{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sinha S"],"funding":["Torey Pines Foundation, La Jolla","Padres Pedal the Cause","United States National Institutes of Health","Torrey Pines Foundation","NCI NIH HHS","W.M. Keck Foundation","NIH HHS","United States National Institute of Health"],"pagination":["e170953"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11645149"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["134(24)"],"pubmed_abstract":["Estrogen receptor-positive (ER+) breast cancer commonly disseminates to bone marrow, where interactions with mesenchymal stromal cells (MSCs) shape disease trajectory. We modeled these interactions with tumor-MSC co-cultures and used an integrated transcriptome-proteome-network-analyses workflow to identify a comprehensive catalog of contact-induced changes. Conditioned media from MSCs failed to recapitulate genes and proteins, some borrowed and others tumor-intrinsic, induced in cancer cells by direct contact. Protein-protein interaction networks revealed the rich connectome between \"borrowed\" and \"intrinsic\" components. Bioinformatics prioritized one of the borrowed components, CCDC88A/GIV, a multi-modular metastasis-related protein that has recently been implicated in driving a hallmark"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Breast cancers that disseminate to bone marrow acquire aggressive phenotypes through CX43-related tumor-stroma tunnels."],"pmcid":["PMC11645149"],"funding_grant_id":["No fund number","R01 CA238042","#PTC2021","R33 CA225549","P30 CA046592","R01 CA238023","R01 CA160911","R37 CA222563","R01 CA100768","S10 OD026929","R01CA238042,R01CA100768,R01CA160911,R50CA221807,U01CA210152,R01CA238023,R33CA225549,R37CA222563","U01 CA210152","994854","R50 CA221807"],"pubmed_authors":["Masotti M","Luker GD","Buschhaus JM","Sinha S","Farfel AP","Callow BW","Luker KE","Ghosh P","Roy S","Espinoza CR","Rajendran S","Chen S"],"additional_accession":[]},"is_claimable":false,"name":"Breast cancers that disseminate to bone marrow acquire aggressive phenotypes through CX43-related tumor-stroma tunnels.","description":"Estrogen receptor-positive (ER+) breast cancer commonly disseminates to bone marrow, where interactions with mesenchymal stromal cells (MSCs) shape disease trajectory. We modeled these interactions with tumor-MSC co-cultures and used an integrated transcriptome-proteome-network-analyses workflow to identify a comprehensive catalog of contact-induced changes. Conditioned media from MSCs failed to recapitulate genes and proteins, some borrowed and others tumor-intrinsic, induced in cancer cells by direct contact. Protein-protein interaction networks revealed the rich connectome between \"borrowed\" and \"intrinsic\" components. Bioinformatics prioritized one of the borrowed components, CCDC88A/GIV, a multi-modular metastasis-related protein that has recently been implicated in driving a hallmark","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-07-15T08:11:17.314Z","creation":"2025-04-04T01:54:36.303Z"},"accession":"S-EPMC11645149","cross_references":{"pubmed":["39480488"],"doi":["10.1172/JCI170953"]}}