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peir.net

peir.net


Pritish Pawar Mail Email this article  
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Previous | Molecular & Cellular Pathology Graduate Student Profiles | Next

After getting my medical degree, I worked for a year as a resident medical officer in a Primary Health Care setting in India. It was an enriching experience with the satisfaction of caring for and treating the sick and the needy. But while I was tackling the diseases at the individual and community level, I was constantly startled by the recurring realization that knowing the disease and understanding it at a molecular level would be the best way to substantiate and consolidate my knowledge base and be able to contribute to the field.


 

The Department of Pathology here at UAB with its invigorating research ambience happened to be the best place for me
to embark on this mid-career shift from
the clinical sciences to the basic sciences.

 






   Hometown:

Nashik, India



Undergraduate/Masters Institution:

Byramjee Jeejeebhoy Medical College
Pune, India



General Research Interests:

Apoptosis



Cholangiocarcinoma is a highly lethal tumor arising from biliary epithelium. Various studies have shown the importance of Fas death receptor in the prognosis of this tumor.

 

I am currently researching Fas mediated apoptosis signaling in Cholangiocarcinoma tumor model.

 
We have established two unique Cholangiocarcinoma cell lines, Fas high and Fas low, based on the surface expression of Fas receptors. Our lab has reported a novel role for Calmodulin (CaM), a Ca++ regulated cytoplasmic protein, in Fas mediated death signaling by showing that CaM antagonists like TFP are able to induce apoptosis in Fas high cells but not in Fas low cells. Now we have observed that the expression of cellular FLICE like inhibitory protein (c-FLIP), a structural homologue and inhibitor of caspase 8, is increased in Fas low cholangiocarcinoma cells.

We believe that c-FLIP could be an important switch in deciding the sensitivity of Cholangiocarcinoma cells to Fas mediated apoptosis as the activity of c-FLIP seems to increase in response to activation of Fas-induced pathway. I am currently working on further characterizing the role of Calmodulin and c-FLIP in this signaling pathway.


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