Journal articles: 'Tumour necrosis; Cancer'

1

Balkwill, Frances. "Tumour necrosis factor and cancer." Nature Reviews Cancer 9, no. 5 (April 3, 2009): 361–71. http://dx.doi.org/10.1038/nrc2628.

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Waters, John P., Jordan S. Pober, and John R. Bradley. "Tumour necrosis factor and cancer." Journal of Pathology 230, no. 3 (June 7, 2013): 241–48. http://dx.doi.org/10.1002/path.4188.

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Balkwill, Frances R. "Tumour necrosis factor and cancer." Progress in Growth Factor Research 4, no. 2 (January 1992): 121–37. http://dx.doi.org/10.1016/0955-2235(92)90027-f.

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4

Szlosarek, Peter, Kellie A. Charles, and Frances R. Balkwill. "Tumour necrosis factor-α as a tumour promoter." European Journal of Cancer 42, no. 6 (April 2006): 745–50. http://dx.doi.org/10.1016/j.ejca.2006.01.012.

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5

Selby, P. J., S. Hobbs, C. Viner, E. Jackson, I. E. Smith, and T. J. Mcelwain. "ENDOGENOUS TUMOUR NECROSIS FACTOR IN CANCER PATIENTS." Lancet 331, no. 8583 (February 1988): 483. http://dx.doi.org/10.1016/s0140-6736(88)91286-x.

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Lui, Philip C. W., Yuen Shan Fan, Guiyan Xu, C. Y. Ngai, Kwok Pui Fung, Gary M. K. Tse, Alex M. C. Yu, and Jian Yi Li. "Apoptotic and necrotic effects of tumour necrosis factor-alpha potentiated with hyperthermia on L929 and tumour necrosis factor-alpha-resistant L929." International Journal of Hyperthermia 26, no. 6 (August 13, 2010): 556–64. http://dx.doi.org/10.3109/02656736.2010.486777.

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Aderka, Dan, Shimshon Fisher, Yoram Levo, Helmut Holtmann, Talia Hahn, and David Wallach. "CACHECTIN/TUMOUR-NECROSIS-FACTOR PRODUCTION BY CANCER PATIENTS." Lancet 326, no. 8465 (November 1985): 1190. http://dx.doi.org/10.1016/s0140-6736(85)92713-8.

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&NA;. "Recent advances in tumour necrosis factor in cancer." Inpharma Weekly &NA;, no. 770 (January 1991): 22–23. http://dx.doi.org/10.2165/00128413-199107700-00065.

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9

Trentin, L., R. Zambello, P. Bulian, A. Cerutti, C. Enthammer, M. Cassatella, D. Nitti, M. Lise, C. Agostini, and G. Semenzato. "Tumour-infiltrating lymphocytes bear the 75 kDa tumour necrosis factor receptor." British Journal of Cancer 71, no. 2 (February 1995): 240–45. http://dx.doi.org/10.1038/bjc.1995.50.

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Wigmore, S. J., D. N. Redhead, B. N. J. Thomson, E. J. Currie, R. W. Parks, K. K. Madhavan, and O. J. Garden. "Postchemoembolisation syndrome – tumour necrosis or hepatocyte injury?" British Journal of Cancer 89, no. 8 (October 2003): 1423–27. http://dx.doi.org/10.1038/sj.bjc.6601329.

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Ocvirk, J., B. Štabuc, Z. Rudolf, V. Galvani, and V. Čurin-Šerbec. "Serum values of tumour necrosis factor-α and of soluble tumour necrosis factor-R55 in melanoma patients." Melanoma Research 10, no. 3 (June 2000): 253–58. http://dx.doi.org/10.1097/00008390-200006000-00007.

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Ocvirk, J., B. Štabuc, Z. Rudolf, V. Galvani, and V. Čurin-Šerbec. "Serum values of tumour necrosis factor-α and of soluble tumour necrosis factor-R55 in melanoma patients." Melanoma Research 10, no. 3 (June 2000): 253–58. http://dx.doi.org/10.1097/00008390-200010030-00007.

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Cross, N. A., M. Papageorgiou, and C. L. Eaton. "Bone marrow stromal cells promote growth and survival of prostate cancer cells." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 698–700. http://dx.doi.org/10.1042/bst0350698.

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Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).

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Nezu, M., H. Iwagaki, H. Aoki, N. Tanaka, and K. Orita. "Tumour Necrosis Factor-α Upregulates Transferrin Receptors in K 562 Cells." Journal of International Medical Research 22, no. 3 (May 1994): 145–52. http://dx.doi.org/10.1177/030006059402200302.

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The effects of tumour necrosis factor-α on transferrin receptor expression in a human chronic myelocytic leukaemia cell line, K 562 cells, were studied. Cytofluorometry studies showed that the numbers of transferrin receptors in exponentially growing K 562 cells were increased when the cells were incubated with tumour necrosis factor-α for 24 h. The induction of transferrin receptors by tumour necrosis factor-α may be mediated by a mechanism that is independent of growth since cell growth in treated cultures did not differ from that in the controls. The DNA contents of K 562 cells treated with tumour necrosis factor-α showed that after 24 h there were less cells in the G1 and S phases and more cells in the G2/M phase than in the control group. The phase of upregulation of transferrin receptors induced by tumour necrosis factor-α may be dependent on the cell cycle. This new evidence that tumour necrosis factor-α upregulates transferrin receptors suggests a cancer-anaemia cascade in which the cancer burden state activates macrophage release of tumour necrosis factor-α as a result of transferrin receptor expression.

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Robinson, Hugh P. C., and Leanne Li. "Autocrine, paracrine and necrotic NMDA receptor signalling in mouse pancreatic neuroendocrine tumour cells." Open Biology 7, no. 12 (December 2017): 170221. http://dx.doi.org/10.1098/rsob.170221.

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N -Methyl- d -aspartate receptor (NMDAR) activation is implicated in the malignant progression of many cancer types, as previously shown by the growth-inhibitory effects of NMDAR antagonists. NMDAR-mediated calcium influx and its downstream signalling depend critically, however, on the dynamics of membrane potential and ambient glutamate concentration, which are poorly characterized in cancer cells. Here, we have used low-noise whole-cell patch-clamp recording to investigate the electrophysiology of glutamate signalling in pancreatic neuroendocrine tumour (PanNET) cells derived from a genetically-engineered mouse model (GEMM) of PanNET, in which NMDAR signalling is known to promote cancer progression. Activating NMDARs caused excitation and intracellular calcium elevation, and intracellular perfusion with physiological levels of glutamate led to VGLUT-dependent autocrine NMDAR activation. Necrotic cells, which are often present in rapidly-growing tumours, were shown to release endogenous cytoplasmic glutamate, and necrosis induced by mechanical rupture of the plasma membrane produced intense NMDAR activation in nearby cells. Computational modelling, based on these results, predicts that NMDARs in cancer cells can be strongly activated in the tumour microenvironment by both autocrine glutamate release and necrosis.

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Männel, DN, A. Kist, AD Ho, U. Räth, P. Reichardt, B. Wiedenmann, E. Schlick, and H. Kirchner. "Tumour necrosis factor production and natural killer cell activity in peripheral blood during treatment with recombinant tumour necrosis factor." British Journal of Cancer 60, no. 4 (October 1989): 585–88. http://dx.doi.org/10.1038/bjc.1989.318.

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17

Balkwill, Frances, Frances Burke, Denis Talbot, Jan Tavernier, Richard Osborne, Stuart Naylor, Helga Durbin, and Walter Fiers. "EVIDENCE FOR TUMOUR NECROSIS FACTOR/CACHECTIN PRODUCTION IN CANCER." Lancet 330, no. 8570 (November 1987): 1229–32. http://dx.doi.org/10.1016/s0140-6736(87)91850-2.

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18

Waterston, Ashita, Marc Feldmann, and R. Charles Coombes. "Tumour Necrosis Factor: A Prometastatic Role in Breast Cancer." Clinical Science 104, s49 (April 1, 2003): 26P. http://dx.doi.org/10.1042/cs104026p.

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19

&NA;. "Tumour necrosis factor: increases metabolic rate in cancer patients." Inpharma Weekly &NA;, no. 737 (May 1990): 6–7. http://dx.doi.org/10.2165/00128413-199007370-00015.

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20

Guthrie, Graeme JK, Campbell SD Roxburgh, Colin H. Richards, Paul G. Horgan, and Donald C. Mcmillan. "The relationship between tumour necrosis, circulating IL-6 concentrations, and inflammatory responses in patients undergoing curative resection for colorectal cancer." Journal of Clinical Oncology 31, no. 4_suppl (February 1, 2013): 404. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.404.

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404 Background: Cancer-associated inflammation, in the form of systemic and local inflammation, and tumour necrosis are known to have prognostic value in colorectal cancer (CRC). In addition, recent work has reported a direct relationship between the systemic inflammatory response and loss of skeletal muscle in patients with CRC. However, the inter-relationships between these inflammatory responses, tumour necrosis, metabolic upset and circulating biochemical mediators are unclear in CRC. Interleukin-6 and its downstream signalling cascades have been implicated in both cancer-associated inflammation and cancer-associated muscle wasting. The aim of the present study was to examine whether circulating IL-6 concentrations may link tumour necrosis, local and systemic inflammatory responses, and metabolic upset in patients undergoing curative resection for colorectal cancer. Methods: The study included 118 patients undergoing surgery for CRC between 2004 and 2009. Data were collected from pre-operative blood tests. Routine pathology specimens were scored for Klintrup criteria and tumour necrosis. Results: Tumour necrosis was associated with increased T-stage (p<0.01), reduced inflammatory cell infiltrate (p<0.05), increased IL-6 (p<0.001), IL-10 (p<0.01), and VEGF (p<0.001) and with markers of the systemic inflammatory response: mGPS (p<0.001), anaemia (p<0.05); increased white cell (p<0.001), neutrophil (p<0.05) and platelet (p<0.001) counts. Circulating IL-6 was associated with increased IL-10 (p<0.01), VEGF (p<0.001), increased mGPS (p<0.001), increased white cell (p<0.01) and platelet (p<0.01) counts and low skeletal muscle index (p<0.01). On Spearman rank correlation there were significant associations between circulating concentrations of IL-6 and IL-10 (rs= 0.39, p<0.001) and CRP (r= 0.42, p<0.001). Conclusions: Interleukin-6 appears to be associated with systemic inflammation, tumour necrosis, and sarcopenia in colorectal cancer. However, the lack of an association between IL-6 and the local inflammatory response suggests a more complex relationship with the tumour inflammatory cell infiltrate.

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21

Tsutsumi, Y., S. Tsunoda, H. Kamada, T. Kihira, S. Nakagawa, Y. Kaneda, T. Kanamori, and T. Mayumi. "Molecular design of hybrid tumour necrosis factor-alpha. II: The molecular size of polyethylene glycol-modified tumour necrosis factor-alpha affects its anti-tumour potency." British Journal of Cancer 74, no. 7 (October 1996): 1090–95. http://dx.doi.org/10.1038/bjc.1996.495.

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22

Melton, R. G., R. F. Sherwood, J. A. Rowland, G. A. Pietersz, and I. F. C. McKenzie. "Tumour necrosis factor increases tumour uptake of Co-administered antibody-carboxypeptidase G2 conjugate." European Journal of Cancer 29, no. 8 (January 1993): 1177–83. http://dx.doi.org/10.1016/s0959-8049(05)80311-9.

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23

BARBER, Matthew D., Kenneth C. H. FEARON, and James A. ROSS. "Relationship of serum levels of interleukin-6, soluble interleukin-6 receptor and tumour necrosis factor receptors to the acute-phase protein response in advanced pancreatic cancer." Clinical Science 96, no. 1 (January 1, 1999): 83–87. http://dx.doi.org/10.1042/cs0960083.

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The level of the acute-phase response is a major predictor of survival in patients with advanced pancreatic cancer. This study examines the association between the acute-phase protein response, as determined by serum C-reactive protein, and serum levels of interleukin-6, soluble interleukin-6 receptor and the soluble tumour necrosis factor receptors in patients with pancreatic cancer. Thirty-four blood samples were collected from 13 patients with advanced pancreatic cancer. Samples were also collected from six healthy subjects. Levels of C-reactive protein, interleukin-6, soluble interleukin-6 receptor and soluble tumour necrosis factor receptors 55 and 75 were measured by indirect ELISA. Serum levels of C-reactive protein, interleukin-6 and soluble tumour necrosis factor receptors 55 and 75 were significantly higher in cancer patients than in controls. Levels of serum soluble interleukin-6 receptor were not significantly different between the two groups. In cancer patients, a significant positive association was found between the level of the acute-phase protein response and serum levels of interleukin-6, soluble tumour necrosis factor receptor 55 and soluble tumour necrosis factor receptor 75. No association was found between levels of soluble interleukin-6 receptor and any other factor. There is no significant relationship between the level of soluble interleukin-6 receptor and the acute-phase protein response in vivo and the biological role of soluble interleukin-6 receptor in the chronic inflammatory component of cachexia remains unclear.

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Mainou-Fowler, Tryfonia, Anne M. Dickinson, Penelope R. A. Taylor, Philip Mounter, Fergus Jack, Steven J. Proctor, Jean Nordon, and Peter G. Middleton. "Tumour Necrosis Factor Gene Polymorphisms in Lymphoproliferative Disease." Leukemia & Lymphoma 38, no. 5-6 (January 2000): 547–52. http://dx.doi.org/10.3109/10428190009059274.

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25

Thomas, H., and K. Sikora. "Biological Approaches to Cancer Therapy." Journal of International Medical Research 17, no. 3 (May 1989): 191–204. http://dx.doi.org/10.1177/030006058901700301.

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Advances in the biological approach to cancer therapy are reviewed. The mechanisms of actions, clinical effects and uses of interferons, the first biological modifiers to be used, are reviewed first. The interleukins and monoclonal antibodies are also mentioned in detail. This review also covers the clinical use and production of lymphokine activated killer cells, which are used in conjunction with interleukin-2. A brief review of tumour infiltrating lymphocytes, which comprise a subset of lymphocytes found within solid tumours is given. In mice, tumour infiltrating lymphocytes have been shown to be more therapeutic than lymphokine activated killer cells. Tumour necrosis factor, a protein released by activated macrophages in response to stimulation by endotoxin, is also briefly mentioned although clinical data are disappointing. Finally, the role which oncogenes may play in cancer therapy and understanding is discussed.

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Pinato, David James, Anu Vallipuram, Joanne Evans, Clement Wong, Hua Zhang, Matthew Brown, Roberto Dina, et al. "Molecular characterization of the tumour microenvironment in neuroendocrine malignancy." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 4107. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.4107.

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4107 Background: A comprehensive characterization of the tumour microenvironment is lacking in neuroendocrine tumors (NETs), where immunotherapy is undergoing efficacy testing. We investigated drivers of cancer-related immunosuppression across NETs of various sites and grade using multi-parameter immunohistochemistry and targeted transcriptomics. Methods: Tissue microarrays (n = 102) were stained for PD-L1 & 2, Indoleamine-deoxygenase-1 (IDO-1) and evaluated in relationship to functional characteristics of tumor-infiltrating T-lymphocytes (TILs) and biomarkers of hypoxia/angiogenesis including VEGF-A, Hif-1α and Carbonic Anhydrase-IX. PD-L1 expression was tested in circulating tumour cell (CTCs, n = 12) to evaluate its relationship with metastatic dissemination. Results: PD-L1 expression was highest in lung NETs (n = 30, p = 0.007), whereas PD-L2 was highest in pNETs (n = 53, p < 0.001) with no correlation with grade, stage or biomarkers of hypoxia. Incubation of QGP-1 and BON-1 NET cells in 1% O2 did not induce PD-L1 expression confirming transcriptional independence from hypoxia. PD-L1+ NETs (n = 26, 25%) had frequent IDO-1 co-expression (p = 0.03), greater CD4+/FOXP3+ and CD8+/PD1+ TILs (p < 0.001) and necrosis (p = 0.02). CD4+/FOXP3+ infiltrate was highest PD-L1/IDO-1 co-expressing tumours (p = 0.006). Survival was predicted by tumour grade (p < 0.001) and necrosis (p < 0.001) but not PD-L1, PD-L2 nor IDO-1. High-grade NETs had lower CD4+/FOXP3+ and CD8+/PD1+ TILs density (p < 0.001) and Nanostring immune-profiling revealed enrichment of macrophage-related transcripts in cases with poorer prognosis. We identified PD-L1(+) CTC subpopulations in 75% of evaluated patients (n = 12). Conclusions: PD-L1 expression correlates with T-cell exhaustion independent of tumour hypoxia and is enhanced in a subpopulation of CTCs, suggesting its relevance to the progression of NETs. These findings support a potential therapeutic role for PD-L1/IDO-1 inhibitors in a subset of NETs.

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Watanabe, T., S. Fuchimoto, N. Matsubara, H. Iwagaki, and K. Orita. "Anti-Proliferative Effect on Human Pancreatic Cancer Cells of Natural Human Tumour Necrosis Factor-β Combined with Natural Human Interferon-α or Interferon-γ." Journal of International Medical Research 20, no. 2 (April 1992): 112–20. http://dx.doi.org/10.1177/030006059202000203.

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The anti-proliferative effects of natural cytokines, human tumour necrosis factor-β, natural human interferon-α and natural human interferon-γ, on three human pancreatic cancer cell lines (PANC-1, MIA PaCa-2 and BxPC-3) were investigated in vitro. The anti-proliferative effect was determined using the dye uptake method and analysed for synergism by the median effect principle. Tumour necrosis factor-β, as a single agent, had little anti-proliferative effect on any of the three cell lines, whereas interferon-α and interferon-γ exhibited a strong anti-proliferative effect against two cell lines (MIA PaCa-2 and BxPC-3) and one cell line (BxPC-3), respectively. When tumour necrosis factor-β and interferon-α were administered together (ratio 1:1), a synergistic effect was observed against PANC-1 cells. The combination of tumour necrosis factor-β and interferon-γ (ratio 10:1) was synergisic against both PANC-1 and MIA PaCa-2 cells. A synergistic anti-proliferative effect of tumour necrosis factor-β and interferons was, therefore, observed even for cell lines that showed little biological response to each cytokine alone. The data suggest that some future improvement in the treatment of pancreatic cancer may be obtained by using combination cytokine therapy.

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Lorusso, Domenica, Paola Malaguti, Giovanni Scambia, Claudio Bordignon, and Francesco Raspagliesi. "NGR-hTNF plus Doxorubicin in Recurrent Ovarian Cancer." European Oncology & Haematology 08, no. 02 (2012): 107. http://dx.doi.org/10.17925/eoh.2012.08.02.107.

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Ovarian cancer is the most lethal gynaecological cancer. Despite surgery and first-line chemotherapy, tumours recur in 6070 % of cases and prognosis is poor. Several studies have indicated that the cytokine tumour necrosis factor (TNF) has antitumour activity when given systematically, but its high toxicity has limited its use. Peptides containing the aspargine-glycine-arginine motif (NGR peptides) selectively bind to the aminopeptidase N ligand CD13, which is overexpressed in the cells of tumour blood vessels. It has been found that the combination of an NGR peptide and human TNF (NGR-hTNF) has the ability to increase intratumoural doxorubicin distribution by altering the tumour vasculature. In this article, we describe the activity and toxicity profile of NGR-hTNF plus doxorubicin as a combination treatment for recurrent ovarian cancer.

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29

Semenzato, G. "Tumour necrosis factor: a cytokine with multiple biological activities." British Journal of Cancer 61, no. 3 (March 1990): 354–61. http://dx.doi.org/10.1038/bjc.1990.78.

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30

Duncombe, A. S., D. J. Gottlieb, A. Bianchi, and M. K. Brenner. "BIOACTIVITY AND IMMUNORHACTIVITY OF TUMOUR NECROSIS FACTOR IN CANCER PATIENTS." Lancet 331, no. 8579 (January 1988): 248. http://dx.doi.org/10.1016/s0140-6736(88)91106-3.

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Reibnegger, Gilbert, Antonio Diez-Ruiz, Dietmar Fuchs, and Helmut Wachter. "Soluble tumour necrosis factor receptors as prognostic factors in cancer." Lancet 344, no. 8923 (September 1994): 681–82. http://dx.doi.org/10.1016/s0140-6736(94)92115-6.

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32

Malik, S. T. A., D. B. Griffin, W. Fiers, and F. R. Balkwill. "Paradoxical effects of tumour necrosis factor in experimental ovarian cancer." International Journal of Cancer 44, no. 5 (November 15, 1989): 918–25. http://dx.doi.org/10.1002/ijc.2910440529.

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33

Hardy, J., A. Jones, M. E. Gore, C. Viner, P. Selby, and E. Wiltshaw. "Treatment of advanced ovarian cancer with intraperitoneal tumour necrosis factor." European Journal of Cancer and Clinical Oncology 26, no. 6 (January 1990): 771. http://dx.doi.org/10.1016/0277-5379(90)90146-k.

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Fujimoto, S., K. Kobayashi, M. Takahashi, C. Konno, M. Kokubun, M. Ohta, RD Shrestha, and S. Kiuchi. "Effects on tumour microcirculation in mice of misonidazole and tumour necrosis factor plus hyperthermia." British Journal of Cancer 65, no. 1 (January 1992): 33–36. http://dx.doi.org/10.1038/bjc.1992.6.

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35

Jackson, Andrew M., Anton B. Alexandrov, S. Prescott, and Keith James. "Production of urinary tumour necrosis factors and soluble tumour necrosis factor receptors in bladder cancer patients afterbacillus Calmette-Guerin immunotherapy." Cancer Immunology Immunotherapy 40, no. 2 (March 1995): 119–24. http://dx.doi.org/10.1007/bf01520294.

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Tse, Brian W. C., Kieran F. Scott, and Pamela J. Russell. "Paradoxical Roles of Tumour Necrosis Factor-Alpha in Prostate Cancer Biology." Prostate Cancer 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/128965.

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Tumour necrosis factor (TNF) is a pleiotropic cytokine with dual roles in cancer biology including prostate cancer (PCa). On the one hand, there is evidence that it stimulates tumour angiogenesis, is involved in the initiation of PCa from an androgen-dependent to a castrate resistant state, plays a role in epithelial to mesenchymal plasticity, and may contribute to the aberrant regulation of eicosanoid pathways. On the other hand, TNF has also been reported to inhibit neovascularisation, induce apoptosis of PCa cells, and stimulate antitumour immunity. Much of the confusion surrounding its seemingly paradoxical roles in cancer biology stems from the dependence of its effects on the biological model within which TNF is investigated. This paper will address some of these issues and also discuss the therapeutic implications.

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37

Dillman, Robert O. "Monoclonal Antibodies as Immune Modulators for Cancer Therapy." Canadian Journal of Infectious Diseases 3, suppl b (1992): 20–25. http://dx.doi.org/10.1155/1992/205769.

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Monoclonal antibodies may modulate immune and/or biological responses alone, or as carriers of specific agents. Monoclonal antibodies directed against tumours may be indirectly cytotoxic by modulation of antibody-dependent, cell-mediated cytotoxicity or complement-mediated cytotoxicity. Monoclonal antibodies directed against certain tumour cell receptors may alter the biological behaviour of tumour cells such as blocking or downregulation of growth factors essential to tumour cell proliferation. Monoclonal antibodies directed to certain receptors on host immune cells. such as the CD3 receptor on T lymphocytes. may activate those cells and increase their cytotoxicity. Antitumour monoclonal antibodies can serve as carriers of interferons, interleukin-2, tumour necrosis factor and other lymphokines and cytokines to modulate selectively the cytotoxic potential of immune cells in the vicinity of tumour cells. Cytotoxic chemotherapy agents conjugated to antitumour monoclonal antibodies may be processed differently so that they bypass certain mechanisms of drug resistance. The penultimate application of monoclonal antibodies in cancer therapy is to combine various monoclonal antibodies and immunoconjugates for selective combination therapy based on known antigenic tumour cell determinants and the status of the host immune system.

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38

Gao, Shan, Jingcheng Jiang, Pan Li, Huijuan Song, Weiwei Wang, Chen Li, and Deling Kong. "Attenuating Tumour Angiogenesis: A Preventive Role of Metformin against Breast Cancer." BioMed Research International 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/592523.

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Metformin is one of the most widely prescribed antidiabetics for type 2 diabetes. A critical role of metformin against tumorigenesis has recently been implicated, although several studies also reported the lack of anticancer property of the antidiabetics. Given the controversies regarding the potential role of metformin against tumour progression, the effect of metformin against breast, cervical, and ovarian tumour cell lines was examined followed byin vivoassessment of metformin on tumour growth using xenograft breast cancer models. Significant inhibitory impact of metformin was observed in MCF-7, HeLa, and SKOV-3 cells, suggesting an antiproliferative property of metformin against breast, cervical, and ovarian tumour cells, respectively, with the breast tumour cells, MCF-7, being the most responsive.In vivoassessment was subsequently carried out, where mice with breast tumours were treated with metformin (20 mg/kg body weight) or sterile PBS solution for 15 consecutive days. No inhibition of breast tumour progression was detected. However, tumour necrosis was significantly increased in the metformin-treated group, accompanied by decreased capillary formation within the tumours. Thus, despite the lack of short-term benefit of metformin against tumour progression, a preventive role of metformin against breast cancer was implicated, which is at partially attributable to the attenuation of tumour angiogenesis.

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Matthews, N., and ML Neale. "Relationship between tumour cell morphology, gap junctions and susceptibility to cytolysis by tumour necrosis factor." British Journal of Cancer 59, no. 2 (February 1989): 189–93. http://dx.doi.org/10.1038/bjc.1989.39.

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40

Mahony, SM, and MJ Tisdale. "Role of prostaglandins in tumour necrosis factor induced weight loss." British Journal of Cancer 60, no. 1 (July 1989): 51–55. http://dx.doi.org/10.1038/bjc.1989.218.

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Waase, Inge, Michael Bergholz, Andrea Iglauer, Stefan Beissert, Manfred Blech, Alfred Schauer, and Martin Krönke. "Heterogeneity of tumour necrosis factor production in renal cell carcinoma." European Journal of Cancer 28, no. 10 (January 1992): 1660–64. http://dx.doi.org/10.1016/0959-8049(92)90063-8.

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42

Mahony, S. M., and M. J. Tisdale. "Reversal of weight loss induced by tumour necrosis factor-alpha." Cancer Letters 45, no. 3 (June 1989): 167–72. http://dx.doi.org/10.1016/0304-3835(89)90072-4.

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Patel, Meera, James Hugh Park, Hester Catharina van Wyk, Joanne Edwards, Paul G. Horgan, and Donald C. McMillan. "The relationship between tumor location, tumor microenvironment, systemic inflammation, and cancer-specific survival in patients undergoing surgery for colon cancer." Journal of Clinical Oncology 35, no. 4_suppl (February 1, 2017): 689. http://dx.doi.org/10.1200/jco.2017.35.4_suppl.689.

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689 Background: Evidence from clinical trials and cohort studies suggest primary tumour location is a prognostic factor in patients with advanced colorectal cancer and that right and left colonic tumours should be considered as distinct clinical and biological entities. The aim of the present study was to examine the relationship between tumour location, tumour microenvironment, systemic inflammatory response (SIR), and cancer-specific survival (CSS) in patients undergoing surgery for colon cancer. Methods: Clinicopathological characteristics were extracted from a prospective database of patients who underwent potentially curative surgery for colon cancer between 1997 and 2016, at a single centre. The tumour microenvironment was assessed retrospectively using routine H&E pathological sections. Results: 722 patients were included. The majority of patients were over the age of 65 years (69%), were male (52%), had right-sided (RS) tumour location (63%), had TNM stage I/II disease (64%) and 25% received adjuvant chemotherapy. RS location was associated with poor tumour differentiation ( p =< 0.001) and high venous invasion ( p =0.003) but not with TNM stage (p= 0.310), perineural invasion ( p= 0.286), tumour budding ( p= 0.568), margin involvement ( p= 0.424), peritoneal involvement ( p= 0.689), tumour necrosis ( p= 0.423) or tumour cell proliferation ( p= 0.605). RS location was not associated with tumour inflammatory cell infiltrate at the margin (CD3+ p= 0.103, CD8+ p= 0.620) or in the tumour (CD3+ p= 0.540, CD8+ p= 0.713) or with tumour stroma percentage ( p= 0.843). RS location was associated with high mGPS ( p =0.007) and neutrophil:platelet score ( p =0.001) but not NLR ( p= 0.387). Finally, there was no difference between RS and left sided tumour location in the administration of adjuvant chemotherapy (p= 0.901) or CSS ( p= 0.951). Conclusions: Few clinicopathological features were associated with tumour location in patients undergoing surgery for colon cancer. However, RS tumour location was consistently associated with a higher SIR. This may account for the poor prognosis associated with RS tumours in patients with advanced colon cancer.

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Heidenreich, A. N., D. Pfister, D. Thüer, U. H. Engelmann, and C. H. Ohlmann. "Prediction of residual retroperitoneal mass histology following postchemotherapy retroperitoneal surgery for metastatic nonseminomatous germ cell tumors: Role of MDR-1 and mismatch repair genes." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 5088. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.5088.

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5088 Background: Following inductive chemotherapy for metastatic nonseminomatous germ cell tumours (NSGCT) about 35% and 15% of patients undergoing residual tumor resection (RTR) demonstrate mature teratoma and vital cancer, respectively. It was the aim of our study to evaluate the expression of mdr-1, hMLH1 and hMLH2 in primary NSGCT and their resected residual tumors. Methods: 185 patients with NSGCT underwent RTR of retroperitoneal masses. Immunohistochemical investigations of mdr-1, hMLH1/2 were performed on paraffin-embedded tissue section of the primary tumour and the resected lymph nodes using monoclonal, commercially available antibodies. Staining was analysed according to a semiquantitative scoring system; furthermore, detailed morphometry was performed. Preoperative serum and clinical parameters were assessed to predict necrosis/fibrosis or teratoma in residual tumors. Statistical analysis was performed by uni- and multivariate analysis to correlate data with histology of the RTR specimens. Parameters were statistically significant if p<0.05. Results: A total of 122 patients (65.9%) had necrosis, 23 patients (12.4%) and 40 patients (21.6%) had viable cancer and mature teratoma, resp. After multivariate analysis pre-chemotherapeutic AFP-levels, tumor size before RTR, mature teratoma in the primary and mdr-1 expression in the primary were independent predictors of final necrosis. Positive predictive values were 74%, 76%, 78% and 88% resp., sensitivity was 81%, 52.8%, 65% and 86%, resp.; specificity was 59%, 79.3%, 81% and 90% resp.. Nonseminomatous elements demonstrated a significantly higher staining intensity for hMLH1 than seminomas, whereas staining intensity for hMLH2 was lower (p=0.03). IHC for hMLH1/2 of GCT with necrosis was higher as compared to GCT exhibiting mature teratoma or vital cancer approaching statistical significance (p=0.07). Conclusions: Pre-chemotherapy AFP levels < 15 ng/ml and a residual mass < 2 cm are associated with a favourable histology in the RTR specimen. The addition of mdr-1 expression in the primary NSGCT improves sensitivity to 88% and represents a clinically useful prediction marker. No significant financial relationships to disclose.

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Morrow, Elizabeth, Antonia Roseweir, Fadia Gujam, Laszlo Romics, Alison Lannigan, Paul Horgan, Donald McMillan, and Joanne Edwards. "31. A combined score of tumour necrosis, tumour budding and tumour-stroma percentage predicts cancer specific survival in primary operable breast cancer." European Journal of Surgical Oncology 45, no. 5 (May 2019): 884–85. http://dx.doi.org/10.1016/j.ejso.2019.01.217.

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Gallagher, Grant, Joyce Eskdale, Debbie Lynch, and Paul Horgan. "Tumour necrosis factor receptor alleles predict metastatic behaviour in colorectal cancer." Gastroenterology 118, no. 4 (April 2000): A766. http://dx.doi.org/10.1016/s0016-5085(00)85202-6.

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Park, K. S., J. W. Mok, H. E. Ko, K. Tokunaga, and M. H. Lee. "Polymorphisms of tumour necrosis factors A and B in breast cancer." European Journal of Immunogenetics 29, no. 1 (February 2002): 7–10. http://dx.doi.org/10.1046/j.0960-7420.2001.00260.x.

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LANGKOPF, F. "Soluble tumour necrosis factor receptors as prognostic factors in cancer patients." Lancet 344, no. 8914 (July 1994): 57–58. http://dx.doi.org/10.1016/s0140-6736(94)91078-2.

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McCall, J. L., J. A. Tuckey, and B. R. Parry. "Serum tumour necrosis factor alpha and insulin resistance in gastrointestinal cancer." British Journal of Surgery 79, no. 12 (December 1992): 1361–63. http://dx.doi.org/10.1002/bjs.1800791240.

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Belizario, JE, JL Tilly, and SW Sherwood. "Caffeine potentiates the lethality of tumour necrosis factor in cancer cells." British Journal of Cancer 67, no. 6 (June 1993): 1229–35. http://dx.doi.org/10.1038/bjc.1993.230.

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Journal articles on the topic 'Tumour necrosis; Cancer'

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