{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T13:57:27Z","timestamp":1791640647178,"version":"4.3.4"},"reference-count":52,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,11,12]],"date-time":"2013-11-12T00:00:00Z","timestamp":1384214400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2013,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:bold>\n                      Peritoneal dissemination is a frequent metastatic route for cancers of the ovary and gastrointestinal tract. Tumour cells metastasize by attaching to and invading through the mesothelial cell (\n                      <jats:styled-content style=\"fixed-case\">MC<\/jats:styled-content>\n                      ) monolayer that lines the peritoneal cavity. Metastases are influenced by carcinoma\u2010associated fibroblasts (\n                      <jats:styled-content style=\"fixed-case\">CAFs<\/jats:styled-content>\n                      ), a cell population that derives from different sources. Hence, we investigated whether\n                      <jats:styled-content style=\"fixed-case\">MCs<\/jats:styled-content>\n                      , through mesothelial\u2013mesenchymal transition (\n                      <jats:styled-content style=\"fixed-case\">MMT<\/jats:styled-content>\n                      ), were a source of\n                      <jats:styled-content style=\"fixed-case\">CAFs<\/jats:styled-content>\n                      during peritoneal carcinomatosis and whether\n                      <jats:styled-content style=\"fixed-case\">MMT<\/jats:styled-content>\n                      affected the adhesion and invasion of tumour cells. Biopsies from patients with peritoneal dissemination revealed the presence of myofibroblasts expressing mesothelial markers in the proximity of carcinoma implants. Prominent new vessel formation was observed in the peritoneal areas harbouring tumour cells when compared with tumour\u2010free regions. The use of a mouse model of peritoneal dissemination confirmed the myofibroblast conversion of\n                      <jats:styled-content style=\"fixed-case\">MCs<\/jats:styled-content>\n                      and the increase in angiogenesis at places of tumour implants. Treatment of omentum\n                      <jats:styled-content style=\"fixed-case\">MCs<\/jats:styled-content>\n                      with conditioned media from carcinoma cell cultures resulted in phenotype changes reminiscent of\n                      <jats:styled-content style=\"fixed-case\">MMT<\/jats:styled-content>\n                      . Adhesion experiments demonstrated that\n                      <jats:styled-content style=\"fixed-case\">MMT<\/jats:styled-content>\n                      enhanced the binding of cancer cells to\n                      <jats:styled-content style=\"fixed-case\">MCs<\/jats:styled-content>\n                      in a\n                      <jats:italic>\u03b2<\/jats:italic>\n                      1\u2010integrin\u2010dependent manner. Scanning electron microscopy imaging showed that the enhanced adhesion was mostly due to increased cell\u2013cell interaction and not to a mere matrix exposure. Invasion assays suggested a reciprocal stimulation of the invasive capacity of tumour cells and\n                      <jats:styled-content style=\"fixed-case\">MCs<\/jats:styled-content>\n                      . Our results demonstrate that\n                      <jats:styled-content style=\"fixed-case\">CAFs<\/jats:styled-content>\n                      can derive from mesothelial cells during peritoneal metastasis. We suggest that\n                      <jats:styled-content style=\"fixed-case\">MMT<\/jats:styled-content>\n                      renders the peritoneum more receptive for tumour cell attachment\/invasion and contributes to secondary tumour growth by promoting its vascularization. Copyright \u00a9 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                    <\/jats:bold>\n                  <\/jats:p>","DOI":"10.1002\/path.4281","type":"journal-article","created":{"date-parts":[[2013,10,11]],"date-time":"2013-10-11T21:51:55Z","timestamp":1381528315000},"page":"517-531","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":179,"title":["Carcinoma\u2010associated fibroblasts derive from mesothelial cells via mesothelial\u2010to\u2010mesenchymal transition in peritoneal metastasis"],"prefix":"10.1002","volume":"231","author":[{"given":"Pilar","family":"Sandoval","sequence":"first","affiliation":[{"name":"Centro de Biolog\u00eda Molecular\u2010Severo Ochoa CSIC\u2013UAM, Cantoblanco Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose Antonio","family":"Jim\u00e9nez\u2010Heffernan","sequence":"additional","affiliation":[{"name":"Servicio de Anatom\u00eda Patol\u00f3gica Hospital Universitario de la 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