MYC, TP53, and chromosome 17 copy-number alterations in multiple gastric cancer cell lines and in their parental primary tumors.

Abstract

We evaluated whether MYC, TP53, and chromosome 17 copy-number alterations occur in ACP02, ACP03, and AGP01 gastric cancer cell lines and in their tumor counterpart. Fluorescence in situ hybridization for MYC and TP53 genes and for chromosome 17 was applied in the 6th, 12th, 60th, and 85th passages of the cell lines and in their parental primary tumors. We observed that three and four MYC signals were the most common alterations in gastric cell lines and tumors. ACP02 presented cells with two copies of chr17 and loss of one copy of TP53 more frequently than ACP03 and AGP01. Only ACP03 and AGP01 presented clonal chr17 trisomy with three or two TP53 copies. The frequency of MYC gain, TP53 loss, and chromosome 17 trisomy seems to increase in gastric cell lines compared to their parental tumors. Our findings reveal that these cell lines retain, in vitro, the genetic alterations presented in their parental primary tumors.

• Authors: Mariana Ferreira Leal, Danielle Queiroz Calcagno, Joana de Fátima Ferreira Borges da Costa, Tanielly Cristina Raiol Silva, André Salim Khayat, Elizabeth Suchi Chen, Paulo Pimentel Assumpção, Marília de Arruda Cardoso Smith, Rommel Rodríguez Burbano
• Journal: Journal of biomedicine & biotechnology (J Biomed Biotechnol) Vol. 2011 Pg. 631268 ( 2011) ISSN: 1110-7251 [Electronic] United States
• PMID: 21528007 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Proto-Oncogene Proteins c-myc
• Tumor Suppressor Protein p53

Topics

• Cell Line, Tumor
• Chromosome Aberrations
• Chromosomes, Human, Pair 17 (genetics)
• Gene Dosage
• Humans
• In Situ Hybridization, Fluorescence
• Proto-Oncogene Proteins c-myc (genetics)
• Stomach Neoplasms (genetics)
• Tumor Suppressor Protein p53 (genetics)