title: [Studies of the origin of malignant rhabdoid tumor(MRT)--experimental researches on the MRT evolving in nude mice inoculated with violently variable HeLa cells].
abstract: Under the prerequisite that the incidence of cancer or tumor in negatively-controlled nude mice inoculated subcutaneously with feline or canine kidney cell cultures purified in vitro at passage 3 or higher (the modal chromosome number of FKC on passage 3 was 38 of diploid at the rate of 80%) was 0%(0/22) and 0%(0/10) respectively, and the incidence of progressively negative growing tumor in controlled nude mice inoculated subcutaneously with repeatedly-frozen- and thawed-HeLa cell cultures of X strain was 20%(1/5), the negative growing malignant tumor (MT) was found in half of the nude mice inoculated subcutaneously with HeLa cell cultures of H strain(with modal chromosome number of 78 +/- 2 of sub-tetraploid at the rate of 40%), the progressively-growing malignant tumor was found in all the other 40 nude mice inoculated subcutaneously with HeLa cell cultures of other strains, with the incidence of MT in nude mice with KB strain (with modal chromosome number of 60 +/- 3 of hyperdiploid at the rate of 72%-76%) 10/10, the incidence of poorly-differentiated MT originated from epithelia in nude mice with X strain (with modal chromosomal number of 62 +/- 3 of hyperdiploid at the rate of 69%) 25/25, and the incidence of MRT in nude mice with in vitro cultured tumor cell NM20/X strain (with modal chromosome number of 68 +/- 3 of both hyperdiploid and subtetraploid at the rate of 52%) 5/5. After being continuously cultivated for 20 passages in vitro, HeLa cell of X strain was subcutaneously inoculated into nude mice and cultivated for 1 passage in vivo within 15 days, and then the developed growing MT was collected as HeLa cell of NM20/X strain on passage 0 and continuously cultivated for 11 passages to prepare for transplanting into nude mice again. Therefore, the highly variable strain of HeLa cells can be successfully selected by alternate cultivation in vitro and in vivo. Occasionally in another experiment, the progressively-growing MRT was found in all the 4 nude mice of one test group inoculated subcutaneously with 0.17 ml cell-cultures of super-high density containing 12.75 x 10(7) HeLa cells of KB strain on passages 10-11(with the rate of chromosome aberration high to 20% on passages 10-11 including 18% dicentric chromosome and 2% breakage chromosome). Although the incidence of MRT in nude mice inoculated subcutaneously with violently variable HeLa cells of NM20/X strain on passage 11, HeLa cells of KB strain on passages 10-11 reaches 100%(5/5) & 100%(4/4) respectively, yet it is requested that the inoculated live cell number is huge (5-12 x 10(7) cells per nude mouse), the tumor emerges immediately, develops violently, grows very fast, and has an extremely aggressive malignancy, the tumor is rich in the blood vessel giving a full supply of blood for it, and the mean value of major diameter X minor diameter of the tumor is essentially up to the standard of 30 mm x 20 mm in 16-22 days after the inoculation of the cells into the nude mice. The first finding of MRT in model animals provides an opportunity for answering the origin problem of MRT. Based on this reason, human uterus vertical epithelium may be an original tissue of MRT, thus opening up a new era for the research of MRT origin. It is also concluded as follows: 1. Cellular tumorigenicity is different among differently-karyotypic cells. 2. Highly variable strain of tumor cell line can be selected quickly and successfully in nude mouse. 3. Cellular tumorigenicity may be increased if chromosome aberration is very high. 4. The genetic characteristics of chromosomes of HeLa cells determines their tumorigenicity, chromosome number variation of HeLa cells has positive relationship with their carcinogenesis or tumorigenicity, and the turn of HeLa cells concerning their tumorigenicity from weak to strong is KB, X and NM20/X strains (excluding H strain, in which tumorigenicity remains to be determined by further experiments) respectively.
authors.affiliation: Peking University Health Science Center, Beijing 100083, China.
authors.forename: D L
authors.initials: DL
authors.lastname: Zhang
authors.forename: G S
authors.initials: GS
authors.lastname: Huang
authors.forename: L J
authors.initials: LJ
authors.lastname: Li
authors.forename: X Y
authors.initials: XY
authors.lastname: He
authors.forename: G T
authors.initials: GT
authors.lastname: Xia
authors.forename: B X
authors.initials: BX
authors.lastname: Gao
authors.forename: X H
authors.initials: XH
authors.lastname: Bai
authors.forename: S G
authors.initials: SG
authors.lastname: Liu
mesh_terms: D000818:Animals; D002415:Cats; D004285:Dogs; D006367:HeLa Cells; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D018335:Rhabdoid Tumor / Q000209:etiology* / Q000235:genetics / Q000473:pathology