Evidence map›Paper›PMID 12618518›Full record

ArticleThe Journal of clinical investigation2003

Chronic myelogenous leukemia shapes host immunity by selective deletion of high-avidity leukemia-specific T cells.

Jeffrey J Molldrem, Peter P Lee, Shreya Kant, Eric Wieder, Weidong Jiang, Sijie Lu, Changqing Wang, Mark M Davis

Registry-linked trialAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03117816 (Efficacy and Safety of Pegylated Proline Interferon Alpha 2b), which is not on this map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing 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.

NCT03117816 phase3completednot on this mapstarted 2017, after this paper: background citation

Efficacy and Safety of Pegylated Proline Interferon Alpha 2b (AOP2014) in Maintaining Deep Molecular Remissions in Patients With Chronic Myeloid Leukemia (CML) Who Discontinue ABL-Kinase Inhibitor Therapy - a Randomized Phase III, Multicenter Trial With Post-study Follow-up

TypeinterventionalSponsorPhilipps University MarburgRan2017 to 2022Enrolled214ConditionsChronic Myeloid Leukemia in RemissionArmsAOP2014 / Pegylated-Proline-interferon alpha-2b, Surveillance
3 · Its place in the literature

Who cites it

77 citing papers in PubMed.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. Article
  9. Vaccines: a promising therapy for myelodysplastic syndrome.Journal of hematology & oncology · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Jeffrey J MolldremSection of Transplantation Immunology, Department of Blood and Marrow Transplantation, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Peter P Lee
Shreya Kant
Eric Wieder
Weidong Jiang
Sijie Lu
Changqing Wang
Mark M Davis

Funding

TOLERANCE INDUCTION BY MEGADOSE STEM CELL TRANSPLANTS IN CML--GVHD AND GVLP01CA049639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ARLINGHAUS, RALPH BERNARD · 1990 to 2014
$41.8M
PROTEINASE 3 SPECIFIC IMMUNOTHERAPY OF LEUKEMIAR01CA081247 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI MOLLDREM, JEFFREY J · 1999 to 2002
$532k
NCI NIH HHS CA49639NCI NIH HHS CA81247NCI NIH HHS P01 CA049639NCI NIH HHS R01 CA081247
6 · The paper itself

Abstract

We have shown that cytotoxic T lymphocytes specific for PR1, an HLA-A2-restricted nonopeptide derived from proteinase 3, kill leukemia cells and may contribute to the elimination of chronic myelogenous leukemia (CML) after treatment with IFN or allogeneic bone marrow transplant. Some patients with persistent disease also have circulating PR1-specific T cells, however, suggesting the likelihood of immune tolerance. Here we show that both high- and low-avidity PR1-specific T cells from the peripheral blood of healthy donors can be identified and selectively expanded in vitro. Although high-avidity PR1-specific T cells killed CML more effectively than low-avidity T cells, only high-avidity T cells underwent apoptosis when stimulated with high PR1 peptide concentration or when exposed to leukemia that overexpressed proteinase 3. No high-avidity PR1-specific T cells could be identified or expanded from newly diagnosed leukemia patients, whereas low-avidity T cells were readily expanded. Circulating high-avidity PR1-specific T cells were identified in IFN-sensitive patients in cytogenetic remission, however. These results provide evidence that CML shapes the host immune response and that leukemia outgrowth may result in part from leukemia-induced selective deletion of high-avidity PR1-specific T cells.

Indexed as

ApoptosisCytotoxicity, ImmunologicHLA-A2 AntigenHumansInterferon-alphaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMyeloblastinSerine EndopeptidasesT-Lymphocytes, CytotoxicHLA-A2 AntigenInterferon-alphaMyeloblastinSerine Endopeptidases

Identifiers

PMID12618518
PMCPMC151894

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.