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Drug Res (Stuttg) 2015; 65(10): 535-539
DOI: 10.1055/s-0034-1390459
Original Article
© Georg Thieme Verlag KG Stuttgart · New York

Increased Angiogenesis and Decreased Programmed Cell Death Increases the Risk of Uterine Cervical Cancer

Z.-l. Qin
1   Department of Gynaecology, Jinan Maternity and Child Care Hospital, Shandong, China
,
X.-x. Zheng
1   Department of Gynaecology, Jinan Maternity and Child Care Hospital, Shandong, China
,
Y.-h. Xu
1   Department of Gynaecology, Jinan Maternity and Child Care Hospital, Shandong, China
› Author Affiliations
Further Information

Publication History

received 02 September 2014

accepted 12 September 2014

Publication Date:
21 October 2014 (online)

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Abstract

Introduction: Cervical cancer is one of the most common female malignancies and leading cause for high mortality rate. In the present study we made an attempt to determine the extent of angiogenesis, apoptosis, accumulation of mutant p53 protein, cell proliferation rate in the uterine cervical cancer tissues.

Materials and Methods: Cervical cancer samples were obtained from patients and they were subjected to PCR analysis and immunocytochemistry.

Results: A total of 30 cervical cancer tissue samples were analyzed, by PCR, we found 25 collected cervical cancer samples showed HPV-16 and E6 positive. Further, we observed the increased CD34 expression was associated with HPV-16 and E6 positive cancer tissues when compared to the corresponding control tissues. This elevated level of CD34 confirms the increased extent of angiogenesis in cervical cancer tissues. Further by immunocytochemistry we have demonstrated that the rate of apoptosis is reduced, over expression of bcl-2, Ki 67 and thus increases rate of cell proliferation.

Discussion: Therefore, our data suggest that development of new anticancer or antiviral drugs could efficiently compromise the HPV-16 mediated angiogenesis and reduced apoptosis in cervical cancer and thus will improve the survival rate of patients.

Key words

cervical cancer - human papilloma virus - angiogenesis - apoptosis - cell proliferation
 

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