Evidence map›Paper›PMID 29417354›Full record

ArticleInternational journal of hematology2018

Clonal dynamics in a case of acute monoblastic leukemia that later developed myeloproliferative neoplasm.

Shinya Sato, Hidehiro Itonaga, Masataka Taguchi, Yasushi Sawayama, Daisuke Imanishi, Hideki Tsushima, Tomoko Hata, Yukiyoshi Moriuchi, Hiroyuki Mishima, Akira Kinoshita and 2 more

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. Protracted Clonal Trajectory of aCase reports in hematology · 2018
    Article
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

12 authors at 4 institutions in 1 country.

Shinya SatoDepartment of Hematology, Nagasaki University Hospital, Nagasaki, Japan.
Hidehiro ItonagaDepartment of Hematology, Nagasaki University Hospital, Nagasaki, Japan.
Masataka TaguchiDepartment of Hematology, Sasebo City General Hospital, Sasebo, Japan.
Yasushi SawayamaDepartment of Hematology, Nagasaki University Hospital, Nagasaki, Japan.
Daisuke ImanishiDepartment of Hematology, Goto Central Hospital, Goto, Japan.
Hideki TsushimaDepartment of Hematology, Nagasaki Harbor Medical Center City Hospital, Nagasaki, Japan.
Tomoko HataDepartment of Hematology, Nagasaki University Hospital, Nagasaki, Japan.
Yukiyoshi MoriuchiDepartment of Hematology, Sasebo City General Hospital, Sasebo, Japan.
Hiroyuki MishimaDepartment of Human Genetics, Atomic Bomb Disease Insutitute, Nagasaki University, Nagasaki, Japan.
Akira KinoshitaDepartment of Human Genetics, Atomic Bomb Disease Insutitute, Nagasaki University, Nagasaki, Japan.
Koh-Ichiro YoshiuraDepartment of Human Genetics, Atomic Bomb Disease Insutitute, Nagasaki University, Nagasaki, Japan.
Yasushi MiyazakiDepartment of Hematology, Nagasaki University Hospital, Nagasaki, Japan. y-miyaza@nagasaki-u.ac.jp.
Nagasaki University · JPNagasaki University Hospital · JPSasebo City General Hospital · JPKanto Central Hospital · JP

Funding

the Ministry of Education, Culture, Sports, Science and Technology of Japan 26461426the Ministry of Health, Labor and Welfare 26271301
6 · The paper itself

Abstract

In acute myeloid leukemia (AML), patients may harbor pre-leukemic hematopoietic stem cells (HSCs) containing some, but not all, of the mutations observed in the leukemic cells. These pre-leukemic HSCs may survive induction chemotherapy and contribute to AML relapse by obtaining additional mutations. We report here an acute monoblastic leukemia (AMoL) patient who later developed an unclassifiable myeloproliferative neoplasm (MPN-U). Whole-exome sequencing and cluster analysis demonstrated the presence of three distinct major clones during the clinical course: (1) an AMoL clone with ASXL1, CBL, and NPM1 somatic mutations, likely associated with the pathogenesis, and GATA2, SRSF2, and TET2 mutations, (2) an AMoL remission clone, with mutated GATA2, SRSF2, and TET2 only (possibly the founding clone (pre-leukemic HSC) that survived chemotherapy), (3) a small subclone which had JAK2 mutation during the AMoL remission, appearing at MPN-U manifestation with additional mutations. These findings suggest that pre-leukemic HSCs in AML patients may give rise to non-AML myeloid malignancies. This is the first report to analyze the clonal evolution from AMoL to MPN-U, which may provide new insight into the development of myeloid malignancies.

Indexed as

AgedClonal EvolutionExome SequencingHematopoietic Stem CellsHumansInduction ChemotherapyLeukemia, Monocytic, AcuteMaleMutationMyeloproliferative DisordersNeoplasm Recurrence, LocalNucleophosminNucleophosminAcute myeloid leukemiaMyeloproliferative neoplasmPre-leukemic hematopoietic stem cellsWhole-exome sequencing

Identifiers

PMID29417354
OpenAlexW2790177040

What OpenQuestion holds

Textmetadata
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.