Please use this identifier to cite or link to this item:
http://hdl.handle.net/10603/123489
Title: | Role of wnt β catenin in dna damage response and telomere associated regulatory function in cancer progression |
Researcher: | Padhi, Swati Shree |
Guide(s): | Banarjee, Birendranath |
Keywords: | Wnt, and#946;-catenin, DNA, telomere, cancer |
University: | KIIT University |
Completed Date: | 2016 |
Abstract: | Head and neck squamous cell carcinoma (HNSCC) is the majority number of cases to be considered under oral cancer. Nearly 40% of oral cancers comprises of head and neck cancer. Head and neck cancer is the sixth most common cancer in the world. Squamous cell carcinoma starts with a series of cellular events, affecting a single epithelial cell called atypia and then with many such cellular alterations leading to dysplasia, progressing into carcinoma in situ and then finally invasion. India reports maximum oral cancer incidences majorly due to betel quid (BQ) intake, bidi smoking and alcohol. Carcinoma Buccal Mucosa or cheek is the most common sub-site of occurrence of the disease in the Odisha population (45.2% in males and 48.2% in females) (Mohanta et al. 2013)as compared to any other sites owing to the habit of betel quid retention, chewing tobacco and keeping them for longer time. This indicates prevalence of HNSCC in the Odisha population and active research has to be taken up for the incidents of oral cancer in this part of the country. newline newlineTumorigenesis is a long process where the cancer cells gains their invasive property by accumulating mutations through generations and keep on acquiring new traits. This evolutionary process prepares the tumor cells to surpass the anti- cancer defence mechanism devised by surrounding normal cells. (Hanahan and Weinberg 2000) These are the hallmarks of cancer explained by Hanahan and Weinberg which transforms a normal cell into neoplastic by acquiring sustaining proliferative signal, resisting cell death, inducing angiogenesis, enabling replicative immortality, activating invasion and metastasis and evading growth suppressors. newline newline |
URI: | http://hdl.handle.net/10603/123489 |
Appears in Departments: | School of Biotechnology |
Files in This Item:
File | Description | Size | Format | |
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acknowledgement.pdf | Attached File | 277.45 kB | Adobe PDF | View/Open |
bibliography.pdf | 3.39 MB | Adobe PDF | View/Open | |
chapter-1.pdf | 865.7 kB | Adobe PDF | View/Open | |
chapter-2.pdf | 1.39 MB | Adobe PDF | View/Open | |
chapter-3.pdf | 923.9 kB | Adobe PDF | View/Open | |
chapter-4.pdf | 1.13 MB | Adobe PDF | View/Open | |
chapter-5.pdf | 1.3 MB | Adobe PDF | View/Open | |
chapter-6.pdf | 291.76 kB | Adobe PDF | View/Open | |
contents.pdf | 315.41 kB | Adobe PDF | View/Open | |
list of figures & tables.pdf | 198.62 kB | Adobe PDF | View/Open | |
title page.pdf | 110.6 kB | Adobe PDF | View/Open |
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