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Detection of survivin and p53 in human oral cancer: Correlation with clinicopathologic findings
Author(s) -
Khan Zakir,
Tiwari Ram P.,
Mulherkar Rita,
Sah Nand K.,
Prasad Godavarthi BKS,
Shrivastava Braj R.,
Bisen Prakash S.
Publication year - 2009
Publication title -
head and neck
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 127
eISSN - 1097-0347
pISSN - 1043-3074
DOI - 10.1002/hed.21071
Subject(s) - survivin , cancer , correlation , medicine , oncology , cancer research , mathematics , geometry
Background Survivin, an inhibitor of apoptosis, is overexpressed in cancer. It has been implicated in both prevention of apoptosis and cell cycle regulation. We investigated the distribution of antiapoptotic protein survivin in 29 oral squamous cell carcinoma (OSCC) and 16 oral premalignant lesions. It has been suggested that wild‐type p53 represses survivin expression. Therefore, we investigated the status of p53 in relation to survivin to determine the potential involvement in oral tumorigenesis. Methods Oral cancer tissues were freshly obtained at the time of surgery and classified as per general rules of head and neck cancer (TNM classification). Immunohistochemistry and reverse transcriptase‐polymerase chain reaction were conducted to study the expression of survivin and p53. The Fisher's exact test was employed to determine the association of survivin and p53 with clinicopathologic parameters of the subjects being studied. Results Positive staining for survivin was found in 72% OSCC and 44% oral premalignant lesions with no immunoreactions in the corresponding normal tissues. For p53, 59% OSCC, 38% premalignant lesions, and 14% normal tissues were positive. Importantly, about half of the p53‐positive OSCC and premalignant tissues also showed survivin positivity (28% OSCC and 18% premalignant lesions). Further, it is observed that the number of survivin positive cells was significantly higher in the p53‐positive group. Survivin is expressed in a varying proportion of cells, and in majority of patients it was localized in cytoplasm, whereas p53 is strictly restricted to the nucleus. The survivin expression levels in both primary OSCC and premalignant lesions were significantly higher than in normal oral tissues (OSCC, p < .0008; premalignant lesions, p < .04). No significant correlations between survivin and p53 expression with clinicopathologic parameters were found. Conclusions Frequent overexpression of apoptosis regulators, survivin and p53, in OSCC as well as in oral premalignant lesions were found. Overexpression of these 2 markers in premalignant lesions suggest a role in early stages of oral carcinogenesis. © 2009 Wiley Periodicals, Inc. Head Neck, 2009