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Mohammed L. Ibrahim, B. Pharm, PhD

Assistant Professor of Immunology

Office Phone: (916) 378-3509
Fax: 916-686-7310
Email: mohammed.ibrahim@cnsu.edu

Mohammed L. Ibrahim, B. Pharm, PhD

Education

  • PhD, Biochemistry and Cancer Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA
  • BS, Pharmaceutical Science, Cairo University, Egypt

About

Dr. Ibrahim is an accomplished scientist in the field of cancer immunology with extensive hands-on experience and several high-impact publications. He is a dedicated educator with a strong record of student mentorship and an interdisciplinary background in various branches of biomedical sciences, including Biochemistry, Immunology, Cancer immunotherapy, Cancer Biology, Molecular Biology, Genetics, and Clinical Nutrition.

His doctoral work centered on defining the potential epigenetic mechanisms and oncogenic signals underlying the development of inflammation-mediated colon tumorigenesis. He completed his postdoctoral training in the Department of Immunology at Moffitt Cancer Center in Tampa, Florida, USA. During his postdoctoral fellowship, Dr. Ibrahim expanded his research into the rapidly evolving fields of targeted therapy and cancer immunotherapy, with a greater emphasis on translational aspects. His work highlighted how newly developed epigenetic modulators—especially HDAC inhibitors—and oncogenic targeted therapies, with a particular emphasis on KRAS inhibitors, reshape the tumor immune microenvironment.

Dr. Ibrahim’s work lays the foundation for innovative therapeutic strategies that integrate cancer-selective KRAS pathway inhibitors, epigenetic modifiers such as DNMT and HDAC inhibitors, and groundbreaking immunotherapies, including immune checkpoint blockade and adoptive cell therapies. His ultimate goal is to enhance the antitumor immunity and improve the clinical outcomes for patients with refractory cancers such as pancreatic, lung, and colorectal malignancies.

Research Interests

Dr. Ibrahim’s laboratory investigates how combination therapies—incorporating KRAS pathway targeted inhibitors (KRASi, SHP2i, MEKi), epigenetic modulators (DNMTi, HDACi, HMTi), and immunotherapies (immune checkpoint inhibition and adoptive T-cell therapy) reshape the tumor immune microenvironment in pancreatic, colorectal, and lung cancers, to achieve the optimum clinical benefit. His research aims to define the immune modulation induced by these therapeutic regimens with insight into T cell effector function and macrophage activation.

A major focus of his research is uncovering the oncogenic and epigenetic mechanisms that underlie resistance to next-generation KRAS inhibitors and developing rational combination strategies targeting upstream and downstream signaling nodes or epigenetic regulators to overcome this resistance.

His work also explores the regulation of TNF-RIP1/NFkB and Type I/II interferon pathways, investigating how KRAS inhibition and epigenetic modulation impact their downstream immune-function genes (like MHC-I and T cell chemokines), cancer cell death (apoptotic genes), and the resultant remodeling in the tumor immune microenvironment, with implications to enhance the clinical outcome from cancer immunotherapies.

Publications

  • Complete list of publications and citation indices on the Google Scholar home page
  • Nana Adjoa Ben-Crentsil, Wazim Mohammed Ismail, Maria Balasis, Hannah Newman, Ariel Quintana, Moritz Binder, Traci Kruer, Surendra Neupane, Meghan Ferrall-Fairbanks, Jenna Fernandez, Terra Lasho, Christy Finke, Mohammed L. Ibrahim, Kathy McGraw, Michael Wysota, Amy Aldrich, Christopher Ryder, Christopher Letson, Joshua Traina, Amy Mclemore, Nathalie Droin, Aditi Shastri,, Seongseok Yun, Eric Solary, David A. Sallman, Amer A. Beg, Li Ma, Alexandre Gaspar-Maia, Mrinal M. Patnaik, and Eric Padron. RNA shielding of P65 is required to potentiate oncogenic inflammation in TET2 mutated clonal hematopoiesis. Cancer Discovery. 2024, CD-24-0093.
  • Mohammed L. Ibrahim*, Hong Zheng*, Margaret L. Barlow*, Yousuf Latif, Zhihua Chen, Xiaoqing Yu, Amer A. Beg. HDAC inhibitors directly modulate T cell gene expression and signaling and promote development of effector-exhausted T cells in murine tumors. J Immunol. 2024, 212: 1–12. *Equal contributions
  • Hong Zheng, Xiaoqing Yu, Mohammed L. Ibrahim, Dana Foresman, Mengyu Xie, Joseph Johnson, Theresa A. Boyle, Brian Ruffell, Bradford A. Perez, Scott J. Antonia, Neal Ready, Andreas N. Saltos, Mark J. Cantwell, Amer A. Beg. Combination IFNβ and membrane-stable CD40L maximize tumor dendritic cell activation and lymph node trafficking to elicit systemic T-cell immunity. Cancer Immunol Res. 2023. CIR-22-0927.
  • Alyssa D. Smith, Chunwan Lu, Daniela Payne, Amy V. Paschall, John D. Klement, Priscilla S. Redd, Mohammed L. Ibrahim, Dafeng Yang, Qimei Han, Zhuoqi Liu, Huidong Shi, Thomas J. Hartney, Asha Nayak-Kapoor, and Kebin Liu. Autocrine IL6-mediated activation of the STAT3–DNMT axis silences the TNFα–RIP1 necroptosis pathway to sustain survival and accumulation of myeloid-derived suppressor cells. Cancer Research. 2020. 80 (15), 3145-3156.