Evidence map›Paper›PMID 26660431›Full record

ReviewBlood2016

Molecular landscape of acute myeloid leukemia in younger adults and its clinical relevance.

David Grimwade, Adam Ivey, Brian J P Huntly

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
225citing papers in PubMed, 3 pooled it
25.3field-weighted citation impact, top 1% 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

225 citing papers in PubMed, 3 syntheses or guidelines pooled it, 458 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
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  18. MALNC: a new mutant NPM1/IDH2Cancer gene therapy · 2025
    Article
  19. Article
  20. Cancers · 2025
    Review

165 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

David GrimwadeDepartment of Medical & Molecular Genetics, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom;
Adam IveyDepartment of Medical & Molecular Genetics, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom;
Brian J P HuntlyDepartment of Haematology, Cambridge Institute for Medical Research and Addenbrookes Hospital, University of Cambridge, and Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute, Cambridge, United Kingdom.ORCID http://orcid.org/0000-0003-0312-161X
King's College London · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Department of Health RP-PG-0108-10093Medical Research Council MR/M010392/1Wellcome Trust 100140Wellcome Trust 97922Worldwide Cancer Research 14-1069
6 · The paper itself

Abstract

Recent major advances in understanding the molecular basis of acute myeloid leukemia (AML) provide a double-edged sword. Although defining the topology and key features of the molecular landscape are fundamental to development of novel treatment approaches and provide opportunities for greater individualization of therapy, confirmation of the genetic complexity presents a huge challenge to successful translation into routine clinical practice. It is now clear that many genes are recurrently mutated in AML; moreover, individual leukemias harbor multiple mutations and are potentially composed of subclones with differing mutational composition, rendering each patient's AML genetically unique. In order to make sense of the overwhelming mutational data and capitalize on this clinically, it is important to identify (1) critical AML-defining molecular abnormalities that distinguish biological disease entities; (2) mutations, typically arising in subclones, that may influence prognosis but are unlikely to be ideal therapeutic targets; (3) mutations associated with preleukemic clones; and (4) mutations that have been robustly shown to confer independent prognostic information or are therapeutically relevant. The reward of identifying AML-defining molecular lesions present in all leukemic populations (including subclones) has been exemplified by acute promyelocytic leukemia, where successful targeting of the underlying PML-RARα oncoprotein has eliminated the need for chemotherapy for disease cure. Despite the molecular heterogeneity and recognizing that treatment options for other forms of AML are limited, this review will consider the scope for using novel molecular information to improve diagnosis, identify subsets of patients eligible for targeted therapies, refine outcome prediction, and track treatment response.

Indexed as

Molecular Targeted TherapyAdultAntineoplastic AgentsHumansLeukemia, Myeloid, AcutePrognosisYoung AdultAntineoplastic Agents

Identifiers

PMID26660431
PMCPMC4705608
OpenAlexW2208333084

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.