Evidence map›Paper›PMID 33562056›Full record

ReviewBiology2021

From Clonal Hematopoiesis to Therapy-Related Myeloid Neoplasms: The Silent Way of Cancer Progression.

Carmelo Gurnari, Emiliano Fabiani, Giulia Falconi, Serena Travaglini, Tiziana Ottone, Antonio Cristiano, Maria Teresa Voso

Open access · goldAbstract readReview
In one paragraph

Review in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. CHIPing Away at Proteomics to Find Correlations with Myeloid Neoplasms.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Bone Marrow Microenvironment Involvement in t-MN: Focus on Mesenchymal Stem Cells.Mediterranean journal of hematology and infectious diseases · 2023
    Review
  9. Article
  10. Clonal Hematopoiesis: Role in Hematologic and Non-Hematologic Malignancies.Mediterranean journal of hematology and infectious diseases · 2022
    Review
  11. Review
  12. Review
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

7 authors at 1 institution in 2 countries.

Carmelo GurnariDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0001-6829-5544
Emiliano FabianiDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0002-6209-8934
Giulia FalconiDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0001-7699-1427
Serena TravagliniDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0002-5411-1502
Tiziana OttoneDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.
Antonio CristianoDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.
Maria Teresa VosoDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0002-6164-4761
University of Rome Tor Vergata · IT

Funding

Harmony GA116026Metastatic disease: the key unmet need in oncology (MYNERVA project) 21267
6 · The paper itself

Abstract

Clonal hematopoiesis (CH) has been recognized as a predisposing factor for the development of myeloid malignancies. Its detection has been reported at different frequencies across studies, based on the type of genome scanning approach used and the population studied, but the latest insights recognize its virtual ubiquitous presence in older individuals. The discovery of CH in recent years paved the way for a shift in the paradigm of our understanding of the biology of therapy-related myeloid malignancies (t-MNs). Indeed, we moved from the concept of a treatment-induced lesion to a model where CH precedes the commencement of any cancer-related treatment in patients who subsequently develop a t-MN. Invariant patterns of genes seem to contribute to the arising of t-MN cases, with differences regarding the type of treatment received. Here, we review the principal studies concerning CH, the relationship with myeloid progression and the mechanisms of secondary t-MN development.

Indexed as

clonal hematopoiesismyeloid progressiontherapy-related myeloid neoplasms

Identifiers

PMID33562056
PMCPMC7914896
OpenAlexW3128618750

What OpenQuestion 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 OpenQuestion graph.