Evidence map›Paper›PMID 19110529›Full record

ReviewThe Keio journal of medicine2008

Biology of chronic graft-versus-host disease: implications for a future therapeutic approach.

Paul J Martin

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Keio journal of medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 6% 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, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Oral manifestations of graft-versus-host disease in patients submitted to allogeneic hematopoietic stem cell transplantation: the experience of a Brazilian Cancer Center.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. State-of-the-art acute and chronic GVHD treatment.International journal of hematology · 2015
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

1 author at 1 institution in 1 country.

Paul J MartinDivision of Clinical Research, Department of Medicine, Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA 98109-1024, USA. pmartin@fhcrc.org
University of Washington · US

Funding

Mycophenylate Mofetil for Treatment of Chronic GVHDR01CA098906 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MARTIN, PAUL J · 2003 to 2008
$2.3M
NCI NIH HHS CA 98906NCI NIH HHS R01 CA098906
6 · The paper itself

Abstract

Hematopoietic cell transplantation (HCT) is frequently complicated by graft-versus-host disease (GVHD). During the past three decades, experimental studies and clinical observations have elucidated the pathophysiology of acute GVHD, but the biology of chronic GVHD is much less well understood. Recommendations of the NIH Consensus Development Project on Criteria for Clinical Trials in Chronic GVHD have begun to standardize the diagnosis and clinical assessment of the disease. These criteria have emphasized the importance of qualitative differences, as opposed to time of onset after HCT, in making the distinction between acute and chronic GVHD. Experimental studies have generated at least four theories to explain the pathophysiology of chronic GVHD. These theories include 1) thymic damage and defective negative selection of T cells generated from marrow progenitors after HCT, 2) aberrant production of transforming growth factor-beta, 3) auto-antibody production, and 4) deficiency of T-regulatory cells. Recent studies in humans have corroborated a possible role for each of these mechanisms in humans. No animal model fully replicates all of the features of chronic GVHD in humans, and it appears likely that multiple biological mechanisms account for the diverse features the disease. Chronic GVHD may represent a "syndrome" with diverse causes among individual patients. In the future, it might become possible to tailor specific therapeutic interventions for patients as individually needed for each distinct pathophysiologic mechanism involved in development of the disease.

Indexed as

AnimalsB-LymphocytesCD4-Positive T-LymphocytesChronic DiseaseDisease Models, AnimalGraft vs Host DiseaseHumansT-Lymphocytes, RegulatoryTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID19110529
PMCPMC2722785
OpenAlexW2020532629

What OpenQuestion holds

Textmetadata
LicenceTDM
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.