Thomas M. Bodenstine, Ph.D.

Assistant Professor

Midwestern University
Department of Biochemistry
College of Osteopathic Medicine
Science Hall 421-G
555 31st Street
Downers Grove, IL 60515
Office: 630-515-6153


B.S. Biotechnology, Pennsylvania State University
Ph.D. Molecular and Cellular Pathology, University of Alabama at Birmingham

Current Teaching Activities

BIOCD 0551: Human Biochemistry (Lipid Metabolism, Cancer Biology)
BIOCD 0530/0580/0581: Human Genetics (Genetic Screening/Gene Therapy)
BIOCD 0510/0560/1554: Biochemistry I (Lipid Metabolism)
BIOCD 0520/0570/1555: Biochemistry II (Cellular Signaling, Cancer Biology)

Research Summary

Gap junctions are regulated intercellular pores formed by the connexin family of proteins that allow for passage of ions, signaling molecules and nutrients between epithelial cells. Proper regulation of gap junction communication contributes to cellular homeostasis and tissue function. During cancer development, the normal roles of connexins are often dysregulated. Expression of connexin genes may be lost or connexin protein function may be altered. Collectively, these changes can affect how cancer cells function and respond to therapy. Interestingly, gap junction communication can be restored within metastatic tumor cells by modulation of signaling pathways without the need for exogenous expression of connexin genes. The focus of my laboratory aims to understand the pathway alterations that lead to changes in connexin function during breast cancer progression, and how this information may be used from a therapeutic standpoint.

Research Opportunities

Research elective opportunities are available for the Master of Arts in Biomedical Sciences program and thesis track positions in the Master of Biomedical Sciences program. Summer research fellowship positions through the Kenneth E. Suarez research program are available for medical students.

Selected Publications

(Full List)
Bodenstine TM, Chandler GS, Reed DW, Margaryan NV, Gilgur A, Atkinson J, Ahmed N, Hyser M, Seftor EA, Strizzi L, Hendrix MJ. Nodal expression in triple-negative breast cancer: cellular effects of its inhibition following doxorubicin treatment. Cell Cycle 2016; 15(9):1295-302.

Bodenstine TM, Chandler GS, Seftor RE, Seftor EA, Hendrix MJ. Plasticity underlies tumor progression: Role of Nodal in Cancer. Cancer and Metastasis Reviews 2016; 35(1):21-39.

Strizzi L, Sandomenico A, Margaryan NV, Foca A, Sanguigno L, Bodenstine TM, Chandler GS, Reed DW, Gilgur A, Seftor EA, Seftor RE, Khalkhali-Ellis Z, Leonardi A, Ruvo M, Hendrix MJ. Effects of a novel Nodal-targeting monoclonal antibody in melanoma. Oncotarget 2015; 6(33):34071-86.

Bodenstine TM, Seftor RE, Seftor EA, Khalkhali-Ellis Z, Samii NA, Monarrez JC, Chandler GS, Pemberton PA, Hendrix MJ. Internalization by multiple endocytic pathways and lysosomal processing impact Maspin-based therapeutics. Molecular Cancer Research 2014; 12:1480-1891.

Bodenstine TM, Seftor RE, Khalkhali-Ellis Z, Seftor EA, Pemberton PA, Hendrix MJ. Maspin: molecular mechanisms and therapeutic implications. Cancer and Metastasis Reviews 2012; 31: 529-551.

Bodenstine TM, Vaidya KS, Ismail A, Beck BH, Cook LM, Diers AR, Landar A, Welch DR. Homotypic gap junctional communication associated with metastasis suppression increases with PKA activity and is unaffected by PI3K inhibition. Cancer Research 2010; 70(23): 10002-10011.

Bodenstine TM, Welch DR. Metastasis suppressors and the tumor microenvironment. Cancer Microenvironment 2008; 1:1-11.

Kim MH, Bodenstine TM, Sumerel LA, Rivera AA, Baker AH, Douglas JT. Tissue inhibitor of metalloproteinases-2 improves antitumor efficacy of a replicating adenovirus in vivo. Cancer Biology and Therapeutics 2006; 5(12):1647-53.