Carey T E, Van Dyke D L, Worsham M J, Bradford C R, Babu V R, Schwartz D R, Hsu S, Baker S R
Department of Otolaryngology/Head and Neck Surgery, University of Michigan, Ann Arbor 48109-0506.
Cancer Res. 1989 Nov 1;49(21):6098-107.
The squamous cell carcinoma (SCC) cell lines UM-SCC-17A and -17B were derived, respectively, from the primary laryngeal cancer and a metastatic neck tumor of a patient who failed to respond to radiation therapy but achieved long-term remission after surgery. The karyotypes of both cell lines and a subline of 17A were pseudodiploid and stable in multiple in vitro passages. Several karyotypic abnormalities were common to all three cell lines and therefore represent mutations present in the tumor before the divergence of the metastatic and subline populations whereas those rearrangements observed only in one cell are more likely to be secondary. The shared mutations include: duplication of the short and proximal long arm of chromosome 2, isochromosome 3q, duplication 7, inversion 8, duplication of the distal long arm of 18, and monosomy 21 or ring 21. Each line had different rearrangements involving chromosome 7 that resulted in three copies of most of the short arm being present in both cell lines, except for high passages of 17B, in which one structurally normal 7 was replaced by a dicentric isochromosome, dic(7)(q11.22), resulting in four copies of 7p. The dic(7) may represent an in vitro mutation. An isochromosome 13q was noted in both the stemline and subline of UM-SCC-17A but not in UM-SCC-17B. A del(11p) and an iso(21q) were present only in the 17A subline. The cell lines expressed the membrane antigen phenotype characteristic of squamous cancers although the UM-SCC-17A subline differed with respect to three markers. Of these, the A9 and blood group antigen changes are thought to be associated with progression. The subline, which carried the del(11)(p13-p15.1), also failed to express the E7 antigen mapped to the band 11p13. It is possible that the two apparently normal 11s in this subline carry a point mutation or microscopically undetected deletion involving the E7 antigen locus.
鳞状细胞癌（SCC）细胞系UM-SCC-17A和-17B分别源自一名喉癌患者的原发性肿瘤和颈部转移瘤，该患者对放疗无反应，但术后实现了长期缓解。这两个细胞系以及17A的一个亚系的核型均为假二倍体，且在多次体外传代中保持稳定。三个细胞系均存在一些常见的核型异常，因此这些异常代表了转移瘤群体和亚系群体分化之前肿瘤中存在的突变，而仅在一个细胞中观察到的那些重排更可能是继发性的。共同的突变包括：染色体2短臂和近端长臂的重复、等臂染色体3q、重复7、倒位8、18号染色体远端长臂的重复以及单体21或环状21。每个细胞系都有涉及染色体7的不同重排，导致两个细胞系中大部分短臂均有三个拷贝，但17B的高代细胞除外，其中一条结构正常的7号染色体被双着丝粒等臂染色体dic(7)(q11.22)取代，导致7p有四个拷贝。dic(7)可能代表一种体外突变。在UM-SCC-17A的主干系和亚系中均发现了等臂染色体13q，但在UM-SCC-17B中未发现。del(11p)和iso(21q)仅存在于17A亚系中。这些细胞系表达了鳞状癌特有的膜抗原表型，尽管UM-SCC-17A亚系在三个标志物方面有所不同。其中，A9和血型抗原的变化被认为与肿瘤进展有关。携带del(11)(p13-p15.1)的亚系也未能表达定位于11p13带的E7抗原。该亚系中两条看似正常的11号染色体可能携带一个点突变或显微镜下未检测到的涉及E7抗原基因座的缺失。
