Evidence map›Paper›PMID 34071283›Full record

ReviewCancers2021

Chromosomal Instability in Acute Myeloid Leukemia.

Mateus de Oliveira Lisboa, Paulo Roberto Slud Brofman, Ana Teresa Schmid-Braz, Aline Rangel-Pozzo, Sabine Mai

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Characterization of neocentromeric marker chromosome derived from chromosome 11: a rare entity in four patients with acute leukemia.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
    Article
  3. Article
  4. Article
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  7. Review
  8. Article
  9. Article
  10. Targeting chromosomal instability in patients with cancer.Nature reviews. Clinical oncology · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
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  20. 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

5 authors at 3 institutions in 2 countries.

Mateus de Oliveira LisboaCore for Cell Technology, School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, Curitiba 80215-901, Paraná, Brazil.ORCID 0000-0002-2811-8356
Paulo Roberto Slud BrofmanCore for Cell Technology, School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, Curitiba 80215-901, Paraná, Brazil.
Ana Teresa Schmid-BrazHospital das Clínicas, Universidade Federal do Paraná, Curitiba 80060-240, Paraná, Brazil.
Aline Rangel-PozzoDepartment of Physiology and Pathophysiology, University of Manitoba, Cell Biology, CancerCare Manitoba Research Institute, Winnipeg, MB R3C 2B7, Canada.
Sabine MaiDepartment of Physiology and Pathophysiology, University of Manitoba, Cell Biology, CancerCare Manitoba Research Institute, Winnipeg, MB R3C 2B7, Canada.ORCID 0000-0002-5797-2201
CancerCare Manitoba · CAPontifícia Universidade Católica do Paraná · BRHospital de Clínicas Universidade Federal do Paraná · BR

Funding

CIHR 000
6 · The paper itself

Abstract

Chromosomal instability (CIN), the increasing rate in which cells acquire new chromosomal alterations, is one of the hallmarks of cancer. Many studies highlighted CIN as an important mechanism in the origin, progression, and relapse of acute myeloid leukemia (AML). The ambivalent feature of CIN as a cancer-promoting or cancer-suppressing mechanism might explain the prognostic variability. The latter, however, is described in very few studies. This review highlights the important CIN mechanisms in AML, showing that CIN signatures can occur largely in all the three major AML types (de novo AML, secondary-AML, and therapy-related-AML). CIN features in AML could also be age-related and reflect the heterogeneity of the disease. Although most of these abnormalities show an adverse prognostic value, they also offer a strong new perspective on personalized therapy approaches, which goes beyond assessing CIN in vitro in patient tumor samples to predict prognosis. Current and emerging AML therapies are exploring CIN to improve AML treatment, which includes blocking CIN or increasing CIN beyond the limit threshold to induce cell death. We argue that the characterization of CIN features, not included yet in the routine diagnostic of AML patients, might provide a better stratification of patients and be extended to a more personalized therapeutic approach.

Indexed as

acute myeloid leukemiaaginganeuploidycentrosome dysfunctionchromosomal instabilitycomplex karyotypecytogenetic heterogeneityMYCsynthetic lethalitytelomere dysfunctiontherapeutic targetsTP53

Identifiers

PMID34071283
PMCPMC8198625
OpenAlexW3164396471

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.