Fusion partner-specific mutation profiles and KRAS mutations as adverse prognostic factors in MLL-rearranged AML.


Journal

Blood advances
ISSN: 2473-9537
Titre abrégé: Blood Adv
Pays: United States
ID NLM: 101698425

Informations de publication

Date de publication:
13 10 2020
Historique:
received: 26 05 2020
accepted: 17 08 2020
entrez: 29 9 2020
pubmed: 30 9 2020
medline: 15 5 2021
Statut: ppublish

Résumé

Mixed-lineage leukemia (MLL) gene rearrangements are among the most frequent chromosomal abnormalities in acute myeloid leukemia (AML). MLL fusion patterns are associated with the patient's prognosis; however, their relationship with driver mutations is unclear. We conducted sequence analyses of 338 genes in pediatric patients with MLL-rearranged (MLL-r) AML (n = 56; JPLSG AML-05 study) alongside data from the TARGET study's pediatric cohorts with MLL-r AML (n = 104), non-MLL-r AML (n = 581), and adult MLL-r AML (n = 81). KRAS mutations were most frequent in pediatric patients with high-risk MLL fusions (MLL-MLLLT10, MLL-MLLT4, and MLL-MLLT1). Pediatric patients with MLL-r AML (n = 160) and a KRAS mutation (KRAS-MT) had a significantly worse prognosis than those without a KRAS mutation (KRAS-WT) (5-year event-free survival [EFS]: 51.8% vs 18.3%, P < .0001; 5-year overall survival [OS]: 67.3% vs 44.3%, P = .003). The adverse prognostic impact of KRAS mutations was confirmed in adult MLL-r AML. KRAS mutations were associated with adverse prognoses in pediatric patients with both high-risk (MLLT10+MLLT4+MLLT1; n = 60) and intermediate-to-low-risk (MLLT3+ELL+others; n = 100) MLL fusions. The prognosis did not differ significantly between patients with non-MLL-r AML with KRAS-WT or KRAS-MT. Multivariate analysis showed the presence of a KRAS mutation to be an independent prognostic factor for EFS (hazard ratio [HR], 2.21; 95% confidence interval [CI], 1.35-3.59; P = .002) and OS (HR, 1.85; 95% CI, 1.01-3.31; P = .045) in MLL-r AML. The mutation is a distinct adverse prognostic factor in MLL-r AML, regardless of risk subgroup, and is potentially useful for accurate treatment stratification. This trial was registered at the UMIN (University Hospital Medical Information Network) Clinical Trials Registry (UMIN-CTR; http://www.umin.ac.jp/ctr/index.htm) as #UMIN000000511.

Identifiants

pubmed: 32991719
pii: S2473-9529(20)31195-2
doi: 10.1182/bloodadvances.2020002457
pmc: PMC7556160
doi:

Substances chimiques

KRAS protein, human 0
Myeloid-Lymphoid Leukemia Protein 149025-06-9
Histone-Lysine N-Methyltransferase EC 2.1.1.43
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4623-4631

Informations de copyright

© 2020 by The American Society of Hematology.

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Auteurs

Hidemasa Matsuo (H)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.

Kenichi Yoshida (K)

Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Kana Nakatani (K)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yutarou Harata (Y)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Moe Higashitani (M)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yuri Ito (Y)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yasuhiko Kamikubo (Y)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yusuke Shiozawa (Y)

Department of Pediatrics, The University of Tokyo, Tokyo, Japan.

Yuichi Shiraishi (Y)

Division of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.

Kenichi Chiba (K)

Division of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.

Hiroko Tanaka (H)

Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Ai Okada (A)

Division of Genome Analysis Platform Development, National Cancer Center Research Institute, Tokyo, Japan.

Yasuhito Nannya (Y)

Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

June Takeda (J)

Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Hiroo Ueno (H)

Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Nobutaka Kiyokawa (N)

Department of Pediatric Hematology and Oncology Research, National Research Institute for Child Health and Development, Tokyo, Japan.

Daisuke Tomizawa (D)

Division of Leukemia and Lymphoma, Children's Cancer Center, National Center for Child Health and Development, Tokyo, Japan.

Takashi Taga (T)

Department of Pediatrics, Shiga University of Medical Science, Otsu, Japan.

Akio Tawa (A)

Higashiosaka Aramoto Heiwa Clinic, Higashiosaka, Japan.

Satoru Miyano (S)

Laboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Manja Meggendorfer (M)

MLL Munich Leukemia Laboratory, Munich, Germany.

Claudia Haferlach (C)

MLL Munich Leukemia Laboratory, Munich, Germany.

Seishi Ogawa (S)

Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Institute for the Advanced Study of Human Biology (WPI ASHBi), Kyoto University, Kyoto, Japan; and.
Department of Medicine, Center for Hematology and Regenerative Medicine, Karolinska Institute, Stockholm, Sweden.

Souichi Adachi (S)

Department of Human Health Sciences, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

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Classifications MeSH