Ramzi Mohammad

Ramzi Mohammad

Professor - Department of Oncology
Director GI-Cancer Research
 

313-576-8329

mohammad@karmanos.org

Ramzi Mohammad

Office Address

Karmanos Cancer Institute
732 HWCRC
4100 John R.
Detroit, MI 48201 

Research Interests

• GI-cancers including pancreatic cancer
• Translational research
• Animal models
• Cancer drug discovery
 

Research Description

Dr. Mohammad has more than 30 years of cancer research experience, including experience in molecular biology, animal models and tissue culture. His lab has established a number of pancreatic cancer and other hematological malignancies cell lines, in which he has years of experience in studying the effects of new anticancer agents, marine products, small molecule inhibitors as well as new natural products. Dr. Mohammad's research is translational in nature through his close work with clinicians.

His lab has introduced several anticancer drugs to the clinic. Among them are new BH3-mimetic small molecule inhibitors (SMIs) that disarm anti-apoptotic Bcl2-family proteins, by displacing natural pro-apoptotic proteins which use their BH3 domain to bind to Bcl-2. We have established mouse xenograft models from pancreatic cancer, colon cancer and lymphoma and leukemia, facilitating studies of drug efficacy and mechanism of action in vivo. Currently, our lab is investigating several SMIs including novel HDM2 inhibitors and Mcl-1 inhibitors. Since these SMIs induce apoptosis, they synergize with traditional cytotoxic drugs commonly used in the clinic, hence increasing the cure rate in some pancreatic and colon cancers.
Dr. Mohammad lab has a long-standing interest in understanding the role of active ingredients in natural products such as Thymoquinone from Black seeds (Nigella sativa) and others. Dr. Mohammad’s lab has demonstrated the synergistic effect of Thymoquinone when combined with several anticancer agents against pancreatic cancer, colon cancer and lymphoma.
The abnormal upregulation or downregulation of specific miRNAs in cancer cells could be due to the hypomethylation or hypermethylation of specific miRNA gene DNAs. Therefore, it is important to reveal the regulatory mechanism(s) in the DNA methylation/miRNA/mRNA/protein axis for a specific miRNA regulation loop in order to design the novel therapeutic strategy for the treatment of pancreatic cancer. Recently Dr. Mohammad’s lab is involved in epigenetic research and has published on the role of DNA-Methylation-caused downregulation of miR-30 and the aggressive growth of pancreatic cancer.
 

Selected Publications

Mohammad RM, Li Y, Muqbil I, Aboukameel A, Senapedis W, Baloglu E, Landesman Y, Philip PA, Azmi AS. Targeting Rho GTPase effector p21 activated kinase 4 (PAK4) suppresses p-Bad-microRNA drug resistance axis leading to inhibition of pancreatic ductal adenocarcinoma proliferation. Small GTPases. 2019;10:367-77.

Muqbil I, Azmi AS, Mohammad RM. Nuclear Export Inhibition for Pancreatic Cancer Therapy. Cancers (Basel). 2018;10:E138.

Azmi AS, Li Y, Aboukameel A, Muqbil I, Philip PA, Mohammad RM. DNA-Methylation-caused downregulation of miR-30 contributes to the high expression of XPO1 and the aggressive growth of tumors in pancreatic cancer ductal adenocarcinoma. Cancers (Basel). 2019;11:E1101.

Diab M, Azmi A, Mohammad R, Philip PA. Pharmacotherapeutic strategies for treating pancreatic cancer: advances and challenges.
Expert Opin Pharmacother. 2019;20:535-46.

Azmi AS, Li Y, Muqbil I, Aboukameel A, Senapedis W, Baloglu E, Landesman Y, Shacham S, Kauffman MG, Philip PA, Mohammad RM. Exportin 1 (XPO1) inhibition leads to restoration of tumor suppressor miR-145 and consequent suppression of pancreatic cancer cell proliferation and migration. Oncotarget. 2017;8:82144-55.

Siveen KS, Uddin S, Mohammad RM. Targeting acute myeloid leukemia stem cell signaling by natural products. Mol Cancer. 2017;16:13.
 

Education/Training

PhD in Stress Physiology (1987): Utah State University, Logan, Utah
Post-Doc in Cancer Biology (1991): Wayne State University, Detroit, Michigan 

Courses Taught

CB7460 Mechanism of Neoplasia: Alterations to Cellular Signaling

 

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