Evidence map›Paper›PMID 32732356›Full record

ArticleHaematologica2021

Monitoring of clonal evolution of acute myeloid leukemia identifies the leukemia subtype, clinical outcome and potential new drug targets for post-remission strategies or relapse.

Esther Onecha, Inmaculada Rapado, María Luz Morales, Gonzalo Carreño-Tarragona, Pilar Martinez-Sanchez, Xabier Gutierrez, José María Sáchez Pina, María Linares, Miguel Gallardo, Joaquín Martinez-López and 1 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Mutations and MRD: clinical implications of clonal ontogeny.Hematology. American Society of Hematology. Education Program · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Point Mutations in theFrontiers in oncology · 2022
    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

11 authors at 1 institution in 1 country.

Esther OnechaHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Inmaculada RapadoHematology Department, Hospital Universitario 12 de Octubre, Madrid.
María Luz MoralesHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Gonzalo Carreño-TarragonaHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Pilar Martinez-SanchezHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Xabier GutierrezHematology Department, Hospital Universitario 12 de Octubre, Madrid.
José María Sáchez PinaHematology Department, Hospital Universitario 12 de Octubre, Madrid.
María LinaresHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Miguel GallardoHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Joaquín Martinez-LópezHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Rosa AyalaHematology Department, Hospital Universitario 12 de Octubre, Madrid.
Hospital Universitario 12 De Octubre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cases of treatment failure in acute myeloid leukemia (AML), the utility of mutational profiling in primary refractoriness and relapse is not established. We undertook a perspective study using next-generation sequencing (NGS) of clinical follow-up samples (n=91) from 23 patients with AML with therapeutic failure to cytarabine plus idarubicin or fludarabine. Cases of primary refractoriness to treatment were associated with a lower number of DNA variants at diagnosis than cases of relapse (median 1.67 and 3.21, respectively, p=0.029). The most frequently affected pathways in patients with primary refractoriness were signaling, transcription and tumor suppression, whereas methylation and splicing pathways were mainly implicated in relapsed patients. New therapeutic targets, either by an approved drug or within clinical trials, were not identified in any of the cases of refractoriness (0/10); however, 8 potential new targets were found in 5 relapsed patients (5/13) (p=0.027): 1 IDH2, 3 SF3B1, 2 KRAS, 1 KIT and 1 JAK2. Sixty-five percent of all variants detected at diagnosis were not detected at complete response (CR). Specifically, 100% of variants in EZH2, RUNX1, VHL, FLT3, ETV6, U2AF1, PHF6 and SF3B1 disappeared at CR, indicating their potential use as markers to evaluate minimal residual disease (MRD) for follow-up of AML. Molecular follow-up using a custom NGS myeloid panel of 32 genes in the post-treatment evaluation of AML can help in the stratification of prognostic risk, the selection of MRD markers to monitor the response to treatment and guide post-remission strategies targeting AML, and the selection of new drugs for leukemia relapse.

Indexed as

Leukemia, Myeloid, AcutePharmaceutical PreparationsClonal EvolutionHumansNeoplasm, ResidualPrognosisRecurrencePharmaceutical Preparations

Identifiers

PMID32732356
PMCPMC8409047
OpenAlexW3046640968

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.