Cristina Migliore

Candiolo Cancer Institute

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Co-Authors

Silvia Giordano

Candiolo Cancer Institute

152

Simona Corso

Candiolo Cancer Institute

140

Filippo Pietrantonio

Fondazione IRCCS Istituto Nazionale dei Tumori

117

Sara E. Bellomo

Candiolo Cancer Institute

116

Caterina Marchiò

University of Turin

115

Federica Morano

Fondazione IRCCS Istituto Nazionale dei Tumori

115

Annalisa Petrelli

University of Turin

114

Maurizio Degiuli

University of Turin

Gian Luca Baiocchi

University of Campania "Luigi Vanvitelli"

Daniela Conticelli

Candiolo Cancer Institute

Cooperative Institutions

Istituti di Ricovero e Cura a Carattere Scientifico

University of Turin

Candiolo Cancer Institute

University of Milan

University of Cagliari

Fondazione IRCCS Istituto Nazionale dei Tumori

Fondazione Piemontese per la Ricerca sul Cancro Onlus

University of Brescia

University of Siena

Azienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia

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Data from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Nil Grunberg Meirav Pevsner‐Fischer Tal Goshen‐Lago Judith Diment Yaniv Stein

<div>AbstractGastric cancer is the third most lethal cancer worldwide, and evaluation of the genomic status of gastric cancer cells has not translated into effective prognostic or therapeutic strategies. We therefore hypothesize that outcomes may depend on the tumor microenvironment (TME), in particular, cancer-associated fibroblasts (CAF). However, very little is known about the role of CAFs in gastric cancer. To address this, we mapped the transcriptional landscape of human gastric cancer stroma by microdissection and RNA sequencing of CAFs from patients with gastric cancer. A stromal gene signature was associated with poor disease outcome, and the transcription factor heat shock factor 1 (HSF1) regulated the signature. HSF1 upregulated inhibin subunit beta A and thrombospondin 2, which were secreted in CAF-derived extracellular vesicles to the TME to promote cancer. Together, our work provides the first transcriptional map of human gastric cancer stroma and highlights HSF1 and its transcriptional targets as potential diagnostic and therapeutic targets in the genomically stable tumor microenvironment.Significance:This study shows how HSF1 regulates a stromal transcriptional program associated with aggressive gastric cancer and identifies multiple proteins within this program as candidates for therapeutic intervention.</div>

Extracellular Vesicles

10.1158/0008-5472.c.6513295

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Table S2 from Optimized EGFR Blockade Strategies in EGFR Addicted Gastroesophageal Adenocarcinomas

Simona Corso Filippo Pietrantonio Maria Apicella Cristina Migliore Daniela Conticelli

Supplementary Table 2

Table (database)

10.1158/1078-0432.22481693

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Supplementary Table S3 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits

Simona Corso Claudio Isella Sara E. Bellomo Maria Apicella Stefania Durando

GC PDXs are annotated for: CNV of HER2, EGFR, FGFR2, MET, KRAS ({greater than or equal to}8 gene copies); COSMIC Mutations/Frameshifts (Allelic frequency >0.3)

10.1158/0008-5472.22422258

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Supplementary Methods1 from HER2 Copy Number and Resistance Mechanisms in Patients with HER2-positive Advanced Gastric Cancer Receiving Initial Trastuzumab-based Therapy in JACOB Trial

Filippo Pietrantonio Paolo Manca Sara E. Bellomo Simona Corso Alessandra Raimondi

Supplementary Methods

Pertuzumab

10.1158/1078-0432.22490099.v1

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Supplementary Table 4 from Cancer-Associated Fibroblasts Promote Aggressive Gastric Cancer Phenotypes via Heat Shock Factor 1–Mediated Secretion of Extracellular Vesicles

Nil Grunberg Meirav Pevsner‐Fischer Tal Goshen‐Lago Judith Diment Yaniv Stein