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体细胞杂种中致瘤性的抑制。IV. 与D98AH2癌细胞杂种中致瘤性抑制相关的正常人细胞染色体。

Suppression of tumorigenicity in somatic cell hybrids. IV. Chromosomes of normal human cells associated with suppression of tumorigenicity in hybrids with D98AH2 carcinoma cells.

作者信息

Klinger H P, Kaelbling M

出版信息

Cytogenet Cell Genet. 1986;42(4):225-35. doi: 10.1159/000132283.

DOI:10.1159/000132283
PMID:3463446
Abstract

An analysis for cosegregation of chromosomes and tumorigenicity in 52 hybrids of human diploid X D98AH2 human carcinoma-derived cells reveals the consistent presence of four copies of chromosome 11 in all nontumorigenic hybrids (two from each of the parental cells) and a consistent loss of one or two copies of the 11 in all tumor cells derived from tumorigenic hybrids that grow in nude mice. In our earlier study, assays with restriction fragment length polymorphic (RFLP) markers for the cell parent origin of the chromosomes 11 in the hybrids indicated that at least one of the Nos. 11 lost in the tumor cells is from the diploid. Thus both Nos. 11 of the diploid seem to be required for complete and stable suppression of the tumorigenic phenotype. The results of the present study suggest that chromosome 2 may also carry suppressor information, but this causes only partial suppression of the tumorigenic phenotype in the absence of both Nos. 11. On the other hand, when the hybrids contain full complements of the 2 and the 11, suppression is very stable. All other chromosomes except for Nos. 1, 16, 17, 19, and 21 are clearly discordant with suppression. The latter chromosomes are not discordant often enough to allow their exclusion as possible carriers of suppressor information, particularly in the absence of RFLP evaluations. It is clear, however, that if they do carry such information it is not adequate for maintaining a stably suppressed phenotype in the absence of both Nos. 11 of the diploid.

摘要

对52个人二倍体X D98AH2人癌衍生细胞杂交体中的染色体共分离和致瘤性进行分析,结果显示,在所有非致瘤性杂交体中均一致存在4条11号染色体(每条亲代细胞各有两条),而在裸鼠中生长的致瘤性杂交体衍生的所有肿瘤细胞中,11号染色体一致缺失1条或2条。在我们早期的研究中,用限制性片段长度多态性(RFLP)标记对杂交体中11号染色体的细胞亲本来源进行分析,结果表明肿瘤细胞中缺失的至少一条11号染色体来自二倍体。因此,二倍体的两条11号染色体似乎都是完全稳定抑制致瘤表型所必需的。本研究结果表明,2号染色体可能也携带抑制信息,但在两条11号染色体均缺失的情况下,这只会部分抑制致瘤表型。另一方面,当杂交体含有完整的2号和11号染色体时,抑制作用非常稳定。除1号、16号、17号、19号和21号染色体外,所有其他染色体与抑制作用明显不一致。后几条染色体与抑制作用不一致的频率不足以使其被排除为可能的抑制信息携带者,特别是在没有RFLP评估的情况下。然而,很明显,如果它们确实携带此类信息,在二倍体的两条11号染色体均缺失的情况下,这些信息不足以维持稳定抑制的表型。

相似文献

1
Suppression of tumorigenicity in somatic cell hybrids. IV. Chromosomes of normal human cells associated with suppression of tumorigenicity in hybrids with D98AH2 carcinoma cells.体细胞杂种中致瘤性的抑制。IV. 与D98AH2癌细胞杂种中致瘤性抑制相关的正常人细胞染色体。
Cytogenet Cell Genet. 1986;42(4):225-35. doi: 10.1159/000132283.
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2
HeLa D98/aH-2 studied by chromosome painting and conventional cytogenetical techniques.
Chromosoma. 1993 Jul;102(7):473-7. doi: 10.1007/BF00357102.
3
Levels of fos, ets2, and myb proto-oncogene RNAs correlate with segregation of chromosome 11 of normal cells and with suppression of tumorigenicity in human cell hybrids.原癌基因fos、ets2和myb的RNA水平与正常细胞11号染色体的分离以及人细胞杂种中致瘤性的抑制相关。
Mol Cell Biol. 1987 Aug;7(8):2941-6. doi: 10.1128/mcb.7.8.2941-2946.1987.
4
Molecular nature of genetic changes resulting in loss of heterozygosity of chromosome 11 in Wilms' tumours.导致肾母细胞瘤11号染色体杂合性缺失的遗传改变的分子本质。
Hum Genet. 1988 Dec;81(1):41-8. doi: 10.1007/BF00283727.
5
Induction of anchorage-independent growth of human embryonic fibroblasts with a deletion in the short arm of chromosome 11 by human papillomavirus type 16 DNA.16型人乳头瘤病毒DNA诱导11号染色体短臂缺失的人胚胎成纤维细胞形成不依赖贴壁的生长
J Virol. 1988 Dec;62(12):4538-43. doi: 10.1128/JVI.62.12.4538-4543.1988.
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