Gotowe bibliografie tematyczne / Cancer cell metastasis

Gotowa bibliografia na temat „Cancer cell metastasis”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Cancer cell metastasis"

Park, Hyung Kyu, Joungho Han, Ghee Young Kwon, Min-Kyung Yeo i Go Eun Bae. "Patterns of Extrathoracic Metastasis in Lung Cancer Patients". Current Oncology 29, nr 11 (16.11.2022): 8794–801. http://dx.doi.org/10.3390/curroncol29110691.

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Metastasis is a major cause of death in lung cancer patients. Therefore, a deeper understanding of the metastatic mechanisms is important for developing better management strategies for lung cancer patients. This study evaluated the patterns of extrathoracic metastases in lung cancer. We retrieved data for 25,103 lung cancer patients from an institutional database and then evaluated the impacts of clinicopathologic factors on metastasis patterns. We found that 36.5% of patients had extrathoracic metastasis. Younger patients had a significantly higher extrathoracic metastasis rate in most histologic subtypes. Metastases to the bone (58.3%), central nervous system (CNS) (44.3%), liver (26.6%) and adrenal gland (18.3%) accounted for 85.5% of all extrathoracic metastases. Patients with nonmucinous adenocarcinoma had significantly higher bone metastasis rate. Patients with small cell carcinoma and large cell neuroendocrine carcinoma (LCNEC) had significantly higher liver metastasis rates. Further, patients with LCNEC also had a significantly lower bone metastasis rate, and patients with squamous cell carcinoma had a significantly lower CNS metastasis rate. Patients with multiple cancers had similar patterns of metastasis compared to patients with only lung cancer. In conclusion, different histologic subtypes of lung cancer have different metastatic patterns. Our study might help clinicians decide on follow-up strategies.

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Voss, Gjendine, Benedikta S. Haflidadóttir, Helena Järemo, Margareta Persson, Tina Catela Ivkovic, Pernilla Wikström i Yvonne Ceder. "Regulation of cell–cell adhesion in prostate cancer cells by microRNA-96 through upregulation of E-Cadherin and EpCAM". Carcinogenesis 41, nr 7 (18.11.2019): 865–74. http://dx.doi.org/10.1093/carcin/bgz191.

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Abstract Prostate cancer is one of the most common cancers in men, yet the biology behind lethal disease progression and bone metastasis is poorly understood. In this study, we found elevated levels of microRNA-96 (miR-96) in prostate cancer bone metastasis samples. To determine the molecular mechanisms by which miR-96 deregulation contributes to metastatic progression, we performed an Argonaute2-immunoprecipitation assay, in which mRNAs associated with cell–cell interaction were enriched. The expression of two cell adhesion molecules, E-Cadherin and EpCAM, was upregulated by miR-96, and potential targets sites were identified in the coding sequences of their mRNAs. We further showed that miR-96 enhanced cell–cell adhesion between prostate cancer cells as well as their ability to bind to osteoblasts. Our findings suggest that increased levels of miR-96 give prostate cancer cells an advantage at forming metastases in the bone microenvironment due to increased cell–cell interaction. We propose that miR-96 promotes bone metastasis in prostate cancer patients by facilitating the outgrowth of macroscopic tumours in the bone.

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Alkhayat, Hana, i Chih-ho Hong. "Cutaneous Metastases from Non-Small Cell Lung Cancer". Journal of Cutaneous Medicine and Surgery 10, nr 6 (listopad 2006): 304–7. http://dx.doi.org/10.2310/7750.2006.00061.

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Background: Cutaneous metastases are an uncommon phenomenon that occurs in a few patients with metastatic disease. Early recognition of a cutaneous metastasis is important as it may be the presenting sign of an underlying malignancy. These metastases usually indicate advanced disease and carry a poor prognosis. Objectives: We present two cases with cutaneous metastasis from primary non-small cell lung cancer. We seek to familiarize dermatologists with the unusual presentations of cutaneous metastases. Conclusion: In our two cases, the diagnosis of the metastatic cutaneous lesion ultimately led to the correct diagnosis of an underlying malignancy.

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Su, ChunXia, Juan Zhou, Xiangling Chu i Jing Zhao. "Genetic mutations associated with lung cancer metastasis to the brain." Journal of Global Oncology 5, suppl (7.10.2019): 41. http://dx.doi.org/10.1200/jgo.2019.5.suppl.41.

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41 Background: Lung cancer is the most common cause of mortality in both men and women, accounting for one-quarter of all cancer deaths. Most lung cancer-associated deaths result from metastasis, especially brain metastasis. Metastasis associated mutations are important biomarkers for metastasis prediction and outcome improvement. The current study aimed to reveal the molecular mechanisms and the genetic alterations involved in metastasis from lung tumors to the brain. Methods: We carried out whole exome sequencing (WES) of the primary tumors and the corresponding brain metastases from 15 patients with metastatic non-small-cell lung carcinoma. Results: We identified novel lung cancer metastases associated genes (CHEK2P2, BAGE2, AHNAK2) and epigenetic factors (miR-4436A, miR-6077). Lung-brain metastasis samples have more similar Ti/Tv(transition/transversion) profile with brain cancer. Focal adhesion, PI3K-Akt signaling pathway, MAPK signaling pathway are some of the most important tumor onset and metastasis pathways. Alternative splicing, Methylation and EGF-like domain are important metabolic abnormal for the lung-metastasis cancers. Conclusions: We conducted a pairwise lung-brain metastasis based WES and identified some novel metastasis related mutations which provided potential biomarkers for prognosis and targeted therapeutics.

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Kiberstis, P. A. "Engineering cancer cell metastasis". Science 347, nr 6221 (29.01.2015): 516. http://dx.doi.org/10.1126/science.347.6221.516-c.

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Hassan, B. B., S. M. Elshafae, W. Supsavhad, J. K. Simmons, W. P. Dirksen, S. M. Sokkar i T. J. Rosol. "Feline Mammary Cancer". Veterinary Pathology 54, nr 1 (11.07.2016): 32–43. http://dx.doi.org/10.1177/0300985816650243.

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Feline mammary carcinoma (FMC) is similar to human breast cancer in the late age of onset, incidence, histopathologic features, biological behavior, and pattern of metastasis. Therefore, FMC has been proposed as a relevant model for aggressive human breast cancer. The goals of this study were to develop a nude mouse model of FMC tumor growth and metastasis and to measure the expression of genes responsible for lymphangiogenesis, angiogenesis, tumor progression, and lymph node metastasis in FMC tissues and cell lines. Two primary FMC tissues were injected subcutaneously, and 6 FMC cell lines were injected into 3 sites (subcutaneous, intratibial, and intracardiac) in nude mice. Tumors and metastases were monitored using bioluminescent imaging and characterized by gross necropsy, radiology, and histopathology. Molecular characterization of invasion and metastasis genes in FMC was conducted using quantitative real-time reverse transcription polymerase chain reaction in 6 primary FMC tissues, 2 subcutaneous FMC xenografts, and 6 FMC cell lines. The histologic appearance of the subcutaneous xenografts resembled the primary tumors. No metastasis was evident following subcutaneous injection of tumor tissues and cell lines, whereas lung, brain, liver, kidney, eye, and bone metastases were confirmed following intratibial and intracardiac injection of FMC cell lines. Finally, 15 genes were differentially expressed in the FMC tissues and cell lines. The highly expressed genes in all samples were PDGFA, PDGFB, PDGFC, FGF2, EGFR, ERBB2, ERBB3, VEGFD, VEGFR3, and MYOF. Three genes ( PDGFD, ANGPT2, and VEGFC) were confirmed to be of stromal origin. This investigation demonstrated the usefulness of nude mouse models of experimental FMC and identified molecular targets of FMC progression and metastasis.

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Hoang, Tien Manh, i Thi Thanh Nguyen. "Comparative analysis of overall survival in non-small cell lung cancer patients with and without different organ metastases". Ministry of Science and Technology, Vietnam 64, nr 3 (15.03.2022): 33–38. http://dx.doi.org/10.31276/vjste.64(1).33-38.

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Lung cancer is the leading cause of cancer death globally. Non-small cell lung cancer (NSCLC) constitutes more than 80% of all lung cancers, and patients with distant metastasis have much higher mortality. The survival times of NSCLC patients with metastasis have been reported in early studies, however, it remains unclear whether there are variations or patterns in survival times of patients with different metastases. Therefore, we assessed risk factors for distant metastases and the effects of different organ metastasis on overall survival (OS) in patients with NSCLC. Methods: demographics and clinical data of NSCLC patients with and without distant metastasis were collected from the Surveillance, Epidemiology, and End Result (SEER) database between 2010 and 2016. We investigated risk factors for distant metastasis patients and compared the difference in OS of NSCLC patients with different metastatic sites. Results: a total of 3849 patients diagnosed with NSCLC were screened from the SEER database with 41% (1577) of the patients having distant metastasis. During the follow-up period, 3221 (83.7%) patients died and, of all the deceased patients, 2935 (88.4%) died of lung cancer while only 286 (11.6%) died from other diseases or causes. The occurrence of distant metastasis was closely related to the patient’s age, primary tumour site, tumour grade, T stage, N stage, surgery of primary site, radiation therapy, and chemotherapy (p<0.05). Compared to patients without metastasis, whose median OS was 13 months, the median OS of patients with metastasis was 6 months (lung), 5 months (liver), 5 months (bone), 4 months (brain), and 3 months (multiple organs). Conclusions: distant metastasis indicates a poor prognosis in NSCLC patients. There were significant differences in the prognosis of different metastatic sites and the order of their OS from high to low was: no metastasis > lung metastasis, liver metastasis, bone metastasis > brain metastasis, multiple organ metastasis.

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V., Ramya, i Sahayaraj J. "Transitional cell carcinoma of urinary bladder with cervical lymph node metastasis: a case report and review of literature". International Journal of Advances in Medicine 6, nr 1 (23.01.2019): 194. http://dx.doi.org/10.18203/2349-3933.ijam20190130.

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Bladder cancer usually spreads via the lymphatic and hematogenous routes, the common sites of metastases of urinary bladder cancers being the regional lymph nodes, liver, lung, bone, peritoneum, pleura, kidney, adrenal gland and intestines. Metastasis to non-regional lymph nodes especially cervical lymph nodes is extremely rare presentation. Metastasis to head and neck region is associated with poor prognosis and low survival rate. Here-in we report a case of cervical lymph node metastasis in patient with muscle invasive bladder cancer.

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Apanovich, Natalya, Maria Peters, Pavel Apanovich, Danzan Mansorunov, Anna Markova, Vsevolod Matveev i Alexander Karpukhin. "The Genes—Candidates for Prognostic Markers of Metastasis by Expression Level in Clear Cell Renal Cell Cancer". Diagnostics 10, nr 1 (8.01.2020): 30. http://dx.doi.org/10.3390/diagnostics10010030.

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The molecular prognostic markers of metastasis are important for personalized approaches to clear cell renal cell carcinoma (ccRCC) treatment but markers for practical use are still missing. To address this gap we studied the expression of ten genes—CA9, NDUFA4L2, VWF, IGFBP3, BHLHE41, EGLN3, SAA1, CSF1R, C1QA, and FN1—through RT-PCR, in 56 ccRCC patients without metastases and with metastases. All of these, excluding CSF1R, showed differential and increased (besides SAA1) expression in non-metastasis tumors. The gene expression levels in metastasis tumors were decreased, besides CSF1R, FN1 (not changed), and SAA1 (increased). There were significant associations of the differentially expressed genes with ccRCC metastasis by ROC analysis and the Fisher exact test. The association of the NDUFA4L2, VWF, EGLN3, SAA1, and C1QA expression with ccRCC metastasis is shown for the first time. The CA9, NDUFA4L2, BHLHE4, and EGLN3 were distinguished as the strongest candidates for ccRCC metastasis biomarkers. We used an approach that presupposed that the metastasis marker was the expression levels of any three genes from the selected panel and received sensitivity (88%) and specificity (73%) levels with a relative risk of RR > 3. In conclusion, a panel of selected genes—the candidates in biomarkers of ccRCC metastasis—was created for the first time. The results might shed some light on the ccRCC metastasis processes.

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Del Vecchio, Sharon, Robert Ellis, Kylie Gallagher, Keng Lim Ng, Li Ma, Geoffrey Strutton i Simon Wood. "A Rare Case of Solitary Kidney Metastasis following Primary Laryngeal Squamous Cell Carcinoma". Journal of Kidney Cancer and VHL 4, nr 2 (2.05.2017): 6–9. http://dx.doi.org/10.15586/jkcvhl.2017.68.

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Laryngeal cancer is the 14th most common malignancy worldwide, and its common subtype squamous cell carcinoma (SCC) is highly associated with tobacco use and long-term alcohol consumption. The incidence of distant metastasis from a primary laryngeal cancer has been reported to be very low, between 6.5% and 8.5%, according to published tumour registry data. Distant metastases of laryngeal SCC most commonly involve the lung, liver, bone and mediastinum, seldom involving the kidney. Renal metastasis has been well established in many other cancers such as lymphoma, lung, breast and gastric carcinoma. This report discusses the rare case of a solitary renal metastasis following a primary laryngeal SCC.

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Rozprawy doktorskie na temat "Cancer cell metastasis"

Park, Se Hyung. "Estrogen in ovarian cancer cell metastasis". Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/1287.

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Benign ovarian tumors and majority of epithelial ovarian cancers possess steroid receptors including estrogen receptors (ERs). However, the estrogen-ER signaling in ovarian carcinomas is not completely understood. Tumorigenesis is a multiple-step process involving dysregulated cell growth and metastasis. Tumor cells acquire the capacity of migration and invasion by temporal phenotypical and genotypical changes termed epithelial-mesenchymal transition (EMT). Considerable evidence implicates a mitogenic action of estrogen in early ovarian carcinogenesis. In contrast, its influence in the metastatic cascade of ovarian tumor cells remains obscure. In this study, I have focused on the role of 17β-estradiol (E2) in ovarian tumorigenesis. EMT related genes including E-cadherin, Snail, Slug, and Twist were examined. E2 treatment led to clear morphological changes and an enhanced cell migratory propensity. These morphologic and functional alterations were associated with changes in the abundance of EMT-related genes. Upon E2 stimulation, expression and promoter activity of the epithelial marker E-cadherin was strikingly suppressed, whereas EMT-associated transcription factors Snail and Slug were significantly up-regulated. This up-regulation was attributed to the increase in gene transcription activated by E2. Depletion of the endogenous Snail or Slug using small interfering RNA (siRNA) attenuated E2-mediated control in E-cadherin. In addition, the E2-induced cell migration was neutralized by Snail and Slug siRNAs, implying that both transcription factors are indispensable for the pro-metastatic actions of E2. Importantly, by using selective ER agonists as well as over-expression and siRNA approaches, it was identified that E2 triggered the metastatic behaviors exclusively through an ER⍺-dependent pathway. In contrast, overexpression of ERβ opposed the phenotypic changes and down-regulation of E-cadherin induced by ER⍺. In addition, microarray analysis was performed to characterize more putative downstream mediators of E2. Expression levels of 486 genes were found to be altered by at least 50% upon E2 treatment, and included several genes involved in oncogenesis, cell cycle control, apoptosis, signal transduction and the gene expression machinery. These candidate genes may be valuable for better delineating the ER pathways and functions. In summary, this study provides compelling arguments that estrogen can potentiate tumor progression by EMT induction, and highlight the crucial role of ER⍺ in ovarian tumorigenesis.

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Oosterhout, Anselmus Gerardus Maria van. "Small cell lung cancer and brain metastasis". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=6643.

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Villafañe, Johann Sebastian Bergholz. "Role of P63 in cell migration and cancer metastasis". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12282.

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Thesis (Ph.D.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
The p53-related p63 protein is expressed as multiple isoforms involved in diverse biological functions, including cell proliferation, survival, apoptosis, differentiation, senescence, and aging. An inverse correlation between p63 expression and cancer progression in a variety of human cancers suggests that p63 functions as a metastasis suppressor. Here, we show that the predominant isoform of p63, ΔNp63α, plays a major role in inhibiting cell migration, invasion, and cancer metastasis by modulating Extracellular signal-regulated protein kinase 1 and 2 (Erk1/2) signaling. We profiled gene expression in human breast cancer Hs-578T cells stably expressing wild type ΔNp63α, or a mutant derivative defective in DNA binding or protein-protein interaction. We observed that wild type ΔNp63α, but not the mutant derivatives, up-regulated Mitogen-activated Protein (MAP) Kinase Phosphatase 3 (MKP3), a negative regulator of Erk1/2 signaling. Accordingly, exogenous ΔNp63α expression in breast cancer MDA-MB-231 cells up-regulated MKP3 expression, decreased nuclear levels of phosphorylated Erk1/2, and down-regulated Matrix Metalloprotease 1 and 9 (MMP1/9) expression. In addition, ΔNp63α inhibited cancer cell invasion, which was significantly rescued by disrupting MKP3 expression. Conversely, pan-p63 knockdown in mammary epithelial MCF-1OA and head and neck squamous cell carcinoma FaDu cells resulted in decreased MKP3 expression and concomitant higher levels of Erk1/2 phosphorylation, while Mek1/2 phosphorylation levels were not affected. Consistently, pan-p63 knockdown led to increased cell motility and invasion, which was reversed either by reintroduction of the ΔNp63α isoform alone, but not by other isoforms, or by expression of MKP3. Interestingly, p63 ablation-induced cell motility is dependent on Erk2, but not Erk1 expression. Moreover, we found that both p63 and MKP3 expression is usually decreased in invasive breast carcinoma, indicating a clinical correlation between p63 and MKP3 down-regulation and cancer progression. Finally, we found that reduced p63 expression in Her2/Neu-transformed MCF-1OA cells dramatically increased metastatic frequency to the lungs in a mouse model of breast cancer. Taken together, these results not only reveal a novel molecular pathway by which p63 plays an important pathological role in cancer metastasis, but also contribute to the design of therapeutic strategies in the treatment of cancer.

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Chan, Pui-man Poemen. "Micrometastases of esophageal cancer /". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36404652.

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Shirure, Venktesh S. "Molecular Mechanisms of Circulating Tumor Cell Adhesion in Breast Cancer Metastasis". Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1357706517.

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Xing, Fei. "ROLE OF NOTCH SIGNALING IN BREAST CANCER METASTASIS". OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/514.

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Notch signaling is often and aberrantly activated by hypoxia during tumor progression; however, the exact pathological role of hypoxia-induced Notch signaling in tumor metastasis is as yet poorly understood. In the first part of this study, we aimed to define the mechanism of Notch ligand activation by hypoxia in both primary tumor and bone stromal cells in the metastatic niche and to clarify their roles in tumor progression. We have analyzed the expression profiles of various Notch liagnds in 779 breast cancer patients in GEO database and found that the expression of Jagged2 among all five ligands is most significantly correlated with the overall- and metastasis-free survival of breast cancer patients. The results of our immunohistochemical (IHC) analysis for Jagged2 in 61 clinical samples also revealed that both Jagged2 and Notch signaling were strongly up-regulated at the hypoxic invasive front. Activation of Jagged2 by hypoxia in tumor cells induced EMT and also promoted cell survival in vitro. Notably, a ã-secretase inhibitor significantly blocked Notch-mediated invasion and survival under hypoxia by promoting expression of E-cadherin and inhibiting Akt phosphorylation. Importantly, Jagged2 was also found to be up-regulated in bone marrow stroma under hypoxia and promoted the growth of cancer stem-like cells by activating their Notch signaling. Therefore, hypoxia-induced Jagged2 activation in both tumor invasive front and normal bone stroma plays a critical role in tumor progression and metastasis, and Jagged2 is considered to be a valuable prognostic marker and may serve as a novel therapeutic target for metastatic breast cancer. In the second part of this study, the role of Notch signaling in brain metastasis was investigated. Metastatic diseases are responsible for the majority of the deaths in breast cancer patients and the brain is one of the most common metastatic sites. The metastatic tumor in the brain profoundly affects the cognitive and sensory functions as well as morbidity of patients, and the one year survival rate among these patients remains less than 20%. However, the pathological mechanism of brain metastasis is as yet poorly understood. In this report, we found that metastatic breast tumor cells in the brain highly expressed IL-1â which can "activate" astrocytes. This activation significantly augmented the expression of JAG1 in the reactive astrocytes, which in turn activated Notch signaling pathway of cancer stem-like cells (CSCs) upon direct interaction. We also found that the activated Notch signaling in CSCs up-regulated Sox2 followed by promoting self-renewal of CSCs. Furthermore, we have shown that the blood-brain barrier permeable Notch inhibitor, Compound E, can significantly suppress the brain metastasis growth in our animal model. These results represent a novel paradigm for the understanding of how metastatic breast CSCs re-establish their niche for their self-renewal in a totally different microenvironment, which opens a new avenue to identify a novel and specific target for the brain metastatic disease

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Lomax-Browne, Hannah Jane. "Interactions between cancer cell glycans and endothelial cells during adhesion events in metastasis". Thesis, Oxford Brookes University, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501906.

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Metastasis, the process by which cancer spreads in the body, is a complex, multi-step cascade which is poorly understood and is the cause of death of most cancer patients. Aberrant glycosylation is an established characteristic of cancer cells and appears to have a role in metastatic mechanisms. The lectin from Helix pomatia, the Ron (Helix pomatia agglutinin, HPA), recognises aberrant glycans terminating in α-N-acetylgalactosamine (GalNAc). The presence of GalNAc-glycans on cancer cell surfaces, detected by HPA binding, is associated with metastasis and consequent poor survival.

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Marshall, John Francis. "The role of integrins in melanoma progression and metastasis". Thesis, Open University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295235.

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Harihar, Sitaram. "The Role of Phosphoinositide Signaling in Breast Cancer Metastasis Suppressor 1-Mediated Metastasis Suppression of Human Breast Carcinoma Cells". DigitalCommons@USU, 2011. https://digitalcommons.usu.edu/etd/870.

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Breast cancer is the most common non-skin cancer in women and the second most common cause of cancer-related death in U.S. women. Despite numerous advances in treatment strategies against breast cancer, the presence of undetected distant metastasis of the primary tumor remains the main cause of mortality. Current screening and detection methods such as mammograms are simply not sensitive enough to detect formation of metastasis. Further, currently available therapies against metastatic breast cancer do not provide a complete cure for the disease. Thus, understanding the biology and molecular factors involved in cancer metastasis will help aid in preventing the onset of metastasis and discovering an effective treatment for this deadly disease. My research focused on understanding the mechanism of action of one such factor, breast cancer metastasis suppressor 1 (BRMS1), a suppressor gene found deleted in late stage breast cancers. The goal of my dissertation was to investigate the role of membrane signaling lipids phosphoinositides, specifically phosphatidylinositol(4,5)bisphosphate (PI(4,5)P2) in BRMS1-mediated metastasis suppression in MDA-MB-435 and MDA-MB-231 human breast carcinoma cells. My studies revealed BRMS1 selectively reduced receptor tyrosine kinases (RTK) and Gprotein coupled receptors (GPCR) expression and downstream signaling in human breast carcinoma cells. My observations are critical as many of these receptors are upregulated in metastatic breast cancer and PI(4,5)P2 is a critical constituent for mediating their downstream signaling events. Further, using immunoblotting studies, I uncovered a possible compensatory mechanism in tumor cells to overcome downregulation of PI(4,5)P2 by BRMS1 and maintain its downstream signaling. When studied for BRMS1 regulation of enzymes involved in PI(4,5)P2 synthesis, I showed BRMS1 completely inhibits phosphatidylinositol 4-phosphate 5-kinase β (PIP5Kβ) expression. Using overexpression studies, I showed PIP5Kβ to be the major contributor to the cellular PI(4,5)P2 pool required for agonist-induced intracellular calcium rise. Taken together, my dissertation research has identified some critical breast cancer markers and revealed signaling pathways altered by BRMS1 in human breast carcinoma cells that can be studied as potential therapeutic targets against breast cancer metastasis.

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Zhang, Hanshuo. "Large-scale identification of functional genes regulating cancer cell migration and metastasis using the self-assembled cell microarray". Diss., Georgia Institute of Technology, 2013. http://hdl.handle.net/1853/49066.

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Metastasis is one of the critical hallmarks of malignancy tumor and the principal cause of death in patients with cancer. Cell migration is the basic and essential step in cancer metastasis process. To systematically investigate functional genes regulating cell migration and cancer metastasis on large scale, we developed a novel on-chip method, SAMcell (self-assembled cell microarray). This method was demonstrated to be particularly suitable for loss-of-function high-throughput screening because of its unique advantages. The first application of SAMcell was to screen human genome miRNAs, considering that more and more miRNAs had been proved to govern cancer metastasis. We found that over 20 % of miRNAs have migratory regulation activity in diverse cell types, indicating a general involvement of miRNAs in migratory regulation. Through triple-round screenings, we discovered miR-23b, which is down-regulated in human colon cancer samples, potently mediates the multiple steps of metastasis, including cell motility, cell growth and cell survival. In parallel, the second application of SAMcell was to screen human genome kinase genes, considering that more and more kinase genes had become successful diagnostic marker or drug targets. We found over 11% migratory kinase genes, suggesting the important role of kinase group in metastasis regulation. Through both functional screening and bioinformatics analysis, we discovered and validated 6 prospective metastasis-related kinase genes, which can be new potential targets in cancer therapy. These findings allow the understanding of regulation mechanism in human cancer progression, especially metastasis and provide the new insight into the biological and therapeutical importance of miRNAs or kinases in cancer.

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Książki na temat "Cancer cell metastasis"

Evans, Clive W. The metastatic cell: Behaviour and biochemistry. London: Chapman and Hall, 1991.

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Oral cancer metastasis. New York: Springer, 2010.

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Failure of apoptosis and cancer metastasis. Austin: R.G. Landes, 1998.

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Wells, Alan, red. Cell Motility in Cancer Invasion and Metastasis. Berlin/Heidelberg: Springer-Verlag, 2006. http://dx.doi.org/10.1007/b103440.

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Jiang, Wen G., red. Electric Cell-Substrate Impedance Sensing and Cancer Metastasis. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4927-6.

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Peter, Thomas. Metastatic potential of human colorectal cancer cell lines. Austin: R.G. Landes Co., 1993.

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S, Lakshmi M., red. The genetics of cancer: Genes associated with cancer invasion, metastasis, and cell proliferation. San Diego: Academic Press, 1997.

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Shrestha, Prashanta. Tenascin: An extracellular matrix protein in cell growth, adhesion and cancer. New York: Chapman & Hall, 1997.

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International, Symposium on Cellular Oncology (2nd 1985 Palm Springs Calif ). Occult nodal metastasis in solid carcinomata. New York: Praeger, 1987.

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Cancer: Between glycolysis and physical constraint. Berlin: Springer, 2004.

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Części książek na temat "Cancer cell metastasis"

Hart, I. R., i R. E. Wilson. "Metastatic Phenotype and Cell Differentiation in Melanoma Cells". W Cancer Metastasis, 62–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_9.

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Dennis, J. W., i S. Laferté. "Importance of Cell Surface Carbohydrates in Tumor Cell Metastasis". W Cancer Metastasis, 86–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_11.

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Danø, K., N. Behrendt, L. R. Lund, E. Rønne, J. Pöllänen, E. M. Salonen, R. W. Stephens, H. Tapiovaara i A. Vaheri. "Cell Surface Plasminogen Activation". W Cancer Metastasis, 98–107. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_13.

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Boon, T. "Metastatic Phenotype and Cell Differentiation". W Cancer Metastasis, 222. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_30.

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Nabi, I. R., i A. Raz. "Cell Shape and the Metastatic Phenotype". W Cancer Metastasis, 92–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_12.

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Rothbard, J. B., R. Busch, R. Lechler, J. Trowsdale i J. R. Lamb. "Recognition of the HLA Class II-Peptide Complex by T cell Receptor: Reversal of MHC Restriction of a T Cell Clone by a Point Mutation in the Peptide Determinant". W Cancer Metastasis, 136–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_18.

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Parris, George E. "Cell-Cell Fusion, Chemotaxis and Metastasis". W Intercellular Communication in Cancer, 227–54. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7380-5_9.

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Schirrmacher, V., P. v. Hoegen, P. Schlag, W. Liebrich, B. Lehner, K. Schumacher, T. Ahlert i G. Bastert. "Active Specific Immunotherapy with Autologous Tumor Cell Vaccines Modified by Newcastle Disease Virus: Experimental and Clinical Studies". W Cancer Metastasis, 157–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74236-1_20.

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Polara, Ruhi, Daphni van Rinsum i Nirmal Robinson. "Autophagy in Cancer Metastasis". W Autophagy in Stem Cell Maintenance and Differentiation, 259–85. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-17362-2_11.

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Thodeti, Charles Kumar, i Kaustabh Ghosh. "Mechanisms of Tumor Cell Migration and Invasion in Lung Cancer Metastasis". W Lung Cancer Metastasis, 93–109. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0772-1_5.

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Streszczenia konferencji na temat "Cancer cell metastasis"

Kraning-Rush, Casey M., Shawn P. Carey i Cynthia A. Reinhart-King. "Molded Collagen Microchannels for the Study of Cancer Cell Invasion". W ASME 2012 10th International Conference on Nanochannels, Microchannels, and Minichannels collocated with the ASME 2012 Heat Transfer Summer Conference and the ASME 2012 Fluids Engineering Division Summer Meeting. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icnmm2012-73093.

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Metastasis is the cause of 90% of cancer-related deaths and yet the precise mechanism of metastasis is poorly understood[1]. To metastasize, cells break free from the primary tumor, migrate through the surrounding tissue, and enter the vascular system to move to a secondary site. To migrate through the stroma, cell can both degrade the tissue and use physical force to move the tissue from its path. However, the relative roles of matrix degradation and cellular force are not well-understood. Previous work has shown that as cell move through the matrix, they create channels that other cells can then use to more easily escape from the primary tumor [2, 3]. To investigate the mechanisms by which metastatic cells move through 3D matrices, we fabricated microchannels from collagen that simulate the paths that are made and used by cells during metastasis. Here, we will present our method for molding channels in compliant collagen gels to investigate cell migration. The channels dimensions approximate the size of a cell and permit cell migration without the need for matrix degradation. We demonstrate that the channels cause persistent, unidirectional cell migration that is significantly faster than the migration observed in 3D matrices without channels. These channels provide a unique platform to probe 3D cellular migration and permit the dissection of the relative roles of matrix degradation and force generation in facilitating cell invasion.

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Yoshimoto, T., T. Ishikawa, N. Matsuki, H. Fujiwara, Y. Imai, H. Ueno, M. Takeda i T. Yamaguchi. "Rheology of Cancer Cells With Different Metastatic Properties". W ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206593.

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Cancer is the leading cause of death in Japan as well as many other countries. One of the most serious problem of cancer is that cancer cells often migrate to a distant part of the body, referred to as metastasis. The rheological properties of cancer cells have been investigated by some reserchers [1,2]. However, the correlations between the metastasis and the rheological properties are still unclear, because of limited number of experimental cases reported so far. In this study, we used two kinds of human breast cancer cell lines, MCF-7 and KPL-4. It is known that KPL-4 has much higher metastatic property than MCF-7. The rheological properties of these cells were measured by a micropipette aspiration method [3,4]. By comparing Young’s modulus between two kinds of cancer cells, we discuss the correlations between the metastasis and the cell deformability.

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Inufusa, H., N. Sagara, K. Nakano i M. Yasutomi. "CHARACTERISATION OF PLATELET AGGREGATING MATERIAL EXTRACTED FROM HUMAN LUNG ADENOCARCINOMA CELL LINE WHICH METASTASIZED IN NUDE MICE S,C, IMPLANTATION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643199.

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It has been reported in animal experimental system that Platelet Aggregating Material (PAM) of cancer cell play important role in cancer metastasis. Many human cancer cell lines has been also studied the platelet aggregation activity of PAM. But correlation between the platelet aggregation activity and metastatic potential of human cancer cells were usually unkncwn. We established a human lung adenocarcinoma cell line KUM-LK-2 which produce spontaneous lung metastasis when cells implanted into subcutaneous of nude mice. PAM was extracted from KUM-LK-2 cells following the method of D.Mbhanty and P.Hilgard. Platelet aggregation study of PAM was performed by human Heparinized platelet rich plasma useing NIKO Hematracer PACT2D. Character of PAM were examined by physical and chemical treatment. KUM-LK-2 PAM shew 80% of platelet aggregation in maximum after 150 sec lag time, and aggregation was not found by Citrated PRP.It is concluded that PAM is high moleculer protein and contain Phospholipid and aggregation activity is concerning with ATP composition of platelet. PAM dose not contain Fibrinogen and Sialic acid, and not concern with Throrriboxan composition. This study is first case of platelet aggregation activity of PAM extracted human canoer cells which contain metastatic potential.

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Stokol, Tracy, Mandy B. Esch, Nozomi Nishimura, Chris Schaffer, Janelle L. Daddona, David J. Post i Dhruv P. Desai. "Little Channels, Big Disease: Using Microfluidics to Investigate Cancer Metastasis". W ASME 2011 9th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2011. http://dx.doi.org/10.1115/icnmm2011-58298.

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The leading cause of death in human patients with malignant cancer is the dissemination of the primary tumor to secondary sites throughout the body. It is well known that cancers metastasize to certain tissues (e.g. breast cancer typically spreads to the lungs. brain and bone), in a pattern that cannot be explained by blood flow from the primary tumor or simple mechanical arrest. Circulating tumor cells usually arrest in the microvasculature of target tissues. At these sites, they must adhere to the endothelium, survive, proliferate and extravasate in order to form a secondary tumor. In vitro tools that appropriately mimic the microvasculature in which cancer metastasis occurs have been largely unavailable. With the advent of microfluidic and nanotechnology, we can now more accurately model the complexity of the microvascular environment, in terms of representative endothelial cells, geometry, shear stress and exposure to organ-specific environmental cues. This talk will focus on the use of microfluidic devices to explore mechanisms involved in tumor-endothelial cell interactions that govern cancer metastasis to organ specific sites.

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Shareef, Sarah J., Mihai Nita-Lazar i Maria A. Kukuruzinska. "E-cadherin N-glycosylation Modulates the Strength of Adherens Junctions". W ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13013.

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Metastasis, the spread of cancer cells throughout the body, claims 90% of solid tumor deaths. During metastasis, cancer cells undergo discohesion. An understanding of how to control and strengthen cell adhesion through junction formation could lead to methods for decreasing metastatic tendencies.

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Tang, Xin, i Taher Saif. "Loss of Cell Adhesion in Colon Cancer Cells During In Vitro Metastasis Measured by Bio-MEMS Force Sensor". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80936.

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Human colon carcinoma (HCT-8) cells show metastatic phenotype when cultured on appropriately soft substrates. Here, we studied the surface non-specific adhesion in HCT-8 cells throughout the in vitro metastasis process. A novel bio-MEMS force sensor was used to measure the cell-probe non-specific adhesion. The adhesion characteristics are analyzed using classical Johnson-Kendall-Roberts (JKR) theory. Our results indicate that the post-metastatic HCT-8 cells (dissociated R cells) display remarkably diminished surface adhesion and are potentially more invasive than original pre-metastatic HCT-8 cells (E cells). To the best of our knowledge, this is the first quantitative data on cancer cells adhesion change as in vitro metastasis proceeds. It is well known that, during in vivo cancer metastasis, malignant cancer cells reduce their surface adhesion (both specific and non-specific) [1] as well as modify their extracellular matrix (ECM) ligands [2] to detach from primary tumor and enhance successful invasion into distant healthy organs. Simultaneously, cancer cells down-regulate their surface cell-cell adhesion molecules, i.e. E-Cadherin, to escape from tumor and initiate metastasis [1]. However, there is no quantitative report on cancer cell adhesion throughout the entire metastasis process, since in vivo metastasis is nearly impossible to detect [3]. We had discovered [4] that human colon cancer cells (HCT-8) can consistently display an in vitro metastasis-like phenotype (MLP) within only 7 days of culture on soft hydrogel substrates with appropriate mechanical stiffness (Poly-acrylamide gels with Elastic modulus: 21∼ 47 kPa [14, 15]). We found that MLP is consistent, repeatable and irreversible (Fig. 1a-1c). In addition, the post MLP cancer cells (referred to here as R cells meaning round-shaped in contrast to the E-cells, i.e., the original HCT-8 cells that are epithelial in nature) up-regulate a number of in vivo tissue-destructive proteinases, such as, MMPs [4]. R cells also express remarkably diminished E-Cadherin patterns compared to HCT8 E cells (Fig. 1d, 1e). Using this model system, we are able to study the kinetics of non-specific and specific surface adhesion change on HCT-8 cancer cells. In this paper, we measure the non-specific adhesion of both pre and post metastatic HCT-8 cells (E and R cells respectively) using a novel bio-MEMS force sensor. The adhesion energy and other mechanical properties are analyzed using classical Johnson-Kendall-Roberts (JKR) theory [5]. We find that after undergoing metastasis (or MLP), the dissociated HCT-8 cells (R cells) down-regulate non-specific adhesion, in contrast to their ancestors, HCT-8 E cells. The reduction of non-specific adhesion is coincident with the immuno-fluorescent staining data of cell-cell specific adhesion molecule E-Cadherin, which shows 4 ∼ 6 times down-regulation after MLP (Fig. 1d-1e). The bio-MEMS sensor consists of a micro cantilever beam with spring constant k = 3.48 nN/ μm. A flat probe is attached with the beam which forms adhesive contact with cells. The sensor is made from single crystal silicon, and is coated with a thin layer of native silicon oxide (SiO2). The probe and the sensor are not functionalized. The sensor is manipulated with an x-y-z piezo stage. To measure the cell adhesion, the flat probe is brought in contact with cells’ lateral convex surface at the boundary. After a 2-minute contact, force sensor is pulled away horizontally from the cell island at a constant quasi-static speed of 2.1 ± 0.4 μm/s (Fig. 2a). Due to the cell-probe adhesion, the sensor beam deforms during retraction. Corresponding restoring force of the cell island is given by F = kδ (Fig. 2a-c). Note the probe is non-functionalized (free of any extra-cellular matrix proteins), and only has a coating of SiO2 on the surface due to air exposure. During probe retraction, the cell is continuously stretched while the cell-probe contact area radius Rc remains unchanged (Fig. 3b-e) and the contact angle θ increases (Fig. 3b). At critical value of force, Fc, the cell suddenly detaches from probe (Fig. 3d). The critical Fc at detachment is optically recorded by video camera and was determined as 27.8 ± 2.2 nN. A similar experiment on cells after MLP shows so measurable adhesion, i.e, the force to detach was zero for all the cells tested. Figure shows the measured adhesion in pre and post metastatic cells.

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Xu, Wenwei, Roman Mezencev, Byungkyu Kim, Lijuan Wang, John McDonald i Todd Sulchek. "Ovarian Cancer Cell Invasiveness Correlates With Increased Cell Deformability". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80624.

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Cancer cells undergo a variety of biochemical and biophysical transformations when compared to identical cells displaying a healthy phenotypic state, cancer cells show a drastic reduction of stiffness upon malignancy[1, 2] and change of stiffness of single cells can indicate the presence of disease [3–6]. Besides, metastatic cancer has a higher deformability than their benign counterparts[7, 8]. Using atomic force microscopy, we demonstrated that cancerous ovarian cells (OVCAR3, OVCAR4, HEY and HEYA8) are substantially softer than the healthy immortalized ovarian surface epithelium (IOSE) cells. In addition, within the different types of cancerous ovarian cells, increased invasiveness and migration are directly correlated with increased cell deformability. These results indicate that stiffness of individual cells can distinguish not only ovarian cancer cells from healthy cells types, but also invasive cancer types from less invasive types. Stiffness may provide an alternative and convenient biomarker to grade the metastasis potential of cancer cells.

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Zielinski, Rachel, Cosmin Mihai i Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition". W ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.

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Moreno, Marcelo, Amauri de Oliveira, Tália Cássia Boff, Gabriela Nogueira Matschinski i Izadora Czarnobai. "SQUAMOUS CELL CARCINOMA METASTASIS OF THE MAMMARY GLAND: CASE REPORT". W Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1007.

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Introduction: Primary squamous cell carcinoma (SCC) of the breast is a rare neoplasm, which represents less than 0.1% of invasive breast cancers. Therefore, it is essential to discriminate between a primary SCC and a metastatic SCC. In order to be considered a primary carcinoma of the breast, a histological examination of the lesion must show more than 90% of squamous neoplastic cells, in addition to the absence of cutaneous SCC or other anatomical sites. Extra-mammary neoplasm metastases are uncommon, representing 0.5% to 2% of breast malignancies. Metastatic SCC in the mammary gland is an uncommon event. To date, only three cases were reported in the literature of secondary involvement of vulvar SCC in the mammary gland. The objective of this work is to report the case of a patient with secondary mammary metastasis to a vulva SCC. Case report: A 74-year-old female patient who underwent radical modified vulvectomy 10 years before. Her pathological stage was characterized as IIIB. For this reason, she was also submitted to adjuvant treatment with chemotherapy associated with radiotherapy to the vulvar region, inguinal lymph node chains and pelvic arteries. On the ninth year of cancer follow-up, she presented recurrence in the vaginal wall. In the complementary image exams, an extentension of neoplasia to pelvic organs was identified, but no distant metastatic lesions were found. She underwent monobloc resection of pelvic organs, with reconstruction of the urinary and intestinal transits. The patient showed a good clinical evolution, with no pelvic complaints. After one year, the patient returned complaining of a nodule in the right breast. On physical examination, a lesion was observed at the junction of the lateral quadrants of the breast, measuring +/- 3.5 cm, with associated inflammatory signs and imprecise limits, with a central region showing a fistulous orifice through which the necrotic material passed. On the mammography, a dense, rounded and partially delimited lesion was identified. She underwent a core biopsy that described a SCC. According to her clinical history, it was considered a remote relapse of the vulvar SCC. The patient was submitted to a quadrantectomy with an ipsilateral axillary lymphadenectomy and reconstruction with a lateral thoracic flap. On an anatomopathological examination there was a description that the neoplasm would invade the underlying muscle tissue; and the resection margins were free. Four out of the fourteen isolated axillary lymph nodes had metastases, without perinodal soft tissue invasion. Six months after breast surgery, the patient evolved metastases to both lungs and soon after she died without response to the systemic treatment employed. This report was approved by the Research Ethics – UFFS (Universidade Federal da Fronteira Sul) (number 4.034.565).

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Tang, Xin, Tony Cappa, Theresa B. Kuhlenschmidt, Mark S. Kuhlenschmidt i Taher A. Saif. "Studying the Mechanical Sensitivity of Human Colon Cancer Cells Through a Novel Bio-MEMS Force Sensor". W ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13237.

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Cancer deaths are primarily caused by metastases, not by the parent tumor. During the metastasis, malignant cancer cells detach from the parent tumor, and spread through the patient’s circulatory system to invade new tissues and organs [1]. To study the role played by the mechanical microenvironment on the cancer cell growth and malignancy promotion, we cultured human colon carcinoma (HCT-8) cells in vitro on substrates with varied mechanical stiffness, from the physiologically relevant 1 kPa, 20 kPa to very stiff 3.5 GPa. A novel and versatile micro-electromechanical systems (Bio-MEMS) force sensor [2] is developed to quantify the strength of non-specific adhesion between living cancer cells membrane and probe, an important hallmark of cancer cell malignancy level. Immunoflurescent staining and Confocal microscopy imaging are used to visualize the cellular organelle organization and cooperate to explore the underlying mechanism.

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Raporty organizacyjne na temat "Cancer cell metastasis"

Henry, Michael. Cell Fusion and Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2008. http://dx.doi.org/10.21236/ada495341.

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Toborek, Michal J. Dietary Lipids, Cell Adhesion and Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, październik 2001. http://dx.doi.org/10.21236/ada403337.

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Toborek, Michal J. Dietary Lipids, Cell Adhesion and Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, październik 2003. http://dx.doi.org/10.21236/ada432548.

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Toborek, Michael J., Bernard Hennig i Larry W. Robertson. Dietary Lipids, Cell Adhesion and Breast Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, październik 2002. http://dx.doi.org/10.21236/ada413683.

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Lazebnik, Yuri. Cell Fusion as a Cause of Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2008. http://dx.doi.org/10.21236/ada501720.

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Lazebnik, Yuri. Cell Fusion as a Cause of Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, marzec 2009. http://dx.doi.org/10.21236/ada502565.

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Ponnazhagan, Selvarangan. Regenerative Stem Cell Therapy for Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2014. http://dx.doi.org/10.21236/ada612699.

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Ponnazhagan, Selvarangan. Regenerative Stem Cell Therapy for Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2012. http://dx.doi.org/10.21236/ada567277.

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Ponnazhagan, Selvarangan. Regenerative Stem Cell Therapy for Breast Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2013. http://dx.doi.org/10.21236/ada592352.

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Lazebnik, Yuri. Cell Fusion as a Cofactor in Prostate Cancer Metastasis. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2010. http://dx.doi.org/10.21236/ada554548.

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