{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,4]],"date-time":"2026-01-04T10:34:38Z","timestamp":1767522878667},"reference-count":35,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2005,4,15]],"date-time":"2005-04-15T00:00:00Z","timestamp":1113523200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/www.springer.com\/tdm"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Cancer"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Familial Adenomatous Polyposis (FAP) is caused by germline mutations in the <jats:italic>APC<\/jats:italic> (Adenomatous Polyposis Coli) gene. The vast majority of <jats:italic>APC<\/jats:italic> mutations are point mutations or small insertions \/ deletions which lead to truncated protein products. Splicing mutations or gross genomic rearrangements are less common inactivating events of the <jats:italic>APC<\/jats:italic> gene.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>In the current study genomic DNA or RNA from ten unrelated FAP suspected patients was examined for germline mutations in the <jats:italic>APC<\/jats:italic> gene. Family history and phenotype were used in order to select the patients. Methods used for testing were dHPLC (denaturing High Performance Liquid Chromatography), sequencing, MLPA (Multiplex Ligation \u2013 dependent Probe Amplification), Karyotyping, FISH (Fluorescence In Situ Hybridization) and RT-PCR (Reverse Transcription \u2013 Polymerase Chain Reaction).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>A 250 Kbp deletion in the <jats:italic>APC<\/jats:italic> gene starting from intron 5 and extending beyond exon 15 was identified in one patient. A substitution of the +5 conserved nucleotide at the splice donor site of intron 9 in the <jats:italic>APC<\/jats:italic> gene was shown to produce frameshift and inefficient exon skipping in a second patient. Four frameshift mutations (1577insT, 1973delAG, 3180delAAAA, 3212delA) and a nonsense mutation (C1690T) were identified in the rest of the patients.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>Screening for <jats:italic>APC<\/jats:italic> mutations in FAP patients should include testing for splicing defects and gross genomic alterations.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2407-5-40","type":"journal-article","created":{"date-parts":[[2005,4,15]],"date-time":"2005-04-15T14:41:23Z","timestamp":1113576083000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Rare mutations predisposing to familial adenomatous polyposis in Greek FAP patients"],"prefix":"10.1186","volume":"5","author":[{"given":"Markos","family":"Mihalatos","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Angela","family":"Apessos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hans","family":"Dauwerse","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Voula","family":"Velissariou","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aristidis","family":"Psychias","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexander","family":"Koliopanos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Konstantinos","family":"Petropoulos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John K","family":"Triantafillidis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ioannis","family":"Danielidis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George","family":"Fountzilas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Niki J","family":"Agnantis","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Georgios","family":"Nasioulas","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2005,4,15]]},"reference":[{"key":"228_CR1","doi-asserted-by":"publisher","first-page":"589","DOI":"10.1016\/0092-8674(81)90021-0","volume":"66","author":"J Groden","year":"1991","unstructured":"Groden J, Thliveris A, Samowitz W, Carlson M, Gelbert L, Albertsen H, Joslyn G, Stevens J, Spirio L, Robertson M: Identification and characterization of the familial adenomatous polyposis coli gene. 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