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Sulagna Banerjee

General Information

Sulagna  Banerjee

Contact

  • .(JavaScript must be enabled to view this email address)

Languages

  • English

Roles

  • Asst. Professor

Education

2004 PhD
Bose Institute, Jadavpur University,
1997 M.Sc
Calcutta University
1995 B.Sc
Presidency College

Publications

Biography

 OMB No. 0925-0001/0002 (Rev. 08/12 Approved Through 8/31/2015)

BIOGRAPHICAL SKETCH

Provide the following information for the Senior/key personnel and other significant contributors.
Follow this format for each person.  DO NOT EXCEED FIVE PAGES.

NAME: Sulagna Banerjee

 

eRA COMMONS USER NAME (credential, e.g., agency login): sbanerje

POSITION TITLE: Assistant Professor, University of Miami, FL

EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, include postdoctoral training and residency training if applicable. Add/delete rows as necessary.)

INSTITUTION AND LOCATION

DEGREE

(if applicable)

 

Completion Date

MM/YYYY

 

FIELD OF STUDY

 

Presidency College, Calcutta, India

B.Sc

09/1995

Botany, Zoology, Chemistry

University of Calcutta, West Bengal, India

M.Sc

09/1997

Botany

Bose Institute, Jadavpur University, Calcutta, India

PhD

08/2004

Life Sciences

Boston University, Boston, MA, USA

Post-doctoral associate

09/2003-01/2008

Molecular and Cell Biology of protozoan parasites

A.           Personal Statement

I am currently an Assistant Professor in the Division of Surgical Oncology at Department of Surgery, University of Miami, FL. My research interest lies in understanding the mechanisms chemo-resistance and tumor initiation in pancreatic cancer. My current research is focused on understanding the pancreatic tumor initiating cells. My research has shown that CD133, one of the surface markers for pancreatic TIC is able to form tumors in an immune compromised syngeneic mice at very low cell numbers. We have also seen that pancreatic TICs represented by CD133+ population have high expression and activity of pro-survival pathways like NF-kB. CD133, a pentaspan membrane glycoprotein, has long been utilized as a TIC marker. However, very little is known about its function in a cancer cell. In the current proposal, we will evaluate the molecular mechanisms that are triggered in a non-stem like cancer cell making it acquire properties that confer survival advantage. This leads to a chemoresistant phenotype within a cancer cell that is capable to “self renewal” and tumor initiation. Previous work from our group has shown the triptolide, an anti-inflammatory, anti -cancer compound reduces tumor burden in mouse models for pancreatic cancer by lowering heat shock protein expression. A water-soluble pro-drug for triptolide, Minnelide, synthesized in University of Minnesota has shown a lot of promise in the pre-clinical evaluation by our group. Prior to joining this group, my post-doctoral training had been focused on understanding glycosylation of cells and their role in different signaling pathways. I will be using this technical expertise in understanding the molecular mechanisms that determine chemoresistance in pancreatic cancer cells as a result of CD133 expression. I look forward to working in this project.

 

 

B. Positions and Honors

Positions and Employment

 

2008-2010

Staff Scientist in Anna University, Chennai, India

2010-2012

Post-doctoral Associate in Div. of Basic and Translational Research, Dept. Of    Surgery, U of Minnesota.    

2012-2013

Research Associate in Div. of Basic and Translational Research, Dept. Of    Surgery, U of Minnesota.    

2013-2016

 

2016- Current

Assistant Professor in Div. of Basic and Translational Research, Dept. Of    Surgery, U of Minnesota.    

Assistant Professor, Div. of Surgical Oncology, Dept. of Surgery, University of Miami, FL

 

 

 

C.    Contribution to Science

 

Research Projects

 

1. Determining the functional significance of pancreatic cancer stem cells

Cancer stem cells are responsible for tumor recurrence, chemoresistance and metastasis. However the mechanism of this remains unknown. This is another aspect of our research. We are actively studying the functional significance of surface markers like CD133 in pancreatic cancer stem cells. Our research is aimed at understanding how these cells evade conventional therapy and is associated with extremely aggressive tumors with poor prognosis. I have been recently awarded an NIH R01 for studying this phenomenon.

 

·       Nomura A, Dauer P, Gupta V, McGinn O, Arora N, Majumdar K, Uhlrich III C, Dalluge J, Dudeja V, Saluja A, Banerjee S*. Microenvironment Mediated Alterations to Metabolic Pathways Confer Increased Chemo-resistance in CD133+ Tumor Initiating Cells, Oncotarget.Jul 26 (*Corresponding Author)

·       Nomura A, McGinn O, Dudeja V, Sangwan V, Saluja AK, Banerjee S*. Minnelide effectively eliminates CD133(+) side population in pancreatic cancer. Mol Cancer. 2015 Nov 23;14(1):200. (*Corresponding Author)

·       Nomura A, Banerjee S, Chugh R, Dudeja V, Yamamoto M, Vickers SM, Saluja AK.CD133 initiates tumors, induces epithelial-mesenchymal transition and increases metastasis in pancreatic cancer. Oncotarget. 2015 Mar 16.

·       Banerjee S, Nomura A, Sangwan V, Chugh R, Dudeja V, Vickers S, Saluja AK. CD133+ tumor initiating cells (TIC) in a syngenic murine model of pancreatic cancer respond to Minnelide. Clin Cancer Res. 2014 Mar 14.

 

2. Understanding the mechanism of action of Minnelide

 

Along with evaluating potential of Minnelide as a therapeutic option for a number of cancers, we are also focused on understanding its mechanism of action. Our studies have shown that the drug downregulates the pro-proliferative pathways in cancer by inhibiting Sp1 activity in pancreatic cancer. This is mediated by altered glycosylation of Sp1. Our studies have further shown that Minnelide also induced chronic ER stress in pancreatic cancer cells that result in apoptotic cell death. Our research on understanding the mechanism of action of Minnelide has shown that multiple interactive cancer pathways are affected upon treatment by this drug, while the normal cells remain unaffected. This has strengthened the potential of Minnelide as a possible therapeutic strategy for multiple cancers.

 

·    Banerjee S, Modi S, McGinn O, Zhao X, Dudeja V, Ramakrishnan S, Saluja AK. Impaired synthesis of stromal components in response to Minnelide improves vascular function, drug delivery and survival in pancreatic cancer. Clin Cancer Res. 2015 Sep 24. pii: clincanres.1155.2015. [Epub ahead of print]

·       Banerjee S, Sangwan V, McGinn O, Chugh R, Dudeja V, Vickers SM, Saluja AK. Triptolide-induced cell death in pancreatic cancer is mediated by O-GlcNAc modification of transcription factor Sp1. J Biol Chem. 2013 Nov 22;288(47):33927-38.

·       Chen Z, Sangwan V, Banerjee S, Mackenzie T, Dudeja V, Li X, Wang H, Vickers SM, Saluja AK.miR-204 mediated loss of Myeloid cell leukemia-1 results in pancreatic cancer cell death. Mol Cancer. 2013 Sep 11;12(1):105.

·       Mackenzie TN, Mujumdar N, Banerjee S, Sangwan V, Sarver A, Vickers S, Subramanian S, Saluja AK.  Triptolide Induces the Expression of miR-142-3p: a Negative Regulator of Heat Shock Protein 70 and Pancreatic Cancer Cell Proliferation. Mol Cancer Ther. 2013 May 1

 

 

3. Preclinical evaluation of Minnelide as a therapy for different GI and non-GI cancers

 

Minnelide, a water-soluble pro-drug of triptolide has been developed by our group at the University of Minnesota. It is currently under Phase 1 clinical trial for GI cancers. Over last 7-8 years we have evaluated Minnelide in a number of cancers. These include pancreatic cancer, osteosarcoma, neuroblastoma, colon cancer, liver cancer and lung cancer. Our preliminary work on renal cancer and prostate cancer are currently under review at different journals. In these different cancers, we have tested the efficacy of Minnelide in a number of cell lines and animal models. Our results have been very promising and they indicate the Minnelide definitely has tremendous potential of developing into a possible therapeutic option for these diseases.

 

·       Isharwal,S, Modi, S, Barlass,U, Soubra, A, Chugh,R, Dudeja,V, Saluja A, Banerjee,S*, Konety, B. Triptolide Inhibits Androgen Dependent, Castration Resistant and Enzalutamide Resistant Prostate Cancer Growth By Decreasing Androgen Receptor Full Length and Splice Variants Expression. Prostate. Under Review * (Corresponding author)

·       Brincks, E, Kucaba, TA, James, BR, Sangwan,V, Banerjee S, Saluja, A and Griffith,TS. Triptolide augments the tumoricial activity of TRAIL against renal cell carcinoma. FEBS J. 2015 Oct 1. doi: 10.1111/febs.13532.

·       Alsaied OA, Sangwan V, Banerjee S, Krosch TC, Chugh R, Saluja A, Vickers SM, Jensen EH.Sorafenib and triptolide as combination therapy for hepatocellular carcinoma. Surgery. 2014 Aug;156(2):270-9.

·       Banerjee S, Thayanithy V, Sangwan V, Mackenzie TN, Saluja AK, Subramanian S.Minnelide reduces tumor burden in preclinical models of osteosarcoma. Cancer Lett. 2013 Mar 14.

·       Krosch TC, Sangwan V, Banerjee S, Mujumdar N, Dudeja V, Saluja AK, Vickers SM.Triptolide-mediated cell death in neuroblastoma occurs by both apoptosis and autophagy pathways and results in inhibition of nuclear factor-kappa B activity. Am J Surg. 2013 Apr; 205(4):387-96

·       Chugh R, Sangwan V, Patil SP, Dudeja V, Dawra RK, Banerjee S, Schumacher RJ, Blazar BR, Georg GI, Vickers SM, Saluja AK. A preclinical evaluation of Minnelide as a therapeutic agent against pancreatic cancer. Sci Transl Med. 2012 Oct 17;4 (156)

 

4.Glycosylation and signaling in disease development

 

As a part of my post-doctoral training, I have worked extensively on glycosylation pathways and their role in mediating cellular signaling in protozoan parasites. My experience in extensive molecular and biochemical characterization of glycosylation pathways have definitely given me the expertise to dissect signaling in cancer in context of their post translational modification.

 

·      Banerjee S, Robbins PW, Samuelson J. Molecular characterization of nucleocytosolic O-GlcNAc transferases of Giardia lamblia and Cryptosporidium parvum. Glycobiology. 2009 Apr;19(4):331-6.

·       Banerjee S, Cui J, Robbins P and Samuelson J.  Use of Giardia, which appears to have a single nucleotide-sugar transporter for UDP-GlcNAc, to identify the UDP-Glc transporter of Entamoeba. Mol Biochem Parasitol. 2008 May; 159(1):44-53

·       Banerjee, S, Vishwanath,P , Robbins, P, Samuelson, J. The evolution of N-glycan-dependent endoplasmic reticulum quality control factors for glycoprotein folding and degradation.
Proc Natl Acad Sci U S A. 2007 July 10;104 (28):11676-11681 .

·       Kelleher DJ, Banerjee S, Cura AJ, Samuelson J, Gilmore R. Dolichol-linked oligosaccharide selection by the oligosaccharyltransferase in protist organisms. J Cell Biol. 2007 Apr 9;177(1):29-37.

·       Samuelson J, Banerjee S, Magnelli P, Cui J, Kelleher DJ, Gilmore R, Robbins PW. (2005)The diversity of dolichol-linked precursors to Asn-linked glycans likely results from secondary loss of sets of glycosyltransferases. Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1548-53.

 

 

Complete List of Published Work in My Bibliography:  

http://www.ncbi.nlm.nih.gov/sites/myncbi/sulagna.banerjee.1/bibliograpahy/40340097/public/?sort=date&direction=ascending

 

D.    Research Support

Ongoing Research Support

 

1R01CA184274-01                              Sulagna Banerjee, PhD, PI

NIH                                                                              (01/2014-12/21/2019)

Functional Significance of CD133 in pancreatic cancer