Somatic mutations of calreticulin in myeloproliferative neoplasms.
By T. Klampfl, H. Gisslinger, A. Harutyunyan, Harini Nivarthi, E. Rumi, J. Milosevic, Nicole C. C. Them, T. Berg, B. Gisslinger, D. Pietra and 19 more. New England Journal of Medicine, 2013
1,902 citations recorded by the source corpus.
Subfields: Genetics, Hematology
View Paper: https://www.semanticscholar.org/paper/77319b3cff4fe23614b775000084553dc5751120
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Citations in the corpus
- The role of mutations in epigenetic regulators in myeloid malignancies (2012, background): “Two groups recently identified CALR mutations in JAK2-wildtype MPN patients, including 25–27% of patients with essential thrombocythemia (ET) and 14–35% of PMF, specifically (108, 109).”
- Evolving cognition of the JAK-STAT signaling pathway: autoimmune disorders and cancer (2023, background): “Whole-exome sequencing identified CALR mutations in ~70% to 80% of JAK2-negative ETs and primary myelofibrosis.(232,233) In vivo research demonstrated that CALR mutation alone was strong enough to initiate an MPN phenotype and increased JAK-STAT signaling activity.”
- Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms. (2014, neutral): “Neutrophils (10(9)/L) average (range) 9 (2-36) 6 (3-16) 8 (3-21)”