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Lalita R. Shevde-Samant, Ph.D.

Associate Professor of Oncologic Sciences

Director, USA-MCI Biobank

Director, Cancer Biology Graduate Track

CABTRAC Member Institution

Office:
USA Mitchell Cancer Institute
1660 Springhill Avenue
Mobile, AL. 36604
(251) 445-9854
lsamant@usouthal.edu

Research Interests:
-Investigation of the molecular mechanisms and signaling pathways that regulate malignant behavior and drug resistance of breast cancer and melanoma.

Honors and Academic Achievements:
-Principal Investigator, IDEA Award, Department of Defense Breast Cancer Research Program, 2007-10.
-Mayer Mitchell Annual Award for Excellence in Cancer Research. In recognition of Outstanding contributions to Research in Oncologic Science, 2010.
-Principal Investigator, Basic, Clinical & Translational Research grant (BCTR0402317), Susan G. Komen Breast Cancer Foundation, 2005-07.
-Principal Investigator, American Cancer Society-IRG, (IRG-60-001-44 and CA 13148-31) University of Alabama at Brimingham, 2003-2004.
-Principal Investigator, UAB Breast SPORE-Pilot Grant (CA89019), University of Alabama at Birmingham, 2003-2004.
-AACR- Genentech, Inc. Scholar-in-Training Award, 92nd Annual Meeting of the American Association of Cancer Research, 2001.
-Susan G. Komen Breast Cancer Foundation, Fellowship Award, 2000-2003.

Education:
-Ph.D., Applied Biology (Tumor Immunology), University of Mumbai, India. (1999)
-M.S., Microbiology, University of Baroda, India. (1994)
-B.S., Microbiology, University of Mumbai, India. (1992)

Professional Appointments:
-Research Instructor, Department of Pathology/ Molecular and Cellular Pathology University of Alabama, Birmingham, AL (2003-2004).
-Associate Scientist, Women’s Cancer Section, Comprehensive Cancer Center, University of Alabama at Birmingham, AL (2002-2004).
-Assistant Professor, Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL (2004-2011).
-Assistant Professor, Department of Cell Biology & Neurosciences, University of South Alabama, Mobile, AL (2007-2011).
-Associate Professor, Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL (2011-present).
-Associate Professor, Department of Cell Biology & Neurosciences, University of South Alabama, Mobile, AL (2011-present).

Service:
-Scientific Reviewer, Department of Defense, Breast Cancer Research Program, 2004-2010
-Scientific Reviewer, Komen Foundation, 2005-2009
-Scientific Reviewer, Cancer Research UK
-Scientific Reviewer, Prostate Cancer Foundation of Australia

Molecular determinants of tumor progression and metastasis of breast cancer.
My laboratory has determined that there exists a yin-and-yang relationship between Merlin (NF2) and OPN in breast cancer. We have determined that the expression of Merlin is post-translationally regulated in breast cancer. Specifically, the research centers on characterizing Merlin as a tumor suppressor in breast cancer, determining the mechanism(s) that lead to post-translational loss of Merlin expression in breast cancer and develop strategies to re-instate the expression and function of Merlin in breast cancer cells as a means of intervening in the treatment breast cancer.

Role of Hedgehog (Hh) pathway in metastasis of breast cancer.
We have characterized the role of Hh signaling in regulating malignant behavior of tumor cells. Our studies focus on understanding the role of autocrine and paracrine Hh signaling in influencing tumor progression and metastasis.

Nuclear protein 1 (NUPR1) in chemoresistance.
We have published our work showing that NUPR1 mediates resistance to conventional chemotherapeutic drugs, likely through the involvement of p21 (Cancer Metastasis Rev (1-2):225-32, 2009 and Curr Cancer Drug Targets 8(5):421-30, 2008.). Studies are in progress to determine the role of p21 in the signaling downstream of NUPR1, with a focus on chemoresistance.

1. Morrow, K. A., Das, S., Metge, B.M., Ye, K., Mulekar, M.S., Tucker, J.A., Samant, R.S., Shevde, L.A. The tumor suppressor Merlin is lost in breast cancer by osteopontin-induced degradation. Accepted for publication in J Biol Chem. September 30th 2011.

2. Harris, L.G., Pannell, L.K., Singh, S., Samant, R.S., Shevde, L.A. Hedgehog signaling promotes breast cancer vascularity and spontaneous hematogenous metastasis by upregulating CYR61. Accepted for publication in Oncogene, September 23rd, 2011.

3. Menezes, M.E., Devine, D.J., Shevde, L.A., Samant, R.S. Dickkopf1: A tumor suppressor or metastasis promoter. Accepted for publication in Int. J. Cancer

4. Harris, L.G., Samant, R.S., Shevde, L.A. Hedgehog signaling: Networking to nurture a pro-malignant tumor microenvironment. Mol. Cancer Res. 9(9): 1169-1174, 2011.

5. Das, S., Samant, R.S., Shevde, L.A. Hedgehog signaling induced by breast cancer cells promotes osteoclastogenesis and osteolysis. J. Biol. Chem. 286(11): 9612-9622, 2011.

6. Mitra, A., Menezes, M.E., Shevde, L.A., Samant R. S. DNAJB6 induces degradation of ß-catenin and causes partial reversal of mesenchymal phenotype. J. Biol. Chem. 285(32): 24686-24694, 2010.

7. Das S., Harris L.G., Metge B.J., Liu S., Riker A.I., Samant R.S., Shevde L.A. The Hedgehog pathway transcription factor, GLI1 promotes malignant behavior of cancer cells by upregulating osteopontin. J Biol Chem 284(34) 22888-22897, 2009

-NCI/NIH 1R01CA138850-01A2 (05/2011 to 03/2016)
Molecular determinants of breast cancer malignancy
Goals: To evaluate the role of the reciprocal relationship between Merlin and Osteopontin in breast cancer.
Role: Principal Investigator

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