<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen Q</submitter><funding>National Natural Science Foundation of China</funding><pagination>786-795</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6889176</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>121(9)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The progression and metastasis of pancreatic ductal adenocarcinoma (PDAC) is highly dependent on the tumour microenvironment. Most tumour-associated macrophages (TAMs) are M2 phenotype macrophages, which normally show anti-inflammatory functions in numerous disorders. Previously, we found that alternatively activated macrophages showed pro-inflammatory characteristics upon stimulation with hepatoma cell-derived debris; however, the molecular mechanism was unclear.&lt;h4>Methods&lt;/h4>In vitro and in vivo experiments were employed to investigate the molecular mechanism. Using pancreatic cancer cell lines, mouse models and human tissues, we obtained a general picture of tumour cell-derived debris promoting metastasis of pancreatic cancer by inducing inflammation via TAMs.&lt;h4>Re</pubmed_abstract><journal>British journal of cancer</journal><pubmed_title>Tumour cell-derived debris and IgG synergistically promote metastasis of pancreatic cancer by inducing inflammation via tumour-associated macrophages.</pubmed_title><pmcid>PMC6889176</pmcid><funding_grant_id>81530079</funding_grant_id><funding_grant_id>2015AA020405</funding_grant_id><pubmed_authors>Fu Q</pubmed_authors><pubmed_authors>Liang T</pubmed_authors><pubmed_authors>Chen Q</pubmed_authors><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Lou Y</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Bai X</pubmed_authors><pubmed_authors>Zhang Q</pubmed_authors><pubmed_authors>Ye M</pubmed_authors><pubmed_authors>Wei T</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Dang X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tumour cell-derived debris and IgG synergistically promote metastasis of pancreatic cancer by inducing inflammation via tumour-associated macrophages.</name><description>&lt;h4>Background&lt;/h4>The progression and metastasis of pancreatic ductal adenocarcinoma (PDAC) is highly dependent on the tumour microenvironment. Most tumour-associated macrophages (TAMs) are M2 phenotype macrophages, which normally show anti-inflammatory functions in numerous disorders. Previously, we found that alternatively activated macrophages showed pro-inflammatory characteristics upon stimulation with hepatoma cell-derived debris; however, the molecular mechanism was unclear.&lt;h4>Methods&lt;/h4>In vitro and in vivo experiments were employed to investigate the molecular mechanism. Using pancreatic cancer cell lines, mouse models and human tissues, we obtained a general picture of tumour cell-derived debris promoting metastasis of pancreatic cancer by inducing inflammation via TAMs.&lt;h4>Re</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Oct</publication><modification>2025-04-18T23:42:40.904Z</modification><creation>2020-05-21T20:33:03Z</creation></dates><accession>S-EPMC6889176</accession><cross_references><pubmed>31588122</pubmed><doi>10.1038/s41416-019-0595-2</doi></cross_references></HashMap>