Evidence map›Paper›PMID 23105141›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Broad cross-presentation of the hematopoietically derived PR1 antigen on solid tumors leads to susceptibility to PR1-targeted immunotherapy.

Gheath Alatrash, Elizabeth A Mittendorf, Anna Sergeeva, Pariya Sukhumalchandra, Na Qiao, Mao Zhang, Lisa S St John, Kathryn Ruisaard, Christine E Haugen, Zein Al-Atrache and 14 more

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  5. Fucosylation Enhances the Efficacy of Adoptively Transferred Antigen-Specific Cytotoxic T Lymphocytes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
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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

24 authors at 1 institution in 1 country.

Gheath AlatrashDepartment of Stem Cell Transplantation and Cellular Therapy, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. galatras@mdanderson.org
Elizabeth A Mittendorf
Anna Sergeeva
Pariya Sukhumalchandra
Na Qiao
Mao Zhang
Lisa S St John
Kathryn Ruisaard
Christine E Haugen
Zein Al-Atrache
Haroon Jakher
Anne V Philips
Xiaoling Ding
Jie Qing Chen
Yun Wu
Rebecca S Patenia
Chantale Bernatchez
Luis M Vence
Laszlo G Radvanyi
Patrick Hwu
Karen Clise-Dwyer
Qing Ma
Sijie Lu
Jeffrey J Molldrem
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
University of Texas M.D. Anderson Cancer SPORE-LeukemiaP50CA100632 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KONOPLEVA, MARINA Y · 2003 to 2023
$43.7M
U OF TEXAS HLTH SCI CTR HOUSTON CENTER FOR CLINICAL AND TRANSLATIONAL SCIENCESUL1RR024148 · NCRR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2006 to 2010
$27.9M
UTMDACC SPORE in Breast CancerP50CA116199 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BERRY, DONALD A · 2005 to 2009
$11.9M
Cyclin E: Implications for targeted therapy in HER2-overexpressing breast cancerR00CA133244 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MITTENDORF, ELIZABETH · 2010 to 2012
$720k
Novel Frailty Phenotype in Older Adults with End-Stage Renal DiseaseF32AG053025 · NIA · JOHNS HOPKINS UNIVERSITY · PI HAUGEN, CHRISTINE · 2016 to 2019
$204k
NCI NIH HHS 4R00CA133244-03200NCI NIH HHS 5P50CA116199-05NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA100632NCI NIH HHS P50 CA116199NCI NIH HHS R00 CA133244NCRR NIH HHS UL1 RR024148NIA NIH HHS F32 AG053025
6 · The paper itself

Abstract

PR1 is a HLA-A2-restricted peptide that has been targeted successfully in myeloid leukemia with immunotherapy. PR1 is derived from the neutrophil granule proteases proteinase 3 (P3) and neutrophil elastase (NE), which are both found in the tumor microenvironment. We recently showed that P3 and NE are taken up and cross-presented by normal and leukemia-derived APCs, and that NE is taken up by breast cancer cells. We now extend our findings to show that P3 and NE are taken up and cross-presented by human solid tumors. We further show that PR1 cross-presentation renders human breast cancer and melanoma cells susceptible to killing by PR1-specific CTLs (PR1-CTL) and the anti-PR1/HLA-A2 Ab 8F4. We also show PR1-CTL in peripheral blood from patients with breast cancer and melanoma. Together, our data identify cross-presentation as a novel mechanism through which cells that lack endogenous expression of an Ag become susceptible to therapies that target cross-presented Ags and suggest PR1 as a broadly expressed tumor Ag.

Indexed as

ImmunotherapyAntibodiesAntigen-Presenting CellsAntigens, NeoplasmBreast NeoplasmsCross-PrimingFemaleHLA-A2 AntigenHumansLeukocyte ElastaseMelanomaMolecular Targeted TherapyMyeloblastinPeptide FragmentsSkin NeoplasmsT-Lymphocytes, CytotoxicAntibodiesAntigens, NeoplasmHLA-A2 AntigenLeukocyte ElastaseMyeloblastinPeptide Fragments

Identifiers

PMID23105141
PMCPMC3504175
OpenAlexW1494334863

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.