Md Wasim Khan, PhD
Office location
Karmanos Cancer Institute
Hudson-Webber Cancer Research Center - 640.2
4100 John R.
Detroit, MI 48201
Mailing address
Karmanos Cancer Institute
4100 John R., HW06AO
Detroit, MI 48201
Biography
Dr. Md. Wasim Khan is an Associate Professor of Oncology at the Barbara Ann Karmanos Cancer Institute and Wayne State University, where he leads a translational research program focused on metabolic reprogramming in liver disease. With a Ph.D. in Biochemistry from Aligarh Muslim University and postdoctoral training at the University of Illinois at Chicago, Dr. Khan has dedicated his career to understanding how altered metabolism drives cancer progression, particularly in hepatocellular carcinoma (HCC). Beyond his research, he is deeply committed to mentoring the next generation of scientists and has trained numerous undergraduate, graduate, and postdoctoral researchers.
Degrees
MS, PhDEducation training
Education
(2006-2010) PhD, Biochemistry, Aligarh Muslim University, Aligarh, India
(2003-2005) MS, Aligarh Muslim University, Aligarh, India
(2000-2003) BS, Aligarh Muslim University, Aligarh, India
Professional experience
Faculty Appointments
(2025-Present) Associate Professor, Karmanos Cancer Institute, Department of Oncology, Wayne State University, Detroit, MI.
(2021-2025) Assistant Professor, University of Illinois at Chicago, Department of Medicine, Division of Endocrinology, Diabetes & Metabolism, Chicago, IL.
Hospital or Other Professional Appointments
(2018-2021) Visiting Scholar, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, IL.
(2017-2018) Research Collaborator, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, IL.
(2012-2016) DST-Inspire Faculty, CSIR-Indian Institute of Chemical Biology, India
(2011) Senior Scientific Officer, Riyadh Military Hospital, Riyadh, KSA
Research
Our laboratory focuses on cancer metabolism, with a particular emphasis on uncovering and targeting metabolic vulnerabilities in hepatocellular carcinoma (HCC)—the most common form of liver cancer and a leading cause of cancer-related deaths worldwide. We have pioneered research on HKDC1, a novel hexokinase that is highly expressed in liver cancer and metabolic dysfunction-associated steatohepatitis (MASH), but is nearly absent in healthy liver tissue. This selective expression makes HKDC1 an exceptional therapeutic target. By integrating mouse models, cellular systems, and innovative PROTAC technology, we are translating fundamental insights into first-in-class precision therapies. Our research spans the full translational continuum—from dissecting molecular mechanisms to developing drug candidates aimed at eliminating HKDC1 and rewiring cancer metabolism. Graduate students in our lab receive interdisciplinary training in cancer metabolism, mitochondrial biology, mouse genetics, cell signaling, medicinal chemistry, and preclinical drug development. Trainees gain hands-on experience with CRISPR gene editing, genetically engineered mouse models, advanced metabolomics and proteomics, live-cell imaging, Seahorse metabolic flux analysis, and PROTAC degrader platforms—preparing them for impactful careers in academia, industry, and biotechnology.
Related websites: https://scholar.google.co.in/citations?user=CmnpwWUAAAAJ&hl=en
Research interests
Active Projects
1. HKDC1 as a Master Regulator of Liver Metabolism
We are investigating how HKDC1 functions as a nutrient sensor and metabolic switch in liver disease. Using cutting-edge single-cell multi-omics (scRNA-seq and spatial metabolomics), this project aims to map HKDC1-driven metabolic shifts across different stages of MASLD and MASH.
2. Targeting Mitochondrial HKDC1 for Therapeutic Intervention
This project focuses on disrupting the interaction between HKDC1 and mitochondrial pathways. We are developing novel PROTACs to selectively degrade HKDC1, aiming to restore mitochondrial function and reverse metabolic dysregulation that underpins liver disease progression.
3. Deciphering Gut-Liver Crosstalk Mediated by HKDC1
Here, we explore the role of HKDC1 in modulating bile acid metabolism within the gut-liver axis. By integrating multi-omics approaches and functional assays, we seek to understand how HKDC1 influences bile acid synthesis, transport, and signaling to reprogram hepatic metabolism.
4. Mechanistic Dissection of Metabolic Reprogramming in Liver Disease
We are using advanced omics, CRISPR-based screens, and metabolic flux analyses to uncover the molecular mechanisms by which HKDC1 drives metabolic reprogramming in liver cells. This project aims to identify key signaling pathways and downstream effectors that could serve as new therapeutic targets.
5. HKDC1 in Liver Regeneration and Tissue Recovery
Recognizing that liver regeneration is intrinsically linked to metabolic reprogramming, this project investigates the role of HKDC1 in regenerative metabolism following liver injury. Through in vivo models, metabolic profiling, and lineage tracing, we aim to elucidate how modulating HKDC1 can enhance liver recovery and regeneration.
Publications
Selected Bibliography
- Xu, Kai, Irene Covila-Corona, María Dolores Frutos, María Ángeles Núñez-Sánchez, Dhruvi Makhanasa, Pratham Viral Shah, Grace Guzman, Bruno-Ramos Molina, Medha Priyadarshini, Md. Wasim Khan. Hepatic Hkdc1 Deletion Alleviates Western Diet-Induced Mash in Mice. bioRxiv 2024.11.26.625530. (2024) (Minor Revision – BBA: Molecular Basis of Disease)
- Pusec, C. M., Ilievski, V., De Jesus, A., Farooq, Z., Zapater, J. L., Sweis, N., Ismail, H., Khan, M. W., Ardehali, H. & Cordoba-Chacon, J. Liver-specific overexpression of HKDC1 increases hepatocyte size and proliferative capacity. Scientific reports 13, 8034 (2023).
- Khan, M. W., Terry, A. R., Priyadarshini, M., Ilievski, V., Farooq, Z., Guzman, G., Cordoba-Chacon, J., Ben-Sahra, I., Wicksteed, B. & Layden, B. T. The hexokinase “HKDC1” interaction with the mitochondria is essential for liver cancer progression. Cell Death & Disease volume 13, 660 (2022).
- Priyadarshini, M., Navarro, G., Reiman, D. J., Sharma, A., Xu, K., Lednovich, K., Manzella, C. R., Khan, M. W., Garcia, M. S. & Allard, S. Gestational Insulin Resistance Is Mediated by the Gut Microbiome–Indoleamine 2, 3-Dioxygenase Axis. Gastroenterology 162, 1675-1689. e1611 (2022).
- Cutler T.Lewandowski, M. W. K., Manel Ben Aissa, Oleksii Dubrovskyia, Martha Ackerman-Berrier, Mary Jo LaDu, Brian T.Layden, Gregory R.J.Thatcher. Metabolomic analysis of a selective ABCA1 inducer in obesogenic challenge provides a rationale for therapeutic development. EBioMedicine 66 (2021).
- Khan, M. W., Priyadarshini, M., Cordoba-Chacon, J., Becker, T. C. & Layden, B. T. Hepatic hexokinase domain containing 1 (HKDC1) improves whole-body glucose tolerance and insulin sensitivity in pregnant mice. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease 1865, 678-687 (2019).
- Pusec, C. M., De Jesus, A., Khan, M. W., Terry, A. R., Ludvik, A. E., Xu, K., Giancola, N., Pervaiz, H., Daviau Smith, E. & Ding, X. Hepatic HKDC1 expression contributes to liver metabolism. Endocrinology 160, 313-330 (2019).
- Khan, M. W., Layden, B. T. & Chakrabarti, P. Inhibition of mTOR complexes protects cancer cells from glutamine starvation-induced cell death by restoring Akt stability. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease (2018).
- Md. Wasim Khan, X. D., Scott J. Cotler, Michael Clarke, Brian T. Layden. Studies on the Tissue Localization of HKDC1, a Putative Novel Fifth Hexokinase, in Humans. Journal of Histochemistry & Cytochemistry (2018).
- Khan, M. W., Biswas, D., Ghosh, M., Mandloi, S., Chakrabarti, S. & Chakrabarti, P. mTORC2 controls cancer cell survival by modulating gluconeogenesis. Cell Death Discovery 1, 1-12 (2015).