Lundgren R, Mandahl N, Heim S, Limon J, Henrikson H, Mitelman F
Department of Urology, University Hospital, Lund, Sweden.
Genes Chromosomes Cancer. 1992 Jan;4(1):16-24. doi: 10.1002/gcc.2870040103.
Cytogenetic analysis after short-term culture in vitro of primary tumor samples was attempted in 82 patients with prostatic cancer. Tumor material was obtained by radical prostatectomy or transurethral resection. Successful cytogenetic studies were performed on 57 tumors of which five were well, 30 moderately, and 22 poorly differentiated adenocarcinomas. Only normal karyotypes were found in 24 tumors. Structural nonclonal aberrations were detected in 18 and clonal karyotypic abnormalities in 15 tumors. The most common clonal numerical aberration was loss of the Y chromosome; a missing Y was found in six tumors, in three of these as the sole anomaly. Clonal structural chromosomal rearrangements, usually accompanied by numerical changes, were detected in 12 tumors. The rearrangements involved 18 of the 22 autosomes and the X chromosome. Chromosomes 1, 7, and 10 were most frequently affected. Deletions, duplications, inversions, insertions, and balanced as well as unbalanced translocations were represented. The breakpoints in chromosome 1 were scattered along both the short and long arms with no obvious clustering, whereas those in chromosomes 7 and 10 were clustered at bands 7q22 (two deletions and two duplications in four different tumors) and 10q24 (two translocations, one deletion, and one inversion in four tumors). One additional tumor displayed a derivative chromosome 10 with a breakpoint in 10q23, and one had monosomy 10. Altogether, these abnormalities resulted in loss of 10q24----qter in five tumors. Monosomy 8 and rearrangements of the short arm of chromosome 8 leading to loss of 8p21----pter were seen in four tumors. Double minute chromosomes were found in two tumors.
对82例前列腺癌患者的原发性肿瘤样本进行体外短期培养后的细胞遗传学分析。肿瘤组织通过根治性前列腺切除术或经尿道切除术获取。对57例肿瘤进行了成功的细胞遗传学研究,其中5例为高分化、30例为中分化、22例为低分化腺癌。24例肿瘤仅发现正常核型。18例检测到结构非克隆性畸变,15例肿瘤检测到克隆性核型异常。最常见的克隆性数目畸变是Y染色体缺失;6例肿瘤发现Y染色体缺失,其中3例以此为唯一异常。12例肿瘤检测到克隆性结构染色体重排,通常伴有数目改变。重排涉及22条常染色体中的18条和X染色体。1号、7号和10号染色体最常受累。出现了缺失、重复、倒位、插入以及平衡和不平衡易位。1号染色体的断点沿短臂和长臂分散,无明显聚集,而7号和10号染色体的断点聚集在7q22带(4例不同肿瘤中有2例缺失和2例重复)和10q24带(4例肿瘤中有2例易位、1例缺失和1例倒位)。另外1例肿瘤显示10号衍生染色体,断点在10q23,1例有10号染色体单体。总之,这些异常导致5例肿瘤中10q24→qter缺失。4例肿瘤出现8号染色体单体和8号染色体短臂重排导致8p21→pter缺失。2例肿瘤发现双微体染色体。