Locus/Chromosome aberrations in intraductal papillary mucinous neoplasms analyzed by fluorescence in situ hybridization.
Locus/Chromosome aberrations in intraductal papillary mucinous neoplasms analyzed by fluorescence in situ hybridization.
复制标题
通过荧光原位杂交分析导管内乳头状粘液性肿瘤中的位点/染色体畸变。
DOI：
10.1097/pas.0000000000000360
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Inagaki H.
中科院分区：
文献类型：
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作者：
Miyabe K;Hori Y;Nakazawa T;Hayashi K;Naitoh I;Shimizu S;Kondo H;Nishi Y;Yoshida M;Umemura S;Kato A;Ohara H;Joh T;Inagaki H.
导管内乳头状黏液性肿瘤(IPMN)的基因定位和染色体异常尚不清楚。这项研究的目的是用荧光原位杂交回溯性地检查这些异常。将28例IPMN分为非侵袭性IPMN组(n=17)和伴侵袭性癌(侵袭性IPMN)组(n=11)。非侵袭性IPMN在组织中有非肿瘤性和非侵袭性斑点，侵袭性IPMN有非肿瘤性、非侵袭性和侵袭性斑点。然后分析非肿瘤性(n=28)、非侵袭性(n=28)和侵袭性(n=11)斑点3、6、7、8、17和18号染色体的非整倍体以及p16和p53基因座的缺失。多态6和p16缺失在非侵袭性斑块中的发生率显著高于非肿瘤性斑块。侵袭性斑块中7号染色体多态、18号染色体多态、p16基因缺失和p53基因缺失的发生率明显高于非侵袭性斑块。对侵袭性IPMN的诊断敏感性为90.9%，特异性为94.1%，准确性为92.5%。我们的研究提示：(1)多态6和p16缺失可能与IPMN的腺瘤性改变有关；(2)多态7、多态18、p16缺失和P53缺失在非侵袭性IPMN恶变中起作用；(3)多态7和P53缺失可能是诊断侵袭性IPMN的良好标志物。
Locus and chromosome abnormalities have not been well clarified in intraductal papillary mucinous neoplasms (IPMNs). The aim of this study was to retrospectively examine these abnormalities using fluorescence in situ hybridization. IPMNs (n= 28) were histopathologically classified into noninvasive IPMN (n= 17) and IPMN with an associated invasive carcinoma (invasive IPMN, n= 11) groups. Noninvasive IPMNs possessed non-neoplastic and noninvasive spots in their tissues, and invasive IPMN cases possessed non-neoplastic, noninvasive, and invasive spots. Non-neoplastic (n= 28), noninvasive (n= 28), and invasive (n= 11) spots were then analyzed for aneuploidy of chromosomes 3, 6, 7, 8, 17, and 18 and deletions of p16 and p53 loci. Polysomy 6 and p16 deletion were significantly more frequent in noninvasive than in non-neoplastic spots. Polysomy 7, polysomy 18, p16 deletion, and p53 deletion were significantly more frequent in invasive than in noninvasive spots. Detection of polysomy 7 and p53 deletion gave a high diagnostic accuracy for invasive IPMN (sensitivity, 90.9%; specificity, 94.1%; and accuracy, 92.5%). Our study suggests that:(1) polysomy 6 and p16 deletion may contribute to adenomatous change of IPMN;(2) polysomy 7, polysomy 18, p16 deletion, and p53 deletion play roles in malignant transformation of noninvasive IPMN; and (3) polysomy 7 and p53 deletion may be excellent diagnostic markers for invasive IPMN.