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Faculty Detail Faculty Entry   
Name LALITA R SHEVDE-SAMANT  
Campus Address WTI 320D
Phone 205-975-6261
E-mail lsamant@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:lsamant@uab.edu">lsamant@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Associate Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Associate Professor
Primary  Pathology   Joint Pathology Associate Professor

Biographical Sketch 
Dr. Lalita Shevde-Samant graduated from the Cancer Research Institute, University of Mumbai, India. She completed her postdoctoral training at the Hershey Medical Center, Penn State University and at the University of Alabama at Birmingham 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.

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)      
 

Research/Clinical Interest
Title
Mechanisms that regulate tumor progression, metastasis and drug resistance; crosstalk between the tumor cells and their microenvironment
Description
Our research goals are to define mechanisms that regulate tumor progression and metastasis, to apply this knowledge to complement and extend current clinical applications and provide additional therapeutic strategies. The microenvironment surrounding the cancer cells is an active participant in regulating tumor cell behavior. We are investigating the dynamics of the interactions between tumor cells and their microenvironment, researching how tumor cells manipulate their milieu and, conversely, how the reactive tumor microenvironment influences tumor cell plasticity, invasion, metastasis, and response to therapy.
Our work identified the tumor suppressor, Merlin, as an important modulator of breast cancer. Further, we have discovered that Merlin is modulated by factors extrinsic to the tumor itself. Work is underway to investigate the impact of the mutually sustaining synergy between tumor and stromal cells and how that impacts the molecular homeostasis and promotes evolution of the malignant phenotype with a focus on determining the mechanisms and implications of post-translation modifications of Merlin protein. Another exciting aspect involves investigations of Hedgehog signaling. We have determined that Hedgehog signaling in tumor cells upregulates the expression of microenvironment modulators that influence tumor vascularization and metastasis. Ongoing investigations are centered on understanding the mechanisms and implications of autocrine and paracrine Hedgehog signaling in influencing tumor progression, metastasis and resistance to therapy.

Postdoc Positions Available
Date Posted Position Title
06/22/2012  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
1. Morrow, K.A. and Shevde L.A. Merlin: The wizard requires protein stability to function as a tumor suppressor. Accepted in BBA- Reviews on Cancer. June 20th, 2012.    
2. Das, S., Tucker, J.A., Khullar, S., Mastro, A., Samant, R.S., Shevde, L. A. Hedgehog Signaling in Tumor Cells Facilitates Osteoblast-Enhanced Osteolytic Metastases. PLoS One 7(3): e34374, 2012.   22479615 
3. Meng, E., Taylor, B.A., Ray, A., Shevde, L.A., Rocconi, R.P. Targeted inhibition of telomerase activity combined with chemotherapy demonstrates synergy in eliminating ovarian cancer spheroid-forming cells. Gyn Oncology 124(3): 598-605; 2012.   22115853 
4. 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, January 23, 2012. doi: 10.1038/onc.2011.610.   22266871 
5. 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 GSK3&#946; to down regulate &#946;-catenin transcription target, osteopontin. Oncogene, 1-12, January 23, 2012.   22266849  
6. 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. Doi:10.1155/2012/298623.  22295244 
7. 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, November 7th 2011, doi: 10.1038/onc.2011.496.  22056874 
8. 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  
9. 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 
10. 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 
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Keywords
Tumor progression, metastasis, signaling, cancer stem cells, chemoresistance, microenvironment, metabolism, osteolysis, Merlin, Hedgehog pathway, Wnt pathway

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