Acute myeloid leukemia ontogeny is defined by distinct somatic mutations.

By R. C. Lindsley, B. Mar, E. Mazzola, Peter V. Grauman, Sarah Shareef, Steven L. Allen, A. Pigneux, M. Wetzler, Robert K. Stuart, H. Erba and 9 more. Blood, 2015

928 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/080cb5465b439265583e6f30a2b865fa6da8c46c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Benjamin L. Ebert
2. Andreas Hochhaus
3. H. Kantarjian

In Hematology

1. J. Apperley
2. Benjamin L. Ebert
3. Andreas Hochhaus
4. H. Kantarjian
5. Brian J. Druker

In Molecular Biology

1. Benjamin L. Ebert

Citations in the corpus

• The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Myeloid and Histiocytic/Dendritic Neoplasms (2022, background): “This AML type is defined as a neoplasm with ≥20% blasts expressing a myeloid immunophenotype and harboring specific cytogenetic and molecular abnormalities associated with MDS, arising de novo or following a known history of MDS or MDS/MPN. Key changes include: (1) removal of morphology alone as a d”
• Cancer therapy shapes the fitness landscape of clonal hematopoiesis (2020, neutral): “In 91% of cases, transformation was associated with acquisition of additional somatic mutations, including chromosomal aneuploidies or mutations in genes (e.g. FLT3, KRAS, NRAS) known to drive late progression to myeloid disease 27,32–34 (Supplementary Figure 11).”
• Diagnosis and management of AML in adults: 2017 ELN recommendations from an international expert panel. (2017, background): “The prognoses of patients with clinically diagnosed de novo AML whose gene mutation profile resembles those of patients with clinically diagnosed secondary AML is more like secondary than de novo AML.(81) Mutations associatedwith secondaryAMLoccur in genes encoding SRSF2, SF3B1, U2AF1, and ZRSR2 (sp”
• Genomic Classification and Prognosis in Acute Myeloid Leukemia (2016, neutral): “AML with t(8;21)(q22;q22); RUNX1–RUNX1T1 60 (4) t(8;21) (100), KIT (38), −Y (33), −9q (18)”
• TP53 and Decitabine in Acute Myeloid Leukemia and Myelodysplastic Syndromes (2016, neutral): “With hematologic improvement 6 (5) 5 (24) 1 (1) 0 0.”