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Comparison of therapy‐related and de novo core binding factor acute myeloid leukemia: A bone marrow pathology group study
Author(s) -
Rogers Heesun J.,
Wang Xiaoqiong,
Xie Yan,
Davis Adam R.,
Thakral Beenu,
Wang Sa A.,
Borthakur Gautam,
Cantu Miguel D.,
Margolskee Elizabeth M.,
Philip John K. S.,
Sukhanova Madina,
Bagg Adam,
BuesoRamos Carlos E.,
Orazi Attilio,
Arber Daniel A.,
Hsi Eric D.,
Hasserjian Robert P.
Publication year - 2020
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.25814
Subject(s) - medicine , core binding factor , trisomy , myeloid leukemia , trisomy 8 , gastroenterology , bone marrow , oncology , leukemia , kras , cytogenetics , pathology , chromosome , cancer , biology , gene , genetics , colorectal cancer , transcription factor
This multi‐institutional study retrospectively evaluated clinicopathologic and genetic characteristics in 351 patients with core‐binding‐factor acute myeloid leukemia (CBF‐AML), comprising 69 therapy‐related (t‐CBF‐AML) and 282 de novo cases. The T‐CBF‐AML patients were older, had lower WBC counts, and slightly higher hemoglobin than patients with de novo disease. Secondary cytogenetic abnormalities were more frequent in patients with de novo disease than t‐CBF‐AML (57.1% vs 41.1%, P = .026). Patients with secondary cytogenetic abnormalities had longer overall survival (OS) than those without abnormalities (median 190 vs 87 months, P = .021); trisomy 8, trisomy 22, and loss of the X or Y chromosome were associated with longer OS. In the 165 cases performed of targeted gene sequencing, pathogenic mutations were detected in 75.7% of cases, and were more frequent in de novo than in therapy‐related disease ( P = .013). Mutations were found in N/KRAS (37.0%), FLT3 (27.8%), KIT (17.2%), TET2 (4.9%), and ASXL1 (3.9%). The TET2 mutations were associated with shorter OS ( P = .012) while N/KRAS mutation was associated with longer OS in t(8;21) AML patients ( P = .001). The KIT mutation did not show prognostic significance in this cohort. Although they received similar therapy, t‐CBF‐AML patients had shorter OS than de novo patients (median 69 vs 190 months, P = .038). In multivariate analysis of all patients, older age and absence of any secondary cytogenetic abnormalities were significant predictors of shorter OS. Among the t‐CBF‐AML subset, age and hemoglobin were significant on multivariate analysis. This study demonstrated that although de novo and t‐CBF‐AML patients share many features, t‐CBF‐AML patients have worse clinical outcome than de novo patients.