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人类前列腺癌中视网膜母细胞瘤和腺瘤性息肉病易感基因位点以及10号染色体短臂、10号染色体长臂和16号染色体长臂的杂合性缺失。

Loss of heterozygosity of the retinoblastoma and adenomatous polyposis susceptibility gene loci and in chromosomes 10p, 10q and 16q in human prostate cancer.

作者信息

Phillips S M, Morton D G, Lee S J, Wallace D M, Neoptolemos J P

机构信息

Department of Surgery Laboratory, Queen Elizabeth Hospital, Birmingham, UK.

出版信息

Br J Urol. 1994 Apr;73(4):390-5. doi: 10.1111/j.1464-410x.1994.tb07602.x.

DOI:10.1111/j.1464-410x.1994.tb07602.x
PMID:7911059
Abstract

OBJECTIVE

To examine prostate tumours for losses of known or suspected tumour suppressor genes to determine some of the important events in the genesis of this common cancer.

MATERIALS AND METHODS

Paired tumour and blood samples were obtained from 21 patients who underwent transurethral resection of malignant prostate glands for urinary outflow obstruction. Paired tumour and normal tissue (leucocytes) DNA was extracted and examined for possible losses of several known or suspected tumour suppressor genes, using restriction fragment length polymorphism techniques to detect loss of heterozygosity.

RESULTS

Deletions of the retinoblastoma susceptibility gene (RB1) locus were found in six of nine informative cases using two intragenic probes (p68RS2.0 and p123m1.8). The locus related to the familial adenomatous polyposis susceptibility (APC) gene demonstrated loss of heterozygosity in three of seven informative cases using the EF5.44 probe. Losses were also noted in loci on chromosome 10p in four of 19 informative cases (probe cTBQ7), chromosome 10q in eight out of 19 informative cases (probes EFD75 and D10S90) and in 16q in three of 17 informative cases (probe D16S7).

CONCLUSION

These findings suggest that losses of the RB1 and APC tumour suppressor genes and suspected tumour suppressor genes on 10p, 10q and 16q may be important events in the genesis of prostatic tumours.

摘要

目的

检测前列腺肿瘤中已知或疑似肿瘤抑制基因的缺失情况,以确定这种常见癌症发生过程中的一些重要事件。

材料与方法

从21例因尿流梗阻接受经尿道前列腺恶性肿瘤切除术的患者中获取肿瘤和血液配对样本。提取肿瘤和正常组织(白细胞)配对DNA,使用限制性片段长度多态性技术检测杂合性缺失,以检查几种已知或疑似肿瘤抑制基因是否可能缺失。

结果

使用两种基因内探针(p68RS2.0和p123m1.8),在9例信息充足的病例中有6例发现视网膜母细胞瘤易感基因(RB1)位点缺失。使用EF5.44探针,在7例信息充足的病例中有3例发现与家族性腺瘤性息肉病易感(APC)基因相关的位点杂合性缺失。在19例信息充足的病例中有4例(探针cTBQ7)在10号染色体短臂位点发现缺失,19例信息充足的病例中有8例(探针EFD75和D10S90)在10号染色体长臂位点发现缺失,17例信息充足的病例中有3例(探针D16S7)在16号染色体位点发现缺失。

结论

这些发现表明,RB1和APC肿瘤抑制基因以及10号染色体短臂、10号染色体长臂和16号染色体上疑似肿瘤抑制基因的缺失可能是前列腺肿瘤发生过程中的重要事件。

相似文献

1
Loss of heterozygosity of the retinoblastoma and adenomatous polyposis susceptibility gene loci and in chromosomes 10p, 10q and 16q in human prostate cancer.人类前列腺癌中视网膜母细胞瘤和腺瘤性息肉病易感基因位点以及10号染色体短臂、10号染色体长臂和16号染色体长臂的杂合性缺失。
Br J Urol. 1994 Apr;73(4):390-5. doi: 10.1111/j.1464-410x.1994.tb07602.x.
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Allelic loss of chromosomes 16q and 10q in human prostate cancer.人类前列腺癌中16号染色体和10号染色体的等位基因缺失。
Proc Natl Acad Sci U S A. 1990 Nov;87(22):8751-5. doi: 10.1073/pnas.87.22.8751.
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Somatic allelic loss at the DCC, APC, nm23-H1 and p53 tumor suppressor gene loci in human prostatic carcinoma.人类前列腺癌中DCC、APC、nm23-H1和p53肿瘤抑制基因位点的体细胞等位基因缺失。
J Urol. 1994 Apr;151(4):1073-7. doi: 10.1016/s0022-5347(17)35186-8.
4
Loss of heterozygosity on chromosomes 10 and 17 in clinically localized prostate carcinoma.临床局限性前列腺癌中10号和17号染色体杂合性缺失
Prostate. 1996 May;28(5):275-81. doi: 10.1002/(SICI)1097-0045(199605)28:5<275::AID-PROS1>3.0.CO;2-B.
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Distinct areas of allelic loss on chromosomal regions 10p and 10q in human prostate cancer.人类前列腺癌中10号染色体区域10p和10q上等位基因缺失的不同区域。
Cancer Res. 1996 May 15;56(10):2263-7.
6
Loss of the retinoblastoma susceptibility gene (RB1) is a frequent and early event in prostatic tumorigenesis.视网膜母细胞瘤易感基因(RB1)的缺失是前列腺肿瘤发生过程中常见的早期事件。
Br J Cancer. 1994 Dec;70(6):1252-7. doi: 10.1038/bjc.1994.482.
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Genetic changes associated with prostate cancer in humans.
Cancer Surv. 1991;11:15-24.
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Three distinct commonly deleted regions of chromosome arm 16q in human primary and metastatic prostate cancers.人类原发性和转移性前列腺癌中16号染色体长臂的三个不同的常见缺失区域。
Genes Chromosomes Cancer. 1996 Dec;17(4):225-33. doi: 10.1002/(SICI)1098-2264(199612)17:4<225::AID-GCC4>3.0.CO;2-5.
9
P53 mutations and loss of heterozygosity on chromosomes 8p, 16q, 17p, and 18q are confined to advanced prostate cancer.8号染色体、16号染色体、17号染色体和18号染色体上的P53突变及杂合性缺失仅限于晚期前列腺癌。
Anticancer Res. 1994 Nov-Dec;14(6B):2785-90.
10
Recessive genetic mechanisms in the oncogenesis of prostatic carcinoma.前列腺癌发生过程中的隐性遗传机制。
Scand J Urol Nephrol Suppl. 1991;138:93-6.

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