Evidence map›Paper›PMID 24859877›Full record

ArticleHaematologica2014

Increased mitochondrial apoptotic priming of human regulatory T cells after allogeneic hematopoietic stem cell transplantation.

Kazuyuki Murase, Haesook T Kim, O R Gregory Bascug, Yutaka Kawano, Jeremy Ryan, Ken-ichi Matsuoka, Matthew S Davids, John Koreth, Vincent T Ho, Corey Cutler and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Haematologica, 2014. 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
1.1field-weighted citation impact, top 24% 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, 19 citations in OpenAlex.

  1. BAK is a predictive and prognostic biomarker for the therapeutic effect of docetaxel treatment in patients with advanced gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2016
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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

17 authors at 4 institutions in 2 countries.

Kazuyuki MuraseDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Haesook T KimDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, MA, USA Cancer Vaccine Center, Dana-Farber Cancer Institute, Boston, MA, USA Harvard School of Public Health, Boston, MA, USA.
O R Gregory BascugDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Yutaka KawanoDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Jeremy RyanDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Ken-ichi MatsuokaDepartment of Hematology and Oncology, Okayama University, Japan.
Matthew S DavidsDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
John KorethDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Vincent T HoDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Corey CutlerDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Philippe ArmandDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Edwin P AlyeaDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Bruce R BlazarMasonic Cancer Center and Department of Pediatrics, Division of Blood and Marrow Transplantation, University of Minnesota, Minneapolis, MN, USA.
Joseph H AntinDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Robert J SoifferDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Anthony LetaiDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA.
Jerome RitzDivision of Hematologic Malignancies and Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Medical School, Boston, MA, USA Cancer Vaccine Center, Dana-Farber Cancer Institute, Boston, MA, USA Harvard Stem Cell Institute, Boston, MA, USA jerome_ritz@dfci.harvard.edu.
Harvard University · USDana-Farber Cancer Institute · USOkayama University · JPUniversity of Minnesota Medical Center · US

Funding

Trial Design and Biostatistical Support CoreP01CA065493 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Mark J Osborn · 1995 to 2026
$48.2M
Transgenic/KnockoutP01AI056299 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SHARPE, ARLENE H. · 2003 to 2023
$42.5M
Targeting Myeloma Cell-Host Bone Marrow InteractionsP01CA078378 · NCI · DANA-FARBER CANCER INSTITUTE · PI RITZ, JEROME · 1998 to 2014
$26.2M
Project 3: Humoral Targets and B Cell Biology in Chronic Graft-vs.-Host DiseaseP01CA142106 · NCI · DANA-FARBER CANCER INST · PI CUTLER, COREY S · 2009 to 2019
$17.5M
Physician Scientist Training in Cancer ResearchT32CA009172 · NCI · DANA-FARBER CANCER INSTITUTE · PI Jennifer R Brown, James A. DeCaprio · 1985 to 2026
$17.1M
Enhancing Treg Therapeutic Efficacy in GVHDR01HL118979 · NHLBI · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R, HIPPEN, KELI L · 2014 to 2025
$6.7M
IN VIVO PREVENTION OF MURINE GVHDR01AI034495 · NIAID · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BLAZAR, BRUCE R · 1993 to 2016
$6.2M
T-CELL TARGETING FOR GVHDR01HL056067 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BLAZAR, BRUCE R · 1995 to 2022
$5.4M
GVL TO REDUCE AML RELAPSE AFTER MURINE ALLOGENEIC BMTR01CA072669 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BLAZAR, BRUCE R · 1997 to 2017
$4.9M
Manipulation of Immune Responsiveness after Hematopoietic Cell TransplantationR01CA183559 · NCI · DANA-FARBER CANCER INST · PI RITZ, JEROME, SOIFFER, ROBERT JON · 2013 to 2017
$3.7M
Reconstitution of Regulatory T Cells After Stem Cell TransplantationR01CA183560 · NCI · DANA-FARBER CANCER INST · PI RITZ, JEROME, SOIFFER, ROBERT JON · 2013 to 2017
$2.5M
NCI NIH HHS CA142106NCI NIH HHS CA183559NCI NIH HHS CA183560NCI NIH HHS P01 CA065493NCI NIH HHS P01 CA078378NCI NIH HHS P01 CA142106NCI NIH HHS R01 CA072669NCI NIH HHS R01 CA183559NCI NIH HHS R01 CA183560NCI NIH HHS T32 CA009172NHLBI NIH HHS R01 HL056067NHLBI NIH HHS R01 HL118979NIAID NIH HHS AI056299NIAID NIH HHS P01 AI056299NIAID NIH HHS R01 AI034495
6 · The paper itself

Abstract

CD4 regulatory T cells play a critical role in establishment of immune tolerance and prevention of graft-versus-host disease after allogeneic hematopoietic stem cell transplantation. The recovery and maintenance of regulatory T cells is dependent on homeostatic factors including the generation of naïve regulatory T cells from hematopoietic precursor cells, the proliferation and expansion of mature regulatory T cells, and the survival of regulatory T cells in vivo. In this study, quantitation of mitochondrial apoptotic priming was used to compare susceptibility of regulatory T cells, conventional CD4 T cells and CD8 T cells to intrinsic pathway apoptosis in 57 patients after allogeneic hematopoietic stem cell transplantation and 25 healthy donors. In healthy donors, regulatory T cells are more susceptible to mitochondrial priming than conventional T cells. Mitochondrial priming is increased after hematopoietic stem cell transplantation in all T-cell subsets and particularly in patients with chronic graft-versus-host disease. Regulatory T cells express high levels of CD95 and are also more susceptible than conventional T cells to apoptosis through the extrinsic pathway. However, CD95 expression and extrinsic pathway apoptosis is not increased after hematopoietic stem cell transplantation. Decreased expression of BCL2 and increased expression of BIM, a mitochondrial cell death activator protein, in regulatory T cells contributes to increased mitochondrial priming in this T-cell subset but additional factors likely contribute to increased mitochondrial priming following hematopoietic stem cell transplantation.

Indexed as

Hematopoietic Stem Cell TransplantationAdultAgedApoptosisCase-Control StudiesCD8-Positive T-LymphocytesChronic Diseasefas ReceptorFemaleGene ExpressionGraft vs Host DiseaseHumansMaleMiddle AgedMitochondriaMyeloproliferative DisordersBax protein (53-86)FAS protein, humanfas ReceptorPeptide FragmentsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID24859877
PMCPMC4562540
OpenAlexW2016269737

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.