Minneapolis VA Health Care System Research Service

Investigator Profile

Khalil Ahmed, PhD

Positions

Senior Research Career Scientist, Minneapolis VA
Professor of Laboratory Medicine and Pathology, University of Minnesota

Education

BSc, MSc Panjab University; PhD McGill University

Contact Information

khalil.ahmed@va.gov

Research Interests

My long-standing interest in protein CK2 (formerly casein kinase 2 or II) has continued to define its diverse functions, with special focus on mechanism of CK2 regulation of cell survival/death in cancer cells. The focus of our research on CK2 signaling in normal and neoplastic cell growth was originally on prostate cancer but now includes several other cancers (such as HNSCC, breast cancer, melanoma). In addition to studying the mechanistic aspects of CK2 functional biology, we are also investigation of its therapeutic targeting for cancer therapy. In our current studies, we are pursuing the hypothesis that induction of CK2 and consequent impact on AR and NFκB pathways promotes therapy resistance to current AR targeting therapies. To that end, we aim to determine molecular mechanisms involved in CK2 promotion of androgen pathway therapy resistance, and establish how CK2 functions as a driving factor for PCa disease progression. This work will pursue the idea that downregulation of CK2 will delay or prevent PCa progression or reverse resistance to androgen pathway targeting therapy. Further, we plan to determine what type of alterations occur in the proteomic landscape under these therapy conditions and related to suppression of cell death pathways which may provide new insights into PCa progression. Our work would suggest that co-treatment with a CK2-blocking drug (such as CX-4945) might be effective for stopping progression to resistant growth or improving response to androgen pathway drugs in men with advanced PCa, setting the stage for potential ground-breaking translation into the clinic.

Publications

Full bibliography on PubMed

VA Research Topics

Cancer; Prostatic Disease

MeSH Key Words

Apoptosis; Breast Neoplasms; Casein Kinase II; Caspases; Cell Proliferation; Head and Neck Neoplasms; Inhibitor of Apoptosis Proteins; Membrane Potential, Mitochondrial; Mitochondria; Molecular Targeted Therapy; Casein Kinase 2, alpha, human; Nanoparticles; Proteome; Signal Transduction

ORCID | ResearchGate | Google Scholar

Links

University of Minnesota profile

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