Journal articles on the topic 'Isolated tumour cells'
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Carli, Camila B. de A., Djamile C. de Matos, Flávia C. M. Lopes, Danielle C. G. Maia, Maristela B. Dias, Miriam Sannomiya, Clenilson M. Rodrigues, et al. "Isolated Flavonoids against Mammary Tumour Cells LM2." Zeitschrift für Naturforschung C 64, no. 1-2 (June 1, 2009): 32–36. http://dx.doi.org/10.1515/znc-2009-1-206.
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1The purpose of the present study was to investigate antitumour and anti-inflammatory activities of flavonoids isolated from Byrsonima crassa, Davilla elliptica and Mouriri pusa. The antitumour activity was measured by the MTT assay in murine mammary tumour cells (LM2) and the IC50 values of the fl avonoids tested ranged from (31.5 ± 2.97) to (203.1 ± 5.9) μg/ml. The fl avonoids (myricetin-3-O-α-L-rhamnopyranoside) and 3 (quercetin-3-Ogalactopyranoside) from D. elliptica were the most active ones against the tumour cells. The same samples were tested to determine the inhibition of the release of nitric oxide (NO) and of the tumour necrosis factor-alpha (TNF-α) in murine macrophages by the Griess and ELISA sandwich assay, respectively. Almost all the samples showed inhibitory activity to the release of NO but not of TNF-α. Of all substances tested, flavonoids 2 (quercetin) and 6 (myricetin) may show promising activity in the treatment of murine breast cancer by immunomodulatory and antiproliferative activities.
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Sørby, Lise Aagaard, Kristin Jonsdottir, Klaus Beiske, Peter Blom, Ida Rashida Khan Bukholm, and Morten Bj Jacobsen. "Cyclin A2 Protein Overexpression Is Not Caused by Gene Amplification in Colon Cancer." ISRN Pathology 2012 (August 29, 2012): 1–7. http://dx.doi.org/10.5402/2012/691430.
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Increased expression of cyclin A2 protein has been detected in different types of cancers. However, its prognostic importance appears to differ between tumours. The significance and precise mechanisms behind cyclin A2 overexpression remain to be elucidated. We used real-time PCR to examine CCNA2 amplification in tumour cells isolated by laser microdissection and in total tumour tissue in colon cancer patients in which overexpression of cyclin A2 protein had been revealed by immunohistochemistry (n=22 patients). The results were verified by FISH. CCNA2 amplification was not detected in either the isolated tumour cells or the total tumour tissue. We verified our methods by demonstrating amplification of CCNA2 by real-time PCR in three out of eight breast tumours that overexpressed cyclin A2 protein (this frequency is consistent with the findings of others). However, FISH did not reveal any CCNA2 amplification in the breast tumours, but it did reveal polysomy of chromosome 4 or segments of chromosome 4 in three tumour tissue samples, indicating the importance of verifying the real-time PCR results with another method. To conclude, the increased cyclin A2 protein expression in these patients could not be explained by CCNA2 amplification in isolated colonic tumour cells.
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Fuhr, Abreu, Carbone, El-Athman, Bianchi, Laukkanen, Mazzoccoli, and Relógio. "The Interplay between Colon Cancer Cells and Tumour-Associated Stromal Cells Impacts the Biological Clock and Enhances Malignant Phenotypes." Cancers 11, no. 7 (July 15, 2019): 988. http://dx.doi.org/10.3390/cancers11070988.
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Cancer cells interrelate with the bordering host microenvironment that encompasses the extracellular matrix and a nontumour cellular component comprising fibroblasts and immune-competent cells. The tumour microenvironment modulates cancer onset and progression, but the molecular factors managing this interaction are not fully understood. Malignant transformation of a benign tumour is among the first crucial events in colorectal carcinogenesis. The role of tumour stroma fibroblasts is well-described in cancer, but less well-characterized in benign tumours. In the current work we utilized fibroblasts isolated from tubulovillous adenoma, which has high risk for malignant transformation, to study the interaction between benign tumour stroma and the circadian clock machinery. We explored the role of the biological clock in this interplay taking advantage of an experimental model, represented by the co-culture of colon cancer cells with normal fibroblasts or tumour-associated fibroblasts, isolated from human colorectal tumour specimens. When co-cultured with tumour-associated fibroblasts, colon cancer cells showed alterations in their circadian and metabolic parameters, with decreased apoptosis, increased colon cancer cell viability, and increased resistance to chemotherapeutic agents. In conclusion, the interactions among colon cancer cells and tumour-associated fibroblasts affect the molecular clockwork and seem to aggravate malignant cell phenotypes, suggesting a detrimental effect of this interplay on cancer dynamics.
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Lenzen, S., G. Klöppel, S. Zielmann, and U. Panten. "Secretory, enzymatic, and morphological characterization of rat pancreatic endocrine tumours induced by streptozotocin and nicotinamide." Acta Endocrinologica 109, no. 3 (July 1985): 361–68. http://dx.doi.org/10.1530/acta.0.1090361.
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Abstract. Rat pancreatic endocrine tumours were induced by administration of streptozotocin plus nicotinamide. Fifteen to eighteen months later tumours with wet weights of 0.1 to 224 mg were isolated. These tumours were compared with normal rat pancreatic islets. Insulin release from perifused tumours was stimulated by d-glucose, l-leucine, 2-ketoisocaproate, and d-glyceraldehyde, potentiated by theophylline and inhibited by norepinephrine. Compared with isolated rat pancreatic islets, however, insulin secretory responsiveness to glucose stimulation and insulin content were reduced in tumour tissue. Hypoglycaemia in tumour bearing rats and impaired diffusion of insulin out of the tumours may explain this difference. The pattern of enzyme activities observed in tumour tissue was typical for pancreatic endocrine tissue. The activities of succinate dehydrogenase, the two types of the monoamine oxidase, and α-glucosidase were in the normal range in tumour tissue. Only the activities of 5'nucleotidase and glutamate dehydrogenase were decreased. Immunocytochemical analysis of the tumours revealed that they contained an average of 91% B-cells. In addition 8% of D-cells were encountered. Proportions of A-cells and PP-cells ranged below 1%. Thus this endocrine tumour of the pancreas with a high proportion of functionally intact B-cells is an interesting model for studying regulation of secretion and endocrine tumour development.
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Rodin, William Carl Ivar, Patrik Sundström, Filip Ahlmanner, Elinor Bexe Lindskog, and Marianne Quiding Järbrink. "Potent anti-tumor effector functions in tumor-infiltrating MAIT and γδ T cells isolated from colon cancer patients." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 138.13. http://dx.doi.org/10.4049/jimmunol.202.supp.138.13.
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Abstract In colon cancer, tumor progression and patient outcome is affected by the cytokine balance in the tumors. IFNγ, TNFα and Granzyme B expression are associated with favorable patient outcome, while high IL-17 expression is associated with accelerated tumor progression. However, knowledge of the regulation and activation of unconventional T cell subsets in colon tumors is limited. The aim of this study was to characterize unconventional T cells in colon tumors and unaffected tissue, determine their capacity to produce cytokines affecting tumor progression as well as the In vitro cytotoxic capabilities of MAIT and γδ T cells. Using flow cytometry, we show that MAIT cells accumulate in colon tumors and that the frequencies of γδ T cells are reduced in the tumor epithelium. Using polyclonal stimulation, we show that IFNγ production by tumour infiltrating MAIT cells is impaired whilst tumour infiltrating γδ T have an increased expression of IFNγ, TNFα and Granzyme B. IL-17 expression was also elevated in tumour infiltrating γδ T cells, but at lower levels than the TH1 - associated cytokines. Tumor infiltrating MAIT cells had an exhausted (PD-1highTim-3+) phenotype compared to MAIT cells from unaffected tissue. Analyzing cytokine expression, we show that while no single molecule is lost the polyfunctional capacity of tumour infiltrating MAIT cells is decreased compared to MAIT cells from unaffected tissue. Altogether, this study shows that γδ T cells and MAIT cells contribute to the cytokine balance in colon tumors with a TH1 – dominated profile and that they have potent cytotoxic capacity, which may reduce tumor progression and improve patient outcome.
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Schilling, David, Tilman Todenhöfer, Jörg Hennenlotter, Christian Schwentner, Tanja Fehm, and Arnulf Stenzl. "Isolated, disseminated and circulating tumour cells in prostate cancer." Nature Reviews Urology 9, no. 8 (July 10, 2012): 448–63. http://dx.doi.org/10.1038/nrurol.2012.136.
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Joseph, Soniamol, Baby Sabulal, Varughese George, Kuttikkadan Antony, and Kainoor Janardhanan. "Antitumor and anti-inflammatory activities of polysaccharides isolated from Ganoderma lucidum." Acta Pharmaceutica 61, no. 3 (September 1, 2011): 335–42. http://dx.doi.org/10.2478/v10007-011-0030-6.
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Antitumor and anti-inflammatory activities of polysaccharides isolated fromGanoderma lucidumIn this study, polysaccharides were isolated fromGanoderma lucidum (Polyporaceae)and their antitumor and anti-inflammatory activities were investigated usingin vivomodels. Potential antitumor activity was shown byG. lucidumpolysaccharides (GLP) against solid tumor induced by Ehrlich's ascites carcinoma cells. GLP at 100 mg kg-1body mass showed 80.8 and 77.6 % reduction in tumour volume and tumour mass, respectively, when administered 24 h after tumour implantation. Again, GLP at the same dose but when administered prior to tumour inoculation, showed 79.5 and 81.2 % inhibition of tumour volume and tumour mass, respectively. GLP showed significant dose-dependent activity in carrageenean-induced (acute) and formalin-induced (chronic) inflammation assays. At 100 mg kg-1, GLP exhibited 57.6 and 58.2 % inhibition in carrageenean-induced and formalin-induced assays, respectively.
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Fossdal, Guri, Einar O. Vik-Mo, Cecilie Sandberg, Mercy Varghese, Mari Kaarbø, Emily Telmo, Iver A. Langmoen, and Wayne Murrell. "Aqp 9 and Brain Tumour Stem Cells." Scientific World Journal 2012 (2012): 1–9. http://dx.doi.org/10.1100/2012/915176.
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Several studies have implicated the aquaporins (aqp) 1, 4, and 9 in the pathogenesis of malignant brain tumours, suggesting that they contribute to motility, invasiveness, and oedema formation and facilitate metabolism in tumour cells under hypoxic conditions. We have studied the expression of aqp1, 4, and 9 in biopsies from glioblastomas, isolated tumour stem cells grown in a tumoursphere assay and analyzed the progenitor and differentiated cells from these cultures. We have compared these to the situation in normal rat brain, its stem cells, and differentiated cells derived thereof. In short, qPCR in tumour tissue showed presence of aqp1, 4, and 9. In the tumour progenitor population, aqp9 was markedly more highly expressed, whilst in tumour-derived differentiated cells, aqp4 was downregulated. However, immunostaining did not reveal increased protein expression of aqp9 in the tumourspheres containing progenitor cells; in contrast, its expression (both mRNA and protein) was high in differentiated cultures. We, therefore, propose that aquaporin 9 may have a central role in the tumorigenesis of glioblastoma.
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Tavares, A., X. Wen, J. Maciel, F. Carneiro, and M. Dinis-Ribeiro. "Occult Tumour Cells in Lymph Nodes from Gastric Cancer Patients: Should Isolated Tumour Cells Also Be Considered?" Annals of Surgical Oncology 27, no. 11 (May 4, 2020): 4204–15. http://dx.doi.org/10.1245/s10434-020-08524-4.
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Zerlauth, G., J. Wesierska-Gadek, and G. Sauermann. "Fibronectin observed in the nuclear matrix of HeLa tumour cells." Journal of Cell Science 89, no. 3 (March 1, 1988): 415–21. http://dx.doi.org/10.1242/jcs.89.3.415.
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We have investigated the intracellular distribution of insoluble fibronectin in HeLa tumour cells. By indirect immunofluorescence microscopy fibronectin was detected in the nuclear region, but not in the region of the cell surface. Isolated nuclei and isolated nuclear matrices also stained for fibronectin. By quantitative enzyme-linked immunosorbent assay (ELISA), fibronectin was found almost exclusively in the subcellular fraction of isolated nuclear matrices. Using immunoblotting techniques fibronectin was detected in nuclear matrices isolated from cells grown in standard and in fibronectin-depleted medium. The data demonstrate that fibronectin in HeLa tumour cells is preferentially associated with the nuclear matrix.
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Zayas, Yareellys Ramos, Moisés Armides Franco Molina, Reyes Tamez Guerra, and Cristina Rodríguez Padilla. "Evaluation of a canine transmissible venereal tumour cell line with tumour immunity capacity but without tumorigenic property." Journal of Veterinary Research 63, no. 2 (June 1, 2019): 225–33. http://dx.doi.org/10.2478/jvetres-2019-0024.
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AbstractIntroduction:Canine transmissible venereal tumour (CTVT) is a sexually transmitted tumour affecting dogs worldwide, imposing a financial burden on dog owners. A stable culture cell line in continuous passages for >18 months has only been achieved once. The present study investigated a stable CTVT cell line isolated from a bitch and its potential as a vaccine.Material and Methods:A biopsy from a 2-year-old mongrel bitch with CTVT was obtained for histopathological confirmation and isolation of tumour cells. The isolated cells were cultured to passage 55 and characterised by flow cytometry, with karyotyping by GTG-banding and by PCR detection of myc S-2 and LINE AS1. The isolated CTVT cell line was also used as a preventive vaccine in a canine model.Results:Histopathological analysis of the isolated tumour cells revealed typical CTVT characteristics. Constant proliferation and stable morphological characteristics were observed during culture. Phenotypic analysis determined the expression of HLA-DR+, CD5.1+, CD14+, CD45+, CD83+, CD163+, and Ly-6G-Ly-6C+. GTG-banding revealed a mean of 57 chromosomes in the karyotype with several complex chromosomal rearrangements. LINE-c-myc insertion in the isolated CTVT cell line at 550 bp was not detected. However, a 340-bp band was amplified. Isolated CTVT cell line inoculation at a concentration of 1×108did not induce tumour growth in bitches, nor did a challenge with primary CTVT cells.Conclusion:The present study successfully identified and isolated a stable CTVT cell line that may be useful in CTVT prevention.
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Treacy, Oliver, Hannah Egan, Kevin Lynch, Niamh Leonard, Kim De Veirman, Karin Vanderkerken, Laurence Egan, et al. "941 Stromal cell sialylation suppresses T cells in inflammatory tumour microenvironments: a new tumour stromal cell immune checkpoint?" Journal for ImmunoTherapy of Cancer 9, Suppl 2 (November 2021): A987. http://dx.doi.org/10.1136/jitc-2021-sitc2021.941.
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BackgroundImmunosuppressive tumour microenvironments (TME) reduce the effectiveness of immune responses in cancer. Non-haematopoietic mesenchymal stromal cells, precursors to cancer-associated fibroblasts (CAFs), dictate tumour progression by enhancing immune cell suppression. Sialic acids, which exist as terminal sugars of glycans (known as sialoglycans), are highly expressed on cancer cells and hyper-sialylation of glycans is known to promote immune evasion in cancer. Sialoglycans are recognized by sialic acid-binding immunoglobulin-like lectins (Siglecs), a family of immunomodulatory receptors, which are analogous to the immune checkpoint inhibitor PD-1.1 The role of sialyation in stromal cell-mediated immunosuppression, however, is unknown. Using models of solid (colorectal cancer - CRC) and haematological (multiple myeloma - MM) stromal-rich tumours in both mouse and human, the aim of this study was to investigate if stromal cell sialylation contributes to enhanced immunosuppression in the TME.MethodsFlow cytometric analysis of sialic acid expression was performed initially on bone marrow-derived stromal cells isolated from healthy human donor bone marrow aspirates, from wild-type Balb/c mice or from 5T33 multiple myeloma mice. Stromal cells were also isolated and expanded from colorectal cancer patient tumour biopsies (CAFs) with matched controls isolated from tumour-adjacent non-cancerous tissue (normal-associated fibroblasts - NAFs) or from whole blood from primary multiple myeloma bone aspirates. Informed consent was obtained from all patients prior to sampling. Immunosuppression assays were performed using these stromal cells with or without exposure to the tumour cell secretome from the mouse and human CRC cell lines CT26 or HCT116 and HT29, respectively, co-cultured with either murine lymphocytes or healthy human donor-derived peripheral blood mononuclear cells (PBMCs).ResultsOur results showed that tumour conditioned stromal cells have increased levels of sialyltransferase gene expression, α2,3/α2,6-linked sialic acid and Siglec ligands. Co-culture assays revealed that CAFs induced significantly higher frequencies of Siglec 7 and Siglec 9-expressing CD8 T cells, as well as Tim-3 and PD-1-expressing CD8 T cells, compared to NAFs. Inhibition of sialyltransferase activity using the inhibitor 3FAXNeu5Ac reversed these CAF-induced effects. Interestingly, sialyltransferase inhibition had no observed effects on T cells co-cultured with NAFs.ConclusionsThese results demonstrate that targeting stromal cell sialylation can reverse immune cell suppression and reactivate exhausted T cells. These novel data support a rationale for the assessment of stromal cell sialylation and Siglec ligand expression in order to better stratify patients for immunotherapeutic combination treatments that aim to reactivate exhausted T cells in stromal-enriched tumour microenvironments.AcknowledgementsThe authors would like to thank the Blood Cancer Network of Ireland Biobank for providing bone marrow aspirates.ReferenceGray MA, Stanczak MA, Mantuano NR, Xiao H, Pijnenborg JFA, Malaker SA, Miller CL, Weidenbacher PA, Tanzo JT, Ahn G, Woods EC, Läubli H, Bertozzi CR. Targeted glycan degradation potentiates the anticancer immune response in vivo. Nat Chem Biol 2020;16:1376–1384.Ethics ApprovalColorectal tumor and adjacent normal mucosal tissue were obtained from patients undergoing colon tumor resection at University Hospital Galway under an ethically approved protocol (Clinical Research Ethics Committee, Ref: C.A. 2074). Samples were collected and isolated by the Blood Cancer Network of Ireland under an ethically approved protocol. Written informed explicit consent was obtained from all patients prior to sampling. Mice were housed and maintained following the conditions approved by the Animals Care Research Ethics Committee of the National University of Ireland, Galway (NUIG) and procedures were conducted under individual and project authorisation licenses from the Health Products Regulatory Authority (HPRA) of Ireland or from the Ethical Committee for Animal Experiments, Vrije Universiteit Brussel (license no. LA1230281, 16-281-6).
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Alexandrova, Evdokia A., and Beltcho G. Beltchev. "Differences between HMG1 proteins isolated from normal and tumour cells." Biochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology 915, no. 3 (October 1987): 399–405. http://dx.doi.org/10.1016/0167-4838(87)90026-4.
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He, S., P. Li, S. He, T. Long, N. Zhang, J. Fang, and Z. Yu. "Detection of circulating tumour cells with the CellSearch system in patients with advanced-stage head and neck cancer: preliminary results." Journal of Laryngology & Otology 127, no. 8 (July 9, 2013): 788–93. http://dx.doi.org/10.1017/s0022215113001412.
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AbstractObjective:To assess the feasibility and clinical value of using the CellSearch system to detect circulating tumour cells in patients with advanced-stage head and neck squamous cell carcinoma.Methods:Circulating tumour cells were isolated and counted via positive selection utilising magnetically labelled anti-epithelial cell adhesion molecule and immunocytochemical staining for cytokeratin. The correlation between circulating tumour cell presence and clinical features was evaluated in nine patients newly diagnosed with advanced-stage (stage III or IV) head and neck squamous cell carcinoma.Results:Circulating tumour cells were detected in three of the nine patients (33 per cent). Circulating tumour cell positivity was more prevalent in node stage 2 to 3 patients (3 of 5, 60 per cent) than node stage 0 to 1 patients (0 of 4, 0 per cent). Recurrent or progressive disease was observed in only one of the six patients (17 per cent) without circulating tumour cells, compared with two of the three patients (67 per cent) with circulating tumour cells.Conclusion:In this preliminary study, circulating tumour cells were successfully isolated in patients with advanced-stage head and neck squamous cell carcinoma, using the CellSearch system. Further investigation is needed to evaluate the prognostic significance of circulating tumour cells.
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Whiteside, Theresa L. "Immune modulation of T-cell and NK (natural killer) cell activities by TEXs (tumour-derived exosomes)." Biochemical Society Transactions 41, no. 1 (January 29, 2013): 245–51. http://dx.doi.org/10.1042/bst20120265.
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Body fluids of cancer patients contain TEXs (tumour-derived exosomes). Tumours release large quantities of TEXs, and the protein content of exosome or MV (microvesicle) fractions isolated from patients’ sera is high. TEXs down-regulate functions of immune cells, thus promoting tumour progression. We isolated TEXs from tumour cell supernatants and sera of patients with solid tumours or AML (acute myelogenous leukaemia). The molecular profile of TEXs was distinct from that of circulating exosomes derived from normal cells. TEXs were co-incubated with activated T-cells, conventional CD4+CD25neg T-cells or CD56+CD16+ NK (natural killer) cells respectively. TEXs down-regulated CD3ζ and JAK3 (Janus kinase 3) expression in primary activated T-cells and mediated Fas/FasL (Fas ligand)-driven apoptosis of CD8+ T-cells. TEXs promoted CD4+CD25neg T-cell proliferation and their conversion into CD4+CD25hiFOXP3+ (FOXP3 is forkhead box P3) Treg cells (regulatory T-cells), which also expressed IL-10 (interleukin 10), TGFβ1 (transforming growth factor β1), CTLA-4 (cytotoxic T-lymphocyte antigen 4), GrB (granzyme B)/perforin and effectively mediated suppression. Neutralizing antibodies specific for TGFβ1 and/or IL-10 inhibited the ability of TEXs to expand Treg cells. TEXs obtained at diagnosis from AML patients’ sera were positive for blast-associated markers CD33, CD34, CD117 and TGFβ1, and they decreased cytotoxic activity of NK cells isolated from NC (normal control) donors, induced Smad phosphorylation and down-regulated NKG2D receptor expression. Correlations between the TEX molecular profile or TEX protein levels and clinical data in cancer patients suggest that TEX-mediated effects on immune cells are prognostically important. In contrast with exosomes released by normal cells, TEXs have immunosuppressive properties and are involved in regulating peripheral tolerance in patients with cancer.
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Rovnak, Joel, Rufina N. Casey, Connie D. Brewster, James W. Casey, and Sandra L. Quackenbush. "Establishment of productively infected walleye dermal sarcoma explant cells." Journal of General Virology 88, no. 9 (September 1, 2007): 2583–89. http://dx.doi.org/10.1099/vir.0.82967-0.
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Walleye dermal sarcoma virus (WDSV) is a complex retrovirus associated with dermal sarcomas in walleye fish. Virus expression is tightly regulated and limited to accessory gene transcripts throughout tumour development. During tumour regression, this regulation is lost and the replication of virus is greatly enhanced. Cultured walleye fibroblasts infected in vitro do not produce significant quantities of infectious virus. Tissue culture cells established by explantation of tumour cells were found to harbour WDSV provirus and to express accessory and structural proteins. The sequence of the provirus showed little variation from a previous WDSV isolate. Retroviral particles were isolated from supernatants from these cells and were able to transfer infection to uninfected walleye fibroblasts. In addition to the virus present in supernatants, much of the virus was cell associated and liberated only by sonication. This virus was found at internal cellular membranes, including mitochondria, and was infectious.
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Joseph, Robiya, Rama Soundararajan, Suhas Vasaikar, Fei Yang, Kendra L. Allton, Lin Tian, Petra den Hollander, et al. "CD8+ T cells inhibit metastasis and CXCL4 regulates its function." British Journal of Cancer 125, no. 2 (April 1, 2021): 176–89. http://dx.doi.org/10.1038/s41416-021-01338-5.
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Abstract Background The mechanism by which immune cells regulate metastasis is unclear. Understanding the role of immune cells in metastasis will guide the development of treatments improving patient survival. Methods We used syngeneic orthotopic mouse tumour models (wild-type, NOD/scid and Nude), employed knockout (CD8 and CD4) models and administered CXCL4. Tumours and lungs were analysed for cancer cells by bioluminescence, and circulating tumour cells were isolated from blood. Immunohistochemistry on the mouse tumours was performed to confirm cell type, and on a tissue microarray with 180 TNBCs for human relevance. TCGA data from over 10,000 patients were analysed as well. Results We reveal that intratumoral immune infiltration differs between metastatic and non-metastatic tumours. The non-metastatic tumours harbour high levels of CD8+ T cells and low levels of platelets, which is reverse in metastatic tumours. During tumour progression, platelets and CXCL4 induce differentiation of monocytes into myeloid-derived suppressor cells (MDSCs), which inhibit CD8+ T-cell function. TCGA pan-cancer data confirmed that CD8lowPlatelethigh patients have a significantly lower survival probability compared to CD8highPlateletlow. Conclusions CD8+ T cells inhibit metastasis. When the balance between CD8+ T cells and platelets is disrupted, platelets produce CXCL4, which induces MDSCs thereby inhibiting the CD8+ T-cell function.
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Babu Pydi, Chinna, and Satyanarayana Rentala. "An Artificial Niche for Circulating Endothelial Cells During Tumor Angiogenesis Mediated by Prostate Cancer Stem Cells." Biomedical and Pharmacology Journal 11, no. 4 (November 6, 2018): 1879–83. http://dx.doi.org/10.13005/bpj/1560.
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Angiogenesis research investigates the formation of new blood vessels in wound healing, tumour growth and embryonic development. The present paper describes the application of circulating endothelial progenitor (CEP) cells expressing CD133 and VEGFR2. To do so, the CEPs were isolated from human peripheral blood and expanded in an artificial niche using in a transwell plate. The migration, adhesion, homing and differentiation of CEPs towards prostate cancer stem cells were studied. This model is more suitable to study tumor metastasis for the development of novel therapeutics.
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Rauniyar, B. P., X. Liu, J. Shrestha, K. R. Devkota, S. Poudel, and S. Thapa. "Isolated myeloid sarcoma." Journal of Chitwan Medical College 4, no. 3 (January 20, 2015): 46–48. http://dx.doi.org/10.3126/jcmc.v4i3.11941.
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Myeloid Sarcoma (MS) is a tumour mass of myeloblasts or immature myeloid cells in an extra-medullary site. Isolated MS is a red disease found only seen in case reports. Here, we present the case of a 25years old man with bilateral cervical lymphadenopathy who was diagnosed as MS on the basis of lymph node biopsy and immunohistochemistry. There is no definite consensus on management of MS and needs prospective trials. DOI: http://dx.doi.org/10.3126/jcmc.v4i3.11941Journal of Chitwan Medical College 2014; 4(3):46-48
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Clarke, B., MH Schmidt, and GE Pickett. "P.043 Presence of infiltrative glioblastoma cells in an isolated area of diffusion restriction." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 44, S2 (June 2017): S24—S25. http://dx.doi.org/10.1017/cjn.2017.128.
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Background: Diffusion weighted imaging (DWI) has useful diagnostic and predictive value in the assessment of glial tumors. Most studies evaluating the use of DWI in glioblastomas have done so in regions that overlap with abnormal T2/fluid attenuation inversion recovery (FLAIR) signal or contrast enhancement. Isolated DWI abnormalities, which do not overlap with contrast enhancing lesions, are less commonly described. Their relationship with the tumour, and implications for prognosis, are not well understood, though it has been speculated that these lesions may represent infiltrative tumour cells. To our knowledge, this is the first reported case where the presence of infiltrative tumour cells in an area of diffusion restriction has been confirmed via biopsy. Methods: A ring enhancing lesion and isolated DWI hyperintensity from a newly diagnosed patient were biopsied separately. Results: Pathological specimens from both targets were identified as glioblastoma (WHO Grade IV), negative for IDH-1 R132H mutation, with methylated MGMT promoter. Conclusions: In patients with glioblastoma, DWI hyperintensities distant from areas of abnormal T2/FLAIR or contrast enhancement can contain infiltrative tumour cells. The presence of isolated diffusion restriction may be a useful predictor of disease progression and prognosis but further investigation into the nature and behavior of isolated DWI lesions is required.
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Stocco, D. M., and M. W. Kilgore. "Induction of mitochondrial proteins in MA-10 Leydig tumour cells with human choriogonadotropin." Biochemical Journal 249, no. 1 (January 1, 1988): 95–103. http://dx.doi.org/10.1042/bj2490095.
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The side-chain cleavage of cholesterol is the rate-limiting enzymic step in steroidogenesis and occurs in the mitochondria of steroid-producing tissues. In these studies, the effect of acute stimulation of MA-10 Leydig-tumour cells on the synthesis of mitochondrial proteins was investigated. Cells were incubated in the presence of stimulating levels of human choriogonadotropin (hCG) and [35S]methionine for 2 h periods. Mitochondria were isolated and their proteins analysed by two-dimensional polyacrylamide-gel electrophoresis and fluorography. At least three mitochondrial-specific proteins were found in cells exposed to gonadotropin, and these proteins were also found in cells treated with dibutyryl cyclic AMP (db cyclic AMP). The appearance of these proteins was prevented by the addition of cycloheximide to the cells, as was the production of progesterone, the major steroid produced in MA-10 cells. In addition, mitochondria isolated from cells stimulated with db cyclic AMP produced progesterone at a rate 3-fold greater than mitochondria isolated from control cells during 3 h of incubation. Lastly, mixing experiments demonstrated that sonicated mitochondria isolated from db cyclic AMP-treated cells stimulated progesterone production in control mitochondria 6-fold. These studies show that hCG and db cyclic AMP stimulation of MA-10 cells results in the rapid induction of cycloheximide-sensitive proteins located in the mitochondria which may be instrumental in the acute regulation of steroidogenesis.
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Marques, Pedro, Sayka Barry, Eivind Carlsen, David Collier, Amy Ronaldson, Sherine Awad, Neil Dorward, et al. "Pituitary tumour fibroblast-derived cytokines influence tumour aggressiveness." Endocrine-Related Cancer 26, no. 12 (December 2019): 853–65. http://dx.doi.org/10.1530/erc-19-0327.
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Tumour-associated fibroblasts (TAFs) are key elements of the tumour microenvironment, but their role in pituitary neuroendocrine tumours (PitNETs) has been little explored. We hypothesised that TAF-derived cytokines may play a role in tumour aggressiveness and that their release can be inhibited by somatostatin analogues. TAFs were isolated and cultured from 16 PitNETs (11 clinically non-functioning tumours and 5 somatotropinomas). The fibroblast secretome was assessed with a 42-plex cytokine array before and after multiligand somatostatin receptor agonist pasireotide treatment. Angiogenesis and epithelial-to-mesenchymal transition pathway assessment included CD31, E-cadherin and ZEB1 expression. GH3 cells treated with TAF- or skin fibroblast-conditioned medium were assessed for migration, invasion and cell morphology changes. PitNET TAFs secreted significant amounts of cytokines including CCL2, CCL11, VEGF-A, CCL22, IL-6, FGF-2 and IL-8. TAFs from PitNETs with cavernous sinus invasion secreted higher IL-6 levels compared to fibroblasts from non-invasive tumours (P = 0.027). Higher CCL2 release from TAFs correlated with more capillaries (r = 0.672, P = 0.004), and TAFs from PitNETs with a higher Ki-67 tended to secrete more CCL2 (P = 0.058). SST1 is the predominant somatostatin receptor in TAFs, and pasireotide decreased TAF-derived IL-6 by 80% (P < 0.001) and CCL2 by 35% (P = 0.038). GH3 cells treated with TAF-conditioned medium showed increased migration and invasion compared to cells treated with skin fibroblast-conditioned medium, with morphological and E-cadherin and ZEB1 expression changes suggesting epithelial-to-mesenchymal transition. TAF-derived cytokines may increase PitNET aggressiveness, alter angiogenesis and induce epithelial-to-mesenchymal transition changes. Pasireotide’s inhibitory effect on TAF-derived cytokines suggest that this effect may play a role in its anti-tumour effects.
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Thomsen, Jorn Bo, Jens Ahm Sorensen, and Annelise Krogdahl. "Sentinel lymph nodes in cancer of the oral cavity - isolated tumour cells." Journal of Oral Pathology and Medicine 34, no. 2 (February 2005): 65–69. http://dx.doi.org/10.1111/j.1600-0714.2004.00289.x.
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Patani, Neill, and Kefah Mokbel. "Clinical significance of sentinel lymph node isolated tumour cells in breast cancer." Breast Cancer Research and Treatment 127, no. 2 (April 1, 2011): 325–34. http://dx.doi.org/10.1007/s10549-011-1476-4.
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Rakover, Yoseph, Michael Bennett, Rephael David, and Gabriel Rosen. "Isolated extramedullary plasmacytoma of the true vocal fold." Journal of Laryngology & Otology 114, no. 7 (July 2000): 540–42. http://dx.doi.org/10.1258/0022215001906093.
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We report a rare case of isolated extramedullary plasmacytoma (EMP) of the right true vocal fold in a 38-year-old male with a one-year history of hoarseness. Immunohistochemical staining of plasma cells in the tumour, showed over 90 per cent of them to be positive for kappa light chains. After two attempts at local surgical excision and recurrence within 10 months, the tumour was irradiated.Only seven reported cases of isolated EMP of the true vocal fold are reported in the literature. The therapeutic options are discussed.
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Lakshmi, S., G. Padmaja, and P. Remani. "Antitumour Effects of Isocurcumenol Isolated from Curcuma zedoaria Rhizomes on Human and Murine Cancer Cells." International Journal of Medicinal Chemistry 2011 (March 2, 2011): 1–13. http://dx.doi.org/10.1155/2011/253962.
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Curcuma zedoaria belonging to the family Zingiberaceae has been used in the traditional system of medicine in India and Southwest Asia in treating many human ailments and is found to possess many biological activities. The rationale of the present study was to isolate, identify, and characterize antitumour principles from the rhizomes of Curcuma zedoaria, to assess its cytotoxic effects on human and murine cancer cells, to determine its apoptosis inducing capacity in cancer cells, and to evaluate its tumour reducing properties in in vivo mice models. Isocurcumenol was characterized as the active compound by spectroscopy and was found to inhibit the proliferation of cancer cells without inducing significant toxicity to the normal cells. Fluorescent staining exhibited the morphological features of apoptosis in the compound-treated cancer cells. In vivo tumour reduction studies revealed that a dose of 35.7 mg/kg body weight significantly reduced the ascitic tumour in DLA-challenged mice and increased the lifespan with respect to untreated control mice.
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Jelinek, F., J. Felsberg, and M. Mestan. "Familial incidence of mammary gland tumours in the Djungarian hamster (Phodopus sungaros): a case report." Veterinární Medicína 58, No. 8 (September 24, 2013): 442–48. http://dx.doi.org/10.17221/6985-vetmed.
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Tumours of the mammary gland were diagnosed in one female Djungarian hamster (Phodopus sungaros) and in two of her daughters from two litters. Altogether, five tumours were diagnosed. Three of them were adenocarcinomas, one was adenoma with disseminated foci of adenocarcinoma and one was diagnosed as an atypical fibrosarcoma derived from cutaneous ganglion cell-like cells. This was a recurrent tumour in the proximity of the previously extirpated adenocarcinoma. Using specific PCR primers for conserved regions of the mouse mammary tumour virus (MMTV) no endogenous provirus DNA could be detected in DNA samples isolated from formalin-fixed paraffin embedded tissue sections.
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Pink, Ryan Charles, Areeg A. Elmusrati, Daniel Lambert, and David Raul Francisco Carter. "Royal Society Scientific Meeting: Extracellular vesicles in the tumour microenvironment." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1737 (November 20, 2017): 20170066. http://dx.doi.org/10.1098/rstb.2017.0066.
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Cancer cells do not grow as an isolated homogeneous mass; tumours are, in fact, complex and heterogeneous collections of cancer and surrounding stromal cells, collectively termed the tumour microenvironment. The interaction between cancer cells and stromal cells in the tumour microenvironment has emerged as a key concept in the regulation of cancer progression. Understanding the intercellular dialogue in the tumour microenvironment is therefore an important goal. One aspect of this dialogue that has not been appreciated until recently is the role of extracellular vesicles (EVs). EVs are small vesicles released by cells under both normal and pathological conditions; they can transfer biological molecules between cells leading to changes in phenotype. EVs have emerged as important regulators of biological processes and can be dysregulated in diseases such as cancer; rapidly growing interest in their biology and therapeutic potential led to the Royal Society hosting a Scientific Meeting to explore the roles of EVs in the tumour microenvironment. This cross-disciplinary meeting explored examples of how aberrant crosstalk between tumour and stromal cells can promote cancer progression, and how such signalling can be targeted for diagnostic, prognostic and therapeutic benefit. In this review, and the special edition of Philosophical Transactions of the Royal Society B that follows, we will provide an overview of the content and outcomes of this exciting meeting. This article is part of the discussion meeting issue ‘Extracellular vesicles and the tumour microenvironment’.
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Kobayashi, S., and J. Sayato-Suzuki. "Isolation of mouse isometallothioneins. A comparison of isometallothioneins in growing cells and post-mitotic cells." Biochemical Journal 251, no. 3 (May 1, 1988): 649–55. http://dx.doi.org/10.1042/bj2510649.
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Mouse metallothioneins (MTs) were separated into three isoforms by an anion-exchange h.p.l.c. column; conventionally isolated MT-1 and MT-2 showed a single peak (MT-1-1) and two peaks (MT-2-1 and MT-2-2), respectively. In growing cells, developing hepatocytes and growing tumour cells, MT-1/MT-2 ratios were less than 0.6, irrespective of the type of MT inducer, whereas adult liver post-mitotic cells had a ratio of more than 1.0. A large amount of the MT-2-2 subfraction was found in dexamethasone-treated FM3A cells; 90% of MTs was MT-2-2, suggesting that glucocorticoid hormone mainly induces MT-2-2 in tumour cells.
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Alotaibi, Faizah, Mark Vincent, Weiping Min, and James Koropatnick. "498 Downregulation of CD5 in CD8+ T tumour-infiltrating lymphocytes associates with increased level of activation and exhaustion." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A533. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0498.
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BackgroundCD5, a member of the scavenger receptor cysteine-rich superfamily, is a marker for T cells and a subset of B cells (B1a). CD5 associates with T-cell and B-cell receptors and impair TCR signaling1 2 and increased CD5 is an indication of B cell activation. Furthermore, CD5 levels on CD8+ T cell splenocytes were significantly increased after TCR/CD3 stimulation using ex vivo treatment with anti-CD3/anti-CD28 MAbs compared to non-stimulated CD8+ T splenocytes.3 Previous studies have shown a correlation between CD5 and anti-tumour immunity where CD5 knockout mice inoculated with B16F10 melanoma cells had delayed tumour growth compared to wild type mice.4 In tumour-infiltrating lymphocytes (TILs) isolated from lung cancer patients, CD5 levels were negatively correlated with anti-tumour activity and tumour-mediated activation-induced T cell death,5 suggesting that CD5 could impair activation of anti-tumour T cells. However, the correlation between CD5 level expression and T cell activation and exhaustion in the tumour microenvironment and in peripheral organs is ill-defined and requires further investigation.MethodsWe determined CD5 levels in T cell subsets in different organs in mice bearing syngeneic 4T1 breast tumour homografts and assessed the relationship between CD5 and increased CD69 and PD-1 (markers of T cell activation and exhaustion) by flow cytometry.ResultsWe report that T cell CD5 levels were higher in CD4+ T cells than in CD8+ T cells in 4T1 tumour-bearing mice, and that high CD5 levels on CD4+ T cells were maintained in peripheral organs (spleen and lymph nodes). However, both CD4+ and CD8+ T cells recruited to tumours had reduced CD5 compared to CD4+ and CD8+ T cells in peripheral organs. In addition, CD5highCD4+ T cells and CD5highCD8+ T cells from peripheral organs exhibited higher levels of activation and associated exhaustion compared to CD5lowCD4+ T cell and CD5lowCD8+ T cell from the same organs. Interestingly, CD8+ T cells among TILs and downregulated CD5 were activated to a higher level, with concomitantly increased exhaustion markers, than CD8+CD5+ TILs.ConclusionsThus, differential CD5 levels among T cells in tumours and lymphoid organs can be associated with different levels of T cell activation and exhaustion, suggesting that CD5 may be a therapeutic target for immunotherapeutic activation in cancer therapy.AcknowledgementsThe author thanks Rene Figueredo and Ronak Zareardalan for their assistance in animal workEthics ApprovalThis study was approved by the Animal Use Subcommittee of the University of Western OntarioReferencesAzzam HS, et al., Fine tuning of TCR signaling by CD5. The Journal of Immunology 2001. 166(9): p. 5464–5472.Voisinne GA, Gonzalez de Peredo and Roncagalli R. CD5, an undercover regulator of TCR signaling. Frontiers in Immunology 2018;9:p. 2900.Alotaibi, F., et al., CD5 blockade enhances ex vivo CD8+ T cell activation and tumour cell cytotoxicity. European journal of immunology 2020;50(5): p. 695–704.Tabbekh, M., et al., Rescue of tumor-infiltrating lymphocytes from activation-induced cell death enhances the antitumor CTL response in CD5-deficient mice. The Journal of Immunology, 2011. 187(1): p. 102–109.Dorothée, G., et al., In situ sensory adaptation of tumor-infiltrating T lymphocytes to peptide-MHC levels elicits strong antitumor reactivity. The Journal of Immunology 2005;174(11): p. 6888–6897.
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Lopes, Cláudia, Paulina Piairo, Alexandre Chícharo, Sara Abalde-Cela, Liliana R. Pires, Patrícia Corredeira, Patrícia Alves, Laura Muinelo-Romay, Luís Costa, and Lorena Diéguez. "HER2 Expression in Circulating Tumour Cells Isolated from Metastatic Breast Cancer Patients Using a Size-Based Microfluidic Device." Cancers 13, no. 17 (September 3, 2021): 4446. http://dx.doi.org/10.3390/cancers13174446.
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HER2 is a prognostic and predictive biomarker in breast cancer, normally assessed in tumour biopsy and used to guide treatment choices. Circulating tumour cells (CTCs) escape the primary tumour and enter the bloodstream, exhibiting great metastatic potential and representing a real-time snapshot of the tumour burden. Liquid biopsy offers the unique opportunity for low invasive sampling in cancer patients and holds the potential to provide valuable information for the clinical management of cancer patients. This study assesses the performance of the RUBYchip™, a microfluidic system for CTC capture based on cell size and deformability, and compares it with the only FDA-approved technology for CTC enumeration, CellSearch®. After optimising device performance, 30 whole blood samples from metastatic breast cancer patients were processed with both technologies. The expression of HER2 was assessed in isolated CTCs and compared to tissue biopsy. Results show that the RUBYchipTM was able to isolate CTCs with higher efficiency than CellSearch®, up to 10 times more, averaging all samples. An accurate evaluation of different CTC subpopulations, including HER2+ CTCs, was provided. Liquid biopsy through the use of the RUBYchipTM in the clinic can overcome the limitations of histological testing and evaluate HER2 status in patients in real-time, helping to tailor treatment during disease evolution.
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Evans, P. M., D. K. Suker, and I. ap Gwynn. "Expression of anionic sites on tumour cells at different stages of tissue invasion in vivo: a comparative study by X-ray microanalysis." Journal of Cell Science 94, no. 3 (November 1, 1989): 561–66. http://dx.doi.org/10.1242/jcs.94.3.561.
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Quantification of colloidal iron hydroxide (CIH) labelling by X-ray microanalysis was used to investigate anionic sites at the surface of Ehrlich carcinoma cells from different locations in the mouse host. Individual tumour cells from peritoneal ascites suspensions (pre-invasion stage) varied up to threefold in their ability to bind CIH and a similar degree of intra-tumour heterogeneity was observed in different experimental animals. Pretreatment of the cells with neuraminidase confirmed that binding was at least partly due to surface sialic acid. Invasive cells isolated from mesenteric tumour nodules were also heterogeneous with regard to the availability of surface anionic sites, as were tumour cells adhering to the surface of the mesentery; however, in both these populations CIH binding was significantly greater on average than for free ascites tumour cells. The results suggest that surface anionic sites are determinants of the invasiveness of malignant cells in vivo, and that both the number and topography of these sites may be important in modulating tumour cell behaviour.
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Coleto, A. F., T. M. Wilson, N. P. Soares, L. F. Gundim, I. P. Castro, E. C. Guimarães, M. B. Bandarra, and A. A. Medeiros-Ronchi. "Prognostic Value of Occult Isolated Tumour Cells within Regional Lymph Nodes of Dogs with Malignant Mammary Tumours." Journal of Comparative Pathology 158 (January 2018): 32–38. http://dx.doi.org/10.1016/j.jcpa.2017.11.001.
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Morcavallo, Alaide, Karen Barker, Colin Kwok, Jessica K. R. Boult, Patricia Benites Goncalves da Silva, Konstantin Okonechnikov, Marc Zuckermann, et al. "MODL-02. A novelCre-conditionalcMYC-driven MB Group 3 transgenic mouse model shows traceable leptomeningeal dissemination." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i168. http://dx.doi.org/10.1093/neuonc/noac079.625.
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Abstract Medulloblastoma (MB), the most common embryonal tumour of the Central Nervous System, occurs in the cerebellum. Treatment regimens involve surgery, craniospinal radiotherapy, and chemotherapy. The greatest mortality is associated with disseminated disease, almost exclusively found in the leptomeningeal space. Unfortunately, knowledge about the aetiology of MB spread is limited and the need for kinder and efficacious therapy remains an unmet goal. Of the four molecular classified MB groups, Group3 (Gr3) MB presents with a high frequency of metastasis at diagnosis, with the worst overall survival. Gr3 MB tumours are dominated by primitive progenitor-like cells and cMYC deregulation; often, p53 deficiency is observed at relapse. To dissect the biology of primary and metastatic Gr3 MB, we have developed a new germline genetically engineered mouse model (GEMM), harbouring cMYC amplification in a Tamoxifen-inducible p53 functional background (Trp53ERTAM strain). A novel LSL-cMYC-CopGFP-Luciferase transgene was integrated into the Rosa-26 locus of the mouse genome. Transgenic mice were crossed with a strain expressing Cre recombinase under the Blbp promoter targeting embryonic neural progenitors, and subsequently bred to Trp53ERTAM mice. As result, the cMYC overexpression was sufficient to generate tumours. Tumour penetrance was observed in all the expected tumour bearing genotypes, with increased aggressiveness in a non-functional p53 background. Bioluminescence imaging demonstrated tumour onset in the brain and dissemination along the spinal cord. CopGFP positive tumour cells were isolated from primary and metastatic tumours. Pathological interrogation confirmed that tumours present large cell/anaplastic (LCA) histology. Analysis of preliminary transcriptional profiling data proved that tumours cluster with human Gr3 MB. Ongoing methylation profiling and multi-omics approaches will inform on the tumour cells of origin and clonal divergence of primary tumour versus metastasis. In conclusion, we have successfully developed a novel immunocompetent mouse model of metastatic Gr3 MB with which we can investigate therapeutic vulnerabilities of MB.
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Quesada, A. R., F. Sanchez-Jimenez, J. Perez-Rodriguez, J. Marquez, M. A. Medina, and I. Nuñez de Castro. "Purification of phosphate-dependent glutaminase from isolated mitochondria of Ehrlich ascites-tumour cells." Biochemical Journal 255, no. 3 (November 1, 1988): 1031–35. http://dx.doi.org/10.1042/bj2551031.
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Phosphate-dependent glutaminase was purified to homogeneity from isolated mitochondria of Ehrlich ascites-tumour cells. The enzyme had an Mr of 135,000 as judged by chromatography on Sephacryl S-300. SDS/polyacrylamide-gel electrophoresis displayed two protein bands, with Mr values of 64,000 and 56,000. Two major immunoreactive peptides of Mr values of 65,000 and 57,000 were found by immunoblot analysis using anti-(rat kidney glutaminase) antibodies. The concentration-dependences for both glutamine and phosphate were sigmoidal, with S0.5 values of 7.6 mM and 48 mM, and Hill coefficients of 1.5 and 1.6, respectively. The glutaminase pH optimum was 9. The activation energy of the enzymic reaction was 58 kJ/mol. The enzyme showed a high specificity towards glutamine. A possible explanation for the different kinetic behaviour found for purified enzyme and for isolated mitochondria [Kovacević (1974) Cancer Res. 34, 3403-3407] should be that a conformational change occurs when the enzyme is extracted from the mitochondrial inner membrane.
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Cserni, G. "Isolated tumour cells versus micrometastases and non-sentinel node involvement in breast cancer." European Journal of Surgical Oncology (EJSO) 35, no. 8 (August 2009): 897–98. http://dx.doi.org/10.1016/j.ejso.2008.12.004.
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Ojugo, ASE, PMJ McSheehy, M. Stubbs, G. Alder, CL Bashford, RJ Maxwell, MO Leach, IR Judson, and JR Griffiths. "Influence of pH on the uptake of 5-fluorouracil into isolated tumour cells." British Journal of Cancer 77, no. 6 (March 1998): 873–79. http://dx.doi.org/10.1038/bjc.1998.144.
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Ruoslahti, E. "Vascular zip codes in angiogenesis and metastasis." Biochemical Society Transactions 32, no. 3 (June 1, 2004): 397–402. http://dx.doi.org/10.1042/bst0320397.
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In vivo screening of phage-displayed peptide libraries has revealed extensive molecular differences in the blood vessels of individual normal tissues. Pathological lesions also put their signature on the vasculature; in tumours, both blood and lymphatic vessels differ from normal vessels. The changes that characterize tumour blood vessels include selective expression of certain integrins. Peptides isolated by in vivo phage display for homing to tumours have been shown to be useful in directing therapeutic agents to experimental tumours. The targeting can enhance the efficacy of the therapy while reducing side effects. Phage screening has also revealed lung-specific vascular markers that promote tumour metastasis to the lungs by mediating specific adherence of tumour cells to the lung vasculature. These phage-screening studies have revealed a previously unsuspected degree of vascular specialization and provide potentially useful guidance devices for targeted therapies.
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Politano, Amanda, Martin Butcher, Melec Zeadin, Peter Gross, Nima Vaezzadeh, and Stephen G. Shaughnessy. "Targeted Knockdown of Tissue Factor in B16F10 Melanoma Cells suppresses their Ability to Metastasize to Bone and cause cancellous Bone Loss." Cancer Growth and Metastasis 3 (January 2010): CGM.S5229. http://dx.doi.org/10.4137/cgm.s5229.
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In this study, we use a well-defined mouse model to examine tissue factor's (TF) role in osteolytic bone metastasis. C57BL/6 mice received either mock siRNA-transfected or TF-specific siRNA-transfected B16F10 melanoma cells by left ventricular injection. A third group served as an age-matched control and did not receive any tumour cells. The effect on tumour burden and bone strength was then determined 14 days later by using bone histomorphometry and biomechanical testing. Based on histomorphometric analysis of the femurs, mice receiving TF-specific siRNA-transfected tumour cells had significantly reduced tumour burden as compared to those from mice that received mock siRNA-transfected tumour cells (2.20 ± 0.58% vs. 9.18 ± 2.20%). Furthermore, the femurs from mice receiving TF siRNA-transfected tumour cells displayed decreased osteoclast surface and consequently, increased cancellous bone volume and strength when compared to those isolated from mice that were injected with mock-transfected tumour cells. More importantly, no differences in osteoclast surface or cancellous bone volume and strength were observed when the femurs of mice that received TF siRNA-transfected tumour cells were compared to control mice that did not receive tumour cells. Based on these findings, we conclude that the expression of TF by tumour cells promotes their ability to metastasize to bone, thereby facilitating tumour cell—induced cancellous bone loss.
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Sun, Honglei, Mei Qin, Yihong Xiao, Feng Yang, Wei Ni, and Sidang Liu. "Haemangiomas, leiomyosarcoma and myeloma caused by subgroup J avian leukosis virus in a commercial layer flock." Acta Veterinaria Hungarica 58, no. 4 (December 1, 2010): 441–51. http://dx.doi.org/10.1556/avet.58.2010.4.5.
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An outbreak of simultaneously occurring haemangiomas, leiomyosarcoma and myeloma was observed in a commercial layer flock in China. The sick chickens were extremely thin and dehydrated. Scattered haemangiomas were found on the claws, breast and wings. At necropsy, haemangiomas and some other nodular tumours were also found in the internal organs. In addition, diffuse enlargement of the liver and spleen appeared in some birds. Histopathologically, haemangiomas were typically cavernous haemangiomas and haemangioendothelioma. In the diffusely swollen liver and spleen, multifocal or widespread marrow tumour cells filled with ball-like acidophilic particles in cytosol were observed, which are the characteristic pathological changes of avian myelocytomatosis. The nodular tumour cells formed by muscle bundles were of variable size, irregular shape, poorly differentiated and malaligned. Immunohistochemistry for vimentin, cytokeratin, actin (smooth muscle) and actin (sarcomeric) and Masson’s staining confirmed the different cell lineage of the nodular tumour, thus leading to the diagnosis of leiomyosarcoma. The seroprevalence of avian leukosis subgroup J (ALV-J) antibodies was 13.46% (7/52), while ALV-A/B and reticuloendotheliosis virus (REV) antibodies were not detectable. The DF-1 cells inoculated by virus extracted from liver samples from 24 infected chickens were cultured and the group-specific antigen (GSA) was identified by ELISA. All samples were positive for ALV, which was further identified as ALV-J by immunofluorescence assay (IFA). PCR analysis revealed that three isolates of ALV-J proviral sequence were close to the HPRS-103 prototype strain and other Chinese field strains isolated in recent years, while one isolate (DP01) had a lower homology with them. This is the first report that ALV-J infection caused the simultaneous occurrence of haemangiomas, leiomyosarcoma and myeloma in a commercial layer flock.
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Hubbard, S., and C. E. Gargett. "417. In vivo and in vitro evidence for cancer stem cells in human endometrial cancer." Reproduction, Fertility and Development 20, no. 9 (2008): 97. http://dx.doi.org/10.1071/srb08abs417.
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Cancer stem cells (CSCs) have been identified in solid human cancers, including breast, colon, and ovary. Recent evidence suggests that the highly regenerative human endometrium harbors rare populations of epithelial stem/progenitor cells1. We hypothesised that CSCs are responsible for the epithelial neoplasia associated with endometrial carcinoma (EC), the most common gynaecological malignancy in women. The aim of this study was to demonstrate that a rare population of EC cells posses CSC properties. Stem cell characteristics were assessed in 25 EC and 2 endometrial hyperplasia tissues obtained from women aged 62 ± 9 yrs. Samples were cultured at clonal densities (100–500 cells/cm2) for 3–5 wks to determine cloning efficiency. Individual clones were serially subcloned (<10 cells/cm2) every 2–4 wks to determine self renewal capacity. Isolated cells in serial dilution (103–106 cells) were placed under the kidney capsule of immunocompromised mice for 12–16 wks to examine for the presence of tumour initiating cells (TIC). Resulting tumours and original parent tumours were examined for markers by immunohistochemistry. Most samples (23/26) contained rare colony forming cells. The cloning efficiency was 0.23% ± 0.28% (n = 11) in G1, 0.78% ± 0.67% (n = 8) in G2, 0.22% ± 0.21% (n = 3) in G3, 0.03% (n = 2) in type II tumours, and 0.14% (n = 2) in hyperplasia samples, and did not differ significantly between grades or between type I EC and normal endometrial epithelial samples 1. Single cell derived clones subcloned 2.5 ± 1.4 (n = 11), 3.2 ± 0.4 (n = 5), 3.5 (n = 2), 3.0 ± 1.7 (n = 3), and 2.5 (n = 2) times in G1, G2, G3, type II tumours and hyperplasia samples respectively, indicating increasing self renewal capacity with increasing tumour grade. Transplanted EC single cell suspensions initiated tumour growth with similar morphology, ERα, PR, EpCAM, cytokeratin, and vimentin expression as the parent tumour, indicating the presence of TIC. This evidence suggests that rare cells possessing the CSC properties of clonogenicty, self renewal, and tumorigenicity, may be responsible for the initiation and progression of EC. (1) Chan RWS et al. (2004). Biology of Reproduction. 70:1738–1750
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Brown, Jo, Malik Zaben, Florian Siebzehnrubl, and William P Gray. "HiSpots®: A novel ex vivo patient-derived 3D model of glioblastoma." Neuro-Oncology 21, Supplement_4 (October 2019): iv17. http://dx.doi.org/10.1093/neuonc/noz167.075.
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Abstract There are limited chemotherapeutic options for glioblastoma, which contributes to its poor prognosis. Established cell lines have many phenotypic differences from their original tumours, and drugs showing success in animal models often fail to translate to humans. HiSpots® aim to provide a representative 3D in vitro model of glioblastoma using ex vivo human tumour samples, suitable for mechanistic studies. HiSpots® are a high-density 3D cell culture technique. Cancer and microenvironment cells are mechanically and enzymatically isolated from fresh resected or biopsied tumours, seeded onto PTFE membranes and cultured on an air-liquid interface. Cultures were stained for beta-III tubulin (TUJ1), glial fibrillary acidic protein (GFAP), nestin, and ionized calcium binding adapter molecule 1 (IBA1) to identify tumour cells and microglia. Serum-containing and serum-free media were compared. HiSpots® were created at three densities: low, medium and high, for comparison. Medium density HiSpots® best supported TUJ1+GFAP+Nestin+ tumour cells, and the density did not affect the proportion of microglia. Medium and high density HiSpots® formed multiple cell layers, creating structures up to 40μm thick with variable cell type distribution. Medium and high density HiSpots® and tumour cells were best supported in serum-free media. Medium density HiSpots® cultured in serum-free media have been demonstrated as the best choice to support the heterogeneity of glioblastoma. These HiSpots® contain mostly tumour cells and microglia. HiSpots® therefore allow for the culture of human glioblastoma cells, including microenvironmental microglia. These HiSpot® models will be evaluated as a model for mechanistic studies in the future.
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Smith, Adam J., Peter J. Gawne, Michelle T. Ma, Philip J. Blower, Richard Southworth, and Nicholas J. Long. "Synthesis, gallium-68 radiolabelling and biological evaluation of a series of triarylphosphonium-functionalized DO3A chelators." Dalton Transactions 47, no. 43 (2018): 15448–57. http://dx.doi.org/10.1039/c8dt02966k.
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Wu, Z., G. Wang, D. Pan, Y. Guo, X. Zeng, Y. Sun, and J. Cao. "Inflammation-related pro-apoptotic activity of exopolysaccharides isolated from Lactococcus lactis subsp. lactis." Beneficial Microbes 7, no. 5 (November 30, 2016): 761–68. http://dx.doi.org/10.3920/bm2015.0192.
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Exopolysaccharides (EPS) have attracted attention recently for possible use in suppressing early stage breast cancer. In this study, a mannan EPS produced by Lactococcus lactis subsp. lactis was found to affect the production of inflammatory cytokines. EPS (300 μg/ml) can significantly enhance tumour necrosis factor alpha and inducible NO synthase release in MCF-7 cells compared to control cells in a concentration-dependent manner. Also the intracellular calcium level was found to increase with the concentration of EPS. After EPS-treatment, a significant reduction in mitochondrial potential was observed, as was nuclear condensation and cell shrinkage. These results may be helpful in further understanding the anti-tumour properties of lactic acid bacteria.
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Molina, M., J. A. Segura, J. C. Aledo, M. A. Medina, I. Núnez de Castro, and J. Márquez. "Glutamine transport by vesicles isolated from tumour-cell mitochondrial inner membrane." Biochemical Journal 308, no. 2 (June 1, 1995): 629–33. http://dx.doi.org/10.1042/bj3080629.
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Mitochondrial-inner-membrane vesicles, isolated from Ehrlich ascites carcinoma cells by titration with detergents, accumulated L-glutamine by a very efficient transport system. The vesicles lack any phosphate-activated glutaminase activity, allowing measurement of transport rates without interference by L-glutamine metabolism. The time course of the transport was linear for the first 60 s, reaching a steady state after 120 min. L-Glutamine transport showed co-operativity, with a Hill coefficient of 2.2; the kinetic parameters S0.5 and Vmax had values of 5 mM and 26 nmol/30 s per mg of protein respectively. The pH-dependence curve showed a bell shape, with a pH optimum about 8.0. The uptake of L-glutamine was not affected by the presence of a 50-fold molar excess of D-glutamine, L-cysteine, L-histidine, L-alanine, L-serine and L-leucine, whereas L-glutamate behaved as a poor inhibitor. The structural analogue L-glutamate gamma-hydroxamate (5mM) inhibited the net uptake by 68%; interestingly, other analogues (6-diazo-5-oxo-L-norleucine, acivicin and L-glutamate gamma-hydrazide) were ineffective. The impermeant thiol reagent p-chloromercuriphenylsulphonic acid (0.5mM) completely abolished the mitochondrial L-glutamine uptake; in contrast, other thiol reagents (mersalyl and N-ethylmaleimide) did not significantly affect the transport. These data confirm the existence of a specific transport system with high capacity for L-glutamine in the mitochondrial inner membrane, a step preceding the highly operative glutaminolysis in tumour cells.
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Wu, Feng, Fuxingzi Li, Xiao Lin, Feng Xu, Rong-Rong Cui, Jia-Yu Zhong, Ting Zhu, et al. "Exosomes increased angiogenesis in papillary thyroid cancer microenvironment." Endocrine-Related Cancer 26, no. 5 (May 2019): 525–38. http://dx.doi.org/10.1530/erc-19-0008.
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Tumour-derived exosomes under hypoxic conditions contain informative miRNAs involved in the interaction of cancer and para-carcinoma cells, thus contributing to tissue remodelling of the tumour microenvironment (TME). Exosomes isolated from hypoxic papillary thyroid cancer cells, BCPAP cells and KTC-1 cells enhanced the angiogenesis of human umbilical vein endothelial cells (HUVECs) compared with exosomes isolated from normal thyroid follicular cell line (Nthy-ori-3-1), normoxic BCPAP or KTC-1 cells both in vitro and in vivo. miR-21-5p was significantly upregulated in exosomes from papillary thyroid cancer BCPAP cells under hypoxic conditions, while the exosomes isolated from hypoxic BCPAP cells with knockdown of miR-21-5p attenuated the promoting effect of angiogenesis. In addition, our experiment revealed that miR-21-5p directly targeted and suppressed TGFBI and COL4A1, thereby increasing endothelial tube formation. Furthermore, elevated levels of exosomal miR-21-5p are found in the sera of papillary thyroid cancer patients, which promote the angiogenesis of HUVECs. Taken together, our study reveals the cell interaction between hypoxic papillary thyroid cancer cells and endothelial cells, elucidating a new mechanism by which hypoxic papillary thyroid cancer cells increase angiogenesis via exosomal miR-21-5p/TGFBI and miR-21-5p/COL4A1 regulatory pathway.
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Chew, Valerie, Yun Hua Lee, Lu Pan, Nurul J. M. Nasir, Chun Jye Lim, Camillus Chua, Liyun Lai, et al. "Immune activation underlies a sustained clinical response to Yttrium-90 radioembolisation in hepatocellular carcinoma." Gut 68, no. 2 (February 13, 2018): 335–46. http://dx.doi.org/10.1136/gutjnl-2017-315485.
Full textAbstract:
ObjectivesYttrium-90 (Y90)-radioembolisation (RE) significantly regresses locally advanced hepatocellular carcinoma and delays disease progression. The current study is designed to deeply interrogate the immunological impact of Y90-RE, which elicits a sustained therapeutic response.DesignTime-of-flight mass cytometry and next-generation sequencing (NGS) were used to analyse the immune landscapes of tumour-infiltrating leucocytes (TILs), tumour tissues and peripheral blood mononuclear cells (PBMCs) at different time points before and after Y90-RE.ResultsTILs isolated after Y90-RE exhibited signs of local immune activation: higher expression of granzyme B (GB) and infiltration of CD8+ T cells, CD56+ NK cells and CD8+ CD56+ NKT cells. NGS confirmed the upregulation of genes involved in innate and adaptive immune activation in Y90-RE-treated tumours. Chemotactic pathways involving CCL5 and CXCL16 correlated with the recruitment of activated GB+CD8+ T cells to the Y90-RE-treated tumours. When comparing PBMCs before and after Y90-RE, we observed an increase in tumour necrosis factor-α on both the CD8+ and CD4+ T cells as well as an increase in percentage of antigen-presenting cells after Y90-RE, implying a systemic immune activation. Interestingly, a high percentage of PD-1+/Tim-3+CD8+ T cells coexpressing the homing receptors CCR5 and CXCR6 denoted Y90-RE responders. A prediction model was also built to identify sustained responders to Y90-RE based on the immune profiles from pretreatment PBMCs.ConclusionHigh-dimensional analysis of tumour and systemic immune landscapes identified local and systemic immune activation that corresponded to the sustained response to Y90-RE. Potential biomarkers associated with a positive clinical response were identified and a prediction model was built to identify sustained responders prior to treatment.
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Cheeseman, K. H., M. Collins, K. Proudfoot, T. F. Slater, G. W. Burton, A. C. Webb, and K. U. Ingold. "Studies on lipid peroxidation in normal and tumour tissues. The Novikoff rat liver tumour." Biochemical Journal 235, no. 2 (April 15, 1986): 507–14. http://dx.doi.org/10.1042/bj2350507.
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A study has been made of the factors that contribute to the decreased rates of lipid peroxidation under different pro-oxidant conditions in intact Novikoff tumour cells, and in microsomal suspensions prepared from Novikoff tumour cells, compared with isolated normal rat hepatocytes and microsomal suspensions prepared from normal rat liver. The pro-oxidant conditions were the addition of either NADPH, NADPH + ADP + iron, NADPH + CCl4 or ascorbate+iron to the experimental systems used, or exposure to gamma-radiation. Contributory factors to the lower rates of lipid peroxidation observed include: a significant decrease in the polyunsaturated fatty acid content of Novikoff cells or Novikoff microsomes; the decreases are especially marked for the C20:4 and C22:6 fatty acids; a very marked reduction in NADPH-cytochrome c reductase; and no detectable content of cytochrome P-450. Another, and in our opinion critical, contribution to the diminished rate of lipid peroxidation in the tumour material is the substantial increase in alpha-tocopherol relative both to total lipid and to methylene-interrupted double bonds in fatty acids. Moreover, the alpha-tocopherol is the major contributor to lipid-soluble chain-breaking antioxidant in lipid extracts of normal liver and of Novikoff tumour material.
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Geetha, B. S., Mangalam S. Nair, P. G. Latha, and P. Remani. "Sesquiterpene Lactones Isolated fromElephantopus scaberL. Inhibits Human Lymphocyte Proliferation and the Growth of Tumour Cell Lines and Induces ApoptosisIn Vitro." Journal of Biomedicine and Biotechnology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/721285.
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This study was designed to isolate the compounds responsible for the cytotoxic properties of South IndianElephantopus scaberL. and further investigate their effects on quiescent and proliferating cells. Bioassay-guided isolation of the whole plant of chloroform extract of South IndianElephantopus scaberafforded the known sesquiterpene lactone, deoxyelephantopin, and isodeoxyelephantopin whose structures were determined by spectroscopic methods. These compounds caused a dose dependent reduction in the viability of L-929 tumour cells in 72 h culture (IC50value of 2.7 μg/mL and 3.3 μg/mL) by the cell viability assay. Both the compounds act selectively on quiescent and PHA-stimulated proliferating human lymphocytes and inhibited tritiated thymidine incorporation into cellular DNA of DLA tumour cells. The compound deoxyelephantopin at a concentration of 3 μg/mL caused maximum apoptotic cells. It also exhibited significantin vivoantitumour efficacy against DLA tumour cells. The results, therefore, indicate that the antiproliferative property of deoxyelephantopin and isodeoxyelephantopin could be used in regimens for treating tumors with extensive proliferative potencies.
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Mao, Hanwen, Wenli Liu, Zhe Gen, Wei Huang, Yicheng Zhang, Jianfeng Zhou, and Hanying Sun. "Cytotoxic Effects of CML28 Specific T Cells on Acute Leukemia Cells In Vitro." Blood 110, no. 11 (November 16, 2007): 4886. http://dx.doi.org/10.1182/blood.v110.11.4886.4886.
Full textAbstract:
Abstract The antigen-specific cytotoxic T lymphocyte activated by antigen presenting cell is widely used in cell immunotherapy recently. CML28, which was screened from chronic myelogenous leukemia (CML) patients, was reported to be a specific tumour antigen and over-expressed on CML cells and acute leukemia cells. Therefore, CML28 could be a potential target for leukemia treatment. Dendritic cells (DC) are the most important antigen present cells, but it is hard to isolate and culture DCs for clinical use, which hampers the specific cell immunotherapy. Our investigation aimed to study the cytotoxic effects of CML28 specific T cells activated by artificial antigen presenting cells, on acute leukemia cells in vitro. Artificial antigen presenting cells were prepared by connecting CML28 to magnetic superbead that containing HLA-A2-Ig and B7-1 molecule. Mononuclear cells were isolated from the bone marrow or peripheral blood of healthy donors with positive HLA-A2. The artificial antigen-presenting cells were co-cultured with isolated mononuclear cells for four weeks. The activation and proliferation of CML28-specific T cells were measured by dimmer binding technique using flow cytometry. The cytotoxic effects of CML28-specific T cells on leukemia cells, which were isolated from leukemia patient, were evaluated by lactate dehydrogenase (LDH) releasing assay. Increased proportion of CML28-specific T cells was observed in artificial antigen-presenting group than in control group (29.27±3.54% vs 2.95±0.66%, p<0.05). For cytotoxic effects assay, significant higher killing efficiency was seen in artificial antigen-presenting group (41.47±4.23%vs3.56±0.71%, when the effector: target ration is 40:1, p<0.01). Therefore, we concluded that the artificial antigen presenting cells could mimic antigen presenting cells to induce specific T cell activation and proliferation, and cytotoxic effects on target cells, indicating that artificial antigen presenting cell-induced cytotocix T cells could be an option for leukemia treatment.