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Abstract

HEAD AND NECK SQUAMOUS CELL CARCINOMA: A MOLECULAR LANDSCAPE

*Pramod Singh Khatri and Sakshi Shukla

ABSTRACT

HNSCC represents about 6% of all cancer. The general 5 year survival rate for patients with HNSCC cancer is among the lowest of the major cancer types and has not enhanced drastically amid the last decade. The pathological staging, specifically the nodal stage, is the most essential component in HNSCC. The absence of progress in head and neck oncology underlines the significance of molecular studies to characterize alterations that may associate with tumor. The molecular alterations that saw in HNSCC are essentially because of oncogene activation and tumor suppressor gene inactivation, prompting deregulation of cell expansion. Propels in the understanding of the molecular basis of HNSCC will help in the identification of new molecular markers that could be utilized for a more precise diagnosis and evaluation of prognosis and may open the path for novel ways to deal with treatment and counteractive action. The genetic modifications seen in head and neck cancer are because of oncogene activation (gain of function transformations) and tumor suppressor gene inactivation (loss of function mutations), prompting deregulation of cell multiplication and death. These genetic changes incorporate gene amplification and overexpression of oncogenes, for example, myc, erbB-2, EGFR and cyclinD1 and transformations, deletion and hyper methylation prompting p16 and TP53 tumor suppressor gene inactivation. Furthermore, loss of heterozygosity in a several chromosomal regions is also found, proposing that other tumor suppressor gene not yet recognized which are involved in the tumorigenic procedure of head and neck cancer. The temporal sequence of the genetic modifications amid HNSCC development and progression has not yet been characterized and HNSCC represents about 6% of all cancer. The general 5 year survival rate for patients with HNSCC cancer is among the lowest of the major cancer types and has not enhanced drastically amid the last decade. The pathological staging, specifically the nodal stage, is the most essential component in HNSCC. The absence of progress in head and neck oncology underlines the significance of molecular studies to characterize alterations that may associate with tumor. The molecular alterations that saw in HNSCC are essentially because of oncogene activation and tumor suppressor gene inactivation, prompting deregulation of cell expansion. Propels in the understanding of the molecular basis of HNSCC will help in the identification of new molecular markers that could be utilized for a more precise diagnosis and evaluation of prognosis and may open the path for novel ways to deal with treatment and counteractive action. The genetic modifications seen in head and neck cancer are because of oncogene activation (gain of function transformations) and tumor suppressor gene inactivation (loss of function mutations), prompting deregulation of cell multiplication and death. These genetic changes incorporate gene amplification and overexpression of oncogenes, for example, myc, erbB-2, EGFR and cyclinD1 and transformations, deletion and hyper methylation prompting p16 and TP53 tumor suppressor gene inactivation. Furthermore, loss of heterozygosity in a several chromosomal regions is also found, proposing that other tumor suppressor gene not yet recognized which are involved in the tumorigenic procedure of head and neck cancer. The temporal sequence of the genetic modifications amid HNSCC development and progression has not yet been characterized and HNSCC represents about 6% of all cancer. The general 5 year survival rate for patients with HNSCC cancer is among the lowest of the major cancer types and has not enhanced drastically amid the last decade. The pathological staging, specifically the nodal stage, is the most essential component in HNSCC. The absence of progress in head and neck oncology underlines the significance of molecular studies to characterize alterations that may associate with tumor. The molecular alterations that saw in HNSCC are essentially because of oncogene activation and tumor suppressor gene inactivation, prompting deregulation of cell expansion. Propels in the understanding of the molecular basis of HNSCC will help in the identification of new molecular markers that could be utilized for a more precise diagnosis and evaluation of prognosis and may open the path for novel ways to deal with treatment and counteractive action. The genetic modifications seen in head and neck cancer are because of oncogene activation (gain of function transformations) and tumor suppressor gene inactivation (loss of function mutations), prompting deregulation of cell multiplication and death. These genetic changes incorporate gene amplification and overexpression of oncogenes, for example, myc, erbB-2, EGFR and cyclinD1 and transformations, deletion and hyper methylation prompting p16 and TP53 tumor suppressor gene inactivation. Furthermore, loss of heterozygosity in a several chromosomal regions is also found, proposing that other tumor suppressor gene not yet recognized which are involved in the tumorigenic procedure of head and neck cancer. The temporal sequence of the genetic modifications amid HNSCC development and progression has not yet been characterized and their prognostic and diagnostic significance is still dubious. Progresses in the comprehension of the molecular basis of head and neck cancer ought to help in the identification of new markers that could be utilized for the prognosis, diagnosis and treatment of the cancer.

Keywords: HNSCC, Loss of heterozygosity, Cyclin D1, TP53 tumor suppressor gene.


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