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Atypon Free PMC Article

Mol Cell Biol. 1992 Apr;12(4):1747-54. doi: 10.1128/mcb.12.4.1747-1754.1992.

Complex intrachromosomal rearrangement in the process of amplification of the L-myc gene in small-cell lung cancer.

Molecular and cellular biology

Y Sekido, T Takahashi, T P Mäkelä, Y Obata, R Ueda, T Hida, K Hibi, K Shimokata, K Alitalo, T Takahashi

Affiliations

  1. First Department of Internal Medicine, Nagoya University School of Medicine, Japan.

PMID: 1312669 PMCID: PMC369618 DOI: 10.1128/mcb.12.4.1747-1754.1992
Free PMC Article

Abstract

The L-myc gene was first isolated from a human small-cell lung cancer (SCLC) cell line on the basis of its amplification and sequence similarity to c-myc and N-myc. A new mechanism of L-myc activation which results from the production of rlf-L-myc fusion protein was recently reported. On the basis of our earlier observation of a rearrangement involving amplified L-myc in an SCLC cell line, ACC-LC-49, we decided to investigate this rearrangement in detail along with the structure of L-myc amplification units in five additional SCLC cell lines. We report here the identification of a novel genomic region, termed jal, which is distinct from rlf and is juxtaposed to and amplified with L-myc during the process of DNA amplification of the region encompassing L-myc. Long-range analysis using pulsed-field gel electrophoresis revealed that the amplified L-myc locus is involved in highly complex intrachromosomal rearrangements with jal and/or rlf. Our results also suggest that the simultaneous presence of rearrangements both in rlf intron 1 and in regions immediately upstream of L-myc may be necessary for the expression of rlf-L-myc chimeric transcripts.

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