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1
Functional deficiency of fibroblasts heterozygous for Bloom syndrome as specific manifestation of the primary defect.布鲁姆综合征杂合子成纤维细胞的功能缺陷作为原发性缺陷的特异性表现。
Am J Hum Genet. 1981 Nov;33(6):928-34.
2
Mutagen-induced sister chromatid exchange rate in Bloom syndrome remains unaltered in the presence of Bloom corrective factor.在存在布鲁姆校正因子的情况下，诱变剂诱导的布鲁姆综合征中的姐妹染色单体交换率保持不变。
Hum Genet. 1981;58(4):432-3. doi: 10.1007/BF00282831.
3
Roles of DNA interstrand crosslinking and its repair in the induction of sister-chromatid exchange and a higher induction in Fanconi's anemia cells.DNA链间交联及其修复在诱导姐妹染色单体交换中的作用以及范科尼贫血细胞中的更高诱导作用。
Mutat Res. 1981 May;81(3):365-75. doi: 10.1016/0027-5107(81)90123-8.
4
Different sensitivities to ultraviolet light-induced cytotoxicity and sister chromatid exchanges in xeroderma pigmentosum and Bloom's syndrome fibroblasts.着色性干皮病和布卢姆综合征成纤维细胞对紫外线诱导的细胞毒性和姐妹染色单体交换的不同敏感性。
Photodermatol. 1989 Jun;6(3):124-30.
5
Cytogenetic demonstration of a corrective factor in Bloom's syndrome.
IARC Sci Publ. 1982(39):137-45.
6
Bloom's syndrome: in vitro correction of the sister chromatid exchange rate by normal cells.布卢姆综合征：正常细胞对姐妹染色单体交换率的体外校正
Cancer Genet Cytogenet. 1984 Jun;12(2):139-43. doi: 10.1016/0165-4608(84)90125-0.
7
Heterozygous manifestations in four autosomal recessive human cancer-prone syndromes: ataxia telangiectasia, xeroderma pigmentosum, Fanconi anemia, and Bloom syndrome.四种常染色体隐性人类癌症易患综合征中的杂合子表现：共济失调毛细血管扩张症、着色性干皮病、范可尼贫血和布卢姆综合征。
Mutat Res. 1992 Dec 1;284(1):25-36. doi: 10.1016/0027-5107(92)90022-t.
8
Disparate effects of 5-bromodeoxyuridine on sister-chromatid exchanges and chromosomal aberrations in Bloom syndrome fibroblasts.5-溴脱氧尿苷对布卢姆综合征成纤维细胞中姐妹染色单体交换和染色体畸变的不同影响。
Mutat Res. 1988 Mar;198(1):241-53. doi: 10.1016/0027-5107(88)90061-9.
9
Rate of sister chromatid exchanges in Bloom syndrome fibroblasts reduced by co-cultivation with normal fibroblasts.通过与正常成纤维细胞共培养，布卢姆综合征成纤维细胞中姐妹染色单体交换率降低。
Am J Hum Genet. 1980 Mar;32(2):150-7.
10
Analyses of bromodeoxyuridine-associated sister chromatid exchanges (SCEs) in Bloom syndrome based on cell fusion: single and twin SCEs in endoreduplication.基于细胞融合对布卢姆综合征中溴脱氧尿苷相关姐妹染色单体交换（SCEs）的分析：核内复制中的单SCE和双SCE
Proc Natl Acad Sci U S A. 1983 Jul;80(14):4369-73. doi: 10.1073/pnas.80.14.4369.

引用本文的文献

1
Mutagen-induced sister chromatid exchange rate in Bloom syndrome remains unaltered in the presence of Bloom corrective factor.在存在布鲁姆校正因子的情况下，诱变剂诱导的布鲁姆综合征中的姐妹染色单体交换率保持不变。
Hum Genet. 1981;58(4):432-3. doi: 10.1007/BF00282831.
2
Heterozygous carriers for Bloom syndrome exhibit a spontaneously increased micronucleus formation in cultured fibroblasts.布卢姆综合征的杂合子携带者在培养的成纤维细胞中表现出自发性微核形成增加。
Hum Genet. 1984;67(1):52-5. doi: 10.1007/BF00270558.

本文引用的文献

1
High rate of sister chromatid exchanges of Bloom's syndrome chromosomes is corrected in rodent human somatic cell hybrids.布卢姆综合征染色体的姐妹染色单体交换高发生率在啮齿动物-人类体细胞杂种中得到纠正。
Cytogenet Cell Genet. 1980;27(1):8-23. doi: 10.1159/000131459.
2
Rate of sister chromatid exchanges in Bloom syndrome fibroblasts reduced by co-cultivation with normal fibroblasts.通过与正常成纤维细胞共培养，布卢姆综合征成纤维细胞中姐妹染色单体交换率降低。
Am J Hum Genet. 1980 Mar;32(2):150-7.
3
Sister chromatid exchange in cells metabolically coupled to Bloom's syndrome cells.与布卢姆综合征细胞代谢偶联的细胞中的姐妹染色单体交换
Nature. 1980 Mar 6;284(5751):72-4. doi: 10.1038/284072a0.
4
A manyfold increase in sister chromatid exchanges in Bloom's syndrome lymphocytes.布卢姆综合征淋巴细胞中姐妹染色单体交换的多重增加。
Proc Natl Acad Sci U S A. 1974 Nov;71(11):4508-12. doi: 10.1073/pnas.71.11.4508.
5
Cytogenetic investigations in a new case of Bloom's syndrome.对一例新的布卢姆综合征病例进行细胞遗传学研究。
Hum Genet. 1976 Jan 28;31(1):47-52. doi: 10.1007/BF00270398.
6
Induction by alkylating agents of sister chromatid exchanges and chromatid breaks in Fanconi's anemia.烷化剂诱导范可尼贫血患者的姐妹染色单体交换和染色单体断裂
Proc Natl Acad Sci U S A. 1975 Oct;72(10):4066-70. doi: 10.1073/pnas.72.10.4066.
7
A retarded rate of DNA chain growth in Bloom's syndrome.布卢姆综合征中DNA链生长速率迟缓。
Proc Natl Acad Sci U S A. 1975 Feb;72(2):758-62. doi: 10.1073/pnas.72.2.758.
8
Chromatid exchanges in ataxia telangiectasia, Bloom syndrome, Werner syndrome, and xeroderma pigmentosum.共济失调毛细血管扩张症、布卢姆综合征、沃纳综合征和着色性干皮病中的染色单体交换。
Ann Hum Genet. 1976 Jul;40(1):79-86. doi: 10.1111/j.1469-1809.1976.tb00166.x.
9
Susceptibility of Fanconi's anaemia fibroblasts to chromosome damage by carcinogens.
Nature. 1976 Jun 10;261(5560):494-6. doi: 10.1038/261494a0.
10
Bloom's syndrome. V. Surveillance for cancer in affected families.布卢姆综合征。五、对患病家族进行癌症监测。
Clin Genet. 1977 Sep;12(3):162-8. doi: 10.1111/j.1399-0004.1977.tb00919.x.

布鲁姆综合征杂合子成纤维细胞的功能缺陷作为原发性缺陷的特异性表现。

Functional deficiency of fibroblasts heterozygous for Bloom syndrome as specific manifestation of the primary defect.

作者信息

Bartram C R, Rüdiger H W, Schmidt-Preuss U, Passarge E

出版信息

Am J Hum Genet. 1981 Nov;33(6):928-34.

PMID:7325155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1685170/
Abstract

The effect on the rate of sister chromatid exchanges (SCEs) in Bloom syndrome fibroblasts by cocultivation with Fanconi anemia and xeroderma pigmentosum fibroblasts and with Bloom syndrome heterozygotes was studied. Cells of Fanconi anemia and xeroderma origin reduced the rate of SCEs in Bloom cells by about 45%-50%, just as control cells do. In contrast, heterozygous Bloom cells reduced the rate of SCEs by only 16%-28%. In absolute figures, Fanconi cells reduced the mean rate of SCE in Bloom cells from 55.7 +/- 5.50- to 27.7 +/- 6.44, xeroderma cells to 30.5 +/- 5.73, and control cells to 28.3 +/- 5.35. Three different cell strains from Bloom syndrome heterozygotes reduced the rate to 40.1 +/- 8.81, 47.0 +/= 6.94, and 47.5 +/- 8.32. There was no effect on any of these cell strains by Bloom syndrome fibroblasts. We interpret the functional deficiency of heterozygous Bloom syndrome fibroblasts as a gene dosis effect. It probably represents a specific manifestation of the yet unknown primary defect, because it suggests the existence of a "corrective factor" that is inactive or absent in homozygous Bloom cells and reduced in heterozygotes. It may be identical with or closely related to the normal gene product at the Bloom locus.

摘要

研究了将布卢姆综合征成纤维细胞与范可尼贫血、着色性干皮病成纤维细胞以及布卢姆综合征杂合子共培养，对布卢姆综合征成纤维细胞姐妹染色单体交换（SCE）率的影响。范可尼贫血和着色性干皮病来源的细胞使布卢姆细胞的SCE率降低了约45%-50%，与对照细胞的作用相同。相比之下，布卢姆综合征杂合细胞仅使SCE率降低了16%-28%。从绝对值来看，范可尼细胞使布卢姆细胞的SCE平均率从55.7±5.50降至27.7±6.44，着色性干皮病细胞使其降至30.5±5.73，对照细胞使其降至28.3±5.35。来自布卢姆综合征杂合子的三种不同细胞株将SCE率分别降至40.1±8.81、47.0±6.94和47.5±8.32。布卢姆综合征成纤维细胞对这些细胞株均无影响。我们将杂合性布卢姆综合征成纤维细胞的功能缺陷解释为基因剂量效应。它可能代表了尚未明确的原发性缺陷的一种特定表现形式，因为这表明存在一种“校正因子”，该因子在纯合性布卢姆细胞中无活性或不存在，而在杂合子中减少。它可能与布卢姆基因座处的正常基因产物相同或密切相关。