Evidence map›Paper›PMID 39091883›Full record

ArticlebioRxiv : the preprint server for biology2024

MYC and p53 alterations cooperate through VEGF signaling to repress cytotoxic T cell and immunotherapy responses in prostate cancer.

Katherine C Murphy, Kelly D DeMarco, Lin Zhou, Yvette Lopez-Diaz, Yu-Jui Ho, Junhui Li, Shi Bai, Karl Simin, Lihua Julie Zhu, Arthur M Mercurio and 1 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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
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.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Katherine C MurphyDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0002-5962-9896
Kelly D DeMarcoDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0009-0007-0469-7932
Lin ZhouDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0003-2581-4345
Yvette Lopez-DiazHorae Gene Therapy Center, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Yu-Jui HoDepartment of Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID 0000-0002-7540-024X
Junhui LiDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Shi BaiDepartment of Pathology, University of Massachusetts Medical Center, Worcester, MA, USA.
Karl SiminDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0002-7431-0939
Lihua Julie ZhuDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0001-7416-0590
Arthur M MercurioDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0003-2762-7519
Marcus RuscettiDepartment of Molecular, Cell, and Cancer Biology, University of Massachusetts Chan Medical School, Worcester, MA, USA.ORCID 0000-0002-4394-2087

Funding

University of Massachusetts Center for Clinical Science and Translational SupplementUL1TR001453 · NCATS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LUZURIAGA, KATHERINE F · 2015 to 2024
$39.0M
Novel Therapeutic Approaches for Aggressive Prostate CancerR01CA276863 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Arthur M Mercurio · 2023 to 2026
$1.5M
NCATS NIH HHS UL1 TR001453NCI NIH HHS R01 CA276863
6 · The paper itself

Abstract

Patients with castration-resistant prostate cancer (CRPC) are generally unresponsive to tumor targeted and immunotherapies. Whether genetic alterations acquired during the evolution of CRPC impact immune and immunotherapy responses is largely unknown. Using our innovative electroporation-based mouse models, we generated distinct genetic subtypes of CRPC found in patients and uncovered unique immune microenvironments. Specifically, mouse and human prostate tumors with Significance: Though immune checkpoint blockade (ICB) therapies can achieve curative responses in many treatment-refractory cancers, they have limited efficacy in CRPC. Here we identify a genetic mechanism by which VEGF contributes to T cell suppression, and demonstrate that VEGFR2 blockade can potentiate the effects of PD-L1 ICB to immunologically treat CRPC.

Identifiers

PMID39091883
PMCPMC11291169

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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.