Post-Doctortal

Visiting-fellow
National Institute of Health (NIH), Bethesda, USA
2003

Doctor of Philosophy (Ph.D.)

Marine Phramacology & Drug Development
University College Of Medicine, Calcutta University, Kolkata, India
2000

Master of Science (M.S.)

Marine Science
Calcutta Univesrity, Kolkata, India
1987

Bachelor of Science (B.S.)

Zoology
Calcutta University, Kolkata, India
1985

Exposure Biology, Genes and Gene Expression, Biomarkers and Validation, Type 2 Diabetes, Alzheimer's Disease, Heath Disparity

Dr Sghosh completed his Graduate Studies from Calcutta University, India, before he joins National Cancer Institute/NIH, Bethesda, where he completed his postdoctoral research. I moved to Howard University, Washington DC, and started working at Biology Department, with an additional position of Assistant Professor at the in the Department of Pediatrics and Child Health, College of Medicine at Howard University. He is an exposure biologist/scientist with more than 20 years working experience in Academics.  As evidence of my accomplishments, I hold 1 patent, and I published 35+ research papers in peer-reviewed journals, with numerous national and international presentations.  I am also an in the Editorial Board of 16 Journals. I am also the also the Lead PI of a recently funded NIGMS-RCMI RO1 and NCI P-20 projects to advance the identification and understanding of the role of Type 2 Diabetes in African American population of USA determining the their health and disease (Gene Environment Interactions, GxE), provide fresh perspectives, and bring new understanding to problems in environmental health through application of innovative knowledge and problem-solving technologies.

BIO 101

Role: Instructor 

Number of Direct Contact Hours*: 20 

Year(s) Taught: 2018-2019 

Number of Students: 423 in each Semester

SEA-PHAGES (HHMI)-BIO-101

Role: Instructor 

Number of Direct Contact Hours*: 150 Hours/in Academic Calendar 

Year(s) Taught: 2018-Present 

Number of Students: 22 per batch

Faculty Author Award, Howard University, 2005-2018

Visiting Postdoctoral Fellowship, National Institute of Health, 2003- 2004

Research Associate, Department of Ocean Development, Govt. of India, 2000-2003

Senior Research Fellowship, Department of Ocean Development, Govt. of India, 1993-2000

Junior Research Fellowship, Department of Ocean Development, Govt. of India, 1991-1993

PATENT

Indian Patent No. AA-2468: A Novel Process for the Extraction of Non-toxic Oil Having High EPA & DHA Content from the Livers of Marine Non-Edible Fishes

Ghosh S., Hazra AK. and Mukherjee B.

Biomarkers of metabolic disorders and neurobehavioral diseases in a PCB- exposed population

Biomarkers of metabolic disorders and neurobehavioral diseases in a PCB- exposed population

The current review is primarily intended to summarize the evidence for the association of PCB exposures with increased risks for metabolic dysfunctions and neurobehavioral disorders. In particular, we present evidence of gene expression alterations in PCB-exposed populations to construct the underlying pathways that may lead to those diseases and disorders in course of life. We conclude the review with future perspectives on biomarker-based research to identify susceptible individuals and populations.

Transcriptional Profiling and Biological Pathway(s) Analysis

Transcriptional Profiling and Biological Pathway(s) Analysis of Type 2 Diabetes Mellitus in a Pakistani Population

The epidemic of type 2 diabetes mellitus (T2DM) is an important global health concern. Our earlier epidemiological investigation in Pakistan prompted us to conduct a molecular investigation to decipher the differential genetic pathways of this health condition in relation to non-diabetic controls. Our microarray studies of global gene expression were conducted on the Affymetrix platform using Human Genome U133 Plus 2.0 Array along with Ingenuity Pathway Analysis (IPA) to associate the affected genes with their canonical pathways. High-throughput qRT-PCR TaqMan Low Density Array (TLDA) was performed to validate the selected differentially expressed genes of our interest.

Differential expression of efferocytosis and phagocytosis associated genes in tumor associated macrophages

Differential expression of efferocytosis and phagocytosis associated genes in tumor associated macrophages exposed to African American patient derived prostate cancer microenvironment

Macrophages are the first line of defense in the cellular environment in response to any antigenic or foreign invasion. Since cancer cells express antigenic molecules and create a tumor microenvironment quite different from the normal cellular environment, macrophages will attack this cancer cells as foreign Invaders. However, the cancer cells adept their ability to suppress macrophage activity by secreting compounds/proteins through unknown mechanisms and train these macrophages to aid in tumorigenesis. These macrophages are commonly known as tumor associated macrophages (TAM). In this study, our goal was to find out key regulatory molecules involved in this conversion of cancer-fighting macrophages to cancer friendly macrophages. We used African American(AA) patient derived established human prostate cancer cells along with the human derived macrophages followed by Affymetrix cDNA microarray analysis.

Non-muscle myosin IIA and IIB differentially modulate migration

Non-muscle myosin IIA and IIB differentially modulate migration and alter gene expression in primary mouse tumorigenic cells

Though many cancers are known to show up-regulation of nonmuscle myosin (NM) IIA and IIB, the mechanism by which NMIIs aid in cancer development remains unexplored. Here we demonstrate that tumor-generating, fibroblast-like cells isolated from 3-methylcholanthrene (3MC)-induced murine tumor exhibit distinct phospho-dependent localization of NMIIA and NMIIB at the perinuclear area and tip of the filopodia and affect cell migration differentially. While NMIIA-KD affects protrusion dynamics and increases cell directionality, NMIIB-KD lowers migration speed and increases filopodial branching. Strategically located NMIIs at the perinuclear area colocalize with the linker of nucleoskeleton and cytoskeleton (LINC) protein Nesprin2 and maintain the integrity of the nuclear-actin cap. Interestingly, knockdown of NMIIs results in altered expression of genes involved in epithelial-to-mesenchymal transition, angiogenesis, and cellular senescence. NMIIB-KD cells display down-regulation of Gsc and Serpinb2, which is strikingly similar to Nesprin2-KD cells as assessed by quantitative PCR analysis. Further gene network analysis predicts that NMIIA and NMIIB may act on similar pathways but through different regulators. Concomitantly, knockdown of NMIIA or NMIIB lowers the growth rate and tumor volume of 3MC-induced tumor in vivo. Altogether, these results open a new window to further investigate the effect of LINC-associated perinuclear actomyosin complex on mechanoresponsive gene expression in the growing tumor.

Epidemiological Investigation of Type 2 Diabetes and Alzheimer's Disease in a Pakistani Population

Epidemiological Investigation of Type 2 Diabetes and Alzheimer's Disease in a Pakistani Population

The epidemic of type 2 diabetes mellitus (T2DM) and the possibility of it contributing to the risk of Alzheimer's disease (AD) have become important health concerns worldwide and in Pakistan, where the co-occurrence of T2DM and AD is becoming more frequent. To gain insights on this phenomenon, a cross-sectional study was initiated. We recruited and interviewed 820 research participants from four cities in Pakistan: 250 controls, 450 T2DM, 100 AD, and 20 with both diseases. Significant differences between groups were observed for age (p < 0.0001), urban vs. rural locality (p = 0.0472) and residing near industrial areas. The average HbA1c (%) level was 10.68 ± 2.34 in the T2DM group, and females had a lower level than males (p = 0.003). In the AD group, significant relationships existed between education and family history. Overall, the results suggest that T2DM and AD were associated with both socio-demographic and environmental factors in Pakistani participants. Detailed molecular investigations are underway in our laboratory to decipher the differential genetic pathways of the two diseases to address their increasing prevalence in this developing nation.

A Review

A Review: Molecular Concepts and Common Pathways Involving Vitamin D in the Pathophysiology of Preeclampsia

Preeclampsia is one of the most serious conditions at the end of pregnancy, causing increased perinatal morbidity and mortality to the pregnant mother and her product of conception. It remains a high-risk disease in ethnic minorities worldwide. Conception involves fetal invasion and implantation, followed by an actively forming and shedding decidua, an important uterine activity facilitating placental development. Dysregulation in conception mediates functional changes that induce onset of preeclampsia. The pathophysiology of preeclampsia primarily results from impaired trophoblastic invasion and implantation with subsequent vasculopathy. These events trigger exaggerated ischemic, inflammatory and immunologic events in the placenta bed that disrupt implantation. As the underlying mechanism(s) of preeclampsia remain obscure, there is increasing evidence that Vitamin D deficiency during pregnancy potentiates hypertensive states that could lead to the development of preeclampsia. As a prohormone, Vitamin D regulates molecular events within central pathophysiological pathways of implantation and vascular development. We review shared pathways involving Vitamin D modulation of pathologic events in implantation associated with preeclampsia. Understanding the causal mechanisms between Vitamin D and preeclampsia during early stages of conception could allude to development of candidate markers for treatment or screening and decipher “hot spots” for research and intervention of, at-risk pregnant mothers.