The DOI matches its Crossref record; 93 of the 93 references it cites were found in a registry or an index.
Diagnosis, risk stratification, and response evaluation in classical myeloproliferative neoplasms
Open accessAbstract
Philadelphia-negative classical myeloproliferative neoplasms (MPNs) include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The 2016 revision of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues includes new criteria for the diagnosis of these disorders. Somatic mutations in the 3 driver genes, that is, JAK2, CALR, and MPL, represent major diagnostic criteria in combination with hematologic and morphological abnormalities. PV is characterized by erythrocytosis with suppressed endogenous erythropoietin production, bone marrow panmyelosis, and JAK2 mutation. Thrombocytosis, bone marrow megakaryocytic proliferation, and presence of JAK2, CALR, or MPL mutation are the main diagnostic criteria for ET. PMF is characterized by bone marrow megakaryocytic proliferation, reticulin and/or collagen fibrosis, and presence of JAK2, CALR, or MPL mutation. Prefibrotic myelofibrosis represents an early phase of myelofibrosis, and is characterized by granulocytic/megakaryocytic proliferation and lack of reticulin fibrosis in the bone marrow. The genomic landscape of MPNs is more complex than initially thought and involves several mutant genes beyond the 3 drivers. Comutated, myeloid tumor-suppressor genes contribute to phenotypic variability, phenotypic shifts, and progression to more aggressive disorders. Patients with myeloid neoplasms are at variable risk of vascular complications, including arterial or venous thrombosis and bleeding. Current prognostic models are mainly based on clinical and hematologic parameters, but innovative models that include genetic data are being developed for both clinical and trial settings. In perspective, molecular profiling of MPNs might also allow for accurate evaluation and monitoring of response to innovative drugs that target the mutant clone.
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Cites
WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues
Swerdlow, S. H. (2017) · Medical Entomology and Zoology · Cited by 12,933
Arber, D. A., Orazi, A., Hasserjian, R., Thiele, J., Borowitz, M. J., Le Beau, M. M., Bloomfield, C. D., Cazzola, M., & Vardiman, J. W. (2016) · Blood · doi:10.1182/blood-2016-03-643544 · Cited by 10,119
Self-citationWHO classification of haematolymphoid tumours
Gaillard, F., Weerakkody, Y., & Sharma, R. (2010) · Radiopaedia.org · doi:10.53347/rid-9250 · Cited by 3,776
Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders
Baxter, E. J., Scott, L. M., Campbell, P. J., East, C., Fourouclas, N., Swanton, S., Vassiliou, G. S., Bench, A. J., Boyd, E. M., Curtin, N., et al. (2005) · The Lancet · doi:10.1016/s0140-6736(05)71142-9 · Cited by 3,548
A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera
James, C., Ugo, V., Le Couédic, J.-P., Staerk, J., Delhommeau, F., Lacout, C., Garçon, L., Raslova, H., Berger, R., Bennaceur-Griscelli, A., et al. (2005) · Nature · doi:10.1038/nature03546 · Cited by 3,544
A Gain-of-Function Mutation of JAK2 in Myeloproliferative Disorders
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Self-citationLevine, R. L., Wadleigh, M., Cools, J., Ebert, B. L., Wernig, G., Huntly, B. J. P., Boggon, T. J., Wlodarska, I., Clark, J. J., Moore, S., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.03.023 · Cited by 2,993
Somatic Mutations of Calreticulin in Myeloproliferative Neoplasms
Klampfl, T., Gisslinger, H., Harutyunyan, A. S., Nivarthi, H., Rumi, E., Milosevic, J. D., Them, N. C. C., Berg, T., Gisslinger, B., Pietra, D., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1311347 · Cited by 2,003
Self-citationSomatic CALR Mutations in Myeloproliferative Neoplasms with Nonmutated JAK2
Nangalia, J., Massie, C. E., Baxter, E. J., Nice, F. L., Gundem, G., Wedge, D. C., Avezov, E., Li, J., Kollmann, K., Kent, D. G., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1312542 · Cited by 1,756
MPLW515L Is a Novel Somatic Activating Mutation in Myelofibrosis with Myeloid Metaplasia
Pikman, Y., Lee, B. H., Mercher, T., McDowell, E., Ebert, B. L., Gozo, M., Cuker, A., Wernig, G., Moore, S., Galinsky, I., et al. (2006) · PLoS Medicine · doi:10.1371/journal.pmed.0030270 · Cited by 1,449
Cited by
Barbui, T., Thiele, J., Gisslinger, H., Kvasnicka, H. M., Vannucchi, A. M., Guglielmelli, P., Orazi, A., & Tefferi, A. (2018) · Blood Cancer Journal · doi:10.1038/s41408-018-0054-y · Cited by 641
ASXL1/EZH2 mutations promote clonal expansion of neoplastic HSC and impair erythropoiesis in PMF
Triviai, I., Zeschke, S., Rentel, J., Spanakis, M., Scherer, T., Gabdoulline, R., Panagiota, V., Thol, F., Heuser, M., Stocking, C., et al. (2019) · Leukemia · doi:10.1038/s41375-018-0159-0 · Cited by 28
Gleitz, H. F., Kramann, R., & Schneider, R. K. (2018) · The Journal of Pathology · doi:10.1002/path.5078 · Cited by 23
Metadata
- Authors
- Rumi, E., & Cazzola, M.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2017-02-09
- Volume
- 129
- Issue
- 6
- Pages
- 680-692
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2567208701
- Cited by
- 258
- References
- 93
- FWCI
- 16.63
- Type
- journal article
- Language
- en
- Open access
- green
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