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Faculty Detail    
Name LALITA R SHEVDE-SAMANT
Director, Cancer Biology Theme
 
Campus Address WTI 320D
Phone  205-975-6261
E-mail  lsamant@uab.edu
Other websites UAB Graduate Biomedical Sciences Cancer Biology Program
Metastasis Research Society
MRS ECAM
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Pathology   Molecular & Cellular Pathology Professor
Center  Biomedical Engineering  Biomatrix Eng Regen Med (BERM) Ctr Professor
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Medical Scientist Training Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
Dr. Lalita Shevde-Samant’s graduate training from the Cancer Research Institute, University of Mumbai, India encompassed the area of innate immunity in the regulation of breast cancer. She completed postdoctoral training at the Hershey Medical Center, Penn State University in the laboratory of Prof. Danny Welch in the area of metastasis suppressors. She was a faculty at the Mitchell Cancer Institute, University of South Alabama (2004-2012) before joining UAB in 2012.
Research in the Shevde-Samant laboratory is aimed at understanding the aberrations intrinsic to the tumor cells and those that are extrinsically manipulated as a result of interaction with cells in the tumor microenvironment.

Society Memberships
Organization Name Position Held Org Link
AACR-Minorities in Cancer Research (AACR-MICR)      
AACR-Women in Cancer Research (AACR-WICR)      
AAMC-Group on Women In Medicine and Science (GWIMS)      
American Association for Cancer Research (AACR)     
Metastasis Research Society (MRS)      
The American Society for Cell Biology (ASCB)     

Research/Clinical Interest
Title
Mechanisms that regulate tumor progression, metastasis and drug resistance; crosstalk between the tumor cells and their microenvironment
Description
Although significant progress in the development of early detection tests has led to improved management of patients diagnosed with organ-confined cancer, the progression to locally invasive and metastatic disease typically is associated with decreased survival rates. This is further complicated by the development of drug resistance, which greatly limits the treatment options and confounds the issue. Therefore, a better understanding of etiological causes responsible for cancer initiation and progression and treatment resistance is needed to identify novel molecular therapeutic targets. Our research goals are to define molecular signaling mechanisms that regulate tumor progression and metastasis and apply this knowledge to complement and improve current clinical protocols with new therapeutic strategies. We are investigating the dynamics of the interactions between tumor cells and their microenvironment, with a predominant focus on carcinoma of the breast. Work is underway to investigate the impact of the mutually sustaining synergy between tumor and the microenvironment and how this impacts the molecular homeostasis and promotes evolution of the malignant phenotype. One major area of investigation centers on the tumor suppressor, Merlin. Our efforts were instrumental in identifying that Merlin is regulated at the post-translational level in breast cancer. Ongoing investigations examine various aspects of Merlin, in particular determining the tumor cell metabolomics, bioenergetics, and cell signaling regulated by Merlin. Another major thrust encompasses developmental signaling pathways: Hedgehog, Wnt/β-catenin, Hippo and TGF-β. In this context, we are conducting studies to understand the mechanisms and implications of autocrine and paracrine Hedgehog signaling in influencing tumor progression, M2 macrophage polarization, bone metastasis, and resistance to therapy.

Positions Available
Date Posted Position Title
3/8/2016  Postdoctoral Fellow 
Please send a CV, three letters of recommendation and a brief statement of your research interests to Dr. Lalita Shevde-Samant, University of Alabama at Birmingham, WTI320D 1824 6th Avenue South, Birmingham, AL35233.    

Selected Publications 
Publication PUBMEDID
Morrow, K. A., Das, S., Meng, E., Menezes M. E., Bailey, S. K., Metge, B. M., Buchsbaum, D. J., Samant, R. S., Shevde, L. A. Loss of tumor suppressor Merlin results in aberrant activation of Wnt/β-catenin signaling in cancer. Oncotarget doi: 10.18632/oncotarget.7494.  26908451 
Shevde, L. A.and Samant, R. S. Non-Classical Hedgehog-GLI Signaling and Its Clinical Implications. Int. J. Cancer-135(1): 1-6, 2014.   23929208 
Devine, D. J., Rostas, J. W., Metge, B. J., Das, S., Mulekar, M. S., Tucker, J. A., Grizzle, W. E., Buchsbaum, D. J., Shevde, L. A., Samant R. S. Loss of N-Myc interactor promotes epithelial-mesenchymal-transition by activation of TGF-beta/SMAD signaling. Oncogene-33(20): 2620-2628, 2014.  23770854 
Das, S., Samant, R. S., Shevde, L.A. Non-Classical Activation of Hedgehog Signaling Enhances Multidrug Resistance and Makes Cancer Cells Refractory to SMOH-Targeting Hedgehog Inhibition. J. Biol. Chem. 288(17): 11824-11833, 2013.   23508962 
Vincent, A. J., Ren, S., Harris, L.G., Devine, D. J., Samant, R.S., Fodstad, O., Shevde, L.A. Cytoplasmic translocation of p21 mediates NUPR1-induced chemoresistance. FEBS Letters 586: 3429-3434, 2012.   22858377 
Morrow, K.A. and Shevde L.A. Merlin: The wizard requires protein stability to function as a tumor suppressor. BBA-Reviews on Cancer. 1826(2): 400-406, 2012.   22750751 
Meng, E., Long, B., Sullivan, P., McClellan, S., Finan, M.A., Reed, E., Shevde, L.A., Rocconi, R.P. CD44+/CD24- ovarian cancer cells demonstrate cancer stem cell-like properties and correlate to survival. Clin. Exp. Metastasis 29(8): 939-948, 2012.  22610780 
Frost, A.R., Hurst, D.R., Shevde L.A. and Samant, R.S. The Influence of the Cancer Microenvironment on the Process of Metastasis (Editorial) Int J Breast cancer, 2012: 756257, 2012.  22570792 
Das, S., Samant, R.S., Shevde, L.A. The Hedgehog Pathway Conditions the Bone Microenvironment for Osteolytic Metastasis of Breast Cancer. Int. J. Breast Cancer. 2012: 298623, 2012.   22295244 
Kudo, K., Amable, L., Gavin, E., Das, S., Denny, W., Shevde, L.A., Reed, E. Inhibition of Gli-1 results in altered c-Jun activation, inhibition of cisplatin-induced up-regulation of ERCC1, XPD, and XRCC1, and inhibition of platinum-DNA adduct repair. Oncogene 31 (44): 4718-4724, 2012.   22266871 
Mitra, A., Menezes, M.E., Pannell, L.K., Mulekar, M.S., Honkanen, R.E., Shevde, L.A., Samant, R.S. DNAJB6 chaperones PP2A mediated dephosphorylation of GSK3β to down regulate β-catenin transcription target, osteopontin. Oncogene 31 (41): 4472-4483, 2012.   22266849 
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. Oncogene 31(28): 3370-3380, 2012.   22056874 
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. J Biol Chem 286(46): 40376-40385, 2011.   21965655 
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.   21775419 
Ray, A., Meng, E., Reed E., Shevde, L.A., Rocconi, R.P. Hedgehog signaling pathway regulates the growth of ovarian cancer spheroid forming cells. Int. J. Oncol 39(4): 797-804, 2011.   21701772 
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.   21169638 
Mitra, A., Menezes, M.E., Shevde, L.A., Samant R. S. DNAJB6 induces degradation of β-catenin and causes partial reversal of mesenchymal phenotype. J. Biol. Chem. 285(32): 24686-24694, 2010.   20522561 
Shevde, L.A., Das, S., Clark, D. W., Samant, R.S. Osteopontin: An effector and an effect of tumor metastasis. Curr Mol Med 10(1): 71-81, 2010.   20205680 
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.  19556240 
Shevde, L.A., Metge, B. M., Mitra, A., Xi, Y., Ju, J., King, J.A., Samant, R.S. Spheroid-forming sub-population of breast cancer cells demonstrates vasculogenic mimicry via hsa-miR-299-5p regulated de novo expression of osteopontin. J Cell Mol Med 14(6B): 1693-1706, 2010  19538464 
Chowdhury, U.R., Samant, R.S., Fodstad, O., Shevde, L.A. Emerging role of Nuclear Protein 1 (NUPR1) in Cancer Biology. Cancer and Metastasis Rev 28: 225-232, 2009.   19153668 
Mbeunkui F., Metge B.M., Shevde L.A.*, Pannell L. K.* Identification of differentially secreted biomarkers using LC-MS/MS in isogenic cell lines representing a progression of breast cancer. J Proteome Res 6(8): 2993-3002, 2007.   17608509 

Keywords
Tumor progression, metastasis, signaling, cancer stem cells, chemoresistance, microenvironment, metabolism, osteolysis, Merlin, Hedgehog pathway, Wnt pathway, innate immunity, macrophage polarization