Mark J. Levis
| Mark J. Levis | |
|---|---|
 File:MarkLevis.webp | |
| Born | |
| 🏫 Education | University of California, Berkeley University of California, San Francisco School of Medicine |
| 💼 Occupation | |
Mark J. Levis is an American physician‑scientist and oncologist[1] known for his work in the treatment and molecular targeting of acute leukemia, particularly acute myeloid leukemia (AML).[2][3] He is a Professor of Oncology at the Johns Hopkins University School of Medicine, Director of the Adult Leukemia Service, and has served as Co‑Director of the Division of Hematologic Malignancies at the Sidney Kimmel Comprehensive Cancer Center.[4] He has served as an ad hoc member of the Oncology Drug Advisory Committee.[5]
Education
Levis earned a B.A. in Genetics from the University of California, Berkeley in 1984. He completed both his Ph.D. in Biochemistry in 1992 and M.D. in 1994 at the University of California, San Francisco School of Medicine, where he participated in the Medical Scientist Training Program and conducted thesis work under Henry Bourne.[6]
Career
Levis joined the Johns Hopkins faculty in 2002. He served as assistant professor from 2002 to 2008 and Associate Professor from 2008 to 2015 before being named full professor of Oncology in 2015. He has directed the Adult Leukemia Program since 2013,[7] and served as the co-leader of the Hematologic Malignancies and Bone Marrow Transplantation Program at the Sidney Kimmel Comprehensive Cancer Center until 2025.[8]
In 2002, he received the Daniel Nathans Research Award from Johns Hopkins University.[9]
Levis is also actively involved in clinical trial and is a member of the American Society of Hematology (ASH),[10] the American Society of Clinical Oncology (ASCO),[11] and the European Hematology Association.[6]
Research
His research focuses on targeted therapies for leukemia, with a focus on FLT3 (FMS‑like tyrosine kinase 3)[12] as a therapeutic target in AML.[13] FLT3 is a receptor tyrosine kinase frequently mutated in AML, and Levis’s early work helped demonstrate that AML cells with FLT3 mutations are dependent on mutant FLT3 signaling for survival, forming the basis for the clinical development of FLT3 inhibitors.[14]
Levis held researches on FLT3 inhibitors, including the clinical development of gilteritinib and quizartinib, both effective FLT3 inhibitors approved for treating FLT3‑mutated AML.[15] He also developed assays to measure plasma inhibitory activity of these drugs and to evaluate their effectiveness as targeted therapies in patients.[16]
References
- ↑ Fine, Bev (2013-02-27). "Leukemia and Lymphoma Society holds Journey of Hope". Baltimore Sun. Retrieved 2026-05-22.
- ↑ Wahner, Ashling (2026-05-22). "Quizartinib May Represent an Additional Therapeutic Option for FLT3-ITD+ AML | OncLive". www.onclive.com. Retrieved 2026-05-22.
- ↑ Doyle, Chase. "Gilteritinib Maintenance Therapy After Transplantation in Patients With FLT3-ITD AML Who Have Measurable Residual Disease". ascopost.com. Retrieved 2026-05-22.
- ↑ "Dr. Mark Levis Discusses Quizartinib in AML | OncLive". www.onclive.com. 2026-05-22. Retrieved 2026-05-22.
- ↑ Stein, Jeffrey. "Dr. Levis will discuss the current landscape of hematology drugs and the dilemmas and risks". firstwordpharma.com. Retrieved 2026-05-22.
- ↑ 6.0 6.1 "Prof. Levis received his medical degree from the University of California San Francisco School of Medicine in San Francisco, CA, in 1994". VJHemOnc. Retrieved 2026-05-22.
- ↑ "Using FLT3 Inhibitors to Treat Acute Myeloid Leukemia". Massachusetts General Hospital. Archived from the original on 2026-01-21. Retrieved 2026-05-22. Unknown parameter
|url-status=ignored (help) - ↑ Doherty, Kyle (2026-05-22). "Quizartinib Plus Chemotherapy Shows Strong Activity in FLT3-ITD–Positive, NPM1-Mutated AML | OncLive". www.onclive.com. Retrieved 2026-05-22.
- ↑ Downer, Joanna. "The Johns Hopkins Gazette: April 8, 2002". The Gazette Online. Retrieved 2026-05-22.
- ↑ "Announcing New ASH Executive Committee Members, ASH Visitor Training Program". ASH. Archived from the original on 2024-11-05. Retrieved 2026-05-22. Unknown parameter
|url-status=ignored (help) - ↑ Ahmed, Kamran A. "Mark J. Levis, MD, PhD, on Acute Myeloid Leukemia: Gilteritinib in FLT3-Mutated Disease". ascopost.com. Retrieved 2026-05-22.
- ↑ University, Mark J. Levis, MD, PhD, Johns Hopkins (2026-05-22). "Dr. Levis on the Challenges of Treating FLT3-ITD AML | OncLive". www.onclive.com. Retrieved 2026-05-22.
- ↑ Levis, Mark J.; Hamadani, Mehdi; Logan, Brent R.; Jones, Richard J.; Singh, Anurag K.; Litzow, Mark R.; Wingard, John R.; Papadopoulos, Esperanza B.; Perl, Alexander E.; Soiffer, Robert J.; Ustun, Celalettin; Oshima, Masumi Ueda; Uy, Geoffrey L.; Waller, Edmund K.; Vasu, Sumithira (2025-05-08). "Measurable residual disease and posttransplantation gilteritinib maintenance for patients with FLT3-ITD–mutated AML". Blood. 145 (19): 2138–2148. doi:10.1182/blood.2024025154. ISSN 0006-4971. PMC 12105721 Check
|pmc=value (help). Archived from the original on 2026-02-20. Retrieved 2026-05-22. Unknown parameter|url-status=ignored (help) - ↑ Unanswered questions that remain in FLT3-mutated AML. Retrieved 2026-05-22 – via www.vjhemonc.com.
- ↑ Erba, Harry P.; Fathi, Amir (2026-05-22). "Second-Generation FLT3 Inhibitors in AML | OncLive". www.onclive.com. Retrieved 2026-05-22.
- ↑ Levis, Mark; Brown, Patrick; Smith, B. Douglas; Stine, Adam; Pham, Rosalyn; Stone, Richard; DeAngelo, Daniel; Galinsky, Ilene; Giles, Frank; Estey, Elihu; Kantarjian, Hagop; Cohen, Pamela; Wang, Yanfeng; Roesel, Johannes; Karp, Judith E. (2006-11-15). "Plasma inhibitory activity (PIA): a pharmacodynamic assay reveals insights into the basis for cytotoxic response to FLT3 inhibitors". Blood. 108 (10): 3477–3483. doi:10.1182/blood-2006-04-015743. ISSN 0006-4971. PMC 1895426. PMID 16857987.
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