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Krishna A, Singh S, Kumar V, et al. Molecular concept in human oral cancer. Natl J Maxillofac Surg. 2015;6(1):9-15doi: 10.4103/0975-5950.168235.
Krishna, A., Singh, S., Kumar, V., & Pal, U. S. (2015). Molecular concept in human oral cancer. National journal of maxillofacial surgery, 6(1), 9-15. https://doi.org/10.4103/0975-5950.168235
Krishna, Akhilesh, et al. "Molecular concept in human oral cancer." National journal of maxillofacial surgery vol. 6,1 (2015): 9-15. doi: https://doi.org/10.4103/0975-5950.168235
Krishna A, Singh S, Kumar V, Pal US. Molecular concept in human oral cancer. Natl J Maxillofac Surg. 2015 Jan-Jun;6(1):9-15. doi: 10.4103/0975-5950.168235. PMID: 26668446; PMCID: PMC4668742.
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Natl J Maxillofac Surg. 2015 Jan-Jun;6(1):9-15. doi: 10.4103/0975-5950.168235.

Molecular concept in human oral cancer.

National journal of maxillofacial surgery

Akhilesh Krishna, Shraddha Singh, Vijay Kumar, U S Pal

Affiliations

  1. Department of Physiology, King George's Medical University, Lucknow, Uttar Pradesh, India.
  2. Department of Surgical Oncology, King George's Medical University, Lucknow, Uttar Pradesh, India.
  3. Department of Oral and Maxillofacial Surgery, King George's Medical University, Lucknow, Uttar Pradesh, India.

PMID: 26668446 PMCID: PMC4668742 DOI: 10.4103/0975-5950.168235

Abstract

The incidence of oral cancer remains high in both Asian and Western countries. Several risk factors associated with development of oral cancer are now well-known, including tobacco chewing, smoking, and alcohol consumption. Cancerous risk factors may cause many genetic events through chromosomal alteration or mutations in genetic material and lead to progression and development of oral cancer through histological progress, carcinogenesis. Oral squamous carcinogenesis is a multistep process in which multiple genetic events occur that alter the normal functions of proto-oncogenes/oncogenes and tumor suppressor genes. Furthermore, these gene alterations can deregulate the normal activity such as increase in the production of growth factors (transforming growth factor-α [TGF-α], TGF-β, platelet-derived growth factor, etc.) or numbers of cell surface receptors (epidermal growth factor receptor, G-protein-coupled receptor, etc.), enhanced intracellular messenger signaling and mutated production of transcription factors (ras gene family, c-myc gene) which results disturb to tightly regulated signaling pathways of normal cell. Several oncogenes and tumor suppressor genes have been implicated in oral cancer especially cyclin family, ras, PRAD-1, cyclin-dependent kinase inhibitors, p53 and RB1. Viral infections, particularly with oncogenic human papilloma virus subtype (16 and 18) and Epstein-Barr virus have tumorigenic effect on oral epithelia. Worldwide, this is an urgent need to initiate oral cancer research programs at molecular and genetic level which investigates the causes of genetic and molecular defect, responsible for malignancy. This approach may lead to development of target dependent tumor-specific drugs and appropriate gene therapy.

Keywords: Growth factor; oncogenes; oral cancer; transcription factor

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