Evidence map›Paper›PMID 31776465›Full record

ArticleLeukemia2020

Mutations associated with age-related clonal hematopoiesis in PMF patients with rapid progression to myelofibrosis.

Stephan Bartels, Muhammad Faisal, Guntram Büsche, Jerome Schlue, Britta Hasemeier, Elisa Schipper, Julia Vogtmann, Lina Westphal, Ulrich Lehmann, Hans Kreipe

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Prevalence ofCancers · 2021
    Review
  8. The Role of Megakaryocytes in Myelofibrosis.Hematology/oncology clinics of North America · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. 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

10 authors at 1 institution in 1 country.

Stephan BartelsInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany. bartels.stephan@mh-hannover.de.ORCID http://orcid.org/0000-0002-8903-2345
Muhammad FaisalInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Guntram BüscheInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Jerome SchlueInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Britta HasemeierInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Elisa SchipperInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Julia VogtmannInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Lina WestphalInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Ulrich LehmannInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Hans KreipeInstitute of Pathology, Hannover Medical School, Carl-Neuberg Str. 1, 30623, Hannover, Germany.
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Besides histopathological findings there are no indicators of increased risk for fibrotic progression in myeloproliferative neoplasms (MPN). Age-related clonal hematopoiesis (ARCH/CHIP) is a frequent finding in the elderly and combinations with MPN driver mutations (JAK2, MPL, and CALR) have been described. To determine the impact of ARCH/CHIP-related mutations for development of fibrosis in primary myelofibrosis (PMF), the mutational status of cases with fibrotic progression from grade 0 to grade 2/3 (n = 77) as evidenced by follow-up bone marrow biopsies (median 6.2 years) was compared with prefibrotic PMF samples without development of fibrosis (n = 27; median follow-up 7.3 years). Frequent ARCH/CHIP-associated mutations (TET2, ASXL1, and DNMT3A) demonstrable at presentation were not connected with fibrotic progression. However, mutations which are rarely found in ARCH/CHIP (SRSF2, U2AF1, SF3B1, IDH1/2, and EZH2) were present in 24.7% of cases with later development of fibrosis and not detectable in cases staying free from fibrosis (P = 0.0028). Determination of the tumor mutational burden (TMB) in a subgroup of cases (n = 32) did not show significant differences (7.68 mutations/MB vs. 6.85 mutations/MB). We conclude that mutations rarely found in ARCH/CHIP provide an independent risk factor for rapid fibrotic progression (median 2.0 years) when manifest already at first presentation.

Indexed as

Clonal EvolutionMutationAge FactorsBiomarkers, TumorBone MarrowDisease ProgressionFemaleFibrosisFollow-Up StudiesHematopoiesisHumansMaleMiddle AgedPrimary MyelofibrosisPrognosisRetrospective StudiesBiomarkers, Tumor

Identifiers

PMID31776465
OpenAlexW2990266223

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.