Oncogenic Calreticulin Induces Immune Escape by Stimulating TGFβ Expression and Regulatory T-cell Expansion in the Bone Marrow Microenvironment.

doi:10.1158/0008-5472.CAN-23-3553

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Article

Oncogenic Calreticulin Induces Immune Escape by Stimulating TGFβ Expression and Regulatory T-cell Expansion in the Bone Marrow Microenvironment.

Cancer research - 16 Sept 2024

Schmidt Dominik, Endres Cornelia, Hoefflin Rouven, Andrieux Geoffroy, Zwick Melissa, Karantzelis Nikolaos, Staehle Hans F, Vinnakota Janaki Manoja, Duquesne Sandra, Mozaffari Jovein Miriam, Pfeifer Dietmar, Becker Heiko, Blazar Bruce R, Zähringer Alexander, Duyster Justus, Brummer Tilman, Boerries Melanie, Baumeister Julian, Shoumariyeh Khalid, Li Juan, Green Anthony R, Heidel Florian H, Tirosh Itay, Pahl Heike L, Leimkühler Nils, Köhler Natalie, de Toledo Marcelo A S, Koschmieder Steffen, Zeiser Robert

Abstract excerpt

Increasing evidence supports the interplay between oncogenic mutations and immune escape mechanisms. Strategies to counteract the immune escape mediated by oncogenic signaling could provide improved therapeutic options for patients with various malignancies. As mutant calreticulin (CALR) is a common driver of myeloproliferative neoplasms (MPN), we analyzed the impact of oncogenic CALRdel52 on the bone marrow (BM)...

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Identifiers

PMID: 38885318
DOI: 10.1158/0008-5472.CAN-23-3553
PMCID: PMC11405138

Genes

CALR
CD4
JAK1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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