Author of

• 11866

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  P2.18 - Poster Session 2 - Pathology (ID 176)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/29/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 11876

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    P2.18-010 - Copy number changes in chromosome 2p are unique events among ALK fusion positive lung adenocarcinomas (ID 1805)

    09:30 - 09:30  |  Author(s): H. Mano
    • Abstract

    Background
    ALK fusion is a unique gene transversion detected among lung adenocarcinomas. It emerged as a target for cancer therapy, but little is known how this genomic abnormality is created. To unveil the underlying mechanisms leading to gene fusion, we compared the genomic structures of the two groups using SNP-array allelokaryotyping analysis.

    Methods
    35 ALK fusion positive and 95 ALK fusion negative cases were involved in this study. Immunohistochemical staining and multiplex RT-PCR was employed for screening and confirmation. Chromosome 2p were closely examined using SNP-array based allelokaryotyping.

    Results
    Copy number changes of the regions including ALK and EML4 were detected among ALK fusion positive tumors (10/35, 29%) in contrast with ALK fusion negative tumors (0/95, 0%). In other words, the genomic regions unnecessary to constitute each fusion gene variants were deleted in ALK fusion positive tumors. And some of them showed copy number gain of fusion gene. In addition, clustered genomic number changes within 2p were more frequently encountered in ALK fusion positive tumors compared with fusion negative ones.

    Conclusion
    Copy number changes within the genomic region including EML4 and ALK are particular findings in ALK fusion positive tumors. In addition, genomic structure of the short arm of chromosome 2 was more unstable than ALK fusion negative tumors. We speculate that clustered chromosomal rearrangements of the short arm of chromosome 2 contribute to EML4-ALK gene fusion.