Evidence map›Paper›PMID 31371322›Full record

ArticleCancer discovery2019

Polyclonal Heterogeneity: The New Norm for Secondary Clinical Resistance to Targeted Monotherapy in Relapsed Leukemia?

Andrew H Wei, Andrew W Roberts

Abstract readComment
PubMed Publisher
In one paragraph

Article in Cancer discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Therapeutic development and current uses of BCL-2 inhibition.Hematology. American Society of Hematology. Education Program · 2020
    Review
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Andrew H WeiThe Alfred Hospital, Melbourne, Victoria, Australia.
Andrew W RobertsRoyal Melbourne Hospital and Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia. roberts@wehi.edu.au.ORCID https://orcid.org/0000-0002-7341-5720

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this issue, McMahon and colleagues demonstrate that secondary clinical resistance to the FLT3 inhibitor gilteritinib in relapsed acute myeloid leukemia is often polyclonal and commonly mediated by heterogeneous mutations that activate downstream RAS-MAPK pathways. These findings and recent data from others indicate that emergence of multiple clones, each with distinct mechanisms of resistance, is a common finding at secondary failure of single-agent-targeted therapies for relapsed leukemias.

Indexed as

Leukemia, Myeloid, Acutefms-Like Tyrosine Kinase 3HumansImmune SystemMutationProtein Kinase InhibitorsFLT3 protein, humanfms-Like Tyrosine Kinase 3Protein Kinase Inhibitors

Identifiers

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.