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前列腺癌细胞遗传学异常的纵向评估:随时间复发的肿瘤显示出非持续性肿瘤和转移性肿瘤之间的中间遗传状态。

Longitudinal evaluation of cytogenetic aberrations in prostatic cancer: tumours that recur in time display an intermediate genetic status between non-persistent and metastatic tumours.

作者信息

Alers J C, Krijtenburg P J, Hop W C, Bolle W A, Schröder F H, van der Kwast T H, Bosman F T, van Dekken H

机构信息

Department of Pathology, Eramus University, Rotterdam, The Netherlands.

出版信息

J Pathol. 1998 Jul;185(3):273-83. doi: 10.1002/(SICI)1096-9896(199807)185:3<273::AID-PATH92>3.0.CO;2-8.


DOI:10.1002/(SICI)1096-9896(199807)185:3<273::AID-PATH92>3.0.CO;2-8
PMID:9771481
Abstract

Only limited data are available on chromosomes specifically involved in prostatic tumour progression. This study has evaluated the cytogenetic status of primary prostatic carcinomas, local tumour recurrences, and distant metastases, representing different time points in prostatic tumour progression. Interphase in situ hybridization (ISH) was applied with a set of (peri) centromeric DNA probes, specific for chromosomes 1, 7, 8 and Y, to routinely processed tissue sections of 73 tumour specimens from 32 patients. Longitudinal evaluation was possible in 11 cases with local recurrence and nine cases with distant metastases. The remaining 12 patients showed no evidence of local recurrence or distant metastasis after radical prostatectomy on follow-up (mean 60.5 months) and served as a reference. Numerical aberrations of at least one chromosome were found in 27 per cent of the local recurrences and 56 per cent of the distant metastases. In decreasing order of frequency, +8, +7, and -Y were observed in the recurrences and +8, +7, -Y, and +1 in the distant metastases. Evaluation of the corresponding primary tumour tissue of the recurrence group showed numerical aberrations in 45 per cent of cases. The aberrations found were, in decreasing order of frequency, -Y, +7, and +8. In the concomitant primary tumour tissue of the distant metastasis group, numerical aberrations were detected in 67 per cent of cases. The aberrations most frequently encountered were +8, -Y, followed by +7. In four cases, a concordance was found between the primary tumour and its recurrence or distant metastasis. Discrepancies might have been caused by cytogenetic heterogeneity. Comparison of the primary tumour tissue of the reference, the recurrence, and the distant metastasis groups showed a significant increase for the percentage of cases with numerical aberrations (Ptrend = 0.02). Likewise, a trend was seen for gain of chromosome 7 and/or 8 (Ptrend < 0.05). The number of DNA aneuploid tumours also increased in these different groups (Ptrend = 0.03). These data suggest that cancers which recur in time display an intermediate position between tumours of disease-free patients and metastatic cancers.

摘要

关于前列腺肿瘤进展中具体涉及的染色体,仅有有限的数据。本研究评估了原发性前列腺癌、局部肿瘤复发和远处转移灶的细胞遗传学状态,它们代表了前列腺肿瘤进展中的不同时间点。运用一组针对1号、7号、8号染色体和Y染色体的(着丝粒周围)着丝粒DNA探针,对32例患者的73个肿瘤标本的常规处理组织切片进行间期原位杂交(ISH)。对11例局部复发和9例远处转移患者进行了纵向评估。其余12例患者在前列腺癌根治术后随访(平均60.5个月)未出现局部复发或远处转移迹象,作为对照。在27%的局部复发和56%的远处转移中发现至少一条染色体的数目异常。按频率递减顺序,在复发中观察到+8、+7和-Y,在远处转移中观察到+8、+7、-Y和+1。对复发组相应的原发性肿瘤组织评估显示,45%的病例存在数目异常。发现的异常按频率递减顺序为-Y、+7和+8。在远处转移组的同期原发性肿瘤组织中,67%的病例检测到数目异常。最常出现的异常是+8、-Y,其次是+7。在4例中,原发性肿瘤与其复发或远处转移之间存在一致性。差异可能是由细胞遗传学异质性引起的。对照、复发和远处转移组的原发性肿瘤组织比较显示,数目异常病例的百分比显著增加(Ptrend = 0.02)。同样,观察到7号和/或8号染色体增加的趋势(Ptrend < 0.05)。这些不同组中DNA非整倍体肿瘤的数量也增加了(Ptrend = 0.03)。这些数据表明,随时间复发的癌症在无病患者的肿瘤和转移性癌症之间处于中间位置。

相似文献

[1]
Longitudinal evaluation of cytogenetic aberrations in prostatic cancer: tumours that recur in time display an intermediate genetic status between non-persistent and metastatic tumours.

J Pathol. 1998-7

[2]
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Lab Invest. 1997-11

[3]
DNA in situ hybridization (interphase cytogenetics) versus comparative genomic hybridization (CGH) in human cancer: detection of numerical and structural chromosome aberrations.

Acta Histochem. 2000-2

[4]
Numerical abnormalities of chromosome 7 in human prostate cancer detected by fluorescence in situ hybridization (FISH) on paraffin-embedded tissue sections with centromere-specific DNA probes.

J Pathol. 1994-4

[5]
Aneusomy of chromosomes 7, 8, and 17 and amplification of HER-2/neu and epidermal growth factor receptor in Gleason score 7 prostate carcinoma: a differential fluorescent in situ hybridization study of Gleason pattern 3 and 4 using tissue microarray.

Hum Pathol. 2001-12

[6]
Identification of numerical chromosome aberrations in archival tumours by in situ hybridization to routine paraffin sections: evaluation of 23 phaeochromocytomas.

J Pathol. 1993-11

[7]
Histological preservation after in situ hybridization to archival solid tumour sections allows discrimination of cells bearing numerical chromosome changes.

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[8]
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[9]
[Significance of numerical chromosome aberrations in prostate cancer].

Verh Dtsch Ges Pathol. 1993

[10]
Fluorescence in situ hybridization analysis of matched primary tumour and lymph-node metastasis of D1 (pT2-3pN1M0) prostate cancer.

BJU Int. 2004-8

引用本文的文献

[1]
High-resolution analysis of paraffin-embedded and formalin-fixed prostate tumors using comparative genomic hybridization to genomic microarrays.

Am J Pathol. 2003-3

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