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Fariborz (Fred) Mortazavi, M.D.
Fariborz (Fred) Mortazavi, M.D.



General Information:

English and Farsi


Assistant Professor in Residence, Department of Medicine
Member, JCCC Signal Transduction and Therapeutics Program Area

Hospital Affiliation(s):

West Los Angeles Veterans Affairs Medical Center


University of Illinois at Chicago, 2003 - 2006
Research Fellowship:
Memorial Sloan Kettering Cancer Center, 2002 - 2003
St. Luke's-Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, 2000-2002
Mt. Sinai Medical Center, 1999-2000
Medical Degree:
M.D., Tehran University of Medical Sciences, Tehran, Iran, 1994


Board Certification(s):
Medical Oncology, American Board of Internal Medicine, 2006
Hematology, American Board of Internal Medicine, 2006
Internal Medicine, American Board of Internal Medicine, 2002

Contact Information:

(310) 268-4567

Practice Information:

Clinical Interest(s):
Thoracic malignancies

Scientific Interest(s):

Studying the signaling pathways that promote invasion and metastasis in lung cancer is currently the focus of Dr. Fred Mortazavi's research. For example, as part of the adherens junction, p120-catenin (p120ctn) plays an important role in the stability of cell-cell adhesions and downregulation of the p120-catenin is reported in a large proportion (60-80 percent) of non-small cell lung cancer (NSCLC) cases. Mortazavi and others reported that p120-catenin is transcriptionally downregulated in NSCLC and identified two signaling pathways that mediate p120-catenin repression. Identifying the prometastatic signaling events in cancer cells could pave the way for the future interventions in order to stop the metastatic process.

Selected Cancer-Related Publications:

Mortazavi F, Dubinett S, Rettig M. c-Crk proto-oncogene contributes to transcriptional repression of p120-catenin in non-small cell lung cancer cells. Clin Exp Metastasis. 2011 Apr;28(4):391-404. Epub 2011 Feb 20.

Mortazavi F, An J, Dubinett S, Rettig M. p120-catenin is transcriptionally downregulated by FOXC2 in non-small cell lung cancer cells. Mol Cancer Res. 2010 May;8(5):762-74. Epub 2010 May 11.