Patricia Berg

Patricia Berg

George Washington University Medical Center, USA

Title: BP1, A potential oncogene over expressed in Cancer


Patricia Berg received her bachelors degree in mathematics from the University of Chicago, her Ph.D. in microbiology at the Illinois Institute of Technology in Chicago, then pursued Post Doctoral studies at the University of Chicago in molecular biology. Further work at the National Institutes of Health followed, where she cloned the first repressor of the human beta-globin gene, with the idea of using it in therapy of sickle cell anemia to repress the mutant beta-globin gene. Currently she is a Professor of Biochemistry and Molecular Medicine at the George Washington University in Washington, DC, where she is director of a cancer research laboratory. Her work centers on the BP1 gene, which she cloned, and its involvement in breast cancer, the topic of her presentation. Dr. Berg research has been featured on network television and in the New York Times, Washington Post, Washington Times, Los Angeles Times, AP, and Reuters among other major media, and Hillary Clinton and congressional leaders have headlined an event supporting her work.


BP1, a gene we identified and cloned, is a member of the homeobox gene family of transcription factors (TF). BP1 is overexpressed in breast cancer, prostate cancer, ovarian cancer, acute myeloid leukemia, non-small cell lung cancer, and possibly other malignancies as well. Important characteristics of BP1 in breast cancer, our main focus, include findings that: (1) BP1 is expressed in 80% of invasive ductal breast tumors, including 89% of the tumors of African American women compared with 57% of the tumors of Caucasian women. (2) BP1 expression correlates with the progression of breast tumors, from 0% in normal breast tissue to 21% in hyperplasia and 46% in ductal carcinoma in situ. (3) Expression of BP1 is associated with larger tumor size in both women and mice. (4) BP1 appears to be associated with metastasis. Forty-six cases of inflammatory breast cancer were examined and all were positive for BP1 expression, as well as matched lymph nodes in the nine metastatic cases. (5) BP1 overexpression induces oncogene expression. BP1 protein (pBP1) activates the BCL-2 gene; high BCL-2 protein levels are associated with resistance to drug and radiation therapy. BP1 also activates VEGF and c-MYC, as well as other genes important in angiogenesis, invasion and metastasis. pBP1 down-regulates BRCA1. (6) BP1 up-regulates ER alpha and induces estrogen independence. High pBP1 levels can lead to estrogen independence in ER positive breast cancer cells and tumors in mice. In summary, BP1 appears to confer properties on breast cancer cells that lead to a more invasive and aggressive phenotype. Since the functions of homeotic TF are highly conserved, it is likely that BP1 regulates many of the same processes and genes in other malignancies.