Sajal K. Ghosh, PhD
Compliance Coordinator
Boston University
Research Compliance

PhD, University of Calcutta
MSc, University of Calcutta

My broad research interest is to study the role of non-coding RNAs in tumorigenesis.
Project 1.
Over the last decade microRNAs have been identified as master regulator of almost all major biochemical pathways that regulate cellular metabolism. Most importantly, their deregulation is closely related to many cancers. In pancreatic cancer, which has the lowest 5-year survival rate, the level of microRNA let-7 is consistently downregulated. We are interested to identify the link between let-7 downregulation and aggressive growth characteristics of pancreatic cancer cells. We identified that let-7 level is inversely proportional with STAT3 signaling in pancreatic cancer. We are working on the detail mechanism of the process and testing in xenograft model whether let-7 reexpression can be a therapeutic option in pancreatic cancer.

Project 2.
My other research interest is to understand the molecular basis of tumorigenesis by leukemia virus and Epstein Barr virus (EBV). Leukemia viruses are oncogene-deficient simple retroviruses but how their infection in animals causes tumor development in a predicable manner still remains poorly understood. We have demonstrated, using feline leukemia virus as a model, that the long-terminal region (LTR) of these viruses independently activates AP-1 and NF?B signaling pathways in the host cells. We hypothesized that such activities may aid in tumorigenesis. We found that the U3-LTR region makes small non-coding RNA, whose production is directly related to the transactivation potential of the LTR. Our recent studies demonstrated that toll-like receptor 3 (TLR3) expression is necessary for such activity. Our current research effort is dedicated to understand the regulation of expression of the LTR-transcript and how it activates TLR3 signaling.
EBV, on the other hand, is a large DNA tumor virus, associated with several human malignancies. However, EBV maintains a latent state of infection in these cancers and it is believed that the latent gene products play a discrete role in the genesis or maintenance of EBV-associated tumors. Our interest is to determine the contribution of EBV latent gene products in tumorigenesis.

Other Projects:
Additionally in collaborative studies we are also interested in indentifying better therapeutic options against EBV-associated tumors. Prognosis of certain type of lymphomas is very poor when EBV is present in them (such as post-transplantation lymphoproliferative disease, Burkitt’s lymphoma, Hodgkin’s disease). A combination approach where lytic EBV replication is first induced by chemicals and then followed by treatment with anti-herpesvirus drugs, has been previously found to be effective in selective killing of EBV-containing tumor cells. We have and continues to characterize novel histone deacetylase inhibitors or other cytotoxic compounds as inducer of lytic replication of EBV and their usefulness in selective killing of EBV-associated tumors in the combinational therapy model. We are validating efficacy of such approach in xenograft tumor model in NOD/SCID mice.

In another collaborative study we are working on the molecular mechanism of anticancer effect of novel chemically modified plumbagin derivative. Especially, we are interested in the autophagic activity of the compound and its relationship to cell death signaling.

Do EBV Encoded Small RNAs Interfere with Tumor Suppressor APC in EBV Associated Breast Cancers?
07/15/2004 - 08/31/2006 (PI)
Department of Defense/Army

Leukemia Virus Long Terminal Repeat-Mediated Cellular Gene Activation and Tumorigenesis
10/01/1999 - 09/30/2000 (PI)
American Cancer Society - MA Division


Yr Title Project-Sub Proj Pubs

Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

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  1. Ghosh SK, Ganta A, Spanjaard RA. Discovery and cellular stress pathway analysis of 1,4-naphthoquinone derivatives with novel, highly potent broad-spectrum anticancer activity. J Biomed Sci. 2018 Feb 08; 25(1):12. PMID: 29422060; PMCID: PMC5804083; DOI: 10.1186/s12929-018-0408-6;
  2. Patel K, Kollory A, Takashima A, Sarkar S, Faller DV, Ghosh SK. MicroRNA let-7 downregulates STAT3 phosphorylation in pancreatic cancer cells by increasing SOCS3 expression. Cancer Lett. 2014 May 28; 347(1):54-64.View Related Profiles. PMID: 24491408; PMCID: PMC3972339; DOI: 10.1016/j.canlet.2014.01.020;
  3. Ghosh SK, Patton JR, Spanjaard RA. A small RNA derived from RNA coactivator SRA blocks steroid receptor signaling via inhibition of Pus1p-mediated pseudouridylation of SRA: evidence of a novel RNA binding domain in the N-terminus of steroid receptors. Biochemistry. 2012 Oct 16; 51(41):8163-72. PMID: 22998747; DOI: 10.1021/bi300602r;
  4. Ghosh SK, Perrine SP, Faller DV. Advances in Virus-Directed Therapeutics against Epstein-Barr Virus-Associated Malignancies. Adv Virol. 2012; 2012:509296.View Related Profiles. PMID: 22500168; PMCID: PMC3303631; DOI: 10.1155/2012/509296;
  5. Ghosh SK, Perrine SP, Williams RM, Faller DV. Histone deacetylase inhibitors are potent inducers of gene expression in latent EBV and sensitize lymphoma cells to nucleoside antiviral agents. Blood. 2012 Jan 26; 119(4):1008-17.View Related Profiles. PMID: 22160379; PMCID: PMC3271713; DOI: 10.1182/blood-2011-06-362434;
  6. Forman LW, Pal-Ghosh R, Spanjaard RA, Faller DV, Ghosh SK. Identification of LTR-specific small non-coding RNA in FeLV infected cells. FEBS Lett. 2009 Apr 17; 583(8):1386-90.View Related Profiles. PMID: 19336234; PMCID: PMC3774839; DOI: 10.1016/j.febslet.2009.03.056;
  7. Zhao X, Patton JR, Ghosh SK, Fischel-Ghodsian N, Shen L, Spanjaard RA. Pus3p- and Pus1p-dependent pseudouridylation of steroid receptor RNA activator controls a functional switch that regulates nuclear receptor signaling. Mol Endocrinol. 2007 Mar; 21(3):686-99. PMID: 17170069
  8. Ghosh SK, Forman LW, Akinsheye I, Perrine SP, Faller DV. Short, discontinuous exposure to butyrate effectively sensitizes latently EBV-infected lymphoma cells to nucleoside analogue antiviral agents. Blood Cells Mol Dis. 2007 Jan-Feb; 38(1):57-65.View Related Profiles. PMID: 17161633; PMCID: PMC1829174; DOI: 10.1016/j.bcmd.2006.10.00;
  9. Abujamra AL, Spanjaard RA, Akinsheye I, Zhao X, Faller DV, Ghosh SK. Leukemia virus long terminal repeat activates NFkappaB pathway by a TLR3-dependent mechanism. Virology. 2006 Feb 20; 345(2):390-403.View Related Profiles. PMID: 16289658; PMCID: PMC3808874; DOI: 10.1016/j.virol.2005.10.003;
  10. Abujamra AL, Faller DV, Ghosh SK. Mutations that abrogate transactivational activity of the feline leukemia virus long terminal repeat do not affect virus replication. Virology. 2003 May 10; 309(2):294-305.View Related Profiles. PMID: 12758176
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This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 22 publications over 17 distinct years, with a maximum of 2 publications in 1989 and 1993 and 1999 and 2006 and 2012


2010-2011 Boston University School of Medicine: Genome Science Institute Seed Grant
2008-2009 Boston University School of Medicine: Department of Medicine Pilot Grant
2004-2006 Department of Defense: Breast Cancer Research Concept Grant
2002-2003 Boston University School of Medicine: Department of Medicine Pilot Grant
1999-2000 Boston University School of Medicine: American Cancer Society New Investigator Award
1999-2000 Boston University School of Medicine: American Cancer Society Institutional Research Grant Award
1984-1989 Council of Scientific & Industrial Research, Govt. of India: Individual Research Fellowship
In addition to these self-described keywords below, a list of MeSH based concepts is available here.

Gene transactivation
Leukemia virus
non-coding RNA
Pancreatic Cancer
Compliance, Protocol
Compliance, Policy
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