Ctirad Radek Skoda, M.D.
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Ctirad Radek Skoda, M.D.
Senior Faculty
Positions
- Senior Faculty
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Dan L Duncan Comprehensive Cancer Center
Molecular and Cell Biology
Baylor College of Medicine
Houston, US
- Professor
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Department of Medicine
Baylor College of Medicine
Houston, United States
Education
- Residency at University Hospital Basel
- 04/1989 - Basel, Switzerland
- Postdoctoral Fellowship at Harvard Medical School, Dept. of Genetics
- 10/1993 - Boston
- MD from University of Zurich
- 01/1983 - Zurich, Switzerland
Honors & Awards
- Ernest Beutler Lecture and Prize
- American Society of Hematology (01/2025)
- David Grimwade Award
- European Hematology Association (01/2020)
- Ham Wasserman Lecture Award
- American Society of Hematology (01/2007)
Professional Interests
- Molecular pathogenesis of myeloproliferative neoplasms
- Clonal hematopoiesis driven by the JAK2-V617F mutation
Professional Statement
We are investigating the pathogenesis of myeloproliferative neoplasms (MPN), a group of chronic leukemias caused by gene mutations that are acquired in hematopoietic stem cells. In 2005, my research group described the JAK2-V617F mutation as the most frequent cause of MPN, which is acquired in approximately 70% of all patients with MPN. We further elucidated the contribution of additional gene mutations, including Ezh2 and Dnmt3a, to MPN outcome and prognosis. We also identified mutations in THPO and EPO genes as the cause of hereditary MPN-like syndromes. Since JAK2-V617F is frequently found in healthy individuals with clonal hematopoiesis of indeterminate potential (CHIP), we are examining the factors that limit or promote the conversion from CHIP to MPN. We developed a JAK2-V617F mouse model that allows us to study MPN disease initiation from single hematopoietic stem cells, and using this system we recently demonstrated that the pro-inflammatory cytokine IL-1 promotes MPN disease initiation and progression to fibrosis. We now investigate the role of immune surveillance in CHIP initiation and the molecular mechanisms of how Dnmt3a mutations accelerate conversion from CHIP to MPN. We also study how JAK2-V617F mutant stem cells gain resistance to therapeutic agents currently used to treat patients with MPN, such as tyrosine kinase inhibitors and interferon-α.Websites
Selected Publications
- Usart, M., Stetka, J., Luque Paz, D., Hansen, N., Kimmerlin, Q., Almeida Fonseca, T., Lock, M., Kubovcakova, L., Karjalainen, R., Hao-Shen, H., Börsch, A., El Taher, A., Schulz , J., Leroux , J.C., Dirnhofer, S., Skoda, R.C,. "Loss of Dnmt3a increased self-renewal and resistance to pegIFNα in JAK2-V617F-positive myeloproliferative neoplasms.." Blood. 2024;143:2490-2503. Pubmed PMID: 38493481
- Stetka, J., Usart, M., Kubovcakova, L., Rao, T.N., Hao-Shen, H., Dirnhofer, S., et al.; Skoda, R.C. "Iron is a modifier of the phenotypes of JAK2-mutant myeloproliferative neoplasms.." Blood. 2023;141:2127-40.
- Rai, S., Grockowiak, E., Hansen, N., Luque Paz, D., Stoll, C.B., Hao-Shen, H., Mild-Schneider, G., Dirnhofer, S., Farady, C.J., Méndez-Ferrer, S., Skoda, R.C. "Inhibition of interleukin-1β reduces myelofibrosis and osteosclerosis in mice with JAK2-V617F driven myeloproliferative neoplasm.." Nature Communications. 2022;13:5346.
- 4) Zmajkovic, J., Lundberg, P., Nienhold, R., Lyngaas Torgersen, M., Sundan, A., Waage, A. Skoda, R.C. "A gain-of-function mutation in EPO in familial erythrocytosis.." N. Engl. J. Med. 2018;378:924-30.
Memberships
- American Society of Hematology (ASH)
- Member (01/1994)
- Swiss Society of Hematology (SGH-SSH)
- Member (01/1995)
- European Hematology Association (EHA)
- Member (01/2005)
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