Co-overexpression of p53 and c-myc proteins linked with advanced stages of betel- and tobacco-related oral squamous cell carcinomas from eastern India
Co-overexpression of p53 and c-myc proteins linked with advanced stages of betel- and tobacco-related oral squamous cell carcinomas from eastern India
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DOI：
10.1046/j.0909-8836.1998.eos106502.x
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发表时间：
1998-10-01
影响因子：
1.9
通讯作者：
Das, BR
中科院分区：
文献类型：
--
作者：
Baral, R;Patnaik, S;Das, BR
流行病学证据表明，大量食用槟榔和槟榔烟草是印度东部人口口腔癌高发的原因，这与西方国家口腔鳞状细胞癌（SCC）的病因明显不同。在这里，p53和c-myc蛋白的表达进行了研究，在口腔鳞状细胞癌从这个病因不同的人口免疫组织化学。在48例口腔鳞癌中，22例（45.8%）p53阳性，27例（56.3%）c-myc阳性。考虑到p53/c-myc表达模式，单独或组合，将群体分为四组，即，p53和c-myc均阳性; p53阳性- c-myc阴性; c-myc阳性- p53阴性;以及p53和c-myc均阴性。p53和c-myc均阳性的肿瘤处于疾病的晚期（低分化，肿瘤3期，核III级），而在既无p53也无c-myc免疫反应性的肿瘤中检测到口腔SCC的最早期，其余两组的传言通常限于早期至中期。这些观察结果表明，槟榔和烟草相关的口腔SCC的快速进展可能与这两种癌蛋白的同时参与有关。本研究还探讨了p53/c-myc表达与自发性细胞凋亡的关系。在c-myc阳性而p53阴性的肿瘤中发现更多的凋亡细胞。这一初步观察需要进一步的分子研究的作用，p53和c-myc基因的进展，这种流行病学上不同的口腔癌。
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, rumours 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.