<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>133(11)</volume><submitter>Lee HJ</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Cancer metastasis, primarily driven by epithelial-to-mesenchymal transition (EMT), is responsible for most cancer-related mortalities. Traditional pre-clinical models fail to fully capture mesenchymal characteristics due to the loss of human stroma. The extracellular matrix (ECM) plays a crucial role in EMT, yet conventional in vitro models often rely on defined ECM components, which may not adequately replicate the human physiological ECM niche.&lt;h4>Methods&lt;/h4>To mimic the in situ dissemination of cancer cells, we employed a patient-derived extracellular matrix (pdECM). We transitioned the culture matrix for patient-derived colorectal cancer organoids from a basement membrane extract (BME) to a patient-derived ECM (pdECM). We performed single-cell multiomic analyses, in</pubmed_abstract><journal>British journal of cancer</journal><pagination>1708-1719</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12644670</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Single-cell multiomic modelling of early metastatic events promoted by the extracellular matrix.</pubmed_title><pmcid>PMC12644670</pmcid><pubmed_authors>Park JE</pubmed_authors><pubmed_authors>Cho Y</pubmed_authors><pubmed_authors>Kim TY</pubmed_authors><pubmed_authors>Park J</pubmed_authors><pubmed_authors>Choi JK</pubmed_authors><pubmed_authors>Kim K</pubmed_authors><pubmed_authors>Park WY</pubmed_authors><pubmed_authors>Kwon J</pubmed_authors><pubmed_authors>Song SH</pubmed_authors><pubmed_authors>Kim P</pubmed_authors><pubmed_authors>Kim YJ</pubmed_authors><pubmed_authors>Lee HJ</pubmed_authors><pubmed_authors>Kang J</pubmed_authors><pubmed_authors>Lee JH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Single-cell multiomic modelling of early metastatic events promoted by the extracellular matrix.</name><description>&lt;h4>Background&lt;/h4>Cancer metastasis, primarily driven by epithelial-to-mesenchymal transition (EMT), is responsible for most cancer-related mortalities. Traditional pre-clinical models fail to fully capture mesenchymal characteristics due to the loss of human stroma. The extracellular matrix (ECM) plays a crucial role in EMT, yet conventional in vitro models often rely on defined ECM components, which may not adequately replicate the human physiological ECM niche.&lt;h4>Methods&lt;/h4>To mimic the in situ dissemination of cancer cells, we employed a patient-derived extracellular matrix (pdECM). We transitioned the culture matrix for patient-derived colorectal cancer organoids from a basement membrane extract (BME) to a patient-derived ECM (pdECM). We performed single-cell multiomic analyses, in</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-06T15:46:38.247Z</modification><creation>2026-06-02T03:09:33.37Z</creation></dates><accession>S-EPMC12644670</accession><cross_references><pubmed>40954257</pubmed><doi>10.1038/s41416-025-03181-4</doi></cross_references></HashMap>