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Faculty Detail Faculty Entry   
Name BORIS C PASCHE  
Campus Address NP 2566 Zip 3300
Phone 205-934-9591
E-mail uifcftu@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:uifcftu@uab.edu">uifcftu@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  General Clinical Research Center  Minority Health & Research Center Professor
Primary  Medicine  Med - Hematology & Oncology Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor

Biographical Sketch 
Education and degrees

1980-1983 University of Lausanne, Lausanne, Switzerland
1983-1989 Karolinska Institute, Stockholm, Sweden
1986 M.D. degree, Karolinska Institute
1987 M.D. degree, University of Lausanne
1989 Ph.D. degree, Karolinska Institute

Board certifications

1994 Diplomate, American Board of Internal Medicine
1997 Diplomate, American Board of Medical Oncology
Recertified through 2018
1999 Diplomate, American Board of Hematology

Postdoctoral Research Training

November 1989- Research fellow in the laboratory of Dr. Joseph Loscalzo,
May 1992 Cardiovascular Division, Brigham and Women's Hospital,
Harvard Medical School
January 1996- Research fellow in the laboratory of Dr. Joan Massagué,
June 2000 Cell Biology Program, Howard Hughes Medical Institute and
Sloan-Kettering Institute for Cancer Research

Graduate Medical Training

June 1992-June 1994 Internship and Residency in Medicine, The New York Hospital
Cornell Medical Center
July 1994-June 1997 Fellowship in Hematology/Oncology, Memorial Sloan-Kettering Cancer
Center and the New York Hospital, Cornell University Medical College

Clinical Appointments

1988-2000 Assistant in Medicine, Clinique Bon Port, Montreux, Switzerland
1993-2000 Assistant Physician I, The New York Hospital and the Memorial Sloan-Kettering Cancer Center-Cornell University Medical College
2001-2008 Attending Physician, Northwestern Memorial Hospital
2009- Attending Physician, UAB Hospitals

Academic Appointments

1989-1992 Research Fellow in Medicine, Harvard Medical School
1992-2000 Clinical Associate in Medicine, Cornell University Medical College
2000-2005 Assistant Professor of Medicine
Northwestern University Feinberg School of Medicine
2002-2008 Director, Cancer Genetics Program, Robert H. Lurie Comprehensive Cancer Center and Feinberg School of Medicine
2006-2008 Associate Professor of Medicine
Northwestern University Feinberg School of Medicine
2006-2007 Co-Leader, Cancer Genes and Molecular Targeting Program, Robert H. Lurie Comprehensive Cancer Center
2008 Leader, Cancer Genes and Molecular Targeting Program, Robert H. Lurie Comprehensive Cancer Center
2008- Professor of Medicine with Tenure and Director, Division of Hematology/Oncology Division, The University of Alabama at Birmingham
2008-2009 Associate Director for Translational Research, The University of Alabama Comprehensive Cancer Center
2009-2011 Deputy Director, The University of Alabama Comprehensive Cancer Center
2008- Martha Ann and David L. May Endowed Chair in Cancer Research

Editorial Positions

2003- Contributing Editor, The Journal of the American Medical Association (JAMA)
2004- Editor, The Journal of Experimental and Clinical Cancer Research

Grant Review Panels

2010 Chair, Department of Defense Colorectal Cancer review panel
2010- Member, NCI Cancer Genetics (CG) Study section
2008- Member (adhoc), NCI Cancer Genetics (CG) Study section
2008- Member, AACR Colorectal Cancer Review Committee
2008 Member, Komen for the Cure Pathobiology-1 Review Panel
2007 Grant reviewer (adhoc), Instituto Toscano Tumori, Florence, Italy
2004- Member, Breast Cancer Center of Excellence and Era of Hope Scholar Award Review Panels, Department of Defense

Society Memberships
Organization Name Position Held Org Link
No records
 

Research/Clinical Interest
Title
Description
Our laboratory focuses on three main projects: 1) The role of Transforming Growth Factor Beta (TGF-beta) in cancer development and progression, 2) The biological effects of amplitude-modulated electromagnetic fields, and 3) The role of variants of the adiponectin pathway in cancer development.
1) TGF-beta is one of the most potent inhibitor of normal cell growth and is also a potent modulator of the immune system. TGF-&#946; signaling and growth-inhibition are mediated by the type I TGF-beta receptor (TGFBR1). We have previously identified a common mutant form of this gene, TGFBR1*6A, that is 9 base pairs shorter than TGFBR1. TGFBR1*6A is shorter than TGFBR1: it has a deletion of three GCG triplets coding for alanine within a nine alanine (9A) repeat of TGFBR1 exon 1 resulting in six alanines (6A) repeats. In normal epithelial cells TGFBR1*6A (*6A) mediates TGF-beta growth inhibitory signals less effectively than TGFBR1 (*9A). In cancer cells *6A is capable of switching TGF-beta growth inhibitory signals into growth stimulatory signals. This appears to be mediated by *6A signal sequence. Our laboratory has shown that *6A is somatically acquired in a large proportion of liver metastases from colon cancer. Epidemiological studies suggest that *6A is a candidate tumor susceptibility allele that is associated with an increased incidence of various types of cancer. Our discovery that decreased TGFBR1 signaling was associated with cancer risk led us to develop a novel mouse model of Tgfbr1 haploinsufficiency to test the hypothesis that constitutively decreased Tgfbr1 signaling enhances cancer risk. This mouse model led to the discovery that constitutively decreased TGFBR1 signaling is a potent modifier of colorectal cancer in mice and in humans. We are studying the molecular mechanisms underlying the biological effects of constitutively decreased TGFBR1 signaling.
2) We have previously shown that the intrabuccal administration of low and safe levels of electromagnetic fields, amplitude-modulated at a frequency of 42.7 Hz by means of a battery-powered portable device modifies the electroencephalographic activity of healthy subject, is associated with subjective and objective relaxation effects. We have also shown that sequential administration of four insomnia-specific frequencies, including 42.7 Hz, results in a significant decrease in sleep latency and a significant increase in total sleep time in patients suffering from chronic insomnia. This approach has been termed Low Energy Emission Therapy (LEET). Dosimetric studies have shown that the amount of electromagnetic fields delivered to the brain with this approach is 100 to 1000 times lower than the amount of electromagnetic fields delivered by handheld cellular phones and does not result in any heating effect within the brain. The U.S. FDA has determined that such a device is not a significant risk device. A long-term follow-up survey of 807 patients who have received this therapy revealed that the rate of adverse reactions were low and were not associated with increases in the incidence of malignancy or coronary heart disease. We hypothesized that the same approach may be used for the treatment of cancer. We have recently identified cancer-specific modulation frequencies, which have yielded therapeutic responses in patients with advanced cancer. We are studying the molecular mechanisms underlying the biological effects of cancer-specific amplitude-modulated electromagnetic fields.
3) Current epidemiologic evidence suggests an association between obesity, hyperinsulinemia and breast as well as colorectal cancer risk. Adiponectin is a hormone secreted by the adipose tissue, and serum levels are inversely correlated with obesity and hyperinsulinemia. We have recently shown that common variants of the adiponectin and type I adiponectin receptor are associated with breast and colorectal cancer risk. We are currently studying the association of the adiponectin pathway with breast and colorectal cancer risk.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Bian, Y., Knobloch, T.J., Sadim, M., Kaklamani, V., Raji, A, Yang, G.-Y., Weghorst, C.M., Pasche, B.
Somatic acquisition of TGFBR1*6A by epithelial and stromal cells during cancer development.
Hum Mol Genetics 2007, 16: 3128-3135
 		 17890272 
Kaklamani, V., Sadim, M., Hsi, A., Offit, K., Oddoux, C., Ostrer, H., Ahsan, H., Pasche, B., Mantzoros, C.
Variants of the Adiponectin and Adiponectin 1 receptor genes and breast cancer risk
Cancer Research 2008, 68:3178-3184
 		 18451143 
Valle, L., Serena-Acedo, T., Liyanarachchi, S., Hampel, H., Comeras, I., Li, Z., Zeng, Q., Zhang, H.T., Pennison, M., Sadim, M., Pasche, B., Tanner, S., de la Chapelle, A.
Germline allele-specific expression of TGFBR1 predisposes to colorectal cancer
Science 2008, 321:1361-1365
 		 1159397 
Kaklamani, V., Sadim, M., Do, A., Wisinski, K., Gulden, C., Offit, K., Baron, J., Ahsan, H., Mantzoros, C., Pasche, B.
Variants of the adiponectin (ADIPOQ) and adiponectin receptor 1 (ADIPOR1) genes and colorectal cancer risk
Journal of the American Medical Association 2008, 300:1523-31
18827209
 		 18827209 
Kaklamani, V.G., Sadim, M., Koumantaki, Y., Kaklamanis, P., Pasche, B.
Role of Polymorphisms in AdamantiadesBehçet's Disease
Journal of Rheumatology 2008,35:2376-8
 		 18925687 
Varga, J., Pasche, B.
Antitransforming growth factor-beta therapy in fibrosis: recent progress and implications for systemic sclerosis.
Curr Opin Rheumatol 2008, 20(6):720-8
 		 18946334 
Zeng, Q., Phukan, S., Xu, Y., Sadim, M., Rosman, D., Pennison, M., Liao, J., Yang, G.-Y., Huang, C.-C., Valle, L., Di Cristofano, A., de la Chapelle, A., Pasche, B.
Tgfbr1 haploinsufficiency is a potent modifier of colon cancer development
Cancer Res 2009, 69:678-686
 		 19147584 
Varga J, Pasche B.
Transforming growth factor beta as a therapeutic target in systemic sclerosis.
Nat Rev Rheumatol. 2009 Apr;5(4):200-6.

 		 19337284 
 

Keywords
TGF-beta cancer susceptibility treatment amplitude-modulated electromagnetic fields TGFBR1*6A

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