Professor of Biochemistry and Molecular Medicine
Office Phone: 202-994-2810
Department: Biochemistry and Molecular Medicine
- BA, University of Chicago, 1965
- PhD, University of Chicago, 1973
BP1, a Potential Oncogene Activated in Breast Cancer and Other Malignancies
We isolated the BP1 gene, a transcription factor belonging to the homeobox gene family, and have discovered that activation of BP1 is associated with a number of malignancies: (1) BP1 protein is present in 80% of invasive ductal breast tumors. (2) BP1 expression correlates with the progression of breast tumors. The frequency of BP1 positivity, distribution and intensity of BP1 expression all increased with the progression of tumor development from 0% (normal) to 21% in hyperplasia, 46% in ductal carcinoma in situ, and 81% in IDC. (3) Increased expression of BP1 is associated with larger tumor size. (4) BP1 expression is associated with metastasis. (5) Overexpression of BP1 confers an aggressive phenotype on breast cancer cells. (6) High BP1 levels are associated with estrogen independence in mice. (7) BP1 overexpression activates oncogenes expression such as BCL-2, a death suppressor, and oncogenes important in angiogenesis, invasion and metastasis, including MET, TWIST, c-FOS and MMP-9. (8) BP1 is activated in other malignancies. We found that BP1 is activated in 70% of prostate cancers and 63% of acute myeloid leukemias. A group in Canada has shown BP1 activation in non-small cell lung cancer. Currently we are developing a blood test for potential early detection of BP1 protein, testing drugs that may repress BP1 and working to better understand the molecular effects of BP1 in breast cancer. If we can turn the gene off, perhaps patients would have a better chance of survival.
View publications by this faculty member.
Fu, S., Ginsberg, E., Kirolikar, S., Rheey, J., Bivona, L., Scwartz, A., Man, Y-G., Pinzone, J. J., Stevenson, H., Simmens, S., Teal, C., Kim, K.S., Vonderhaar, B.K., and Berg, P.E. BP1 Promotes Aggressiveness of ER Positive Breast Cancer Cells. Submitted.
Hwang, B.-J., Nguyen, T., Bivona, L. and Berg, P.E. BP1 Upregulates Twist and Induces the Epithelial to Mesenchymal Transition in Breast Cancer Cells. Submitted.
Kirolikar, S. and Berg, P.E. BP1 (Beta-Protein 1). Atlas Genet. Cytogenet. Oncol. Haematol. 2011. Updated 2012.
Kluk, N.J., Fu, Y., Formolo, T.A., Zhang, L., Hindle, A.K., Man, Y-G., Siegel, R.S., Berg, P.E., Deng, C., McCaffrey, T.A., and Fu, S.W. BP1, an isoform of the DLX4 homeoprotein, negatively regulates BRCA1 in sporadic breast cancer. Int. J. Biol. Sciences 6: 491-503, 2010.
Tigli, O., Bivona, L., Berg, P. and Zaghloul, M. Fabrication and characterization of a surface acoustic wave biosensor in CMOS technology for cancer biomarker detection. IEEE Transactions on Biomedical Circuits and Systems 4; 62-73, 2010.
Scwartz, A.A., Man, Y-G., Rezai, M.K., Simmens, S., and Berg, P.E. BP1, a homeoprotein, is significantly expressed in prostate adenocarcinoma and is concordant with prostatic intraepithelial neoplasia (PIN). Modern Pathol. 22: 1-6, 2009.
Man, Y-G., Scwartz, A., Levine, P.H., Teal, C. and Berg, P.E. BP1, a putative signature marker for inflammatory breast cancer or tumor aggressiveness. Cancer Biomarkers 5: 9-17, 2009.
Cavalli, L.R., Man, Y-G., Scwartz, A., Rone, J.D., Zhang, Y., Urban, C.A., Lima, R.S., Haddad, B.R., and Berg, P.E. Amplification of the BP1 homeobox gene in breast cancer. Cancer Genetics and Cytogenetics 187: 19-24, 2008.
Awwad, R.T., Do, K., Stevenson, H., Fu, S.W., LoCoco, F., Costello, M., Campbell, C.L., and Berg, P.E. Overexpression of BP1, a homeobox gene, is associated with resistance to all-trans retinoic acid in acute promyelocytic leukemia cells. Ann. Hematol. 87: 195-203, 2008.
Stevenson, H.S., Fu, S., Pinzone, J.J., Campbell, C.L., Simmens, S.J. and Berg, P.E. BP1 transcriptionally activates bcl-2 and inhibits TNF?-induced cell death in MCF7 breast cancer cells. Br. Ca. Res. 9: R60-69, 2007.
Industry Relationships and Collaborations
This faculty member (or a member of their immediate family) has reported a financial interest with the health care related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.