Dickkopf-4血清蛋白在卵巢浆液性乳头状癌中的表达意义

目的研究Dickkopf-4(DKK-4)血清蛋白在卵巢癌中的表达及意义。方法收集2015年1月至2016年6月在中国医科大学附属盛京医院40例卵巢浆液性乳头状癌和40例正常自愿者血清。采用ELISA的方法检测DKK-4血清蛋白的表达情况,分析其与各临床病理参数的关系。结果 DKK-4蛋白在人卵巢浆液性乳头癌患者血清中的表达含量明显高于正常自愿者血清,其表达含量与卵巢浆液性乳头癌细胞分化程度明显呈正相关。结论 DKK-4蛋白可能参与卵巢浆液性乳头癌发病机制。     

免疫组织化学和电镜在腹膜间皮瘤和浆液性癌鉴别诊断中的价值

上皮样间皮瘤，特别是那些呈乳头状和管状乳头状生长的间皮瘤，与原发性或转移性浆液性乳头状癌弥漫累及腹膜者很难鉴别。1998年一个研究报道有16种标记在间皮瘤的诊断中有一定的价值，该项研究认为，calretinin、thrombomodulin和CK5／6是间皮瘤最好的诊断指标，MOC-31、B72．3、Ber—EP4、CA19—9和Leu—M1（CD15）在间皮瘤中表达阴性，可用于区分腹膜上皮样恶性间皮瘤和乳头状浆液性癌弥漫累及腹膜。D2-40和podoplanin是2个最近认识的淋巴管内皮细胞标记物，它们也表达于正常间皮细胞和间皮瘤。为了比较这两种新的间皮细胞标记和以前其他用于间皮瘤和浆液性癌鉴别诊断的标记的特异性，     

女性盆腔浆液性癌20例临床病理分析

目的：探讨女性盆腔浆液性癌( pelvic serous carcinoma, PSC)的临床病理学特征、免疫表型、发病机制及鉴别诊断。方法回顾性分析20例PSC 的临床病理资料、组织学形态及免疫表型,并复习相关文献。结果20例PSC,年龄23~87岁,平均58.9岁。PSC 可发生于输卵管、卵巢和腹膜,常因腹胀、腹痛或盆腔占位就诊,发现时常广泛累及盆腔多个脏器,不易明确原发部位。输卵管浆液性癌原发灶小,易种植,卵巢和腹膜浆液性癌常伴有浆液性输卵管上皮内癌(serous tubal intraepithelial carcinoma, STIC)。结论输卵管黏膜上皮细胞可能是PSC 的主要来源。诊断PSC 时需仔细检查输卵管以明确其原发部位,病变广泛累及腹膜时需与腹膜间皮瘤和盆腔外腺癌腹膜转移相鉴别。     

miRNA-200c在IIIc期卵巢浆液性囊腺癌中的表达及其参与癌转移中的作用

研究miR-200c在IIIc期卵巢浆液性囊腺癌中的表达格局,探索其参与转移癌形成的相关机制。选取2010年1月至2013年12月上海交通大学医学院附属仁济医院妇科卵巢肿瘤组织标本(IIIc期卵巢浆液性囊腺癌40例(其中选择自身配对的原发灶40例、转移灶40例)、卵巢浆液性囊腺瘤30例为对照),采用real time-qPCR法检测miR-200c的表达;采用CCK8法、Transwell小室分别检测细胞过表达miR-200c后增殖、迁移和侵袭能力的改变;采用western blot法检测相关蛋白表达量。结果发现:(1)IIIc期卵巢浆液性囊腺癌转移灶肿瘤与原发灶肿瘤相比,miR-200c表达是升高的(490.37±78.32cf.157.46±17.21),P0.01;而且这两者均高于对照组(卵巢浆液性囊腺瘤)的表达(25.32±10.17),P0.01。SKOV3细胞过表达miRNA-200c后(2)细胞迁移能力降低(35.6±4.3cf.18.6±1.9),P0.05;侵袭能力降低(26.7±3.1cf.15.4±2.4)P0.05;但是增殖能力不改变。(3)在蛋白水平检测ZEB1蛋白表达下降(0.3023±0.0251cf.0.6753±0.0262)P0.05、E-cad蛋白表达升高(1.274±0.0331cf.0.6140±0.0460)P0.05、Vimentin蛋白表达降低(0.0957±0.0049cf.0.1767±0.0158)P0.05。可见,miR-200c在IIIc期卵巢浆液性囊腺癌组织样本中表达增高,检测miR-200c的表达格局对于临床上监测上皮性卵巢癌的临床进展和转移有重要意义;也为开拓过表达miR-200c作为卵巢癌治疗手段,提供了理论与实验依据。     

卵巢微乳头浆液性交界瘤4例临床病理分析

1996年Burks[1]报道在卵巢浆液性交界瘤内有一类微乳头状交界瘤,肿瘤虽无明显卵巢间质浸润,但常伴有浸润性腹膜种植,病变多进行性发展为浸润性肿瘤.Burks称其为卵巢微乳头浆液性癌(micropapillary serous carcinoma, MPSC).此后许多学者[2～4]对MPSC进行了研究,并提出了不同的看法.Deavers[5]认为MPSC常伴浸润性种植,复发率高,但其总生存率和浆液性交界瘤相当,因而将它保留在交界的范围内是正确的.我们复查了近10年来诊断为卵巢浆液性交界瘤和卵巢浆液性癌的病例,发现符合MPSC的诊断标准有4例,本文称之为微乳头浆液性交界瘤(micropapillary serous borderline tumors, MSBTs),现将其临床病理学特点报道如下.     

浅谈妇产科病理诊断

2．8．1卵巢浆液性囊腺癌与宫内膜样囊腺癌前者囊壁常分布大小不等乳头、簇状结节，光镜下除衬覆1～3层不等异型浆液性上皮外，及1～3级乳头状分枝或筛状结构，常伴砂砾体沉着，后者往往呈钝、粗、宽乳头状结构，及大小不等腺腔为主，衬覆异型子宫内膜型上皮，高分化者常伴有鳞状分化，或伴发透明细胞癌，若同时伴发子宫体子宫内膜样腺癌，     

卵巢浆液性表面乳头状瘤6例

卵巢浆液性表面乳头状瘤６例宋蔚青，赵承洛卵巢浆液性表面乳头状瘤，是卵巢表面上皮外向性乳头状增生形成的，为卵巢浆液性上皮性肿瘤结构类型之一，比较少见。临床上缺乏特殊症状和体征，往往在手术中偶然发现。近５年来本院遇见６例，分析报道如下。１临床资料见附表。...     

卵巢微乳头浆液惟交界瘤4例临床病理分析

1996年Burks报道在卵巢浆液性交界瘤内有一类微乳头状交界瘤，肿瘤虽无明显卵巢间质浸润，但常伴有浸润性腹膜种植，病变多进行性发展为浸润性肿瘤。Burks称其为卵巢微乳头浆液性癌（micropapillary scrous curcinoma,MPSC）。此后许多学者对MPSC进行了研究，并提出了不同的看法。Deavers认为MPSC常伴浸润性种植，复发率高，但其总生存率和浆液性交界瘤相当，     

卵巢恶性甲状腺肿2例并文献复习

目的探讨卵巢恶性甲状腺肿(malignant struma ovarii,MSO)病因、临床病理特点、诊断与鉴别诊断及其命名。方法对2例MSO进行组织病理学观察及S-P法免疫组化标记,并复习有关文献。结果卵巢恶性甲状腺肿2例患者年龄分别为59岁和41岁。2例TG、PCNA、p53均阳性;例2CK19乳头状癌阳性,例1CK19滤泡癌阴性。冷冻切片诊断困难,结合甲状腺癌的形态特点及免疫组化标记有助于确诊。结论MSO是一类转移率低、进展缓慢的卵巢恶性肿瘤,分为单纯型和癌变型。在组织学上分为乳头状型和滤泡型,在冷冻切片诊断时应引起注意。     

Numb蛋白在卵巢浆液性肿瘤中的表达及临床意义

目的检测Numb蛋白在卵巢浆液性肿瘤组织中的表达及其临床意义。方法用免疫组织化方法检测Numb蛋白在卵巢浆液性囊腺癌、交界性浆液性囊腺瘤、浆液性囊腺瘤及正常卵巢组织中的表达情况,并与患者的临床病理资料进行分析。结果Numb蛋白在卵巢浆液性囊腺癌中表达阳性率明显低于卵巢正常组织和卵巢浆液性囊腺瘤及交界性浆液性囊腺瘤的阳性率(P0.01),但与肿瘤分化程度、临床病理分期、淋巴结转移及年龄均无明显相关性(P0.05)。结论Numb蛋白在卵巢浆液性囊腺癌中低表达,可能参与浆液性囊腺癌的发生过程。     

Pathological, cytological and immunohistochemical study of normal-sized ovary carcinoma syndrome

Normal-sized ovary carcinoma syndrome(NOCS) is characterized by diffuse metastatic malignant disease of the abdominal cavity in females, with normal-sized ovaries, and no origin assigned definitively by intraoperative evaluation. To elucidate the characteristics of NOCS arising from ovarian carcinoma, we investigated the immunohistochemical reactivities of keratin, epithelial membrane antigen(EMA), vimentin, and proliferative cell nuclear antigen(PCNA) in 4 cases of ovarian carcinoma with NOCS(NOCS group), including 3 cases of serous surface papillary adenocarcinoma(SSPC) and 1 case of small ovarian primary serous papillary adenocarcinoma(SPC). These cases were compared with 3 cases of ovarian carcinoma without NOCS(non-NOCS group), including 3 cases of SPC. Cytological and histological testing of the NOCS and non-NOCS groups showed the same findings. Similar reactivities for keratin, EMA and vimentin were observed in the NOCS and non-NOCS groups. No significant change of PCNA labeling index between the groups was seen. However, clinical stage of the NOCS group was higher than that of non-NOCS group. It was hypothesized that exposure of cancer cells to peritoneal cavity in ovarian SSPC leads to the spread. In NOCS case arising from small-sized ovarian carcinoma, another factor was thought to be involved, such as genetic alteration, but it is not known.     

Value of mesothelial and epithelial antibodies in distinguishing diffuse peritoneal mesothelioma in females from serous papillary carcinoma of the ovary and peritoneum

AIMS: To evaluate the role of mesothelial markers (calretinin, thrombomodulin, cytokeratin 5/6, and CD44H) and carcinoma markers (polyclonal and monoclonal carcinoembryonic antigen, Leu-M1, CA-125 and Ber-EP4) in distinguishing diffuse peritoneal malignant mesothelioma from primary serous papillary adenocarcinoma of the ovary and peritoneum. METHODS AND RESULTS: Paraffin-embedded formalin-fixed blocks from 32 diffuse peritoneal mesotheliomas of epithelial subtype (all females), 20 serous papillary ovarian carcinomas and three primary peritoneal serous papillary carcinomas were studied. Calretinin and Ber-EP4 appeared to be the best positive mesothelial and carcinoma marker, respectively. Nuclear calretinin expression was identified in 28 of 32 malignant mesotheliomas with no nuclear immunoreactivity in the cohorts of serous papillary ovarian and peritoneal carcinomas, thus yielding 88% sensitivity and 100% specificity. Ber-EP4 showed 95% sensitivity and 91% specificity for serous papillary ovarian carcinoma. Thrombomodulin, cytokeratin 5/6 and CD44H immunoreactivities were seen in 18 (56%), 17 (53%) and 15 (47%) of peritoneal mesotheliomas, respectively, and in six (30%), five (25%) and five (25%) of the ovarian tumours, respectively. None of the three primary peritoneal serous papillary carcinomas expressed calretinin, thrombomodulin, cytokeratin 5/6 or CD44H. Polyclonal and monoclonal CEA, and Leu-M1 were expressed by two (10%), one (5%) and seven (35%) serous papillary ovarian carcinomas, respectively. None of the serous papillary peritoneal carcinomas expressed polyclonal CEA, monoclonal CEA or Leu-M1. CA-125 was positive in 19 (95%) and two (67%) ovarian and peritoneal carcinomas, respectively, and in eight (25%) peritoneal mesotheliomas. CONCLUSIONS: Calretinin and Ber-EP4 are useful discriminant markers in distinguishing peritoneal mesothelioma in women from serous papillary ovarian and peritoneal carcinoma. The other mesothelial markers (thrombomodulin, cytokeratin 5/6, and CD44H) and carcinoma markers (polyclonal and monoclonal CEA, and Leu-M1) yielded a too low sensitivity for practical use.     

Fine-needle aspiration cytology of metastatic ovarian carcinoma to the breast

Metastatic ovarian carcinoma to the breast is rare. It represents a diagnostic challenge to the cytologist. It usually signifies a progressive widespread metastatic ovarian tumor with a poor prognosis. This report evaluates the breast fine-needle aspiration (FNA) cytomorphologic features of six cases of metastatic ovarian carcinoma and compares them to those reported in the literature. The cytologic features included hypercellularity, abundant papillary fragments, and necrotic background. The tumor cells showed high nuclear/cytoplasmic ratio, anisonucleosis, prominent nucleoli, and psammoma bodies in cases of serous papillary carcinoma. In addition, the clear-cell carcinoma had prominent finely vacuolated and clear cytoplasm, multinucleated giant cells, and papillary fragments with hobnail nuclei. Recognition of these unusual patterns in a breast FNA cytology should raise the suspicion of a metastatic ovarian tumor. Direct comparison between the breast FNA cytology and the original primary ovarian tumor should confirm the diagnosis. The proper diagnosis of metastatic ovarian cancer to the breast will prevent unnecessary surgical treatment and ensure the appropriate therapy. Diagn Cytopathol 1996;15:1–6. © 1996 Wiley-Liss, Inc.     

Primary Peritoneal Serous Carcinoma: A Rare Case and Palliative Approach

Primary peritoneal serous carcinoma (PPSC) is a rare primary malignancy that diffusely involves the peritoneum, indistinguishable clinically and histopathologically from primary serous ovarian carcinoma. The origin of PPSC has not been well characterized. Here we present a case of PPSC diagnosed in ultrasonography-guided fine needle aspiration cytology (FNAC) in a 76- old female presenting with ascites, abdominal pain, distension and constipation. PPSC is an unusual tumour but cytomorphology is distinctive enough to diagnose preoperatively. In the case report hereby described PPSC is an inoperable malignancy, hence chemotherapy and palliative care are the only offered treatment.     

CA125 and thyroglobulin staining in papillary carcinomas of thyroid and ovarian origin is not completely specific for site of origin

AIMS: A 70-year-old woman presented with metastatic psammoma body-rich papillary carcinoma in a supraclavicular lymph node. No primary site was evident. The tumour showed strong staining for CA125 and weak staining for thyroglobulin. Prompted by this case we aimed to assess the reliability of immunostaining for CA125 and thyroglobulin in making the distinction between thyroid and ovarian papillary carcinoma. METHODS AND RESULTS: Nine papillary carcinomas of the thyroid and 17 serous papillary carcinomas of the ovary were stained for CA125 and thyroglobulin, as well as CAM 5.2, LP 34, carcinoembryonic antigen (CEA), S100 and diastase/periodic acid-Schiff. Nine of nine thyroid carcinomas stained for thyroglobulin; in addition CA125 was positive in four of nine. Normal surrounding thyroid also showed some reaction. Seventeen of 17 ovarian serous carcinomas were positive for CA125; in addition one case showed moderately strong staining for thyroglobulin. Mucin stains were positive in 14/17 ovarian serous carcinomas, but negative in all thyroid carcinomas. The other antibodies assessed showed no useful differences in staining frequency. Conclusion: Many cases of papillary carcinoma of the thyroid show CA125 staining, and this feature therefore has little positive predictive value for an ovarian origin. Occasional cases of ovarian papillary carcinoma may show staining for thyroglobulin, and this result should therefore be interpreted cautiously.     

Serous papillary adenocarcinoma of the female genital organs and invasive micropapillary carcinoma of the breast. Are WT1, CA125, and GCDFP-15 useful in differential diagnosis?

Serous papillary adenocarcinoma of the female genital organs and invasive micropapillary carcinoma of the breast have close histologic similarities. Thus, when these cancers occur synchronously or metachronously in the same patient, it is difficult to determine the primary site. We examined 23 serous papillary adenocarcinomas (16 ovarian, 5 endometrial, and 2 peritoneal) and 37 invasive micropapillary carcinomas of the breast (12 pure and 25 mixed types) on immunohistochemical expression of Wilm's tumor antigen-1 (WT1), CA125, and gross cystic disease fluid protein-15 (GCDFP-15), which have been reported to be useful in the differential diagnosis of primary ovarian carcinomas versus metastatic breast cancer to the ovary. The positive rates of WT1, CA125, and GCDFP-15 in serous papillary adenocarcinomas were 78%, 78%, and 0%, respectively, and the corresponding rates in invasive micropapillary carcinomas were 3%, 40%, and 38%. The CA125-positive rate of invasive micropapillary carcinoma was higher than the rate reported for other types of breast carcinomas. We consider CA125 to be not always useful in the differential diagnosis of serous papillary adenocarcinoma and invasive micropapillary carcinoma. Although the positive rate of WT1 was significantly higher in serous papillary adenocarcinoma than in invasive micropapillary carcinoma, WT1 expression in endometrial serous papillary adenocarcinoma was infrequent (20%). WT1 and GCDFP-15 could be useful markers for the differential diagnosis of ovarian and peritoneal serous papillary adenocarcinoma versus breast invasive micropapillary adenocarcinoma. However, the availability of GCDFP-15 is limited because of the low positive rate of GCDFP-15 in invasive micropapillary carcinomas.     

Expression of Rsf-1, a chromatin-remodeling gene, in ovarian and breast carcinoma

Rsf-1 protein is a member of a chromatin-remodeling complex that plays an important role in regulating gene expression and cell proliferation. Our previous study showed that Rsf-1 was an amplified gene that participated in the development of ovarian serous carcinoma. To further elucidate the role of Rsf-1 in ovarian cancer, we studied Rsf-1 immunoreactivity in 294 ovarian tumors of various histologic types. Because the Rsf-1 amplicon overlaps an amplified region reported in breast cancer, we included 782 neoplastic and normal breast tissues for comparison. Immunohistochemistry was performed on tissue microarrays using a 4-tiered scoring system. Overexpression of Rsf-1 was defined as a nuclear immunointensity of 3+ to 4+ because of a strong correlation between 3+ and 4+ immunointensity and Rsf-1 gene amplification, based on our previous fluorescence in situ hybridization analysis. Rsf-1 overexpression was observed in 25% of high-grade ovarian serous carcinomas and in only rare cases (<7%) of low-grade ovarian serous, ovarian endometrioid, and invasive breast carcinomas but not in any ovarian serous borderline tumors, ovarian clear cell carcinomas, ovarian mucinous carcinomas, intraductal carcinomas of the breast, and normal ovaries and breast tissues. Thus, overexpression of Rsf-1 was significantly associated with high-grade ovarian serous carcinoma (P < .05), as compared with other types of ovarian tumors and breast carcinomas. Our results provide evidence that Rsf-1 expression is primarily confined to high-grade serous carcinoma, the most aggressive ovarian cancer. Because Rsf-1 overexpression occurs in only a small number of breast carcinomas, it is unlikely that Rsf-1 is a critical gene in the development of breast carcinoma.     

Atypical papillary proliferation in gynecologic patients: a study of 32 pelvic washes

Papillary clusters in gynecologic pelvic washes frequently cause diagnostic challenges because they can be associated with borderline or malignant ovarian tumors, as well as benign pelvic diseases. The objective of our study was to review all pelvic washes with atypical papillary proliferation (APP) and investigate whether cytomorphology and/or immunohistochemistry on cell block could determine their origin. Thirty-two pelvic washes from 31 patients containing APP were reviewed and correlated with their corresponding gynecologic or pelvic disease. Previously obtained cell blocks with immunohistochemical (IHC) stains were reviewed also. Nine of 32 washes (28%) were overcalled as malignant and were from patients with 5 borderline serous ovarian tumors (BSTO), 1 ovarian follicular cyst, 1 serous cystadenofibroma, and 1 endometrial carcinoma with ovarian seromucinous cystadenoma. BSTO and endometriosis were the most common sources of APP. Cell blocks could not discriminate further the etiology of APP. Immunohistochemistry was performed rarely and not fully contributory. Caution in interpreting papillary groups and cytohistological correlation is recommended to prevent a high false positive rate.     

肿瘤坏死因子-α在卵巢肿瘤患者腹水中的表达及意义

目的 探讨卵巢肿瘤患者腹水中肿瘤坏死因子-α(TNF-α)与卵巢癌之间的关系,探讨其对腹水性质鉴别的价值.方法 采用酶联免疫吸附法(ELISA)检测59例卵巢上皮性肿瘤、9例原发性腹膜癌、6例卵巢子宫内膜异位囊肿患者腹水TNF-α水平.结果 腹水TNF-α水平在卵巢恶性上皮性肿瘤、卵巢交界性肿瘤、原发性腹膜癌中的水平明显高于卵巢良性上皮性肿瘤、卵巢子宫内膜异位囊肿,且与肿瘤的恶性行为包括临床分期、组织分化程度、淋巴转移及腹水量等有关.结论 腹水TNF-α对诊断卵巢癌有较高的敏感性和特异性,可能成为卵巢恶性肿瘤的标志物.     

WT-1 assists in distinguishing ovarian from uterine serous carcinoma and in distinguishing between serous and endometrioid ovarian carcinoma

AIMS: It has been suggested that WT-1 is helpful in distinguishing a primary ovarian serous carcinoma (OSC) from a primary uterine serous carcinoma (USC). Since both neoplasms are often disseminated at diagnosis and since USC often spreads to the ovary and vice versa, it may be difficult to ascertain the primary site. This is important, since adjuvant therapies for OSC and USC may differ. WT-1 staining patterns also differ between OSC and ovarian endometrioid carcinoma and so it is possible that WT-1 may assist in the distinction of these two neoplasms, which is sometimes problematic, especially with poorly differentiated tumours. This study aims to document the value of WT-1 in these settings. Cases of ovarian borderline serous tumour, primary peritoneal serous carcinoma (PPSC) and uterine endometrioid carcinoma were also studied. METHODS AND RESULTS: Cases of OSC (n = 38), USC (n = 25) (in five of these cases there was also a component of endometrioid adenocarcinoma), ovarian endometrioid carcinoma (n = 13), uterine endometrioid carcinoma (n = 7), ovarian borderline serous tumour (n = 16) and PPSC (n = 6) were stained with WT-1. Cases were scored on a scale of 0-3, depending on the percentage of positive cells. The intensity of staining was scored as weak, moderate or strong. There was positive nuclear staining of 36 of 38 (94.7%) OSC with WT-1. In most OSC (68.4%), >50% of cells stained positively and staining was usually strong. Five of 25 (20%) USC were positive with only two cases exhibiting staining of >50% of cells. All primary ovarian and uterine endometrioid carcinomas were negative. All PPSC were positive, usually with diffuse strong immunoreactivity. Fourteen of 16 borderline serous tumours exhibited positivity with WT-1. CONCLUSIONS: WT-1 is useful in distinguishing OSC (characteristically diffuse strong nuclear positivity) from USC (characteristically negative). However, rarely OSC is negative and occasional cases of USC are positive. WT-1 may also be helpful in differentiating poorly differentiated OSC from poorly differentiated ovarian endometrioid carcinoma.