Evidence map›Paper›PMID 35874659›Full record

ArticleFrontiers in immunology2022

SIRPα Mismatch Is Associated With Relapse Protection and Chronic Graft-Versus-Host Disease After Related Hematopoietic Stem Cell Transplantation for Lymphoid Malignancies.

Rima M Saliba, Samer A Srour, Uri Greenbaum, Qing Ma, Yudith Carmazzi, Michael Moller, Janet Wood, Stefan O Ciurea, Piyanuch Kongtim, Gabriela Rondon and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 92% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

18 authors at 3 institutions in 3 countries.

Rima M SalibaDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Samer A SrourDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Uri GreenbaumDepartment of Hematology, Soroka University Medical Center, Beer Sheva, Israel.
Qing MaDepartment of Hematopoietic Biology and Malignancy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Yudith CarmazziDepartment of Laboratory Medicine, Division of Pathology/Laboratory Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Michael MollerSchool of Health Professions, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Janet WoodDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Stefan O CiureaDivision of Hematology/Oncology, Department of Medicine, Chao Family Comprehensive Cancer Center, University of California, Irvine, CA, United States.
Piyanuch KongtimDivision of Hematology/Oncology, Department of Medicine, Chao Family Comprehensive Cancer Center, University of California, Irvine, CA, United States.
Gabriela RondonDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Dan LiDepartment of Hematopoietic Biology and Malignancy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Supawee SaengboonDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Amin M AlousiDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Katayoun RezvaniDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Elizabeth J ShpallDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Kai CaoDepartment of Laboratory Medicine, Division of Pathology/Laboratory Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Richard E ChamplinDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Jun ZouDepartment of Laboratory Medicine, Division of Pathology/Laboratory Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
The University of Texas MD Anderson Cancer Center · USUniversity of California, Irvine · USBen-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a potentially curative therapy for hematologic malignancies. Alloreactivity after HSCT is known to be mediated by adaptive immune cells expressing rearranging receptors. Recent studies demonstrated that the innate immune system could likewise sense the non-self signals and subsequently enhance the alloimmune response. We recently demonstrated that the donor/recipient mismatch of signal regulatory protein α (SIRPα), an immunoglobulin receptor exclusively expressed on innate cells, is associated with a higher risk of cGVHD and relapse protection in a cohort of acute myeloid leukemia patients who underwent allo-HSCT. Whether these effects also occur in other hematologic malignancies remains unclear. In the present study, we compared outcomes by SIRPα match status in a cohort of 310 patients who received allo-HSCT from an HLA matched-related donor for the treatment of lymphoid malignancies. Multivariable analysis showed that SIRPα mismatch was associated with a significantly higher rate of cGVHD (hazard ratio [HR] 1.8, P= .002), cGVHD requiring systemic immunosuppressive therapy (HR 1.9, P= .005), a lower rate of disease progression (HR 0.5, P= .003) and improved progression-free survival (HR 0.5, P= .001). Notably, the effects of SIRPα mismatch were observed only in the patients who achieved >95% of donor T-cell chimerism. The mismatch in SIRPα is associated with favorable relapse protection and concurrently increased risk of cGVHD in patients who undergo allo-HSCT for lymphoid malignancies, and the optimal donor could be selected based on the finding of the study to mitigate the risk of GVHD and relapse.

Indexed as

Graft vs Host DiseaseHematologic NeoplasmsHematopoietic Stem Cell TransplantationLeukemia, Myeloid, AcuteHistocompatibilityHumansRecurrencecGVHDHSCTinnate immunitylymphoid malignanciesmismatchrelapse protectionsignal regulatory protein alpha

Identifiers

PMID35874659
PMCPMC9301275
OpenAlexW4284675779

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.