Wolman S R, Lanfrancone L, Dalla-Favera R, Ripley S, Henderson A S
Cancer Genet Cytogenet. 1985 Jun;17(2):133-41. doi: 10.1016/0165-4608(85)90023-8.
HL-60, a cell line derived from a human promyelocytic leukemia, shows amplification of the oncogene c-myc. Chromosome aberrations reported in HL-60 include double minutes (DMs) and an abnormally banded region (ABR) on chromosome #8. A relationship between these chromosomal aberrations and amplification of c-myc DNA has been suggested. We report the localization by cytologic hybridization of amplified c-myc DNA to a marker chromosome, M3q+, in an early passage of HL-60. The localization of c-myc to an ABR on an 8q+ chromosome was confirmed in later passage clones. The most probable derivation of the M3q+ chromosome is t(5p;17q) with additional material associated with c-myc amplification inserted into 17q. This localization is of interest in light of the association between t(15:17) and promyelocytic leukemia. The results indicate that amplification and chromosome integration can occur at a site other than the native gene locus and at different integration sites in different lineages of the same tumor.
HL-60是一种源自人类早幼粒细胞白血病的细胞系,显示癌基因c-myc扩增。HL-60中报道的染色体畸变包括双微体(DMs)和8号染色体上的异常带纹区域(ABR)。有人提出这些染色体畸变与c-myc DNA扩增之间存在关联。我们报告了在HL-60早期传代中,通过细胞杂交将扩增的c-myc DNA定位到一条标记染色体M3q+上。在后期传代克隆中证实了c-myc定位于8q+染色体上的ABR。M3q+染色体最可能的来源是t(5p;17q),有与c-myc扩增相关的额外物质插入到17q中。鉴于t(15:17)与早幼粒细胞白血病之间的关联,这一定位很有意思。结果表明,扩增和染色体整合可发生在天然基因座以外的位点,且在同一肿瘤的不同谱系中发生在不同的整合位点。