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International Journal of Biological Markers 2016-May

Expression of PTEN and its correlation with proliferation marker Ki-67 in head and neck cancer.

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Il collegamento viene salvato negli appunti
Malik W Ahmed
Mahmood A Kayani
Ghulam Shabbir
Syed M Ali
Wajih-Ud-Din Shinwari
Ishrat Mahjabeen

Parole chiave

Astratto

BACKGROUND

PTEN is part of large family of tyrosine phosphatases and has been found inactivated in a wide variety of human cancers.

OBJECTIVE

In the present study we have tried to determine the association of the expression patterns of this gene with carcinogenesis.

METHODS

First, a systematic review was carried out to ascertain the importance of the PTEN gene and its role in carcinogenesis. In the second phase, a case-control study was designed using different expression analysis techniques. Expression of PTEN mRNA was analyzed using reverse transcriptase polymerase chain reaction (RT-PCR).

RESULTS

Significantly downregulated expression of PTEN was observed in patients with head and neck cancer (HNC) compared to adjacent normal-tissue controls. These results were confirmed with quantitative polymerase chain reaction (qPCR). Significant downregulation of the gene was observed in HNC patients compared to adjacent normal-tissue controls. PTEN expression was correlated with different histopathological parameters of the study cohort by Spearman's correlation coefficient and a significant negative correlation was observed with pT stage (r = -0.271*; p<0.02) and grade (r = -0.228*; p<0.02) of HNC tissues. Furthermore, the expression variations of PTEN were correlated with the expression pattern of the proliferation marker Ki-67. Significantly (p<0.008) upregulated expression of Ki-67 was observed in HNC patients compared with adjacent normal-tissue controls This upregulation of Ki-67 was confirmed at the protein level by immunohistochemistry in HNC patients. When Spearman's correlation was carried out a significant negative correlation was observed between PTEN and Ki-67 (r = -0.230*; p<0.03).

CONCLUSIONS

Our data suggest that downregulation of PTEN and overexpression of Ki-67 may contribute to the initiation and progression of HNC.

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