Different Types Of Ovarian Tumors Research Articles

Deep convolutional neural networks for multiple histologic types of ovarian tumors classification in ultrasound images.

This study aimed to evaluate and validate the performance of deep convolutional neural networks when discriminating different histologic types of ovarian tumor in ultrasound (US) images. Our retrospective study took 1142 US images from 328 patients from January 2019 to June 2021. Two tasks were proposed based on US images. Task 1 was to classify benign and high-grade serous carcinoma in original ovarian tumor US images, in which benign ovarian tumor was divided into six classes: mature cystic teratoma, endometriotic cyst, serous cystadenoma, granulosa-theca cell tumor, mucinous cystadenoma and simple cyst. The US images in task 2 were segmented. Deep convolutional neural networks (DCNN) were applied to classify different types of ovarian tumors in detail. We used transfer learning on six pre-trained DCNNs: VGG16, GoogleNet, ResNet34, ResNext50, DensNet121 and DensNet201. Several metrics were adopted to assess the model performance: accuracy, sensitivity, specificity, FI-score and the area under the receiver operating characteristic curve (AUC). The DCNN performed better in labeled US images than in original US images. The best predictive performance came from the ResNext50 model. The model had an overall accuracy of 0.952 for in directly classifying the seven histologic types of ovarian tumors. It achieved a sensitivity of 90% and a specificity of 99.2% for high-grade serous carcinoma, and a sensitivity of over 90% and a specificity of over 95% in most benign pathological categories. DCNN is a promising technique for classifying different histologic types of ovarian tumors in US images, and provide valuable computer-aided information.

Significance of Endocan Expression in Various Types of Epithelial Ovarian Tumors.

Background & Objective:Ovarian cancer is associated with the highest mortality rate among gynecologic malignancies. Despite new therapeutic strategies, ovarian cancer still has a high risk of metastasis and mortality. Endocan is a newly identified endothelial cell activation marker, which is responsible for angiogenesis, tumor invasion, and aggressive behavior of tumors. The aim of this study was to assess Endocan expression in different types of ovarian tumors and to identify its relationship with clinicopathologic characteristics of ovarian tumors. Methods:This cross-sectional study was conducted on 183 tissue samples, including benign, borderline, and malignant ovarian tumors collected from the University Kebangsaan Malaysia Medical Center archive of Pathology during 2005-2015. Mouse monoclonal anti-human Endocan/ESM-1 Clone MEP08 was used at a dilution of 1:400 for immunohistochemical (IHC) staining. All the information was collected by a checklist, and the association between clinicopathological features and high or low levels of Endocan -MVD was evaluated using Pearson chi-square, Fischer's exact, or Monte Carlo tests.Results:The prevalence of Endocan positivity was significantly higher in malignant compared to borderline and benign ovarian tumors (P<0.001). There was also a significant association between type of tumor and Endocan status in malignant ovarian tumors (P=0.02), indicating that Endocan positivity was more likely in serous malignant ovarian tumors compared to other ovarian tumor types. However, the tumor stage was not significantly associated with Endocan status (P=0.31). Conclusion:This study showed that Endocan positivity may show the highest prevalence among malignant tumors suggesting that high Endocan expression would be negatively associated with ovarian tumor behavior.

Retrospective study of histopathological changes in ovarian tumors

Introduction: Tumors of ovary are of prime importance because of its increasing occurrence and its late diagnosis due to the very vague clinical features presented by the tumor. Its occurrence starts from the thirties, and attains its peak in the seventies. Objectives: To study the different types of ovarian tumors and its pathology and correlating it with age, sex and other important factors. Materials and Methods: This study was done by taking 50 cases of ovarian masses which was sent to department of pathology, from the past year July 2017 – July 2018 in Saveetha Medical College and hospitals, Chennai. Expected outcome: To find out the most prevalent type of ovarian tumor and the age group when its affected the most. Keywords: Benign serous cyst, Biopsy, Benign,Borderline, Malignant, Neoplasm.

Activation of hedgehog signaling and its association with cisplatin resistance in ovarian epithelial tumors.

Few studies have evaluated Hedgehog (Hh) signaling pathway activation in different types of ovarian tumors including benign, borderline and malignant ovarian tumors. The present study investigated the expression of Hh signaling pathway components (SHH, SMO, PTCH, and GLI1) in 193 ovarian epithelial tumor specimens (including 147 malignant epithelial ovarian cancers, 30 borderline ovarian tumors, 16 benign ovarian epithelial tumors) and 11 normal ovarian epithelial tissues by immunohistochemistry. The results demonstrated widespread expression of Hh pathway molecules in ovarian tumors. However, there was no significant difference in the expression intensity of SHH among the four groups (P>0.05). Statistically significant differences were identified in the expression intensity of the SMO, PICH and GLI1 among groups (P<0.001). In addition, significant differences were also revealed in the expression levels of SMO (P=0.013) and GLI1 (P=0.0005) between the platinum drug-sensitive and drug-resistant groups. The overexpression of SMO and GLI1 was further confirmed in the cisplatin-resistant ovarian cancer cell line A2780/DDP by immunofluorescence, flow cytometry and western blotting. The results revealed that the Hh pathway components SMO, PICH and GLI1 are activated in ovarian epithelial tumors. Novel potential associations between cisplatin resistance and the overexpression of SMO and Gli1 in malignant epithelial ovarian cancer were also observed, which may provide an innovative approach to the treatment of drug resistant ovarian epithelial cancer.

PTCH1 gene polymorphisms in ovarian tumors: Potential protective role of c.3944T allele

In this study we investigated the types and role of different genetic changes of PTCH1 gene in three different types of ovarian tumors: carcinomas, fibromas and dermoids. LOH of the PTCH1 region was detected in 27.3% ovarian carcinoma samples, 18.18% ovarian fibroma samples and 55.56% ovarian dermoid samples. No point mutations were detected in any of the three types of ovarian tumors. SNP c.3944C>T showed significant differences between ovarian carcinoma and control samples with the minor T allele being significantly higher in controls compared to ovarian carcinomas. Interestingly, a new polymorphism c.−1184G>A was found only in tumor samples and further analyses should be performed in order to elucidate its potential role in ovarian tumors.

P53 expression in ovarian tumors: (an immunohistochemical study)

Objectives: The aim of this study, first, to evaluate the frequency of immunohistochemical expression of p53 in different types of ovarian tumors, second, to correlate p53 expression with age of patients, histological type and grade of tumors, and third, to compare the results with those of others. Methods: This study was performed on 60 primary ovarian tumors. Samples were obtained in a prospective and retrospective fashion (cross sectional study). The samples were collected from Al-Jumhuri Teaching Hospital, Al-Salaam General Hospital, Al-Khansaa Teaching Hospital, and some private Laboratories, during a period of eight months, from June 2009 through January 2010. P53 expression was assessed immunohistochemically. Results: The patients' age ranged from 13 to 80 years, with a mean of 43.88 year. Most of them were in the fifth decade (28.3%). Data concerning the age were missing in five patients. P53 immunoreactivity was observed in 48.1% of the malignant tumors. It was positive in 13 of 20 cases of serous adenocarcinoma, in all of the 5 cases of mucinous adenocarcinoma, in 3 of 12 granulosa cell tumors, in 2 of 4 endometrioid carcinomas, in 1 of 3 clear cell carcinoma, in 1 of 2 dysgerminomas, and in the one case of Sertoli-Leydig cell tumor. It was negative in malignant thecoma, malignant teratoma and in all borderline and benign tumors. Statistically p53 expression was not significantly related to the age of the patients, grade, or to the histological type of the tumors. It was mainly found in malignant serous tumors (50%), in the poorly differentiated tumors (47.6%), and in the 6th decade of age (30.8%). Conclusions: P53 was expressed in 48.1% of malignant ovarian tumors, 80.8% were epithelial tumors, 15.4% were sex cord-stromal tumors, and 3.8% were germ cell tumors, and it was negative in benign and borderline tumors.

Benign mucinous cystadenoma with stromal luteinization responsible for maternal virilization and fetal intrauterine growth restriction

Virilization caused by ovarian tumors with functioning stroma during pregnancy is extremely rare and has been reported to be due to different types of ovarian tumors. In mucinous cystadenomas with maternal virilization during pregnancy, the stromal cells responsible for hormone secretion resemble lutein or Leydig cells and have been referred to as luteinized stromal cells. Here we present a rare case of mucinous cystadenoma accompanied by virilization, which was also the cause of fetal intrauterine growth restriction during pregnancy and discuss the mechanisms of hormone production in these tumors in the light of the literature.

Variant HNF1 Modulates Epithelial Plasticity of Normal and Transformed Ovary Cells

Ovarian carcinoma arises from the ovarian surface epithelium, which undergoes phenotypic changes characteristic of müllerian epithelium during the first stages of tumorigenesis. The variant isoform of the hepatocyte nuclear factor 1 (vHNF1) is a transcription factor involved in the development of tissues derived from the müllerian duct. Here, we show that vHNF1 knockdown in two ovarian carcinoma cell lines, SKOV3 and IGROV1, leads to reduced E-cadherin (E-cadh) expression and decreased proliferation rate. Accordingly, SKOV3 cells ectopically expressing a dominant-negative (DN) vHNF1 mutant undergo an epithelial-mesenchymal-like transition, acquiring a spindle-like morphology, loss of E-cadh, and disrupted cell-cell contacts. Gene expression profiling of DNvHNF1 cells on the basis of a newly compiled list of epithelial-mesenchymal transition-related genes revealed a correlation between vHNF1 loss-of-function and acquisition of the mesenchymal phenotype. Indeed, phenotypic changes were associated with increased Slug transcription and functionality. Accordingly, vHNF1-transfected immortalized ovarian surface epithelial cells showed down-regulation of Snail and Slug transcripts. In DNvHNF1-transfected SKOV3 cells, growth rate decreased, and in vHNF1-transfected immortalized ovarian surface epithelial cells, growth rate increased. By immunohistochemistry, we found a strong association of vHNF1 with E-cadh in clear cell and in a subset of serous carcinomas, data that could potentially contribute in distinguishing different types of ovarian tumors. Our results may help in understanding the biology of ovarian carcinoma, identifying early detection markers, and opening potential avenues for therapeutic intervention.

Molekulares Profiling und prädiktive Signaturen

The identification of tissue-based biomarkers is a major task for molecular cancer research. As ovarian cancer is a malignancy with a particular poor prognosis, new diagnostic tests are needed for the planning of an individualized therapy. Diagnostic biomarkers are investigated on different biological levels using genomics, transcriptomics, proteomics or metabolomics as a major approach. Protein biomarkers as well as RNA biomarkers can be measured in formalin-fixed tissue using immunohistochemistry as well as new techniques for isolation of nucleic acids. Furthermore, gene expression as well as metabolic signatures can be determined using frozen tissue. In a first evaluation, metabolomics has been used to investigate different types of ovarian tumors. In a systems pathology approach the results from the different biological levels are integrated to a combined signature that reflects the biological behaviour of the tumor.

Changes in mRNA and protein levels of human HtrA1, HtrA2 and HtrA3 in ovarian cancer

Objectives Expression of human HtrA1, HtrA2, HtrA3 and TGF-β1 genes was examined in ovarian tissue specimens including 19 normal ovaries, 20 benign tumors, 7 borderline tumors, 44 cancers and 8 Krukenberg tumors. Design and methods mRNA and protein levels were evaluated by semi-quantitative RT-PCR and Western-blotting methods, respectively. Results A statistically significant decrease of HtrA1 and HtrA3 expression in ovarian tumors comparing to normal tissues was observed. A dramatic decrease of HtrA3 mRNA and protein levels in all tumor tissue groups, and a loss of HtrA3 protein in 30% malignant tumors were found. A significant decrease of HtrA1 mRNA, and of HtrA3 mRNA and protein in malignant tumors compared to benign tumors was revealed. HtrA2 expression in tumor tissues was slightly decreased. Expression of TGF-β1 in tumor tissues was not significantly different compared to control tissues. Conclusions Our results show downregulation of HtrA1 and HtrA3 genes' expression in different types of ovarian tumors and give additional evidence that these genes may function as tumor suppressors.

Methylation profile in benign, borderline and malignant ovarian tumors

Promoter hypermethylation is a common phenomenon in neoplasm. The aims of this study were (a) to compare the methylation profiles in different types of ovarian tumors and (b) to determine the possible relationship between the methylation status and different clinicopathologic characteristics. We examined the promoter methylation status of 9 tumor suppressor genes (RARbeta2, TMS1, RIZ1, P15, P16, PTEN, MINT31, APC and HIC1) in 89 ovarian cancers, 16 borderline ovarian tumors, 19 benign ovarian tumors, 16 normal ovarian tissue and 5 ovarian cancer cell lines. The methylation status was examined with respect to clinicopathologic characteristics of the ovarian cancer patients. Methylation indices for ovarian cancer, borderline ovarian tumor, benign ovarian tumor, normal ovarian tissue and ovarian cancer cell lines were 28.8, 20.1, 10.5, 11.8 and 42.2%, respectively. It was significantly higher in ovarian cancer, borderline ovarian tumor and ovarian cancer cell lines (X (2) test, P < 0.001, P = 0.01 and P < 0.001, respectively) than benign or normal ovarian tissues. In ovarian cancer, concurrent methylation of at least two genes (CM2) was associated with early stage disease (X (2) test, P = 0.035) and less recurrence (X (2) test, P = 0.020). When the methylation statuses of the nine genes as well as CM2 were included in multivariate Cox Regression analysis, CM2 was the only independent predictor for survival (P = 0.013). CM2 was an independent predictor for survival in ovarian cancer.

Differential Expression of Claudin Family Proteins in Mouse Ovarian Serous Papillary Epithelial Adenoma in Aging FSH Receptor-Deficient Mutants

Ovarian cancer is a deadly disease with long latency. To understand the consequences of loss of folliclestimulating hormone receptor (FSH-R) signaling and to explore why the atrophic and anovulatory ovaries of follitropin receptor knockout (FORKO) mice develop different types of ovarian tumors, including serous papillary epithelial adenoma later in life, we used mRNA expression profiling to gain a comprehensive view of misregulated genes. Using real-time quantitative reverse transcription-polymerase chain reaction, protein analysis, and cellular localization, we show, for the first time, in vivo evidence that, in the absence of FSH-R signaling, claudin-3, claudin-4, and claudin-11 are selectively upregulated, whereas claudin-1 decreases in ovarian surface epithelium and tumors in comparison to wild type. In vitro experiments using a mouse ovarian surface epithelial cell line derived from wild-type females reveal direct hormonal influence on claudin proteins. Although recent studies suggest that cell junction proteins are differentially expressed in ovarian tumors in women, the etiology of such changes remains unclear. Our results suggest an altered hormonal environment resulting from FSH-R loss as a cause of early changes in tight junction proteins that predispose the ovary to late-onset tumors that occur with aging. More importantly, this study identifies claudin-11 overexpression in mouse ovarian serous cystadenoma.

Genetic and cytogenetic observations among different types of ovarian tumors are compatible with a progression model underlying ovarian tumorigenesis

In this report we present the characterization of ovarian neoplasms including benign tumors, borderline tumors, and invasive carcinomas in order to assess whether a sharing of cytogenetic abnormalities is present in all three types of tumors. A cohort of 114 newly diagnosed and untreated ovarian epithelial tumors were analyzed by cytogenetic and molecular cytogenetic approaches with probes specific for chromosome 6. Three groups of chromosome abnormalities were identified: the first group included abnormalities common to all tumor classes (losses of chromosomes 6, 8, 10, 11, 15, 16, 17, 18, 19, 20, 21, 22, and X; gains of chromosomes 1, 3, 5, and 12; 6q24∼qter deletions); the second group presented specific abnormalities present in malignant but not in benign tumors (losses of chromosomes 2, 7, 13, and 14; gains of chromosome 4 and chromosome markers); and the last group included abnormalities unique to invasive carcinomas (loss of chromosome 4; gains of chromosomes 2, 7, 8, 9, 10, 16, 17, 18, 19, 20, and 21; 6q16∼q24 deletions; rearrangements of 3p, 3q, 13q, and 21q regions). The presence of shared chromosomal alterations in all three types of ovarian neoplasms investigated in this report seems therefore to suggest a progression model for these types of tumors.

Macrophages and Microvessel Density in Tumors of the Ovary

Macrophages are members of the mononuclear phagocyte system and synthesize and release many angiogenesis stimulators and inhibitors. Previous studies have demonstrated heterogeneous macrophage populations in ovarian tumors. The aim of this study was to compare macrophage number between different types of ovarian tumors and between regions of high (HVD) and average (AVD) microvessel density (MVD). Macrophages were visualized using CD68 antibody. Previously determined regions of HVD and AVD were located on CD68 immunostained sections and image analysis software was used to count the number of positively stained cells per square millimeter. CD68-positive macrophage number did not differ between benign, mucinous, and serous ovarian tumors or between regions of HVD and AVD (ANOVA;P> 0.05). In both HVD and AVD regions of benign tumors, macrophage number positively correlated with MVD (Spearman rank correlation coefficient;P< 0.03). In contrast, a small but significant negative correlation between macrophage number and MVD was observed in HVD regions of serous tumors (Spearman rank correlation coefficient;P> 0.05). Macrophage infiltration does not appear to differ between ovarian tumor types; however, macrophages may have a positive influence on the vascularization of benign ovarian tumors.

Mutation, ageing, and ovarian cancer

The most significant risk factor for cancer is age. 1 Cohen HJ Biology of aging as related to cancer. Cancer. 1994; 74: 2092-2100 Crossref PubMed Scopus (75) Google Scholar One potential contributing cause may be an age-related accumulation of somatic cell mutations. If this putative accumulation is due to an increase in a specific mutational event, it should be possible to detect an altered mutational spectrum in cancers removed from older patients. We have searched for such a mutational signature in primary ovarian tumours of epithelial origin obtained from 113 patients treated at the University of Kentucky from 1990 to 1994. The mean and median age at diagnosis of these patients was 55·3 and 56 years, respectively. Our study focused on loss of heterozygosity on chromosome 17 because this type of genetic alteration is common in ovarian cancer. 2 Pieretti M Cavalieri C Conway PS Gallion HH Powell DE Turker MS Genetic alterations distinguish different types of ovarian tumors. Int J Cancer. 1995; 64: 434-440 Crossref PubMed Scopus (68) Google Scholar

Genetic alterations distinguish different types of ovarian tumors.

Seventy-four sporadic ovarian tumors were studied for loss of heterozygosity (LOH) and microsatellite instability (MI) with 20 polymorphic markers on chromosome 17 and at least I marker on every other chromosome. Additionally, activation of the K-ras oncogene was examined through mutation analysis of codon 12. A majority of the tumors analyzed were low grade and/or of the mucinous histologic type. A negative correlation between LOH on chromosome 17 and K-ras activation was observed, with the former alteration present in the majority of high grade serous and endometrioid tumors and the latter most commonly found in the mucinous and low malignant potential (LMP) tumors. In 60% of cases where LOH on chromosome 17 was present, it was observed at all informative markers, indicating chromosome loss. In these cases, frequent events of LOH were observed on the other chromosomes. When confined events of LOH were observed on chromosome 17, fewer events of LOH were observed on the other chromosomes. In the absence of LOH on chromosome 17, LOH on other chromosomes was rare. K-ras activation was most commonly observed in tumors with no LOH events. Two endometrioid tumors and 2 mucinous tumors demonstrated MI. Our data support the involvement of different molecular pathways in the development of different types of ovarian tumors.

Trans-vaginal ultrasound examination of ovarian masses in premenopausal women

Objective: Two scoring systems based on trans-vaginal sonographic findings of ovarian tumors were evaluated with respect to the prediction of ovarian malignancy. Study design: In this retrospective study, 64 premenopausal non-pregnant patients with an ovarian tumor underwent trans-vaginal sonography from 1991 to 1993. In each women a numerical score was calculated using two methods. Method A included four variables: inner wall structure, wall thickness, presence of septa and echogenicity. The point scale ranged from 4 to 15 points. Method B included three morphological characteristics: volume, wall structure and septal structure, the point scale ranging from 0 to 12 points. The threshold values for predictability of malignancy were 9 and 5 points for methods A and B, respectively. Results: The mean age of the patients was 32.2 years (range 22–44). The mean gravidity was 2.6 (range 0–5) in 45 women, 19 women being nulliparous. Fifty-five masses were surgically proven to be benign and 9 women had primary malignant tumors. Sensitivity and specificity for prediction of malignancy were 89% and 73%, respectively, for method A, and 89% and 70%, respectively, for method B. Positive predictive value and negative predictive value for malignancy were 35% and 97% for method A and 29% and 64% for method B. The mean morphology scores on benign and malignant masses, calculated by method A, were 6.94 ± 2.36 S.D. and 12.0 ± 2.4 S.D. ( P < 0.01). The same scores, calculated by method B, were 4.16 ± 1.16 S.D. and 9.44 ± 2.96 S.D. ( P < 0.01). We found a considerable overlap in the scores of different types of ovarian tumors. Conclusions: Both methods are easy to apply and provided explicit data. Method A was shown to be more effective. The number of false positive results was relatively high. The most important single sonographic characteristic of the malignant masses are the wall structure abnormalities.

Ovarian tumors in childhood and adolescents - Our eight years experiences

Aims: To study the distribution of different types of ovarian tumors seen in adolescents and children and evaluate the commonest tumor during this period. Methods: A prospective study conducted at Dept of Ob/Gyn, Tribhuvan University Teaching Hospital form January 1999 - January 2008. Results: There were a total of 80 cases of ovarian tumors in childhood and adolescents. Most of the cases had presented to the outpatient department of Ob/Gyn (54%), Medicine (10%), Surgery (21%) and Emergency Unit (15%). Majority of the cases were between the ages of 15 to 19 and tumors in childhood age up to 14 represented 21% of the total ( &lt; 10year being 4). The most frequently occurring tumor was Germ cell tumors accounting for 59 (73.7%) of the total. Out of which dermoid was the most frequently occurring in 45(76.2%). Nineteen (23.71 %) of the total tumor were malignant. All of them underwent laparatomy followed by enucleation (14); Unilateral ophoorectomy (28), unilateral salphingooophorectomy (36) and TAHBSO (2). Conclusion: This study shows the preponderance of germ cell tumor and high percentages of malignancies within germ cell tumor in young children and adolescents. Keywords: childhood, adolescent, ovarian tumors, malignancy doi:10.3126/njog.v3i1.1438 NJOG 2008 May-June; 3(1): 39 - 42