Co‐overexpression of p53 and c‐myc proteins linked with advanced stages of betel‐ and tobacco‐related oral squamous cell carcinomas from eastern India

Abstract

Epidemiological evidence suggests that heavy consumption of betel quid and tobacco with areca nuts is the cause of high incidence of oral cancer in eastern part of Indian population, which is distinctly different from the etiology of oral squamous cell carcinomas (SCCs) in western countries. Here, expression of p53 and c-myc protein was studied in oral SCCs from this etiologically distinct population by immunohistochemistry. Out of 48 specimens of oral SCCs, 22 (45.8%) exhibited p53 positivity and 27 (56.3%) showed immunoreactivity with c-myc antibody. Considering the p53/c-myc expression pattern, either alone or in combination, the population was divided into four groups, i.e., both p53 and c-myc positive; p53 positive-c-myc negative; c-myc positive - p53 negative; and both p53 and c-myc negative. Tumours with both p53 and c-myc positivity were in advanced stages of the disease (poorly differentiated, tumour stage 3, nuclear grade III), whereas earliest stage of oral SCCs was detected in tumours with neither p53 nor c-myc immunoreactivity. Tumours of remaining two groups were generally restricted to early to moderate stages. These observations suggest that rapid progression of the betel- and tobacco-related oral SCCs may be associated with a simultaneous involvement of these two oncoproteins. The study also attempted to find out the relationship of p53/c-myc expression with spontaneous apoptosis. More apoptotic cells were found in c-myc positive but p53 negative tumours. This preliminary observation requires further molecular investigation of the role of p53 and c-myc genes for the progression of this epidemiologically distinct oral carcinogenesis.

Proteomics Analysis Identifies Molecular Targets Related to Diabetes Mellitus-associated Bladder Dysfunction

“…These immunoblot results for the two transcriptional factors are consistent with the network analysis prediction. These data are also consistent with the existing literature documenting that the induction of the tumor suppressor p53 is involved in negative regulation of c-Myc expression (37), although there are also reported cases where both p53 and c-Myc are co-expressed in colorectal and oral cancer (38,39).…”

Molecular Alterations in Oral Carcinogenesis: Significant Risk Predictors in Malignant Transformation and Tumor Progression

“…We observed a significant correlation between c-myc and p53 in early stage oral carcinoma. A similar correlation was noted in oral carcinomas by Baral et al (19).…”

“…Also, data concerning the role of Stat3 in oral carcinogenesis and its interaction with the cell cycle machinery are limited (13)(14)(15)(16). Activated c-myc has been shown to contribute to the stepwise progression of tumorigenesis both in vitro and in vivo (17), but there are few reports on its role in oral carcinogenesis (18,19). Ras proteins play a key role in integrating mitogenic signals with cell cycle progression (20), but the role of H-ras in oral carcinogenesis is unclear.…”

Quantitative determination of c-myc facilitates the assessment of prognosis of OSCC patients

“…Several studies have analyzed c-myc expression in this type of tumor showing different results, with an average positivity of 41.28% (2.4-75%) between the different studies (6,(26)(27)(28)(29)(30)(31)(32)(33)(34). The results are extremely contradictory, as well as the variation in the quantification methods.…”