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Characterization of human laryngeal primary and metastatic squamous cell carcinoma cell lines UM-SCC-17A and UM-SCC-17B.

Cancer research (1989-11-01)
T E Carey, D L Van Dyke, M J Worsham, C R Bradford, V R Babu, D R Schwartz, S Hsu, S R Baker
RÉSUMÉ

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.