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303 E. Superior St.

Lurie 7-125

Chicago, IL 60611

 

676 N. Saint Clair St.

Suite 1260

Chicago, IL 60611

 

303 E. Chicago Ave.

Ward 9-148

Chicago, IL 60611

 

Ph: 312.503.5600

Fax: 312.503.5603

 

Faculty

 

Boris Pasche, MD, PhD
Assistant Professor
Department of Hematology Oncology

To Contact Dr. Pasche:
phone: 312-695-0320
e-mail: b-pasche@northwestern.edu
Dr. Pasche's website
PubMed Reference Lookup


Research Interests
Dr. Pasche’s research work focuses on the role of Transforming Growth Factor Beta (TGF-b ) in cancer development and progression. TGF-b signaling and growth-inhibition are mediated by the type I TGF-b receptor (Tb R-I). In a search for mutations of this receptor, a polymorphic allele has been discovered, Tb R-I(6A), that has a deletion of three alanines from a nine-alanine stretch. To investigate the possible association of this mutant allele with neoplasms, a case-control study was designed to determine the relative frequency of this allele in patients with various malignancies. There were 123 of 851 (14.6%) Tb R-I(6A) heterozygotes among cases and 78 of 735 (10.6%) heterozygotes among controls (p<0.02, Fisher’s exact test). Further, a higher than expected number of Tb R-I(6A) homozygotes was observed among cases (9 out of 851) whereas there were no Tb R-I(6A) homozygotes among 735 controls of similar ethnic background (p< 0.01, Fisher’s exact test). A subset analysis revealed the presence of four Tb R-I(6A) homozygotes among 112 patients with colon cancer (p< 0.01, Fisher’s exact test). Signal transduction of Tb R-I and Tb R-I(6A) was assessed in stably transfected cell lines by means of TGF-b growth-inhibition assays. Tb R-I(6A) cells were less effectively inhibited by TGF-b than Tb R-I cells (p< 0.01). Using the Smad4-specific DNA binding element reporter gene construct, pSBE4, other investigators have recently corroborated these findings.

 


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