Common genetic evolutionary pathways in familial adenomatous polyposis tumors

Gemma Tarafa, Esther Prat, Rosa Ana Risques, Sara González, Jordi Camps, Mónica Grau, Elisabeth Guinó, Víctor Moreno, Manel Esteller, James G. Herman, Josep Ramon Germà, Rosa Miró, Miguel Angel Peinado, Gabriel Capellá

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Cancer cells progress through the accumulation of genetic alterations. Familial adenomatous polyposis (FAP) tumors provide an excellent model to unravel the molecular steps underlying malignant transformation. Global genomic damage was assessed in 56 adenomas and 3 carcinomas from six FAP patients and compared with that of sporadic adenomas and carcinomas. Evolutive trees were traced after application of maximum likelihood clustering and split decomposition methods to the analysis of comprehensive genetic profiles generated by diverse molecular approaches: arbitrarily primed PCR, comparative genomic hybridization, and flow cytometry. Overall, genomic damage as assessed by arbitrarily primed PCR was lower in familial adenomas than in sporadic adenomas and carcinomas. Comparative genomic hybridization data also show a low number of alterations in the majority of FAP adenomas. Tumors of the same patient were likely to share specific genetic alterations and may be grouped into one or two clusters. Putative common pathways were also identified, which included tumors of up to three different patients. According to our data, FAP tumors accumulate specific genetic alterations and in a preferred order that is characteristic of each individual. Moreover, the particular genetic background and environmental conditions of a FAP patient restrain the molecular evolution portrait of synchronous tumors.

Original languageEnglish (US)
Pages (from-to)5731-5737
Number of pages7
JournalCancer Research
Issue number18
StatePublished - Sep 15 2003

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


Dive into the research topics of 'Common genetic evolutionary pathways in familial adenomatous polyposis tumors'. Together they form a unique fingerprint.

Cite this