Please use this identifier to cite or link to this item: http://hdl.handle.net/10603/14385
Title: A study on crosstalk between lung carcinoma and immune cells
Researcher: Qazi Danish Mushtaq
Guide(s): Raies Ahmad Qadri
Keywords: Cross-Talk
Immune Cells
Lung Carcinoma
Upload Date: 31-Dec-2013
University: University of Kashmir
Completed Date: 12/09/2012
Abstract: newlineTumor cells are seen to modulate the phenotype of all major immune cells to newlineexpress tumor favouring phenotypes. Inflammation associated with tumors, a result of newlinesuch interaction, is increasingly being believed to play a major role in tumor initiation, newlineprogression and even metastasis. This modulation is achieved very early when newlineMonocytes, precursors of Macrophages and DCs, from the circulating pool are recruited newlinetowards tumors and selectively differentiated. Monocytes, in particular, are thought to newlinegenerate a cytokine milieu in the microenvironment favourable to tumor. Such a newlinecrosstalk and the pathways involved therein are not well established, especially in human newlinemodels. Using representative human carcinoma cells of different origin including Lung, newlineColon and Cervix, we show that factor(s) associated with these cells can activate newlinesecretion of tumor-associated cytokines, TNF-and#945;, IL-6, IL-10, IL-12p40 but not IL-12p70 newlineor IL-1and#946; from human monocytes. Comparative murine co-cultures are also able to induce newlinesimilar responses. Treatment of monocytes with TLR-2 blocking antibody inhibits these newlineinflammatory responses upon encountering cell-associated as well as secretory ligand(s) newlinefrom tumor cells. Pharmacological inhibition of intracellular MAP kinase pathway in newlinecarcinoma cells ablates the TLR-2 agonistic activity of carcinoma cells. However, newlineinhibition of EGFR and Ras, two major oncogenic players, had no such effect. Early newlineinflammatory response tends to enhance the proliferation and invasiveness of tumor cells newlineand concurrently, increase the viability of monocytes. These tumor associated newlineinflammatory responses may well be one of the mechanisms to manipulate effector T-cell newlineresponse against tumors. These results suggest a previously unrecognized pathway that newlinemay regulate inflammatory responses triggered by cancer cells from monocytes. Our newlinefindings have important implications for understanding Cancer related Inflammation.
Pagination: 
URI: http://hdl.handle.net/10603/14385
Appears in Departments:Department of Biotechnology

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acknowledgment.pdfAttached File79.4 kBAdobe PDFView/Open
bibliography.pdf225.73 kBAdobe PDFView/Open
certificate.pdf113.54 kBAdobe PDFView/Open
chapter 1.pdf215.74 kBAdobe PDFView/Open
chapter 2.pdf594.42 kBAdobe PDFView/Open
chapter 3.pdf73.58 kBAdobe PDFView/Open
chapter 4.pdf212.05 kBAdobe PDFView/Open
chapter 5.pdf718.38 kBAdobe PDFView/Open
conclusions.pdf91.51 kBAdobe PDFView/Open
contents.pdf117.65 kBAdobe PDFView/Open
discussion.pdf567.55 kBAdobe PDFView/Open
list of figures.pdf133.81 kBAdobe PDFView/Open
title page.pdf129.65 kBAdobe PDFView/Open


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