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Sandra J. Gendler
Professor of Biochemistry & Molecular Biology at Mayo Clinic College
of Medicine, Mayo Clinic Scottsdale, and Adjunct Professor, Department
of Molecular & Cellular Biology
Ph.D., University of Southern California
Mucin glycoproteins in disease.
Research Interests
Our laboratory is interested in the role of the MUC1 mucin
in cancer. MUC1 is over-expressed and aberrantly glycosylated in most
adenocarcinomas of the mammary gland, lung, colon, pancreas, stomach,
endometrium, ovary and multiple myelomas and other hematopoietic malignancies.
Alterations in MUC1 expression or glycosylation accompany the development
of cancer and influence cellular growth, transformation, adhesion,
invasion, and immune surveillance. Our primary research goals are
to determine the function of the transmembrane MUC1 mucin in cell
adhesion, tumor progression, metastasis, and modulation of the immune
system and to characterize tumor antigens as tumor vaccines. Over-expression
of MUC1 in the mouse mammary gland results in tumor formation, indicating
that MUC1 is an oncogene. The tumorigenic function of MUC1 appears
to be dependent on the cytoplasmic tail, which is tyrosine phosphorylated
and binds to many proteins capable of transducing signals and/or interacting
with the cytoskeleton. MUC1 appears to function as an oncogene whereby
the cytoplasmic tail acts as a scaffolding protein to coordinate and
enhance multiple growth-promoting and oncogenic signals.
The ubiquitous and aberrant expression of MUC1 on most solid tumors
and some hematological tumors suggests that MUC1 is an immunotherapeutic
target. We are testing powerful new approaches to immunize animals
to MUC1 and other tumor antigens. The goal is the prevention and
treatment of spontaneous tumors and metastases of mammary gland,
pancreas, and colon. Clinical trials in breast cancer patients,
utilizing MUC1/Her-2 peptides, will begin shortly.
Select Publications
Any link on the below references will take you off
of the BMCB site and to an abstract of that particular paper.
Hattrup, C.L., and S.J. Gendler. 2006. MUC1 alters oncogenic events
and transcription in human breast cancer cells. Breast
Cancer Research 8: R37.
Thompson, E.J., K. Shanmugam, C.L. Hattrup, K.L. Kotlarczyk, A.
Gutierrez, J.M. Bradley, P. Mukherjee, and S.J. Gendler. 2006. Tyrosines
in the MUC1 cytoplasmic tail modulate transcription via the ERK1/2
and NF-kappaB pathways. Molecular
Cancer Research 4: 489-497.
Al Masri, A., and S.J. Gendler. 2005. MUC1 affects c-Src signaling
in PyV MT-induced mammary tumorigenesis. Oncogene 24: 5799-5808.
Mukherjee, P., T.L. Tinder, G.D. Basu, and S.J. Gendler. 2005.
MUC1 (CD227) interacts with lck tyrosine kinase in Jurkat lymphoma
cells and normal T cells. Journal
of Leukocyte Biology 77: 90-99.
Schroeder, J.A., A. Al Masri, M.C. Adriance, J.C. Tessier, K.L.
Kotlarczyk, M.C. Thompson, and S.J. Gendler. 2004. MUC1 overexpression
results in mammary gland tumorigenesis and prolonged alveolar differentiation. Oncogene 23: 5739-5747.
Contact Information
Mailing:
Sandra J. Gendler, Professor
Department of Biochemistry & Molecular Biology
Johnson Research Building
Mayo Clinic Scottsdale
13400 East Shea Boulevard
Scottsdale, AZ 85259
Web Site: Home
Page |
Telephone:
480-301-7137
Fax:
480-301-7017
Email:
gendler.sandra@mayo.edu |
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