Evidence map›Paper›PMID 31808847›Full record

ReviewHematology. American Society of Hematology. Education Program2019

Clonal evolution and immune evasion in posttransplantation relapses.

Luca Vago

Abstract readCase ReportsReview
In one paragraph

Review in Hematology. American Society of Hematology. Education Program, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Biology of post-transplant relapse: actionable features.Hematology. American Society of Hematology. Education Program · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

1 author.

Luca VagoUnit of Immunogenetics, Leukemia Genomics and Immunobiology, and.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the considerable improvements witnessed over the last few decades in the feasibility and safety of allogeneic hematopoietic cell transplantation (allo-HCT) for hematological malignancies, disease relapse continues to represent a frequent occurrence, with largely unsatisfactory salvage options. Recent studies have shed new light on the biology of posttransplantation relapses, demonstrating that they can frequently be explained using an evolutionary perspective: The changes in disease clonal structure and immunogenicity that are often documented at relapse may in fact represent the end results of a process of selection, allowing the outgrowth of variants that are more capable of resisting the therapeutic control of allo-HCT. This review provides an overview of the mechanisms forming the basis of relapse, including clonal evolution, gain of tropism for privileged sites, genomic and nongenomic changes in the HLA asset, and enforcement of immune checkpoints. Finally, this review discusses how these mechanisms may combine in complex patterns and how understanding and untangling these interactions may provide key knowledge for the selection of personalized therapeutic approaches.

Indexed as

Hematopoietic Stem Cell TransplantationLeukemia, Myeloid, AcuteTumor EscapeAdultAllograftsHumansMaleRecurrence

Identifiers

PMID31808847
PMCPMC6913457

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.