Molecular genetic evidence of an independent origin of serous low malignant potential implants and lymph node inclusions
Molecular genetic evidence of an independent origin of serous low malignant potential implants and lymph node inclusions
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DOI：
10.1097/pgp.0b013e3180336287
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发表时间：
2007-10-01
影响因子：
2.4
通讯作者：
Cheng, Liang
中科院分区：
文献类型：
--
作者：
Emerson, Robert E.;Wang, Mingsheng;Cheng, Liang
患有低度恶性潜能（LMP）卵巢浆液性肿瘤的患者通常发现有腹膜植入物。不太常见的是，类似的病变也可见于淋巴结，有时与输卵管内膜异位症有关。我们将这些病变与共存的卵巢 LMP 肿瘤进行比较，以确定它们是否与卵巢肿瘤有克隆相关。确定了 17 名患者的 2 个或更多部位存在浆液性 LMP 肿瘤。从福尔马林固定、石蜡包埋的组织块中显微解剖组织样本。获得正常组织、卵巢 LMP 肿瘤、腹膜 LMP 植入物和淋巴结内 LMP 包涵体的样本。从样本中提取基因组 DNA，并进行聚合酶链式反应和 X 染色体失活（人类雄激素受体测定）分析。 17 例中的 15 例可以确定 X 染色体失活模式，其中 13 例观察到非随机 X 染色体失活。其中 12 例包括卵巢和卵巢外 LMP 肿瘤。在这 12 例中的 9 例中，卵巢外 LMP 肿瘤与卵巢肿瘤具有相似的非随机 X 染色体失活模式。在这些病例中，共有的失活模式见于 1 个卵巢外部位（3 例）、2 个卵巢外部位（4 例）、5 个卵巢外部位（1 例）和 8 个卵巢外部位中的 7 个（1 例）。在其余 3 例中，观察到相反的非随机 X 染色体失活模式。这些数据表明，在大多数情况下，浆液性 LMP 肿瘤植入物和淋巴结内含物与相关卵巢肿瘤具有共同的克隆起源。然而，至少在某些情况下，植入物和内含物似乎独立于相关的卵巢浆液性 LMP 肿瘤。
Patients with ovarian serous tumors of low malignant potential (LMP) are commonly found to have peritoneal implants. Less commonly, similar lesions are seen in lymph nodes, sometimes in association with endosalpingiosis. We compared these lesions to the coexisting ovarian LMP tumors to determine whether they are clonally related to the ovarian neoplasm. Seventeen patients with serous LMP tumors present at 2 or more sites were identified. Tissue samples were microdissected from formalin-fixed paraffin-embedded tissue blocks. Samples of normal tissue, the ovarian LMP tumors, peritoneal LMP implants, and LMP inclusions within lymph nodes were obtained. Genomic DNA was, extracted from the samples, and polymerase chain reaction and X-chromosome inactivation (human androgen receptor assay) analysis were performed. The pattern of X-chromosome inactivation could be determined in 15 of the 17 cases, and nonrandom X-chromosome inactivation was observed in 13 of these cases. Twelve of these cases included both, ovarian and extraovarian LMP tumors. In 9 of these 12 cases, the extraovarian LMP tumor shared a similar pattern of nonrandom X-chromosome inactivation with the ovarian tumor. In these cases, the shared inactivation pattern was seen at 1 extraovarian site (3 cases), 2 extraovarian sites (4 cases), 5 extraovarian sites (1 case), and 7 of 8 extraovarian sites (1 case). In the remaining 3 cases, opposite patterns of nonrandom X-chromosome inactivation were seen. These data suggest that, in most cases, serous LMP tumor implants and lymph node inclusions share a common clonal origin with the associated ovarian tumors. However, in at least some cases, the implants and inclusions seem to arise independently from the associated ovarian serous LMP tumors.