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These cells were used to provide the following evidence  that fibroblast growth factor (FGF)2 is a paracrine chemoattractant during  PANC-1 cell clustering: (\n                    <jats:italic>i<\/jats:italic>\n                    ) FGF2 is secreted and remains bound to the  extracellular matrix from where it may diffuse to form chemoattractive  gradients; (\n                    <jats:italic>ii<\/jats:italic>\n                    ) a subset of cells expresses FGF receptors (FGFRs) -1,  -2, -3, and -4; (\n                    <jats:italic>iii<\/jats:italic>\n                    ) inhibition of FGFR tyrosine kinase inhibits  cell clustering; and (\n                    <jats:italic>iv<\/jats:italic>\n                    ) FGF2 neutralizing antibody inhibits  clustering. In addition, adult human islet-derived precursor cells, which  cluster and differentiate in a manner similar to PANC-1 cells, also secrete  FGF2 and express FGFRs. We conclude that FGF2, acting as a paracrine  chemoattractant, stimulates clustering of precursor cells, an early step  leading to islet-like cell aggregate formation. Similar processes may occur  during development of the islet of Langerhans in humans.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1232230100","type":"journal-article","created":{"date-parts":[[2003,6,10]],"date-time":"2003-06-10T13:06:36Z","timestamp":1055250396000},"page":"7117-7122","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":143,"title":["Human pancreatic precursor cells secrete FGF2 to stimulate clustering  into hormone-expressing islet-like cell aggregates"],"prefix":"10.1073","volume":"100","author":[{"given":"Anandwardhan A.","family":"Hardikar","sequence":"first","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases,  National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernice","family":"Marcus-Samuels","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases,  National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Geras-Raaka","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases,  National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce M.","family":"Raaka","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases,  National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marvin C.","family":"Gershengorn","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes and Digestive and Kidney Diseases,  National Institutes of Health, Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2003,5,30]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(62)90042-8"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0012-1606(67)90042-5"},{"key":"e_1_3_2_3_2","first-page":"4243","volume":"124","unstructured":"Kim, S. 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