MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients.

By A. Pardanani, Ross L. Levine, T. Lasho, Yana Pikman, R. Mesa, M. Wadleigh, D. Steensma, M. Elliott, A. Wolanskyj, W. Hogan and 4 more. Blood, 2006

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Project DRIVE: A Compendium of Cancer Dependencies and Synthetic Lethal Relationships Uncovered by Large-Scale, Deep RNAi Screening. (2017, neutral): “MPL is the receptor for thrombopoietin and sustains gain-of-function mutations in myeloproliferative neoplasms including essential thrombocythemia and primary myelofibrosis (Pardanani et al., 2006).”
Evolving cognition of the JAK-STAT signaling pathway: autoimmune disorders and cancer (2023, background): “Moreover, a study of a cohort of 1182 patients with MPN and the exploration of bone marrow-derived DNA from different disease courses consistently showed that MPL and JAK2 occurred concurrently in MPNs, suggesting that the functions of these driver mutations may be relatively complementary in the co”
The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. (2009, background): “B lymphoblastic leukemia/lymphoma with t(12;21)(p13;q22) TEL-AML1”