Abstract
Cancer is caused by mutation(s) in driver gene(s), leading to the transformation of normal cell into malignant one, followed by rapid proliferation. Head and neck cancers (HNCs) comprise epithelial malignancies of the mucosal lining in upper aero-digestive tract. These cancers are heterogeneous in nature. Carcinogenesis therein is correlated with the use of tobacco, chewing of areca nut (betel quid), alcohol consumption and infection with the human papillomavirus (HPV). These factors in conjunction with molecular variations contribute to tumour development, pathology and response to treatment. Thus, the carcinogenesis of head and neck cancers comprise a complex system of gene-gene and geneenvironment interactions.
Highlights
Cancer is caused by mutation(s) in driver gene(s), leading to the transformation of normal cell into malignant one, followed by rapid proliferation [1]
Carcinogenesis therein is correlated with the use of tobacco, chewing of areca nut, alcohol consumption and infection with the human papillomavirus (HPV) [4]
In phase I, a polar group is introduced into the molecule
Summary
Cancer is caused by mutation(s) in driver gene(s), leading to the transformation of normal cell into malignant one, followed by rapid proliferation [1]. Head and neck cancers (HNCs) comprise epithelial malignancies of the mucosal lining in upper aerodigestive tract [2]. Carcinogenesis therein is correlated with the use of tobacco, chewing of areca nut (betel quid), alcohol consumption and infection with the human papillomavirus (HPV) [4]. The carcinogenesis of head and neck cancers comprise a complex system of gene-gene and gene-environment interactions.
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