Nuclear findings of ovarian surface epithelial tumors

While cytoplasmic features of ovarian surface epithelial tumors are well-known, the nuclear findings have received little attention. We reviewed imprint cytology materials of the ovary which were collected at the Kawasaki Medical School Hospital between January 1989-July 1999, and identified 15 mucinous cystadenomas, 3 borderline mucinous tumors, 4 mucinous cystadenocarcinomas, 4 serous cystadenomas, 4 borderline serous tumors, 7 serous cystadenocarcinomas, 6 endometrioid carcinomas, and 2 clear-cell adenocarcinomas. We microscopically observed nuclear findings of the 45 cases. Coffee-bean nuclei were observed in 15.0%, 15.8%, and 10.1% of the tumor cells in mucinous adenomas, borderline mucinous tumors, and borderline serous tumors, respectively. The frequencies of the coffee-bean nuclei in the three tumors were higher than in the remaining tumors (P < 0.001). Intranuclear cytoplasmic inclusions were observed in 2.1% of the tumor cells in mucinous cystadenoma, and their frequency was significantly higher than that in cases of other surface epithelial ovarian tumors (P < 0.001). Semilunar-shaped nuclei were seen in all cases of mucinous cystadenomas and borderline mucinous tumors, and in 3 of 4 mucinous adenocarcinomas. The remaining surface epithelial tumors did not reveal the semilunar-shaped nuclei. In the cytology of the ovary, the semilunar nuclei are characteristic of mucinous tumors, and the intranuclear cytoplasmic inclusion may be a diagnostic clue to mucinous cystadenoma, when it is conspicuous. The coffee-bean nuclei can be seen in mucinous cystadenoma, borderline mucinous tumors, and borderline serous tumors.     

Alpha-lactalbumin in "common" epithelial tumors of the ovary. An immunohistochemical study

Alpha-lactalbumin (AL) has been widely used as an immunohistochemical marker for mammary carcinoma. The authors have investigated the AL reactivity of 36 unselected ovarian epithelial neoplasms using the avidin-biotin-peroxidase immunoperoxidase technic. In eight serous cystadenocarcinomas, both the primary neoplasm and its metastases were examined. Of the 36 tumors, 7 (19.4%) showed positive staining for AL and 5 were of the serous type. The serous tumors showed moderate to strong staining reaction. Three serous cystadenocarcinomas were AL positive in both primary and metastatic sites, while the remaining five were negative in all sites. One mucinous cystadenoma and one clear cell carcinoma showed weak to moderately positive AL reactivity. There was no good correlation between AL positivity and the presence of malignancy or between AL positivity and tumor grade. In view of the relatively high AL reactivity in ovarian neoplasms, it is advisable to exercise caution in interpreting the presence of AL positivity as specific marker for mammary carcinoma.     

Association of cortactin, fascin-1 and epidermal growth factor receptor (EGFR) expression in ovarian carcinomas: correlation with clinicopathological parameters

Cortactin, fascin-1 and EGFR are recognized as important factors in tumor progression. We tested the hypothesis that cortactin, fascin-1 and EGFR expression correlates with clinicopathological parameters of the four most common ovarian surface epithelial carcinomas--serous cystadenocarcinoma, mucinous cystadenocarcinoma, endometrioid adenocarcinoma, and clear cell carcinoma. Immunohistochemical analysis of cortactin, fascin-1 and EGFR was performed using tissue microarrays of 172 specimens comprising 69 serous cystadenocarcinomas, 44 mucinous cystadenocarcinomas, 45 endometrioid adenocarcinomas and 14 clear cell carcinomas. All ovarian carcinomas showed significant expression of cortactin, fascin-1 and EGFR in staining intensity, tumor percentages and immunostaining scores. In addition, higher immunostaining scores of fascin-1 correlated with more advanced cancer stages (TNM), poorer histological differentiation and poorer survival rate of mucinous cystadenocarcinoma. Similarly, higher immunostaining scores of cortactin correlated with T stages and histological differentiation of serous cystadenocarcinoma. The immunostaining scores of EGFR did not correlate with TNM stages, tumor differentiation or prognosis in the four ovarian surface epithelial carcinomas. Our findings suggest that cortactin and fascin-1 may serve as good biomarkers in evaluating aggressiveness of ovarian serous and mucinous cystadenocarcinoma. And the pharmacological inhibitors of fascin-1 activity may slow down tumor progression and prolong survival time in patients with mucinous cystadenocarcinoma.     

Aberrant hypermethylation of RASSF1A promoter in ovarian borderline tumors and carcinomas

The newly identified 3p21.3 tumor suppressor gene RASSF1A is inactivated by hypermethylation in variable solid tumors, including those of the lung, breast, prostate, kidney, and ovary. The purpose of this study was to evaluate the methylation status of RASSF1A in various types and stages of ovarian epithelial tumors. We analyzed the DNA methylation status of ovarian tumors using methylation-specific polymerase chain reaction in 54 frozen ovarian tumor tissues and in 97 cases of archival ovarian serous epithelial tumors using a microdissection procedure. Hypermethylation statuses were examined vs clinicopathologic findings. RASSF1A promoter methylation rates in the various types of fresh ovarian tissues were as follows: serous cystadenoma (1/5), serous tumor of borderline malignancy (2/7), serous adenocarcinoma (4/10), mucinous cystadenoma (0/5), mucinous tumor of borderline malignancy (2/7), mucinous adenocarcinoma (3/6), transitional-cell carcinoma (1/3), clear-cell carcinoma (3/3), and malignant müllerian mixed tumor (3/3). In archived serous tumor tissues, RASSF1A promoter hypermethylation was detected in serous cystadenoma (1/6, 16.6%), serous tumor of borderline malignancy (20/41, 48.8%), and in serous adenocarcinoma (25/50, 50%). The status of RASSF1A hypermethylation in borderline tumors was found to correlate statistically with the presence of microinvasion (p=0.002), peritoneal implant (p<0.001), and bilaterality (p=0.019). The RASSF1A promoter hypermethylation was frequently found in borderline tumors and carcinomas, suggesting that RASSF1A promoter hypermethylation may be a useful molecular marker for the early detection of ovarian tumors.     

NQO1过表达在卵巢黏液性囊腺癌预后评估中的意义

目的:探讨NAD(P)H醌氧化还原酶1[NAD(P)H-quinone oxidoreductase 1,NQO1]过表达在卵巢黏液性囊腺癌临床预后评估中的意义。方法:应用免疫组化En Vision法检测NQO1蛋白在162例卵巢黏液性囊腺癌组织、35例卵巢黏液性囊腺瘤组织和29例正常卵巢上皮组织中的表达,并分析其过表达与卵巢黏液性囊腺癌临床病理学特点之间的关系,通过Kaplan-Meier方法进行生存分析。结果:NQO1蛋白在卵巢黏液性囊腺癌组织中的阳性率及强阳性率分别为85.8%和64.2%,显著高于卵巢黏液性囊腺瘤和正常卵巢上皮组织(P0.01)。卡方检验结果显示,NQO1蛋白高表达与卵巢黏液性囊腺癌组织学分级和FIGO分期密切相关(P0.05)。Kaplan-Meier生存分析显示,NQO1蛋白高表达的卵巢黏液性囊腺癌患者总生存期和无病生存期均明显低于NQO1蛋白低表达患者。结论:NQO1蛋白在卵巢黏液性囊腺癌组织中呈高表达,可能成为卵巢黏液性囊腺癌预后评估的有效生物学指标。     

卵巢囊腺肿瘤的凝集素受体分布

55 cases of ovarian cystadenoma and cystadenocarcinoma were investigated with a panel of twelve various lectins and ABC technique. Results showed that RCA and WGA reacted with all the tumors, indicating that these two lectins are possibly functional differential markers of both ovarian mucinous and serous tumors. LCA, DBA and SJA might be of considerable help in differential diagnosis of serous cystadenoma and cystadenocarcinoma. PSA probably was a marker indicating malignant change of mucinous cystadenmas. Since there were different reactivities in mucinous and serous cystadenoma, SJA, DBA and SBA might be considered as the functional markers in differentiating these two different types of ovarian cystadenoma.     

Inhibitory role of prohibitin in human ovarian epithelial cancer

Objectives: To characterize the exact individual roles of gonadotropins on ovarian epithelial carcinogenesis, an earlier study showed that prohibitin was significantly up-regulated by luteinizing hormone (LH). To further clarify the role of prohibitin in ovarian carcinogenesis and its association with LH, herein we studied the expression of prohibitin in various ovarian tissues including different developmental stages of ovarian epithelial tumors. Methods: A total of 135 samples were studied by immunohistochemistry. These included benign ovarian cases with follicles, ovarian surface epithelia and ovarian epithelial inclusions (OEI) (n=30), serous cystadenoma (n=14), serous borderline tumor (n=12), serous carcinoma (n=20), mucinous cystadenoma (n=10), mucinous borderline tumor (n=10), mucinous carcinomas (n=10), endometrioid carcinomas (n=12), poorly/undifferentiated carcinomas (n=5), and fallopian tube (n=12). Results: Strong and diffuse staining of prohibitin was detected in luteinized ovarian stromal cells, follicular cells, fallopian tube, and OEI with serous differentiation. A significantly higher prohibitin expression in luteinized stromal cells than in non-luteinized stromal cells was observed (P<.01). Within the ovarian epithelium, the level of prohibitin expression was basically negative in ovarian surface epithelia, but highly expressed in OEI. However, compared to the level of prohibitin expression in OEI, it showed a trend of gradual loss from benign ovarian tumors, to borderline tumors and to carcinomas (P<.0001). Compared to the serous tumors, epithelial tumors with mucinous differentiation showed a significant lower level of prohibitin (P<.0001). An inverse correlation was noted between prohibitin expression and cancer grade. It is interesting to note that a high prohibitin expression level was seen in the fallopian tube, which is similar to OEI. Conclusions: These data further suggest that prohibitin plays a tumor suppressing role, which is probably associated with LH mediated protection role against ovarian epithelial carcinoma. In addition to the tumor suppressive role of prohibitin, it also plays a role in cellular differentiation, which may be helpful to differentiate ovarian mucinous tumors from the tumors with serous differentiation in clinical settings. More importantly, our findings are supportive that the ovarian epithelial cancers, particularly the serous cancers including those precursors with serous differentiation are likely to be derived from fallopian tube instead of ovarian surface epithelia.     

基质金属蛋白酶-7在卵巢浆液性肿瘤中的表达

目的：探讨MMP－7在卵巢浆液性肿瘤中的表达情况。方法：采用免疫组化SP法对6例正常卵巢、12例卵巢浆液性囊腺瘤、6例交界性囊腺瘤及22例卵巢浆液性囊腺癌MMP－7的表达进行了研究。结果：正常卵巢不表达MMP－7。大部分卵巢浆液性肿瘤的胞浆及间质中都有MMP－7的阳性表达。MMP－7的卵巢良性，恶性及交界性浆液性肿瘤胞浆中的表达无明显差异；而在肿瘤间质中，恶性及交界性卵巢浆液性肿瘤中的表达远高于良性肿瘤（P＜0．05）。在交界性及恶性浆液性卵巢肿瘤中，部分肿瘤细胞的细胞核中也有MMP－7的表达，为国内外首次报道。结论：MMP－7可能在卵巢浆液性肿瘤的进展中发挥重要作用。     

Clinical and prognostic significances of nuclear and cytoplasmic KIT expressions in extrahepatic bile duct carcinomas.

After receiving FDA approval as a therapeutic regimen in gastrointestinal stromal tumors, the tyrosine kinase inhibitor imatinib mesylate has been applied to the treatment of other solid malignant neoplasms. To evaluate the usefulness of imatinib mesylate as a possible therapeutic regimen in extrahepatic bile duct carcinomas, an immunohistochemical study for KIT was performed in 289 cases of extrahepatic bile duct carcinomas, and mutational analysis of exon 11 of the c-kit gene was performed in 20 cases that were arbitrarily retrieved from the cases with KIT expression. Cytoplasmic KIT expression was observed in 54 cases (19%) and nuclear KIT in 58 cases (20%) of extrahepatic bile duct carcinoma. Nuclear KIT expression was more frequent in cases with vascular invasion (P<0.001), whereas cytoplasmic KIT expression was more common in tumors of T1-T3 than in those of T4 (P=0.04), and was more frequently observed in cases with a papillary growth pattern (P=0.03). Patients with cytoplasmic KIT-positive tumors had significantly better survival both by univariate (P=0.01) and multivariate analyses (P=0.04). Infrequent cytoplasmic KIT expression without mutation of exon 11 suggests that imatinib mesylate may not be effective for the treatment of extrahepatic bile duct carcinoma. However, immunohistochemical study for KIT may be helpful in routine pathologic examinations for evaluating better prognosis for patients with extrahepatic bile duct carcinoma. In addition, more frequent nuclear expression of KIT in cases with vascular invasion suggests that nuclear KIT expression may contribute to the progression of extrahepatic bile duct carcinoma.     

Positive immunohistochemical staining of KIT in solid-pseudopapillary neoplasms of the pancreas is not associated with KIT/PDGFRA mutations.

Solid-pseudopapillary neoplasms of the pancreas are uncommon neoplasms of low malignant potential and of uncertain histogenesis. A small percentage of patients develop metastatic disease and some succumb to disease. The management of patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates is problematic. Novel therapy targets are needed. Successful treatment of metastatic and unresectable gastrointestinal stromal tumors with KIT kinase inhibitor, imatinib mesylate (Gleevec), makes it intriguing to look at the status of KIT in solid-pseudopapillary neoplasms of the pancreas. In this study, we investigated KIT expression in 50 solid-pseudopapillary neoplasms by immunohistochemical staining. Of the 50 (50%) solid-pseudopapillary neoplasms, 25 showed diffuse expression (in >50% neoplastic cells) of KIT and additional five (10%) cases showed focal staining (in 10-50% neoplastic cells). Expression of KIT was not associated with tumor behavior and prognosis. A subset of 11 cases showing diffuse KIT expression detected by immunohistochemical staining were further evaluated for the presence of activating mutations in KIT exons 9, 11, 13 and 17, and PDGFRA exons 12 and 18 using PCR amplification followed by direct sequencing. However, no KIT or PDGFRA mutations were identified in any of these 11 cases tested, suggesting that the overexpression of KIT is probably not due to activating mutations in KIT or PDGFRA. The exact mechanism of KIT overexpression in solid-pseudopapillary neoplasms remains to be elucidated. One possible mechanism is gene dose effect (increased copies of KIT gene). Experience in gastrointestinal stromal tumors and other tumors have shown that mutation-mediated activation of KIT or PDGFRA is a prerequisite for clinical response with imatinib mesylate. Thus, lack of mutations in KIT or PDGFRA in solid-pseudopapillary neoplasms suggests that imatinib mesylate is less likely to be effective in the treatment for patients with metastatic disease or unresectable tumor, and patients who are just not good surgical candidates.     

LMX1A as a prognostic marker in ovarian mucinous cystadenocarcinoma

This study aimed to evaluate the relationship of LMX1A and osteopontin (OPN) expression with clinicopathologic parameters for the 4 most common ovarian surface epithelial carcinomas. Both biomarkers were investigated immunohistochemically using tissue microarrays of 249 specimens including 91 serous cystadenocarcinomas, 56 mucinous cystadenocarcinomas, 64 endometrioid adenocarcinomas, 26 clear cell carcinomas, and 12 normal ovarian tissues. All 4 carcinomas showed significant expression of LMX1A and OPN. In addition, higher immunostaining scores and percentage of cells stained for LMX1A in mucinous cystadenocarcinomas correlated with T stage, American Joint Committee on Cancer clinical stage, poorer tumor differentiation, and poorer survival rate. In serous cystadenocarcinoma, higher percentage of staining for OPN and higher intensity or immunostaining scores for LMX1A correlated with poorer tumor differentiation. Thus, the expression of LMX1A may be an independent prognostic risk factor in mucinous cystadenocarcinoma and a helpful marker in evaluating this tumor's aggressiveness.     

Clarification of the active gelatinolytic sites in human ovarian neoplasms using in situ zymography

Tissues from 26 human ovarian common epithelial tumors were examined to determine where and how gelatinolytic activity was present, in relation to tumor-stromal interaction and histologic types. For this purpose, we used in situ zymography, a newly developed technique using gelatin-coated film. Gelatinolytic activity was evident in ovarian carcinomas and in borderline tumors. Benign tumors had no or only weak activity. Four tissue localization patterns of gelatinolysis were identified: pattern A, tumor cytoplasm; pattern B, tumor-stromal junction; pattern C, stroma; and pattern D, cystic fluid. Mucinous cystadenocarcinomas showed A and/or D patterns. One mucinous and one serous adenocarcinoma and one mucinous borderline tumor had a B pattern. Most serous and all clear cell adenocarcinomas showed strong gelatinolysis of C pattern, especially in the desmoplastic stroma, an area where the tumor cells were dispersed. Immunohistochemically in 12 adenocarcinomas and 3 borderline tumors, the tumor cytoplasm was positive for matrix metalloproteinases (MMP-2) (5 cases), MMP-7 (9 cases), and MMP-9 (6 cases). Stromal components were positive for MMP-2 in 5 cases and for MMP-9 in 3 cases, but they were not positive for MMP-7. MMP antigens were mostly distributed in an almost identical pattern consistent with that seen with in situ zymography. In situ zymography clarified the cellular localization of active gelatinolysis in human ovarian neoplasms, a finding which supports the view that interaction between tumor and stroma is critical for tumor growth. This newly developed method contributes to a better understanding of biologic features of ovarian malignancies.     

K-ras activation occurs frequently in mucinous adenocarcinomas and rarely in other common epithelial tumors of the human ovary.

To explore the role of mutational activation of members of the ras family of cellular protooncogenes in the development of human ovarian neoplasms, a series of 37 ovarian tumors from Japanese patients was studied. These included 30 common epithelial tumors (1 mucinous tumor of borderline malignancy, 7 mucinous adenocarcinomas, and 22 nonmucinous carcinomas: 10 serous, 3 clear cell, 8 endometrioid, and 1 undifferentiated), 5 tumors of germ cell origin, and 2 sex cord/stromal cell tumors. Polymerase chain reaction was performed from selected areas of deparaffinized sections of formalin-fixed paraffin-embedded tissue, and the presence of activating point mutations in codons 12, 13, and 61 of the H-, N-, and K-ras genes was probed by dot-blot hybridization analysis with mutation specific oligonucleotides. Mutations in K-ras were also looked for by direct genomic sequencing. The overall frequency of ras gene mutations was 10/37 (27%). Mutations were detected only in K-ras, and were found in most of the mucinous tumors, including the one such tumor of borderline malignancy (6/8; 75%). In one mucinous adenocarcinoma, two mutations were detected in paraffin-embedded material that had not previously been found in high molecular weight DNA isolated from frozen tissue from the same case. K-ras mutations occurred significantly more frequently in mucinous tumors (6/8, 75%) than in serous carcinomas (2/10, 20%; P = 0.031) or in all nonmucinous types of epithelial ovarian tumors combined (3/22, 14%; P = 0.0031).     

卵巢粘液性及浆液性囊腺瘤癌胚抗原的免疫组化研究

以CEA单克隆抗体,双PAP法研究卵巢粘液性和浆液性囊腺瘤组织内CEA的定位。结果表明:良性瘤23例,CEA全部(-)。交界性肿瘤中粘液性22例,CEA(+)者21例;浆液性15例,CEA(+)者7例。恶性肿瘤中粘液性23例,CEA(+)者18例,浆液性37例,CEA(+)者7例。由于粘液性交界性肿瘤有较高的CEA检出率,可作为诊断参考指标。     

KIT mutations are common in testicular seminomas

Expression of KIT tyrosine kinase is critical for normal germ cell development and is observed in the majority of seminomas. Activating mutations in KIT are common in gastrointestinal stromal tumors and mastocytosis. In this study we examined the frequency and spectrum of KIT mutations in 54 testicular seminomas, 1 ovarian dysgerminoma and 37 non-seminomatous germ cell tumors (NSGCT). Fourteen seminomas (25.9%) contained exon 17 point mutations including D816V (6 cases), D816H (3 cases), Y823D (2 cases), and single examples of Y823C, N822K, and T801I. No KIT mutations were found in the ovarian dysgerminoma or the NSGCTs. In transient transfection assays, mutant isoforms D816V, D816H, Y823D, and N822K were constitutively phosphorylated in the absence of the natural ligand for KIT, stem cell factor (SCF). In contrast, activation of T801I and wild-type KIT required SCF. Mutants N822K and Y823D were inhibited by imatinib mesylate (Gleevec, previously STI571) whereas D816V and D816H were both resistant to imatinib mesylate. Biochemical evidence of KIT activation, as assessed by KIT phosphorylation and KIT association with phosphatidylinositol (PI) 3-kinase in tumor cell lysates, was largely confined to seminomas with a genomic KIT mutation. These findings suggest that activating KIT mutations may contribute to tumorigenesis in a subset of seminomas, but are not involved in NSGCT.     

Testicular and paratesticular tumors and tumor-like lesions of ovarian common epithelial and müllerian types. A report of four cases and review of the literature

Three new and eleven previously reported testicular or paratesticular tumors that resembled ovarian tumors of common epithelial type are discussed. The 14 tumors occurred in patients ages 11-68 (average 47) years of age. The exact location for 12 of the tumors is known; 5 involved primarily the testicular parenchyma, 3, the tunica vaginalis, and 4, paratesticular tissue. Five tumors were serous, four of which were in the borderline category. Four tumors were Brenner tumors, admixed in one case with an adenomatoid tumor. Single examples of mucinous cystadenoma, mucinous cystadenocarcinoma, endometrioid adenoacanthoma, clear cell adenocarcinoma, and a benign tumor of mixed cell types complete the list. Follow-up of from 3 months to 14 years is available in eight cases; only one tumor, the clear cell adenocarcinoma, is known to have been clinically malignant. A fourth lesion in this article was a paratesticular mass composed of endometrial glands and stroma and bundles of smooth muscle. It arose in an 82-year-old man who had been treated with estrogens for prostatic adenocarcinoma.     

Neoplastic transformation of endocervicosis into an extraovarian mucinous cystadenocarcinoma

Although extraovarian mucinous cystadenocarcinomas resemble primary ovarian carcinomas, both histologically and clinically, their specific etiology is not clear. This is the first report to show neoplastic transformation of endocervicosis into an extraovarian mucinous cystadenocarcinoma. The histologic spectrum and specific KRAS mutational analysis for this tumor were the same as for their ovarian counterparts. This supports a müllerian origin and the current approach to extrapolate the results from ovarian mucinous cystadenocarcinoma trials in prescribing treatment for patients with extraovarian mucinous cystadenocarcinomas.     

卵巢良性和恶性粘液性囊腺瘤酸性粘蛋白的组化改变

用4种酸性粘蛋白组织化学染色法,观察90例卵巢良性和恶性粘渡性囊腺瘤酸性粘蛋白的含量和成分。发现粘液性囊腺癌酸性粘蛋白含量明显高于交界性粘液性囊腺瘤和钻液性囊腺瘤。绝大多数粘液性囊腺瘤酸性粘蛋白的主要成分是唾液酸粘蛋白,或唾液酸和硫酸两种粘蛋白的混合,仅少数瘤含有较多硫酸粘蛋白。与囊腺癌上皮比较,良性囊腺瘤上皮中唾液酸粘蛋白含量增多,或两种酸性粘蛋白均减少。据认为:①当囊腺瘤恶变时,酸性粘蛋白逐渐增加;②唾液酸粘蛋白(部分肿瘤含硫酸粘蛋白)增多是卵巢粘液性囊腺癌的组化特点;③酸性粘蛋白含量可能与肿瘤生物学行为有关。     

Amylase in fallopian tube and serous ovarian neoplasms: immunohistochemical localization

We studied the cellular localization of amylase in normal Fallopian tubes and serous ovarian neoplasms using an indirect immunoperoxidase technique. The primary antiserum was against human pancreatic amylase, and was found to inhibit ovarian tumor amylase as well. Amylase was present in normal endosalpingeal epithelium and in the epithelial cells of benign, borderline, and malignant serous ovarian tumors. A mucinous cystadenoma was also studied and contained no amylase. This localization suggests that amylase production by serous ovarian neoplasms reflects the endosalpingeal differentiation of these tumors. Antibody to amylase may be potentially useful in distinguishing serous ovarian tumors from other forms of ovarian neoplasia.     

Fascin and EMMPRIN expression in primary mucinous tumors of ovary: A tissue microarray study

ObjectivesThe aim of this study was to compare the expressions of fascin and EMMPRIN in primary malignant, borderline and benign mucinous ovarian tumors, and to investigate the relationship of these markers with tumor progression and their applicability to differential diagnosis.Materials and methodsAn immunohistochemical study was performed for fascin and EMMPRIN using the tissue microarray technique. Eighty-one cases were included in the study; there were 37 benign, 25 borderline and 19 malignant primary mucinous ovarian tumors. For each case, a total staining score was determined, consisting of scores for extent of staining and intensity of staining. The cases were allocated to negative, weakly positive and strongly positive staining categories, according to the total staining score.ResultsBoth of the markers were significantly negative in benign tumors as compared with borderline and malignant tumors. There was no significant difference between borderline and malignant groups for both markers. Sixty-eight percent of malignant tumors were stained positive by fascin, while this rate was 40% for borderline mucinous tumors. All malignant tumors were strongly stained positive for EMMPRIN, while this rate was 92% for borderline mucinous tumors. The rest of the cases stained weakly positive. No significant difference in staining score was found between fascin and EMMPRIN expression.ConclusionsIn ovarian primary mucinous tumors, fascin and EMMPRIN may play an important role in tumor progression from benign tumor to carcinoma. In that context, EMMPRIN and fascin expression may have potential application in the differential diagnosis of some diagnostically problematic mucinous ovarian tumors. However, the differential diagnostic applicability of EMMPRIN appears to be more limited than that of fascin due to its wide spectrum of staining in mucinous ovarian tumors.