Evidence map›Paper›PMID 36572814›Full record

ArticleInternational journal of hematology2023

Clinical features of complex karyotype in newly diagnosed acute myeloid leukemia.

Shota Yoshida, Masahiro Onozawa, Naoki Miyashita, Hiroyuki Kimura, Shogo Takahashi, Shota Yokoyama, Toshihiro Matsukawa, Shinsuke Hirabayashi, Akio Mori, Daisuke Hidaka and 15 more

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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. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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

25 authors at 14 institutions in 1 country.

Shota YoshidaDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Masahiro OnozawaDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan. masahiro.onozawa@nifty.ne.jp.ORCID http://orcid.org/0000-0001-9267-2864
Naoki MiyashitaDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Hiroyuki KimuraDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Shogo TakahashiDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Shota YokoyamaDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Toshihiro MatsukawaDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Shinsuke HirabayashiDepartment of Pediatrics, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Akio MoriBlood Disorders Center, Aiiku Hospital, Sapporo, Japan.
Daisuke HidakaDepartment of Hematology, Sapporo Hokuyu Hospital, Sapporo, Japan.
Koichiro MinauchiDepartment of Hematology, Sapporo City General Hospital, Sapporo, Japan.
Akio ShigematsuDepartment of Hematology, Kushiro Rosai Hospital, Kushiro, Japan.
Junichi HashiguchiDepartment of Internal Medicine/General Medicine, Kitami Red Cross Hospital, Kitami, Japan.
Tetsuyuki IgarashiDepartment of Hematology, Tenshi Hospital, Sapporo, Japan.
Yasutaka KakinokiDepartment of Hematology, Asahikawa City Hospital, Asahikawa, Japan.
Yutaka TsutsumiDepartment of Hematology, Hakodate Municipal Hospital, Hakodate, Japan.
Makoto IbataDepartment of Hematology, Sapporo Kosei General Hospital, Sapporo, Japan.
Hajime KobayashiDepartment of Hematology, Obihiro Kosei Hospital, Obihiro, Japan.
Yoshihito HaseyamaDepartment of Hematology, Tonan Hospital, Sapporo, Japan.
Katsuya FujimotoDepartment of Hematology, National Hospital Organization Hokkaido Cancer Center, Sapporo, Japan.
Toshimichi IshiharaDepartment of Hematology, Kin-Ikyo Chuo Hospital, Sapporo, Japan.
Hajime SakaiDepartment of Hematology, Teine Keijinkai Hospital, Sapporo, Japan.
Shuichi OtaDepartment of Hematology, Sapporo Hokuyu Hospital, Sapporo, Japan.
Takeshi KondoBlood Disorders Center, Aiiku Hospital, Sapporo, Japan.
Takanori TeshimaDepartment of Hematology, Faculty of Medicine, Graduate School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-Ku, Sapporo, 0608638, Japan.
Hokkaido University · JPSapporo Hokuyu Hospital · JPAsahikawa City Hospital · JPHakodate National Hospital · JPJapanese Red Cross Hokkaido College of Nursing · JPKin-ikyo Chuo Hospital · JPKushiro Rosai Hospital · JPNational Hospital Organization Hokkaido Medical Center · JPObihiro Kosei General Hospital · JPSapporo City General Hospital · JPSapporo Kosei General Hospital · JPTeine Keijinkai Hospital · JPTenshi Hospital · JPTonan Hospital · JP

Funding

the Japan Society for the Promotion of Science 20K08745
6 · The paper itself

Abstract

Complex karyotype acute myeloid leukemia (CK-AML) has been classified as an adverse-risk subtype. Although a few reports have further classified CK-AML as typical (including monosomy of chromosomes 5, 7 and 17 or deletion of 5q, 7q and/or 17p) or atypical, the clinical features of these subtypes in Japanese patients remain unclear. We retrospectively analyzed a total of 115 patients with CK-AML, including 77 with typical CK-AML and 38 with atypical CK-AML. Median overall survival (OS) was significantly shorter in patients with typical CK-AML than atypical CK-AML (143 days vs. 369 days, P = 0.009). Among patients with typical CK-AML, those with monosomy 17 or deletion of 17p had significantly shorter OS than patients without such abnormalities (105 days vs. 165 days, P = 0.033). TP53 mutations were more predominant in patients with typical CK-AML than in patients with atypical CK-AML (69.7% vs. 32.4%, P < 0.001). Patients with typical CK-AML had a poor prognosis regardless of TP53 mutation status. Among patients with atypical CK-AML, however, prognosis was worse for those with the TP53 mutation than those without the mutation. In conclusion, prognosis is extremely poor for both typical CK-AML and atypical CK-AML with TP53 mutation.

Indexed as

Leukemia, Myeloid, AcuteAbnormal KaryotypeHumansKaryotypeMonosomyMutationPrognosisRetrospective StudiesTumor Suppressor Protein p53Tumor Suppressor Protein p53CK-AMLComplex karyotypeDeletion of 17pMonosomy 17TP53 mutationTypical CK-AML

Identifiers

PMID36572814
OpenAlexW4312211925

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.