the THP1 cells nor induce expression of endothelial markers. We examined whether PTN induced monocytes from human peripheral blood to transdifferentiate. Normal human blood monocytes were highly purified using density centrifugation followed by anti-CD14 micro-bead affinity column selection. These purified monocytes also showed transdifferentiation into endothelial cells in the presence of PTN with m-CSF unlike cells treated with m-CSF-alone or cells without these factors present. We determined whether PTN could also stimulate differentiation of bone marrow stem cells into endothelial cells. The stem cells were derived from bone marrow selected for CD34 using magnetic bead selection, and were stimulated with either m-CSF or PTN alone or a combination of m-CSF and PTN or no treatment for 7 days. Real time PCR analysis showed that the m-CSF and PTN combination markedly increased endothelial cell marker expression and decreased monocyte marker (CD68 and c-fms) expression in this stem cell population. When induced with PTN alone, the stem cells exhibited slightly increasing expression of endothelial markers with no change in monocyte marker expression whereas m-CSF alone and no treatment had no effect on either endothelial or monocyte marker expression. These experiments define a previously unrecognized novel mechanism leading to angiogenesis in cancer patients- the transdifferentiation of monocytes into endothelial cells by a factor highly produced by tumor cells. They also suggest a potential new specific target to inhibit angiogenesis-pleitrophin which may have profound clinical implications.
16
Foudah, Dana, Juliana Redondo, Cristina Caldara, Fabrizio Carini, Giovanni Tredici, and Mariarosaria Miloso. "Expression of Neural Markers by Undifferentiated Rat Mesenchymal Stem Cells." Journal of Biomedicine and Biotechnology 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/820821.
Повний текст джерелаАнотація:
The spontaneous expression of neural markers by mesenchymal stem cells (MSCs) has been considered to be a demonstration of MSCs’ predisposition to differentiate towards neural lineages. In view of their application in cell therapy for neurodegenerative diseases, it is very important to deepen the knowledge about this distinctive biological property of MSCs. In this study, we evaluated the expression of neuronal and glial markers in undifferentiated rat MSCs (rMSCs) at different culture passages (from early to late). rMSCs spontaneously expressed neural markers depending on culture passage, and they were coexpressed or not with the neural progenitor marker nestin. In contrast, the number of rMSCs expressing mesengenic differentiation markers was very low or even completely absent. Moreover, rMSCs at late culture passages were not senescent cells and maintained the MSC immunophenotype. However, their differentiation capabilities were altered. In conclusion, our results support the concept of MSCs as multidifferentiated cells and suggest the existence of immature and mature neurally fated rMSC subpopulations. A possible correlation between specific MSC subpopulations and specific neural lineages could optimize the use of MSCs in cell transplantation therapy for the treatment of neurological diseases.
17
Xi, Liqiang, Daniel G. Nicastri, Talal El-Hefnawy, Steven J. Hughes, James D. Luketich, and Tony E. Godfrey. "Optimal Markers for Real-Time Quantitative Reverse Transcription PCR Detection of Circulating Tumor Cells from Melanoma, Breast, Colon, Esophageal, Head and Neck, and Lung Cancers." Clinical Chemistry 53, no. 7 (July 1, 2007): 1206–15. http://dx.doi.org/10.1373/clinchem.2006.081828.
Повний текст джерелаАнотація:
Abstract Background: The detection of circulating tumor cells (CTCs) may prove useful for screening, prognostication, and monitoring of response to therapy. However, given the large background of circulating cells, it is probably necessary to detect 1 cancer cell in >106 leukocytes. Although reverse transcription (RT)-PCR is potentially sensitive and specific enough to achieve this goal, success will require the use of appropriate mRNA markers. The goal of this study was to identify optimal marker combinations for detection of CTCs. Methods: An extensive literature and internet database survey was conducted to identify potential markers. We then used real-time quantitative RT-PCR to test for expression of selected potential markers in tissue samples from primary tumors of breast, colon, esophagus, head and neck, lung, and melanoma and normal blood samples. Markers with high expression in tumors and a median 1000-fold lower expression in normal blood were considered potentially useful for CTC detection and were tested further in an expanded sample set. Results: A total of 52 potential markers were screened, and 3–8 potentially useful markers were identified for each tumor type. The mRNAs for all but 2 markers were found in normal blood. Marker combinations were identified for each tumor type that had a minimum 1000-fold higher expression in tumors than in normal blood. Conclusions: Several mRNA markers may be useful for RT-PCR–based detection of CTCs from each of 6 cancer types. Quantification of these mRNAs is essential to distinguish normal expression in blood from that due to the presence of CTCs. Few markers provide adequate sensitivity individually, but combinations of markers may produce good sensitivity for detection of the presence of these 6 neoplasms.
18
Chang, Kyung Hoon, Hong Lim Do, Chan Seung Hwang, Hoon Shik Yang, Young Ho Hong, Hoon Kim, and Chun Gil Kim. "Expression of Proliferative Markers in Cholesteatoma." Journal of Clinical Otolaryngology Head and Neck Surgery 7, no. 2 (November 1996): 340–48. http://dx.doi.org/10.35420/jcohns.1996.7.2.340.
Повний текст джерела
19
Wang, Lei, Wei Yuan, Songmei Geng, Ya Xiong, Dezhi Zhang, Xiaoqing Zhao, Shenqiu Li, Xinling Bi, Tianwen Gao, and Gang Wang. "Expression of lymphatic markers in angiokeratomas." Journal of Cutaneous Pathology 41, no. 7 (May 6, 2014): 576–81. http://dx.doi.org/10.1111/cup.12349.
Повний текст джерела
20
ISHII, Yoshiyuki, Yasuhiro FUJISAWA, Yasuhiro NAKAMURA, Junichi FURUTA, Eiko ICHIKAWA, Yasuhiro KAWACHI, and Fujio OTSUKA. "Expression of endothelial markers in angiosarcomas." Skin Cancer 24, no. 1 (2009): 96–98. http://dx.doi.org/10.5227/skincancer.24.96.
Повний текст джерела
21
Heba Ahmed Elhendawy, Heba Allah Ibrahim Taher, and Nadia Mostafa Lotfy. "Utilization of cell proliferation markers to diagnose cystic jaw pathologies." GSC Biological and Pharmaceutical Sciences 16, no. 3 (September 30, 2021): 129–44. http://dx.doi.org/10.30574/gscbps.2021.16.3.0274.
Повний текст джерелаАнотація:
Markers of cell proliferation are widely used as diagnostic and prognostic tools. Coincident estimation of these markers increases the precise evaluation of the proliferative status of different tissues and can also be helpful in determining progression, aggressiveness and prognosis of the lesions. The current study investigated the expression of PCNA and MCM3 cell proliferation markers in 40 formalin fixed paraffin embedded tissue blocks of odontogenic keratocyst (OKC) and unicystic ameloblastoma (UA) cases using immunohistochemistry method. Markers` expression based on the intensity, percentage of positively stained cells and localization of reaction through the cyst lining epithelium was separately analyzed for each marker using Chi square test, the results of which were significant for the two markers (P < 0.05). Both markers revealed statistically significant differences between OKC and UA cases regarding markers expression intensity, positivity score and localization of reaction through the epithelium. Mural UA histologic variant was significantly different than luminal and intraluminal variants. The correlation coefficient between the two markers was found to be 0.86.
22
Hamon, Morgan, Hsiao-Min Cheng, Ming Johnson, Norimoto Yanagawa, and Peter V. Hauser. "Effect of Hypoxia on Branching Characteristics and Cell Subpopulations during Kidney Organ Culture." Bioengineering 9, no. 12 (December 14, 2022): 801. http://dx.doi.org/10.3390/bioengineering9120801.
Повний текст джерелаАнотація:
During early developmental stages, embryonic kidneys are not fully vascularized and are potentially exposed to hypoxic conditions, which is known to influence cell proliferation and survival, ureteric bud branching, and vascularization of the developing kidney. To optimize the culture conditions of in vitro cultured kidneys and gain further insight into the effect of hypoxia on kidney development, we exposed mouse embryonic kidneys isolated at E11.5, E12.5, and E13.5 to hypoxic and normal culture conditions and compared ureteric bud branching patterns, the growth of the progenitor subpopulation hoxb7+, and the expression patterns of progenitor and differentiation markers. Branching patterns were quantified using whole organ confocal imaging and gradient-vector-based analysis. In our model, hypoxia causes an earlier expression of UB tip cell markers, and a delay in stalk cell marker gene expression. The metanephric mesenchyme (MM) exhibited a later expression of differentiation marker FGF8, marking a delay in nephron formation. Hypoxia further delayed the expression of stroma cell progenitor markers, a delay in cortical differentiation markers, as well as an earlier expression of medullary and ureteral differentiation markers. We conclude that standard conditions do not apply universally and that tissue engineering strategies need to optimize suitable culture conditions for each application. We also conclude that adapting culture conditions to specific aspects of organ development in tissue engineering can help to improve individual stages of tissue generation.
23
Kim, Sun Il, and Ja Seung Koo. "Expression of cancer stem cell markers in breast phyllodes tumor." Cancer Biomarkers 29, no. 2 (October 9, 2020): 235–43. http://dx.doi.org/10.3233/cbm-191276.
Повний текст джерелаАнотація:
BACKGROUND: Phyllodes tumor (PT) is a rare tumor showing various malignant potential. The histological grade of PT is related to clinical outcome, but its relationship between gaining of malignant potential and underlying mechanism including cancer stem cell factor was not understood yet. OBJECTIVE: The main purpose of this study was to determine the expression pattern of cancer stem cell marker in PT and to understand its clinical and pathological implications. METHODS: CD44, CD166, ALDH1, and Ki-67 immunohistochemistry were performed on a tissue microarray from 185 cases of PT specimens (138 benign, 32 borderline, 15 malignant). The immunohistochemistry result and clinicopathological parameter of each cases were compared to analyze the implications of cancer stem cell markers on PT. RESULTS: Borderline/malignant PT showed higher CD44 expression of the stromal component than benign PT (p< 0.001). In lower histologic grade PT, CD166 showed increased expression in the epithelial component (p= 0.019), but decreased in the stromal component (p< 0.001). Stromal overgrowth was rarely observed as the number of positive cancer stem cell markers increased in the epithelial component (p< 0.001). In the stromal component, the number of positive cancer stem cell markers was related to higher histologic grade (p< 0.001), and increased stromal cellularity (p< 0.001), stromal atypia (p= 0.003), and stromal mitosis (p= 0.002). In benign PT, CD44 negativity (p= 0.013) and a decreased number of positive cancer stem cell markers (p= 0.012) in the epithelial component were related to poor prognosis. CONCLUSIONS: The cancer stem cell markers, CD44 and CD166, are expressed in both the epithelial and stromal components of phyllodes tumor. Besides, ALDH1 is only expressed in stromal component. In the stromal component, expression of cancer stem cell markers increases with higher PT histologic grade. In the epithelial component, the absence of cancer stem cell marker expression is related to poor clinical prognosis.
24
Jha, Alok, Shourav Saha, Kamesh Ayasolla, Himanshu Vashistha, Ashwani Malhotra, Karl Skorecki, and Pravin C. Singhal. "MiR193a Modulation and Podocyte Phenotype." Cells 9, no. 4 (April 17, 2020): 1004. http://dx.doi.org/10.3390/cells9041004.
Повний текст джерелаАнотація:
Apolipoprotein L1 (APOL1)-miR193a axis has been reported to play a role in the maintenance of podocyte homeostasis. In the present study, we analyzed transcription factors relevant to miR193a in human podocytes and their effects on podocytes’ molecular phenotype. The motif scan of the miR193a gene provided information about transcription factors, including YY1, WT1, Sox2, and VDR-RXR heterodimer, which could potentially bind to the miR193a promoter region to regulate miR193a expression. All structure models of these transcription factors and the tertiary structures of the miR193a promoter region were generated and refined using computational tools. The DNA-protein complexes of the miR193a promoter region and transcription factors were created using a docking approach. To determine the modulatory role of miR193a on APOL1 mRNA, the structural components of APOL1 3’ UTR and miR193a-5p were studied. Molecular Dynamic (MD) simulations validated interactions between miR193a and YY1/WT1/Sox2/VDR/APOL1 3′ UTR region. Undifferentiated podocytes (UPDs) displayed enhanced miR193a, YY1, and Sox2 but attenuated WT1, VDR, and APOL1 expressions, whereas differentiated podocytes (DPDs) exhibited attenuated miR193a, YY1, and Sox2 but increased WT1, VDR, APOL1 expressions. Inhibition of miR193a in UPDs enhanced the expression of APOL1 as well as of podocyte molecular markers; on the other hand, DPD-transfected with miR193a plasmid showed downing of APOL1 as well as podocyte molecular markers suggesting a causal relationship between miR193a and podocyte molecular markers. Silencing of YY1 and Sox2 in UPDs decreased the expression of miR193a but increased the expression of VDR, and CD2AP (a marker of DPDs); in contrast, silencing of WT1 and VDR in DPDs enhanced the expression of miR193a, YY1, and Sox2. Since miR193a-downing by Vitamin D receptor (VDR) agonist not only enhanced the mRNA expression of APOL1 but also of podocyte differentiating markers, suggest that down-regulation of miR193a could be used to enhance the expression of podocyte differentiating markers as a therapeutic strategy.
25
Choccalingam, Chidambharam, Lakshmi Rao, and Sruti Rao. "Clinico-Pathological Characteristics of Triple Negative and Non Triple Negative High Grade Breast Carcinomas with and without Basal Marker (CK5/6 and EGFR) Expression at a Rural Tertiary Hospital in India." Breast Cancer: Basic and Clinical Research 6 (January 2012): BCBCR.S8611. http://dx.doi.org/10.4137/bcbcr.s8611.
Повний текст джерелаАнотація:
Aims of the study were to evaluate the expression Cytokeratin 5/6(CK5/6) and Epidermal Growth Factor Receptor (EGFR) among triple negative breast cancers and high grade infiltrating duct carcinomas. Further to probe if triple negative phenotype can be a surrogate marker for basal phenotype and to correlate the expression of basal markers with disease free survivals among triple negative phenotype and high grade infiltrating duct carcinomas. Methods Expression of CK5/6 and EGFR were studied by Immunohistochemistry (IHC) in 31 triple negative and 19 non-triple negative high grade breast carcinomas. Results 21 of the 31 triple negative phenotype (67.7%) breast carcinomas and 7 out of 19 non-triple negative (36.8%) breast carcinomas showed expression of basal markers (CK5/6 and/or over-expression of EGFR). There were statistically significant associations of all the basal-like tumors with negative hormonal status. The basal markers positive phenotype subjects had a shorter disease free interval as compared to basal markers negative phenotype subjects. Conclusion Basal-like breast carcinomas constitute a unique clinical and pathological entity, characterized by high tumor grade and a propensity for lack of ER, PR and HER2 expression. Basal phenotypes have a more aggressive course than non-basal phenotype. “Triple negative” status cannot be used as a surrogate for “basal marker expression”.
26
Culen, Martin, Marianna Romzova, Dagmar Smitalova, Tomas Loja, and Jiri Mayer. "Multicolor Immunophenotyping of Candidate Leukemic Stem Cell Markers in CD34+CD38- Chronic Myeloid Leukemia Stem Cells." Blood 134, Supplement_1 (November 13, 2019): 2922. http://dx.doi.org/10.1182/blood-2019-127809.
Повний текст джерелаАнотація:
Introduction: Detection of leukemic stem cells (LSCs) may represent a new potential prognostic parameter in chronic myeloid leukemia (CML) and a tool for minimal residual disease monitoring in combination with standard qPCR method. To date CD26 is studied as a most specific marker for CML LSC detection. Several other candidate LSC markers have been reported, such as IL1-RAP, CD25 and CD93, however a side-by-side testing of their specificity is lacking. Recently, we have identified CD69 molecule to be overexpressed in CD34+CD38-CD26+ cells, which makes this antigen another candidate marker for LSC. Aim: To compare the surface expression of LSC markers CD69, CD26, CD25, CD56, IL1-RAP, CD56, CD93 in bulk CD34+CD38- population at diagnosis using a multicolor phenotypization assay Methods: In total, 44 patients were analyzed at diagnosis of chronic phase CML before administration of any treatment. Fresh (n=38) or cryopreserved (n=6) leukocytes obtained by erythrolysis were stained with CD45, CD34, CD38, CD25, CD26, CD56, CD69, CD93, IL1-RAP antibodies and 7-AAD for selection of live cells. Analysis was performed on FACSAria Fusion (BD Biosciences). Acquisition of live mononuclear cells ranged from 2×104 to 2.5×106. Results: Expression of candidate LSC markers CD26, CD25, CD56, IL1-RAP, CD56, CD93 was analyzed in BM of 35 patients who carried at least 30 CD34+CD38- cells. Median percentage of marker positive cells was 34% for IL1-RAP, 31% for CD25, 23% for CD26, 16% for CD56 and 2% for CD93, from the parent CD34+CD38- population. Next we analyzed the overlap and combination for the three best markers - IL1-RAP, CD25 and CD26. The 3-combination (defined as IL1-RAP or CD25 or CD26 expression) identified 40% of CD34+CD38- positive cells, which was more than any of the markers alone. Expression of the three markers showed good overlap and ruled out mutually exclusive expression of the markers. This was demonstrated by median difference of 0.4% of CD34+CD38- cells (range: 0-18%) and a correlation coefficient r2=0.9914, when comparing the 3-combination and the best performing marker in each patient. In contrast, in 12/35 (34%) of patients, one of the three markers failed to identify at least half of the cells positive for another marker. In 21/35 patients, we also analyzed the expression of CD69 in the CD34+CD38- compartment. The CD69 showed similar performance as the 3-combination of CD26, CD25, and IL1-RAP, 59% vs 54% positive cells, respectively. We observed excellent overlap between CD69 and 3-combination expression in individual patients with median difference of 0% of CD34+CD38- cells (range 0-15%) and correlation coefficient r2=0.9890. Furthermore, we compared marker positivity in BM vs PB in 19 paired samples. Both, sample types showed similar frequency of CD34+CD38- cells (5×10-3 in BM, and 2×10-3 for PB), but PB carried higher percentage of LSCs identified by the 3-combination - median 76 vs 52% cells. Conclusions: We show an overlap in surface expression of three previously reported CML LSC markers - IL1-RAP, CD25 and CD26. Nevertheless, a combination of these markers can detect more positive cells than any of the markers alone. Moreover, we demonstrate that CD69 identifies the same cells within the CD34+CD38- compartment as the combination of three above mentioned markers, which makes CD69 the best candidate for routine CML LSC quantification. Disclosures Mayer: AOP Orphan Pharmaceuticals AG: Research Funding.
27
Bicknese, Alma R., Holly S. Goodwin, Cheryl O. Quinn, Verneake C. D. Henderson, Shin-Nan Chien, and Donna A. Wall. "Human Umbilical Cord Blood Cells can be Induced to Express Markers for Neurons and Glia." Cell Transplantation 11, no. 3 (April 2002): 261–64. http://dx.doi.org/10.3727/096020197390022.
Повний текст джерелаАнотація:
Rare cells are present in human umbilical cord blood that do not express the hematopoietic marker CD45 and in culture do not produce cells of hematopoietic lineage. These umbilical cord multipotent stem cells (UC-MC) behave as multilineage progenitor cells (stem cells) and can be expanded in tissue culture. Exposure to basic fibroblast growth factor (bFGF) and human epidermal growth factor (hEGF) for a minimum of 7 days in culture induces expression of neural and glial markers. Western immunoblots demonstrate expression of both β-tubulin III and glial fibrillary acidic protein (GFAP). Immunocytochemistry of the cells showed intense labeling to both compounds on the intracellular cytoskeleton. The oligodendrocyte cell surface marker galactocerebroside (Gal-C) was present on most cells. Many cells show dual labeling, expressing both neuronal and glial markers.
28
Garcia, Jesús R., Dan S. Gombos, Claudia M. Prospero, Aravindh Ganapathy, Rebecca L. Penland, and Patricia Chévez-Barrios. "Expression of Angiogenic Factors in Invasive Retinoblastoma Tumors Is Associated With Increase in Tumor Cells Expressing Stem Cell Marker Sox2." Archives of Pathology & Laboratory Medicine 139, no. 12 (December 1, 2015): 1531–38. http://dx.doi.org/10.5858/arpa.2014-0262-oa.
Повний текст джерелаАнотація:
Context Progression of retinoblastoma is associated with increased tumor angiogenesis. However, a clear relationship between the expression of angiogenic markers in specific regions of the tumor and tumor progression has not been established. This study investigates the association between angiogenic factors in retinoblastomas with choroidal and/or optic nerve invasion (high-risk/invasive retinoblastoma) and expression of Sox2, a stem cell marker. Objective To investigate the association between the expression of angiogenic factors and markers of tumor invasiveness, such as the stem cell marker Sox2, in retinoblastoma tissues. Design Immunohistochemistry was used to evaluate coexpression of the angiogenic growth factors vascular endothelial growth factor A (VEGF-A), VEGF receptor 2 (VEGFR-2), and endoglin (CD105); markers of glial differentiation (vimentin and glial fibrillary acidic protein); and a neural stem cell marker (Sox2). Expression was assessed in nonneoplastic and neoplastic ocular tissues collected from enucleated eyes of patients with retinoblastoma. During qualitative data interpretation, evaluating pathologists were masked to patient grouping. Results Expression of VEGF-A and VEGFR-2 in noninvasive (non–high-risk feature) retinoblastoma tumors was lower than in the invasive, or high-risk feature tumors. Moreover, our data indicate that the tumor cells, and not the surrounding stroma, secrete VEGF-A and that angiogenesis is mostly localized to the iris. Finally, our data showed that the expression of the neural stem cell marker Sox2 is associated with eyes with increased VEGF-A expression and tumor invasiveness. Conclusions Increased expression of angiogenic factors, with a concomitant increase in expression of the stem cell marker Sox2 observed in retinoblastoma tissues, may partially explain the aggressiveness of these tumors. The complex interaction of angiogenic and stem cell–related pathways in these tumors, especially in high-risk feature retinoblastoma, suggests that targeting tumor cells capable of secreting vasculogenic factors, as well as proangiogenic genes and signaling pathways, may be necessary for development of effective antimetastatic retinoblastoma drugs.
29
Gay, S. "I18 Microrna’s regulating gene expression as novel markers and therapeutic markers." Cytokine 59, no. 3 (September 2012): 495. http://dx.doi.org/10.1016/j.cyto.2012.06.308.
Повний текст джерела
30
Kalinina, Tatiana S., Vladislav V. Kononchuk, Alisa K. Yakovleva, Efim Y. Alekseenok, Sergey V. Sidorov, and Lyudmila F. Gulyaeva. "Association between Lymph Node Status and Expression Levels of Androgen Receptor, miR-185, miR-205, and miR-21 in Breast Cancer Subtypes." International Journal of Breast Cancer 2020 (April 23, 2020): 1–7. http://dx.doi.org/10.1155/2020/3259393.
Повний текст джерелаАнотація:
Breast cancer is the most commonly diagnosed cancer among women. Difficulties in treating breast cancer are associated with the occurrence of metastases at early stages of disease, leading to its further progression. Recent studies have shown that changes in androgen receptor (AR) and microRNAs’ expressions are associated with mammary gland carcinogenesis, in particular, with the formation of metastases. Thus, to identify novel metastatic markers, we evaluated the expression levels of AR; miR-185 and miR-205, both of which have been confirmed to target AR; and miR-21, transcription of which is regulated by AR, in breast cancer samples (n=89). Here, we show that the molecular subtypes of breast cancer differ in the expression profiles of AR and AR-associated microRNAs. In addition, the expression of AR and these microRNAs may depend on the expression of PR, ER, and HER2 receptors. Our results show that the possibility of using AR and microRNAs as markers depends on the tumor subtype: a decrease in AR expression may be the marker for the presence of lymph node metastases in patients with HER2-positive subtypes of breast cancer, and disturbance of miR-205, miR-185, and miR-21 expressions may be the marker in patients with a luminal B HER2-positive subtype. Cases with metastases in this type of breast cancer are characterized by a higher level of miR-205 and a lower level of miR-185 and miR-21 in tumor tissues compared to nonmetastatic cases. A decrease in the miR-185 level is also associated with lymph node metastasis in luminal B HER2-negative breast cancer. Thus, the expression levels of AR, miR-185, miR-205, and miR-21 can serve as markers to predict cancer spread to the lymph node in luminal B- and HER2-positive subtypes of breast cancer.
31
Gaspari-Pezzopane, Cristiana de, Nemailla Bonturi, Oliveiro Guerreiro Filho, José Laércio Favarin, and Mirian Perez Maluf. "Gene expression profile during coffee fruit development and identification of candidate markers for phenological stages." Pesquisa Agropecuária Brasileira 47, no. 7 (July 2012): 972–82. http://dx.doi.org/10.1590/s0100-204x2012000700014.
Повний текст джерелаАнотація:
The objective of this work was to identify genes that could be used as suitable markers for molecular recognition of phenological stages during coffee (Coffea arabica) fruit development. Four cultivars were evaluated as to their differential expression of genes associated to fruit development and maturation processes. Gene expression was characterized by both semi-quantitative and quantitative RT-PCR, in fruit harvested at seven different developmental stages, during three different seasons. No size polymorphisms or differential expression were observed among the cultivars for the evaluated genes; however, distinct expression profiles along fruit development were determined for each gene. Four out of the 28 evaluated genes exhibited a regular expression profile in all cultivars and harvest seasons, and, therefore, they were validated as candidate phenological markers of coffee fruit. The gene α-galactosidase can be used as a marker of green stage, caffeine synthase as a marker of transition to green and yellowish-green stages, and isocitrate lyase and ethylene receptor 3 as markers of late maturation.
32
Raghav, Kanwal Pratap Singh, Hesham M. Amin, Wenting Wang, Ganiraju C. Manyam, Bradley Broom, Cathy Eng, Michael J. Overman, and Scott Kopetz. "MET overexpression as a hallmark of the epithelial-mesenchymal transition (EMT) phenotype in colorectal cancer." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 3529. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.3529.
Повний текст джерелаАнотація:
3529 Background: Epithelial-mesenchymal transition (EMT) has been identified as a dominant molecular subtype of colorectal cancer (CRC). This EMT phenotype as recognized by complex gene signatures is prognostic and associated with chemoresistance, but a biomarker for EMT suitable for clinical utilization has not yet been validated. The purpose of this study was to compare MET protein expression with protein/gene expression of EMT markers and to evaluate its impact on overall survival (OS). Methods: We performed an exploratory analysis of 139 untreated primary CRC samples using data from The Cancer Genome Atlas. Protein and gene expressions were measured using reverse-phase protein array (RPPA) and RNA-sequencing, respectively. MET high/overexpressed group was defined by protein level in the highest quartile. Mann-Whitney U-test and Spearman rank correlation was used to determine association between MET protein expression and protein/gene expression of EMT markers and EMT gene signature scores. Regression tree method and Kaplan-Meier estimates were used to assess overall survival (OS). Results: The MET protein distribution is right skewed, demonstrating a unique population of MET high expressing tumors (P < 0.01). Colon tumors had higher MET protein levels compared to rectal tumors (P < 0.01). MET overexpression was associated with decreased OS (HR 2.92; 95% CI: 1.45 - 5.92). MET protein expression correlated strongly with protein expressions of SLUG (transcription factor for EMT) (r = 0.6) and ERCC1 (a marker for oxaliplatin chemo-resistance) (r = 0.6) (P < 0.01). Higher MET protein levels were associated with higher gene expression of 28 EMT markers including AXL, VIM, ZEB1, ZEB2, FGF1, TGFB1I1 and MMP11 (P < 0.05). Higher MET protein levels were also associated with higher gene scores derived from three published EMT gene signatures (P < 0.05). MET protein expression did not correlate with MET gene expression (r = 0.16). Conclusions: Increased MET protein expression strongly correlates with a molecular EMT phenotype and poor survival in patients with CRC. MET protein expression may be used as a surrogate biomarker to represent and select for this unique molecular subset of CRC driven by EMT biology.
33
Chen, Kai, Xianqi Li, Ni Li, Hongwei Dong, Yiming Zhang, Michiko Yoshizawa, and Hideaki Kagami. "Spontaneously Formed Spheroids from Mouse Compact Bone-Derived Cells Retain Highly Potent Stem Cells with Enhanced Differentiation Capability." Stem Cells International 2019 (May 5, 2019): 1–13. http://dx.doi.org/10.1155/2019/8469012.
Повний текст джерелаАнотація:
The results from our recent study showed the presence of two distinct spheroid-forming mechanisms, i.e., spontaneous and mechanical. In this study, we focused on the spontaneously formed spheroids, and the character of spontaneously formed spheroids from mouse compact bone-derived cells (CBDCs) was explored. Cells from (C57BL/6J) mouse leg bones were isolated, and compact bone-derived cells were cultured after enzymatic digestion. Spontaneous spheroid formation was achieved on a culture plate with specific water contact angle as reported. The expression levels of embryonic stem cell markers were analyzed using immunofluorescence and quantitative reverse transcription polymerase chain reaction. Then, the cells from spheroids were induced into osteogenic and neurogenic lineages. The spontaneously formed spheroids from CBDCs were positive for ES cell markers such as SSEA1, Sox2, Oct4, and Nanog. Additionally, the expressions of fucosyltransferase 4/FUT4 (SSEA1), Sox2, and Nanog were significantly higher than those in monolayer cultured cells. The gene expression of mesenchymal stem cell markers was almost identical in both spheroids and monolayer-cultured cells, but the expression of Sca-1 was higher in spheroids. Spheroid-derived cells showed significantly higher osteogenic and neurogenic marker expression than monolayer-cultured cells after induction. Spontaneously formed spheroids expressed stem cell markers and showed enhanced osteogenic and neurogenic differentiation capabilities than cells from the conventional monolayer culture, which supports the superior stemness.
34
Mazor, Marija, Eric Lespessailles, Thomas M. Best, Mazen Ali, and Hechmi Toumi. "Gene Expression and Chondrogenic Potential of Cartilage Cells: Osteoarthritis Grade Differences." International Journal of Molecular Sciences 23, no. 18 (September 13, 2022): 10610. http://dx.doi.org/10.3390/ijms231810610.
Повний текст джерелаАнотація:
Recent data suggest that cells isolated from osteoarthritic (OA) cartilage express mesenchymal progenitor cell (MPC) markers that have the capacity to form hyaline-like cartilage tissue. Whether or not these cells are influenced by the severity of OA remains unexplored. Therefore, we analyzed MPC marker expression and chondrogenetic potential of cells from mild, moderate and severe OA tissue. Human osteoarthritic tibial plateaus were obtained from 25 patients undergoing total knee replacement. Each sample was classified as mild, moderate or severe OA according to OARSI scoring. mRNA expression levels of MPC markers—CD105, CD166, Notch 1, Sox9; mature chondrocyte markers—Aggrecan (Acan), Col II A1, hypertrophic chondrocyte and osteoarthritis-related markers—Col I A1, MMP-13 and ALPL were measured at the tissue level (day 0), after 2 weeks of in vitro expansion (day 14) and following chondrogenic in vitro re-differentiation (day 35). Pellet matrix composition after in vitro chondrogenesis of different OA-derived cells was tested for proteoglycans, collagen II and I by safranin O and immunofluorescence staining. Multiple MPC markers were found in OA cartilage resident tissue within a single OA joint with no significant difference between grades except for Notch1, which was higher in severe OA tissues. Expression levels of CD105 and Notch 1 were comparable between OA cartilage-derived cells of different disease grades and bone marrow mesenchymal stem cell (BM-MSC) line (healthy control). However, the MPC marker Sox 9 was conserved after in vitro expansion and significantly higher in OA cartilage-derived cells compared to its levels in the BM-MSC. The in vitro expansion of cartilage-derived cells resulted in enrichment while re–differentiation in reduction of MPC markers for all three analyzed grades. However, only moderate OA-derived cells after the in vitro chondrogenesis resulted in the formation of hyaline cartilage-like tissue. The latter tissue samples were also highly positive for collagen II and proteoglycans with no expression of osteoarthritis-related markers (collagen I, ALPL and MMP13). MPC marker expression did not differ between OA grades at the tissue level. Interestingly after in vitro re-differentiation, only moderate OA-derived cells showed the capacity to form hyaline cartilage-like tissue. These findings may have implications for clinical practice to understand the intrinsic repair capacity of articular cartilage in OA tissues and raises the possibility of these progenitor cells as a candidate for articular cartilage repair.
35
Mishra, A., A. Pandey, and S. C. Mishra. "Variable expression of molecular markers in juvenile nasopharyngeal angiofibroma." Journal of Laryngology & Otology 131, no. 9 (July 7, 2017): 752–59. http://dx.doi.org/10.1017/s0022215117001372.
Повний текст джерелаАнотація:
AbstractBackground:Molecular categorisation may explain the wide variation in the clinical characteristics of juvenile nasopharyngeal angiofibroma.Methods:Variations in molecular markers in juvenile nasopharyngeal angiofibroma in an Indian population were investigated and compared with global reports.Results:Variable molecular marker expression was demonstrated at the regional and global levels. A wide variation in molecular characteristics is evident. Molecular data have been reported for only 11 countries, indicating a clear geographical bias. Only 58 markers have been studied, and most are yet to be validated.Conclusion:Research into the molecular epidemiology of juvenile nasopharyngeal angiofibroma is still in its infancy. Although the molecular variation is not well understood, data obtained so far have prompted important research questions. Hence, multicentre collaborative molecular studies are needed to establish the aetiopathogenesis and establish molecular surrogates for clinical characteristics.
36
He, Ke-Fei, Lu Zhang, Cong-Fa Huang, Si-Rui Ma, Yu-Fan Wang, Wei-Ming Wang, Zhi-Li Zhao, et al. "CD163+ Tumor-Associated Macrophages Correlated with Poor Prognosis and Cancer Stem Cells in Oral Squamous Cell Carcinoma." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/838632.
Повний текст джерелаАнотація:
Tumor-associated macrophages (TAMs) play an important role in the progression and prognostication of numerous cancers. However, the role and clinical significance of TAM markers in oral squamous cell carcinoma (OSCC) has not been elucidated. The present study was designed to investigate the correlation between the expression of TAM markers and pathological features in OSCC by tissue microarray. Tissue microarrays containing 16 normal oral mucosa, 6 oral epithelial dysplasia, and 43 OSCC specimens were studied by immunohistochemistry. We observed that the protein expression of the TAM markers CD68 and CD163 as well as the cancer stem cell (CSC) markers ALDH1, CD44, and SOX2 increased successively from the normal oral mucosa to OSCC. The expressions of CD68 and CD163 were significantly associated with lymph node status, and SOX2 was significantly correlated with pathological grade and lymph node status, whereas ALDH1 was correlated with tumor stage. Furthermore, CD68 was significantly correlated with CD163, SOX2, and ALDH1 (P<0.05). Kaplan-Meier analysis revealed that OSCC patients overexpressing CD163 had significantly worse overall survival (P<0.05). TAM markers are associated with cancer stem cell marker and OSCC overall survival, suggesting their potential prognostic value in OSCC.
37
Kopparapu, Prasad R., Melinda Duplessis, Edward Lo, Yingjun Yan, Wade T. Iams, Josh Nordberg, Arturo Ramirez, Tad George, and Christine Lovly. "Abstract 3375: Molecular subtyping of circulating tumor cells in patients with small cell lung cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3375. http://dx.doi.org/10.1158/1538-7445.am2022-3375.
Повний текст джерелаАнотація:
Abstract Background: Recently, a new molecular classification of small cell lung cancer (SCLC), defined by expression of four key transcription regulators - ASCL1, NEUROD1, YAP1 and POU2F3 - has been proposed. These molecular subtypes may confer differential biology and therapeutic vulnerabilities, however, studies to date have been constrained by the paucity of available longitudinal tumor biopsy samples obtained from patients with SCLC. Herein, we utilized circulating tumor cells (CTCs) to characterize subtype marker heterogeneity at the time of diagnosis and evaluate the dynamic nature of marker expression during treatment in patients with SCLC. Methods: Informed consent was obtained from patients with SCLC using an IRB approved protocol (IRB#030763). We have collected blood samples from 32 patients, including treatment naïve samples from the entire cohort as well as on-treatment samples (median of 4 collections per patient). We utilized the RareCyte rare-cell analysis platform to isolate and quantify CTCs, which were defined as CK/EpCAM positive and CD45 negative. Each sample was also evaluated for expression of neuroendocrine markers (ASCL1, NEUROD1) and non-neuroendocrine markers (YAP1, POU2F3). Each set of neuroendocrine and non-neuroendocrine markers were co-stained along with the CTC markers. Mean fluorescence intensity of each marker was extracted using a python program. Results: To date, we have analyzed 22/32 (69%) treatment naïve samples, including n=6 patients with early stage disease and n=16 patients with advanced/metastatic disease. We detected CTCs from 16/22 (73%) patients, with quantities ranging from 1 - 3406 (median = 66) per 7.5ml of blood. CTCs were positive for the neuroendocrine markers ASCL1 in 16/16 (100%) and NEUROD1 in 10/16 (62%); all NEUROD1 positive CTCs were also positive for ASCL1. The non-neuroendocrine markers YAP1 and POU2F3 were detected in 6/16 (37%) and 11/16 (69%) samples, respectively, including YAP1/POU2F3 double positives in 6/16 (37%). Analysis of on-treatment samples is ongoing. Conclusion: We have developed a protocol for monitoring expression of subtype markers on CTCs isolated from patients with SCLC. We found CTCs expressing both neuroendocrine and non-neuroendocrine markers at the time of diagnosis. Ongoing work will attempt to delineate the dynamic nature of subtype marker expression during therapy, to correlate with clinical outcomes. These studies have the potential to offer critical insights regarding the heterogeneity and evolution of SCLC, a tumor type in which novel disease insights and innovative treatment strategies are urgently needed to improve patient survival. Citation Format: Prasad R. Kopparapu, Melinda Duplessis, Edward Lo, Yingjun Yan, Wade T. Iams, Josh Nordberg, Arturo Ramirez, Tad George, Christine Lovly. Molecular subtyping of circulating tumor cells in patients with small cell lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3375.
38
Miyashita, Hirotaka, Nicholas J. Bevins, Kartheeswaran Thangathurai, Suzanna Lee, Sarabjot Pabla, Mary Nesline, Sean Glenn, et al. "Comprehensive transcriptomic analysis of immune checkpoint markers in a pancancer cohort: Implications for response and resistance." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): 2555. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.2555.
Повний текст джерелаАнотація:
2555 Background: Although immune checkpoint blockade (ICB) has revolutionized cancer treatment, not all patients with cancer benefit from ICB. One possible explanation for poor responders/resistance is the variable expression level of the target molecules (e.g., PD-1 and PD-L1) in the tumor microenvironment. There are recent or ongoing trials targeting variable pathways for immune evasion (e.g., LAG3 or IDO1). It is therefore of interest to know the expression levels related to variable immune checkpoints so that clinical trials can focus on the patients who can benefit from the cognate treatment. Methods: Overall, 514 patients with various solid tumors seen at the University of San Diego, Moores Center for Personalized Cancer Therapy were analyzed. The expression levels of checkpoint markers (ADORA2A, BTLA, CD276, CTLA4, IDO1, IDO2, LAG3, NOS2, PD-1, PD-L1, PD-L2, PVR, TIGIT, TIM3, VISTA, and VTCN) in the tumor samples were measured through RNA sequencing and normalized to internal housekeeping gene profiles, and ranked from 0 to 100 percentile based on a reference population. The expressions of each checkpoint marker were correlated with cancer types, microsatellite instability (MSI), tumor mutational burden (TMB), and programmed death-ligand 1 (PD-L1) status on immunohistochemistry. Results: In this cohort, 60% were female, median age of 60, and included 30 different tumor types, with colorectal cancer being the most common (27%). The rank values of all checkpoint markers were distributed broadly from 0 to 99 or 100. CD276 and NOS2 had the highest (68th percentile) and lowest (13.5 percentile) median rank values, respectively. When rank values were categorized to “Low” (0-24), “Intermediate” (25-74), and “High” (75-100), 41.6% of patients showed high expression of CD276 while only 13% showed high expression of PD-L1. Each patient had a distinctive protfolio of the categorical expression levels of 16 checkpoint markers. Several checkpoint markers, especially NOS2, showed a significant correlation with cancer type. (median rank values in colorectal, stomach, pancreatic, and breast cancer were 79, 76, 5 and 0 respectively, p < 0.001) Five markers (IDO1, LAG3, PD-1, PD-L1, and TIGIT) showed significant correlation with MSI, while seven markers (CTLA4, IDO1, LAG3, PD-1, PD-L1, PD-L2, and TIGIT) were significantly associated with positive PD-L1 status. However, no significant association was seen based on TMB or tissue-specific grouping of patients. Conclusions: The expression of immune checkpoint markers varies from patient to patient, though transcript expression of several markers correlates with cancer type, MSI, and PD-L1 status. Clinical trials with patient selection based on the expression level of checkpoint markers matched to the corresponding ICB drug are warranted.
39
El-Hussien, Mahmoud Tag, and Mohamed Abdelfattah Hassan. "Neuroendocrine Differentiation in Non-Small Cell Lung Cancer and its Relation to Different Pathologic Features: An Immunohistochemical Study." Asian Pacific Journal of Cancer Biology 6, no. 1 (March 21, 2021): 49–55. http://dx.doi.org/10.31557/apjcb.2021.6.1.49-55.
Повний текст джерелаАнотація:
Objectives: To identify the relevance of neuroendocrine differentiation in non-small cell lung cancer and its correlation with different pathological features. Materials and Methods: A total number of 30 cases of per cutaneous CT guided biopsies of primary non-small lung cancer were collected in the pathology department of Misr University for Science and Technology Giza, Egypt and private practice in the time period from January 2018 till December 2020. Immunohistochemical study for neuroendocrine differentiation was performed using mono clonal antibodies against synaptophysin, chromogranin A and CD56. For all selected cases, clinical and pathological data such as age, gender, histologic types, grade and clinical stage were collected, tabulated and statistically analyzed with the results of neuroendocrine markers expression. Cases with incomplete pathological data and cases with histologic picture of neuroendocrine differentiation were excluded. Results: A total number of 30 cases of primary non-small lung cancer were enrolled in this study. The median age of patients was 61.5 years. There were 21 (70%) males and 9 (30%) females. Regarding neuroendocrine markers, positivity for either marker was identified in 23.3% of non-small cell lung cancer. Chromogranin A was positively expressed in 9 (30%) of cases, synaptophysin was positively expressed in 7 (23.3%) of cases and CD56 was positively expressed in 5 (16.7%) of cases. Only 2 cases (6.7%) showed co-expression of two markers. It was found that there was a high significant relation between chromogranin A expression and clinical stage. Chromogranin A expression was significantly higher in stage III than stage I and II (P<0.001). There was no statistical significant difference between synaptophysin, chromogranin A and CD56 expressions and the rest of the studied pathologic data. Conclusion: A considerable number of non-small cell lung cancer has neuroendocrine differentiation for at least one neuroendocrine marker despite absence of morphologic features. Much less number of cases showed expression of two markers. A reasonable panel of neuroendocrine markers is recommended to detect this differentiation which may have a clinical impact and optimize an alternative therapeutic option.
40
Kaderi, Mohd Arifin, Meena Kanduri, Mahmoud Mansouri, Anne Mette Buhl, Marie Sevov, Nicola Cahill, Rebeqa Gunnarsson, et al. "LPL Is the Strongest Prognostic Factor in a Comparative Study of RNA-Based Markers in Chronic Lymphocytic Leukemia." Blood 114, no. 22 (November 20, 2009): 1254. http://dx.doi.org/10.1182/blood.v114.22.1254.1254.
Повний текст джерелаАнотація:
Abstract Abstract 1254 Poster Board I-276 Introduction Chronic lymphocytic leukemia (CLL) is a heterogeneous disease with varying clinical outcome, where many patients have an indolent course for many years, whereas others show a more aggressive disease despite treatment. This has prompted the search for biomarkers that can predict outcome in this disease. Recent studies have proposed the RNA expression levels of certain genes, i.e. LPL, CLLU1, TCL1, MCL1 and ZAP70 to be novel predictors of clinical outcome in CLL. However, a comprehensive assessment of these RNA-based markers is still lacking. The current study aimed to investigate the potential of these markers in CLL prognostication, either as single markers or in combination with established markers. Patients and Methods By applying real-time quantitative PCR, we measured the RNA expression levels of LPL, CLLU1, TCL1, MCL1 and ZAP70 in 256 newly diagnosed CLL samples from a Scandinavian population-based cohort collected from 1999 to 2002 (median follow-up, 89 months) and correlated with clinical outcome. The expression cut-offs for each RNA marker was determined by constructing ROC curves. Additionally, Binet stage, IGHV mutation status, CD38 expression (cut-off 7%) and the presence of recurrent genomic aberrations (i.e. 11q-, 17p-, 13q- and +12) were evaluated for all cases. Results High expression of all RNA-based markers except MCL1 predicted significantly shorter overall survival (OS) and time to treatment (TTT), with LPL being the most significant prognostic marker in both log-rank (Table 1) and Cox univariate regression analyses. In multivariate analysis including the RNA markers, LPL expression was the only independent prognostic factor for OS, whereas both LPL and CLLU1 could predict TTT. When including all established markers, LPL lost its significance in the model, due to its close association to the IGHV mutation status. Once the mutation status was excluded from the analysis, LPL regained its prognostic power in addition to genomic aberrations and CD38. Interestingly, all of the RNA-based markers added further prognostic information to established markers in subgroups of patients, with LPL expression status giving the most significant results. Notably, high LPL expression predicted a worse outcome in favorable prognostic subgroups such as patients with Binet stage A, CD38 negativity or favorable genomic aberrations (Table 2). Conclusions Altogether, we conclude that LPL expression appear to be the strongest among the RNA-based markers for prediction of clinical outcome in CLL and thus could potentially be applied in the clinical laboratory to predict outcome, particularly in combination with established markers. Disclosures No relevant conflicts of interest to declare.
41
Jensen, Christina T., Josefine Åhsberg, Mikael N. E. Sommarin, Tobias Strid, Rajesh Somasundaram, Kazuki Okuyama, Jonas Ungerbäck, et al. "Dissection of progenitor compartments resolves developmental trajectories in B-lymphopoiesis." Journal of Experimental Medicine 215, no. 7 (June 13, 2018): 1947–63. http://dx.doi.org/10.1084/jem.20171384.
Повний текст джерелаАнотація:
To understand the developmental trajectories in early lymphocyte differentiation, we identified differentially expressed surface markers on lineage-negative lymphoid progenitors (LPs). Single-cell polymerase chain reaction experiments allowed us to link surface marker expression to that of lineage-associated transcription factors (TFs) and identify GFRA2 and BST1 as markers of early B cells. Functional analyses in vitro and in vivo as well as single-cell gene expression analyses supported that surface expression of these proteins defined distinct subpopulations that include cells from both the classical common LPs (CLPs) and Fraction A compartments. The formation of the GFRA2-expressing stages of development depended on the TF EBF1, critical both for the activation of stage-specific target genes and modulation of the epigenetic landscape. Our data show that consecutive expression of Ly6D, GFRA2, and BST1 defines a developmental trajectory linking the CLP to the CD19+ progenitor compartment.
42
Rookledge, M., M. Colgrave, S. Stockwell, and S. Schmoelzl. "328. CLAUDIN-8 IS EXPRESSED IN BOVINE TESTIS GERM CELLS." Reproduction, Fertility and Development 22, no. 9 (2010): 128. http://dx.doi.org/10.1071/srb10abs328.
Повний текст джерелаАнотація:
Germline stem cells in the testis allow for the continued production of spermatozoa throughout a male’s life. These cells are capable of self-renewal and have the ability to colonise testis tissue and give rise to spermatocytes after transplantation. Identification of germ cells and other cell types within testis tissue is important for increasing understanding of germ cell biology. Work in this lab is focused on the bovine testis, and we use both germ and non-germ cell markers for cell identification and germ cell enrichment. Such markers are also used for monitoring physiological and pathological changes in testis tissue after treatments such as irradiation. At present cell type markers for germ cells are limited, particularly in livestock species. This study has therefore investigated candidate marker genes for expression in testis cells. Here, we present quantitative gene expression data for Claudin-8 (CLDN8) in testis tissue. Claudin-8 is a membrane protein involved in the formation of tight junctions, such as are formed by germ cells in the testis. We used qRT-PCR to examine the expression of CLDN8 and other candidate genes in germ cell enriched and non-enriched testis cell fractions. Our qRT-PCR analysis shows that CLDN8 is preferentially expressed in germ cell enriched fractions. Testis cell fractions were also analysed for expression of established germ cell markers such as PLZF (ZBTB16) and VASA (DDX4), as well as for Sertoli cell marker GATA4. Our analysis shows a positive correlation between expression of CLDN8 and established germ cell markers, and a negative correlation between expression of CLDN8 and established Sertoli cells markers.
43
Inzani, Frediano, Angela Santoro, Giuseppe Angelico, Angela Feraco, Saveria Spadola, Damiano Arciuolo, Michele Valente, et al. "Neuroendocrine Carcinoma of the Uterine Cervix: A Clinicopathologic and Immunohistochemical Study with Focus on Novel Markers (Sst2–Sst5)." Cancers 12, no. 5 (May 12, 2020): 1211. http://dx.doi.org/10.3390/cancers12051211.
Повний текст джерелаАнотація:
Background. Gynecological neuroendocrine neoplasms (NENs) are extremely rare, accounting for 1.2–2.4% of the NENs. The aim of this study was to test cervical NENs for novel markers of potential utility for differential diagnosis and target therapy. Methods. All cases of our center (n = 16) were retrieved and tested by immunohistochemistry (IHC) for 12 markers including markers of neuroendocrine differentiation (chromogranin A, synaptophysin, CD56), transcription factors (CDX2 and TTF1), proteins p40, p63, p16INK4a, and p53, somatostatin receptors subtypes (SST2-SST5) and the proliferation marker Ki67 (MIB1). Results. All cases were poorly differentiated neuroendocrine carcinomas (NECs), 10 small cell types (small cell–neuroendocrine carcinomas, SCNECs) and 6 large cell types (large cell–neuroendocrine carcinomas, LCNECs); in 3 cases a predominant associated adenocarcinoma component was observed. Neuroendocrine cancer cells expressed at least 2 of the 3 tested neuroendocrine markers; p16 was intensely expressed in 14 (87.5%) cases; SST5 in 11 (56.25%, score 2–3, in 9 cases); SST2 in 8 (50%, score 2–3 in 8), CDX2 in 8 (50%), TTF1 in 5 (31.25%), and p53 in 1 case (0.06%). P63 and p40 expressions were negative, with the exception of one case that showed moderate expression for p63. Conclusions. P40 is a more useful marker for the differential diagnosis compared to squamous cell carcinoma. Neither CDX2 nor TTF1 expression may help the differential diagnosis versus potential cervical metastasis. P16 expression may suggest a cervical origin of NEC; however, it must be always integrated by clinical and instrumental data. The expression of SST2 and SST5 could support a role for SSAs (Somatostatin Analogues) in the diagnosis and therapy of patients with cervical NECs.
44
Saad, Aly G., and Margaret H. Collins. "Prognostic Value of MIB-1, E-Cadherin, and CD44 in Pediatric Chordomas." Pediatric and Developmental Pathology 8, no. 3 (May 2005): 362–68. http://dx.doi.org/10.1007/s10024-005-1127-z.
Повний текст джерелаАнотація:
The prognosis of pediatric chordomas is difficult to predict based on histology. The objective of this study was to assess the expression of a proliferation marker and adhesion molecules in pediatric chordomas and relate the expressions to outcome. In 8 pediatric chordomas, we calculated the MIB-1 labeling index (LI) by counting the number of MIB-1–positive tumor cells in 100 tumor cells. The grade of expression of E-cadherin and CD44 was calculated by estimating the percentage of tumor cells expressing these markers. MIB-1 LI correlated with tumor recurrence ( P = 0.007) and low survival rate ( P = 0.007). The expression of E-cadherin correlated with disease-free survival ( P = 0.009), tumor recurrence ( P > 0.0007), and low survival rate ( P > 0.0007). CD44 expression did not correlate with recurrence ( P = 0.056) or survival rate ( P = 0.056). Our results suggest that MIB-1 LI and expression of E-cadherin are helpful to predict outcome in pediatric chordomas.
45
Verburg, Melissa, Ingrid B. Renes, Danielle J. P. M. Van Nispen, Sacha Ferdinandusse, Marieke Jorritsma, Hans A. Büller, Alexandra W. C. Einerhand, and Jan Dekker. "Specific Responses in Rat Small Intestinal Epithelial mRNA Expression and Protein Levels During Chemotherapeutic Damage and Regeneration." Journal of Histochemistry & Cytochemistry 50, no. 11 (November 2002): 1525–36. http://dx.doi.org/10.1177/002215540205001113.
Повний текст джерелаАнотація:
The rapidly dividing small intestinal epithelium is very sensitive to the cytostatic drug methotrexate. We investigated the regulation of epithelial gene expression in rat jejunum during methotrexate-induced damage and regeneration. Ten differentiation markers were localized on tissue sections and quantified at mRNA and protein levels relative to control levels. We analyzed correlations in temporal expression patterns between markers. mRNA expression of enterocyte and goblet cell markers decreased significantly during damage for a specific period. Of these, sucrase-isomaltase (-62%) and CPS (-82%) were correlated. Correlations were also found between lactase (−76%) and SGLT1 (−77%) and between I-FABP (−52%) and L-FABP (-45%). Decreases in GLUT5 (−53%), MUC2 (-43%), and TFF3 (−54%) mRNAs occurred independently of any of the other markers. In contrast, lysozyme mRNA present in Paneth cells increased (+76%). At the protein level, qualitative and quantitative changes were in agreement with mRNA expression, except for Muc2 (+115%) and TFF3 (+81%), which increased significantly during damage, following independent patterns. During regeneration, expression of each marker returned to control levels. The enhanced expression of cytoprotective molecules (Muc2, TFF3, lysozyme) during damage represents maintenance of goblet cell and Paneth cell functions, most likely to protect the epithelium. Decreased expression of enterocyte-specific markers represents decreased enterocyte function, of which fatty acid transporters were least affected.
46
Kamel, Faddy, Nathalie Schneider, Pasha Nisar, and Mikhail Soloviev. "Bottom-Up Approach to the Discovery of Clinically Relevant Biomarker Genes: The Case of Colorectal Cancer." Cancers 14, no. 11 (May 27, 2022): 2654. http://dx.doi.org/10.3390/cancers14112654.
Повний текст джерелаАнотація:
Traditional approaches to genome-wide marker discovery often follow a common top-down strategy, where a large scale ‘omics’ investigation is followed by the analysis of functional pathways involved, to narrow down the list of identified putative biomarkers, and to deconvolute gene expression networks, or to obtain an insight into genetic alterations observed in cancer. We set out to investigate whether a reverse approach would allow full or partial reconstruction of the transcriptional programs and biological pathways specific to a given cancer and whether the full or substantially expanded list of putative markers could thus be identified by starting with the partial knowledge of a few disease-specific markers. To this end, we used 10 well-documented differentially expressed markers of colorectal cancer (CRC), analyzed their transcription factor networks and biological pathways, and predicted the existence of 193 new putative markers. Incredibly, the use of a validation marker set of 10 other completely different known CRC markers and the same procedure resulted in a very similar set of 143 predicted markers. Of these, 138 were identical to those found using the training set, confirming our main hypothesis that a much-expanded set of disease markers can be predicted by starting with just a small subset of validated markers. Further to this, we validated the expression of 42 out of 138 top-ranked predicted markers experimentally using qPCR in surgically removed CRC tissues. We showed that 41 out of 42 mRNAs tested have significantly altered levels of mRNA expression in surgically excised CRC tissues. Of the markers tested, 36 have been reported to be associated with aspects of CRC in the past, whilst only limited published evidence exists for another three genes (BCL2, PDGFRB and TSC2), and no published evidence directly linking genes to CRC was found for CCNA1, SHC1 and TGFB3. Whilst we used CRC to test and validate our marker discovery strategy, the reported procedures apply more generally to cancer marker discovery.
47
He, Yue, Kristina B. V. Døssing, Ane Beth Sloth, Xuening He, Maria Rossing, and Andreas Kjaer. "Quantitative Evaluation of Stem-like Markers of Human Glioblastoma Using Single-Cell RNA Sequencing Datasets." Cancers 15, no. 5 (March 2, 2023): 1557. http://dx.doi.org/10.3390/cancers15051557.
Повний текст джерелаАнотація:
Targeting glioblastoma (GBM) stem-like cells (GSCs) is a common interest in both the laboratory investigation and clinical treatment of GBM. Most of the currently applied GBM stem-like markers lack validation and comparison with common standards regarding their efficiency and feasibility in various targeting methods. Using single-cell RNA sequencing datasets from 37 GBM patients, we obtained a large pool of 2173 GBM stem-like marker candidates. To evaluate and select these candidates quantitatively, we characterized the efficiency of the candidate markers in targeting the GBM stem-like cells by their frequencies and significance of being the stem-like cluster markers. This was followed by further selection based on either their differential expression in GBM stem-like cells compared with normal brain cells or their relative expression level compared with other expressed genes. The cellular location of the translated protein was also considered. Different combinations of selection criteria highlight different markers for different application scenarios. By comparing the commonly used GSCs marker CD133 (PROM1) with markers selected by our method regarding their universality, significance, and abundance, we revealed the limitations of CD133 as a GBM stem-like marker. Overall, we propose BCAN, PTPRZ1, SOX4, etc. for laboratory-based assays with samples free of normal cells. For in vivo targeting applications that require high efficiency in targeting the stem-like subtype, the ability to distinguish GSCs from normal brain cells, and a high expression level, we recommend the intracellular marker TUBB3 and the surface markers PTPRS and GPR56.
48
Livingston, B. T., and F. H. Wilt. "Range and stability of cell fate determination in isolated sea urchin blastomeres." Development 108, no. 3 (March 1, 1990): 403–10. http://dx.doi.org/10.1242/dev.108.3.403.
Повний текст джерелаАнотація:
We have examined the developmental potential of blastomeres isolated from either the animal (mesomeres) or vegetal (macromeres-micromeres) half of 16-cell embryos of the sea urchin Lytechinus pictus. We have also examined the effects of two known vegetalizing agents on the development of isolated mesomeres; LiCl treatment and combination with micromeres, the small blastomeres found at the vegetal pole of the 16-cell embryo. The markers for differentiation used were both morphological (invaginations, spicules and pigment cells) and molecular (gut-specific alkaline phosphatase activity, and monoclonal antibodies against antigens specific for gut and oral ectoderm). Embryoids derived from isolated mesomeres expressed markers characteristic of vegetal differentiation only at very low levels. They did express an antigen characteristic of animal development, the oral ectoderm antigen, but with an altered pattern. Isolated macromere-micromere pairs expressed all markers characteristic of vegetal development, but did not express the marker characteristic of animal development. Increasing concentrations of LiCl caused isolated mesomeres to give rise to embryoids with an increasing tendency to express vegetal markers of differentiation, and it was found that expression of different vegetal markers begin to appear at different concentrations of LiCl. LiCl also caused the marker for oral ectoderm to be expressed in a more normal pattern. Combining micromeres with mesomeres also induced mesomere derivatives to differentiate in a vegetal manner. Micromeres were not completely effective in inducing a more normal pattern of expression of the marker for oral ectoderm. The treatment of isolated mesomeres with both LiCl and micromeres produces a synergistic effect resulting in embryoids expressing markers not induced by either treatment alone.
49
Stutterheim, Janine, Annemieke Gerritsen, Lily Zappeij-Kannegieter, Bilgehan Yalcin, Rob Dee, Max M. van Noesel, Frank Berthold, et al. "Detecting Minimal Residual Disease in Neuroblastoma: The Superiority of a Panel of Real-Time Quantitative PCR Markers." Clinical Chemistry 55, no. 7 (July 1, 2009): 1316–26. http://dx.doi.org/10.1373/clinchem.2008.117945.
Повний текст джерелаАнотація:
Abstract Background: PCR-based detection of minimal residual disease (MRD) in neuroblastoma (NB) patients can be used for initial staging and monitoring therapy response in bone marrow (BM) and peripheral blood (PB). PHOX2B has been identified as a sensitive and specific MRD marker; however, its expression varies between tumors. Therefore, a panel of markers could increase sensitivity. Methods: To identify additional MRD markers for NB, we selected genes by comparing SAGE (serial analysis of gene expression) libraries of healthy and NB tissues followed by extensive real-time quantitative PCR (RQ-PCR) testing in samples of tumors (n = 56), control BM (n = 51), PB (n = 37), and cell subsets. The additional value of a panel was determined in 222 NB samples from 82 Dutch stage 4 NB patients (54 diagnosis BM samples, 143 BM samples during/after treatment, and 25 PB samples). Results: We identified 2 panels of specific RQ-PCR markers for MRD detection in NB patients: 1 for analysis of BM samples (PHOX2B, TH, DDC, CHRNA3, and GAP43) and 1 for analysis of PB samples (PHOX2B, TH, DDC, DBH, and CHRNA3). These markers all showed high expression in NB tumors and no or low expression in control BM or PB samples. In patients’ samples, the PHOX2B marker detected most positive samples. In PB samples, however, 3 of 7 PHOX2B-negative samples were positive for 1 or more markers, and in BM examinations during treatment, 7% (6 of 86) of the PHOX2B-negative samples were positive for another marker. Conclusions: Because of differences in the sensitivities of the markers in BM and PB, we advise the use of 2 different panels to detect MRD in these compartments.
50
Qu, Yuan-Yuan, Xi Tian, Wenhao Xu, Aihemutaijiang Anwaier, Dingwei Ye, and Hailiang Zhang. "Prognostic value of epithelial-mesenchymal transition markers in clear cell renal cell carcinoma." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 739. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.739.
Повний текст джерелаАнотація:
739 Background: Epithelial-to-mesenchymal transition (EMT) in important in tumor invasiveness and metastasis. We aimed to determine prognostic value of six key EMT markers (CDH1, CDH2, SNAI1, SNAI2, VIM, TWIST1) in clear cell renal cell carcinoma (ccRCC). Methods: A total of 533 ccRCC patients with RNASeq data from The Cancer Genome Atlas (TCGA) cohort were included for analysis. Gene expression of these EMT markers was compared between tumor and normal tissues based on Oncomine database and TCGA cohort. Their correlations with progression-free survival (PFS) and overall survival (OS) were also examined in both TCGA cohort and FUSCC (Fudan University Shanghai Cancer Center) cohort. Cox proportional hazards regression model and Kaplan-Meier plot were used to assess the relative factors. Functional enrichment analyses were utilized to describe biologic function annotations and significantly involved hallmarks pathways of each gene. Results: We found that Epithelial marker, CDH1 expression was lower, while mesenchymal markers (CDH2, SNAI1, VIM, TWIST1) expression was higher in ccRCC primary tumors. In the TCGA cohort, we found that patients with higher expression of VIM, TWIST1 or lower expression of CDH1 had worse prognosis. Further, in the FUSCC cohort, we confirmed the predictive ability of mesenchymal markers and epithelial marker expression in PFS and OS of ccRCC patients. After generating Cox regression models, EMT markers (CDH1, SNAI1, VIM, and TWIST1) were independent prognostic factors of both PFS and OS in ccRCC patients. Conclusions: Our preliminary EMT prediction model can facilitate further screening of EMT biomarkers and cast a better understanding of EMT gene function in ccRCC.