Bif-1 and Bax expression in cutaneous Merkel cell carcinoma.

J Cutan Pathol

Department of Pathology, University of South Florida, College of Medicine, Tampa, FL 33612, USA.

Published: January 2009

Background: Bax-interacting factor-1 (Bif-1) binds to Bax, which in turn activates this proapoptotic protein. In the absence of Bif-1, the ability to induce apoptosis through the intrinsic pathway is greatly reduced. Merkel cell carcinoma (MCC) classically shows an aggressive behavior and lack of response to chemotherapy, which remains unexplained. Previous studies have documented the presence of Bax in MCC, but Bif-1 expression has not been evaluated. Herein, the expression of Bif-1 and Bax in cutaneous MCC is examined.

Materials And Methods: The immunohistochemical expression of Bif-1 and Bax protein was examined in nine cases of MCC. Both positive and negative controls were conducted. All the cases were reviewed by a single dermatopathologist.

Results: Bif-1 was detected in nine cases (100%), and Bax was expressed in six cases (66%). The percent positive cells for Bif-1 in MCC ranged from 85% to 98% positive (mean 93.9%). At the same time, decreased Bax expression was shown with 0-8% positive cells (mean 3.45%).

Conclusion: The increased expression of Bif-1 in MCC is associated with low levels of Bax staining. These findings suggest that the upregulation of Bif-1 could in part be responsible for tumorigenesis in cutaneous MCC. As shown, Bax and Bif-1 expression are not exclusively antithetical; therefore, future studies evaluating the expression of both proteins should be conducted.

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1600-0560.2007.00945.xDOI Listing

Publication Analysis

Top Keywords

bif-1 bax
12
expression bif-1
12
bif-1
11
expression
8
bax expression
8
merkel cell
8
cell carcinoma
8
bax
8
bif-1 expression
8
cutaneous mcc
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!