Evidence map›Paper›PMID 37314622›Full record

ArticleInternational journal of hematology2023

Acute monocytic leukemia with KMT2A::LASP1 developed 9 months after diagnosis of acute megakaryoblastic leukemia in a 2-year-old boy.

Takashi Fujita, Hiroko Fukushima, Toru Nanmoku, Yuki Arakawa, Takao Deguchi, Ryoko Suzuki, Yuni Yamaki, Sho Hosaka, Hidetoshi Takada

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In one paragraph

Article in International journal of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Takashi FujitaDepartment of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
Hiroko FukushimaDepartment of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan. fkhiroko@md.tsukuba.ac.jp.ORCID http://orcid.org/0000-0002-1290-3501
Toru NanmokuDepartment of Clinical Laboratory, University of Tsukuba Hospital, Tsukuba, Japan.
Yuki ArakawaDepartment of Hematology and Oncology, Saitama Children's Medical Center, Saitama, Japan.
Takao DeguchiDivision of Cancer Immunodiagnostics, Children's Cancer Center, National Center for Child Health and Development, Tokyo, Japan.
Ryoko SuzukiDepartment of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
Yuni YamakiDepartment of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
Sho HosakaDepartment of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
Hidetoshi TakadaDepartment of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
University of Tsukuba Hospital · JPUniversity of Tsukuba · JPNational Center For Child Health and Development · JPSaitama Children's Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is known as one of the subsequent malignant neoplasms that can develop after cancer treatment, but it is difficult to distinguish from relapse when the preceding cancer is leukemia. We report a 2-year-old boy who developed acute megakaryoblastic leukemia (AMKL, French-American-British classification [FAB]: M7) at 18 months of age and achieved complete remission with multi-agent chemotherapy without hematopoietic stem cell transplantation. Nine months after diagnosis and 4 months after completing treatment for AMKL, he developed acute monocytic leukemia (AMoL) with the KMT2A::LASP1 chimeric gene (FAB: M5b). The second complete remission was achieved using multi-agent chemotherapy and he underwent cord blood transplantation 4 months after AMoL was diagnosed. He is currently alive and disease free at 39 and 48 months since his AMoL and AMKL diagnoses, respectively. Retrospective analysis revealed that the KMT2A::LASP1 chimeric gene was detected 4 months after diagnosis of AMKL. Common somatic mutations were not detected in AMKL or AMoL and no germline pathogenic variants were detected. Since the patient's AMoL was different from his primary leukemia of AMKL in terms of morphological, genomic, and molecular analysis, we concluded that he developed a subsequent leukemia rather than a relapse of his primary leukemia.

Indexed as

Leukemia, Megakaryoblastic, AcuteLeukemia, Monocytic, AcuteAdaptor Proteins, Signal TransducingChild, PreschoolCytoskeletal ProteinsHistone-Lysine N-MethyltransferaseHumansLIM Domain ProteinsMaleMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionRecurrenceRemission InductionRetrospective StudiesAdaptor Proteins, Signal TransducingCytoskeletal ProteinsHistone-Lysine N-MethyltransferaseKMT2A protein, humanLASP1 protein, humanLIM Domain ProteinsMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionAcute megakaryoblastic leukemiaAcute monocytic leukemiaSecond primary cancerSubsequent leukemiaTherapy-related leukemia

Identifiers

PMID37314622
OpenAlexW4380576277

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.