Cathepsins B, L and cystatin C in cyst fluid of ovarian tumors

Introduction

In cancer, an extracellular and membrane bound localization of cathepsins contribute to the invasion of tumor cells at the basement membrane.

Methods

This is the first study that explored levels of cathepsins B (CatB), L (CatL) and their inhibitor cystatin C (CysC) in the cystic fluid (CF) of ovarian tumors (n = 110).

Results

CF contained considerable amounts of CatB, CatL and CysC. Remarkable differences in CatB and CatL and CysC CF levels were found between different histopathological tumor subtypes. Levels of CatB and CysC were significantly higher in CF of malignant serous tumors compared to those found in benign serous tumors (p = 0.010 and p = 0.001 respectively), whereas levels of CatL were significantly higher in CF of malignant mucinous tumors compared to those found in benign mucinous tumors (p = 0.035). CatB and CysC showed a strong correlation in the group of patients with malignant serous tumors (p < 0.001; R = 0.921) suggesting that the increase in CatB might be balanced by a corresponding increase in CysC.

Conclusion

Further studies are warranted to investigate cathepsins as possible prognostic biomarkers for the aggressiveness of ovarian cancer.     

Effects of histologic type on levels of macrophage colony-stimulating factor in liquid contents of benign ovarian tumors

BACKGROUND: Normal ovarian tissue is rich in cytokines. Cytokines are important in the physiology of ovarian function. Most of the same cytokines that are found in normal ovarian tissue are also found in association with benign and malignant tumors in contrast to their functions in normal tissues. Thus, we measured macrophage colony-stimulating factor (M-CSF) levels in the liquid contents of benign ovarian tumors--serous cystadenoma, mucinous cystadenoma, and mature cystic teratoma--and investigated whether M-CSF levels were associated with the histologic type of the ovarian tumors. METHODS: We enrolled 65 patients, 52 with benign ovarian tumor and 13 in the early postmenopausal period with symptoms of a menopausal disorder. Among the 52 patients with benign ovarian tumor, 16 had serous cystadenoma, 21 had mucinous cystadenoma, and 15 had mature cystic teratoma. Immediately after surgery, the liquid content was drawn from the ovarian tumor, then centrifuged, and the separated supernatant was stored at -30 degrees C. The M-CSF level was determined by the sandwich enzyme-linked immunosorbent assay method with use of three antibodies. RESULTS: The level of M-CSF was 12,513 U/mL (median) (range, 0-169,000 U/mL) in serous cystadenoma, 915 U/mL (0-82,500 U/mL) in mucinous cystadenoma, and 149 U/mL (0-6,230 U/mL) in mature cystic teratoma. The M-CSF levels increased significantly from mature cystic teratoma to mucinous cystadenoma to serous cystadenoma. The serum M-CSF levels were 308 to 499 U/mL in patients with benign ovarian tumor. The M-CSF levels did not differ significantly among the three groups. The serum M-CSF levels were 162 U/mL (0-473 U/mL) in menopausal patients. CONCLUSIONS: Elevation of levels of M-CSF varies according to histologic type in benign ovarian tumors. This implies that the antitumor activities of M-CSF for serous cystadenoma, mucinous cystadenoma, and mature cystic teratoma differ by histologic type.     

Increased lipoperoxide levels and antioxidant system in colorectal cancer

In this study, lipid peroxide and glutathione (GSH) levels, GSH peroxidase, GSH S-transferase, superoxide dismutase, γ-glutamylcysteine synthetase and γ-glutamyl transpeptidase activities were investigated in tumorous and nontumorous colorectal tissues obtained from ten patients diagnosed with colon and rectum cancer. Histopathological evaluations, including type, stage, necrosis and lymphocyte infiltration, were also performed for each patient. According to the results, lipid peroxide and GSH levels and the activities of GSH peroxidase, superoxide dismutase, γ-glutamylcysteine synthetase were found to be increased, while GSH S-transferase and γ-glutamyl transpeptidase activities remained unchanged in tumors compared to adjacent normal tissues of subjects with colorectal cancer. However, the considerable interindividual variations were found in these parameters. A definite interrelation between histopathological results with lipid peroxidation and antioxidant system was not observed. Received: 22 December 1997 / Accepted: 7 May 1998     

Effect of quercetin on galactose-induced hyperglycaemic oxidative stress in hepatic and neuronal tissues of Wistar rats

Abstract In recent times there has been great demand for natural products that have possible preventive action against diabetes and its secondary complications. Keeping this in mind, this study was undertaken to investigate the influence of the flavonoid, quercetin, on oxidative stress markers and the antioxidant defence system of hepatic and neuronal tissues from galactose-induced hyperglycaemic rats. Weanling male Wistar rats were treated with 30% galactose in AIN 93 diet (group B, n=8) to induce hyperglycaemia. Control rats received normal Stock AIN 93 diet (group A, n=8). The third set of rats received group B diet with quercetin at 400 mg/100 g diet (group C, n=8). Glucose levels and body weights were measured on a weekly basis for four weeks to monitor the hyperglycaemia induced by galactose feeding. Parameters involved in the pathogenesis of galactose-induced hyperglycaemia, which included organosomatic index, protein content, antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), tryptophan fluorescence, content of protein carbonyls, prooxidant malonaldehyde (MDA) and glutathione (GSH) in hepatic and neuronal tissues were determined at the end of the fourth week. The study suggest that quercetin counters the pro-oxidant effects of galactose-induced hyperglycaemic stress, as there was a significant reversal of changes with respect to body weights, organosomatic index of hepatic and neuronal tissues, lipid peroxidation, protein carbonyl content, reduced glutathione and activities of antioxidant enzymes. In addition, treatment with quercetin appears to reduce the osmotic stress induced by hyperglycaemia, as assessed by polyol pathway enzyme aldose reductase. These results imply that inclusion of quercetin in the diet controls, to some extent, galactose-induced hyperglycaemia and its attendant complications.     

Evidence for oxidative stress in tissues derived from succinate semialdehyde dehydrogenase-deficient mice

Summary Animal models of inborn errors of metabolism are useful for investigating the pathogenesis associated with the corresponding human disease. Since the mechanisms involved in the pathophysiology of succinate semialdehyde dehydrogenase (SSADH) deficiency (Aldh5a1; OMIM 271980) are still not established, in the present study we evaluated the tissue antioxidant defences and lipid peroxidation in various cerebral structures (cortex, cerebellum, thalamus and hippocampus) and in the liver of SSADH-deficient mice. The parameters analysed were total radical-trapping antioxidant potential (TRAP) and glutathione (GSH) levels, the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), as well as thiobarbituric acid-reactive substances (TBARS). We first observed that the tissue nonenzymatic antioxidant defences were significantly reduced in the SSADH-deficient animals, particularly in the liver (decreased TRAP and GSH) and in the cerebral cortex (decreased GSH), as compared to the wild-type mice. Furthermore, SOD activity was significantly increased in the liver and cerebellum, whereas the activity of CAT was significantly higher in the thalamus. In contrast, GPx activity was significantly diminished in the hippocampus. Finally, we observed that lipid peroxidation (TBARS levels) was markedly increased in the liver and cerebral cortex, reflecting a high lipid oxidative damage in these tissues. Our data showing an imbalance between tissue antioxidant defences and oxidative attack strongly indicate that oxidative stress is involved in the pathophysiology of SSADH deficiency in mice, and likely the corresponding human disorder. Competing interests: None declared References to electronic databases: Succinic semialdehyde dehydrogenase (SSADH) deficiency, OMIM 271980.     

Surgery of ovarian tumors in children

Surgery of ovarian tumors in children requires a good knowledge of these lesions. Complete resection is mandatory for malignant lesions, and in the case of benign tumors preservation of healthy ovarian tissue is crucial. Diagnosis is based on clinical features (age and hormonal status), imaging and tumor marker levels. Laparoscopy is of great help in making a diagnosis and staging when the lesion is malignant. Laparotomy by a supra-pubic approach is, however, the only way to ensure a safe treatment of the lesion by avoiding any risk of tumor spillage, which constitutes a chance loss. Surgical treatment consists of complete ovariectomy for a malignant tumor and partial ovariectomy when the lesion is surely benign. Preservation of fertility is based on conservative surgery for uni- or bilateral benign lesions, and may be discussed in some selected cases of bilateral malignant tumors. When the remaining ovarian tissue predicts precocious ovarian failure, ovarian tissue or oocyte cryopreservation may be proposed to patients and their families.     

Enzyme Activity in Invasive Tumors of Human Breast and Colon

Elevated levels of glycoprotein:sialyltransferase activity (EC 2.4.99.1; CMP-N-acetylneuraminate: D-galactosyl-glycoprotein N-acetylneuraminyltransferase) were found in human malignant neoplastic tissues compared to normal, benign, and "preneoplastic" tissues. This increase was not due to the cell density of the tissue. Elevated levels of certain proteases and glycosidases were also found. The increase in transferase activity may be associated with altered membrane synthesis in the neoplastic state; changes in the activity of degradative enzymes may be associated with tumor invasiveness and maintenance of the neoplastic state. Measurements on human tumors are possibly more directly relevant to cancer than those described for transformed fibroblastic cells in vitro.     

卵巢浆液性腺癌组织中MMP-2、MT1-MMP的表达变化及意义

目的观察卵巢浆液性腺癌中的基质金属蛋白酶-2（MMP-2）、膜型基质金属蛋白酶-1（MT1-MMP）的表达变化。方法采用免疫组化PV6000法检测50例卵巢浆液性腺癌、30例卵巢交界性浆液性腺瘤和30例卵巢良性浆液性腺瘤组织中的MMP-2、MT1-MMP。结果MMP-2和MT1-MMP在卵巢浆液性腺癌和交界性浆液性腺瘤中的表达阳性率高于良性浆液性腺瘤（P〈0．05）。卵巢良性浆液性腺瘤组织中的MMP-2、MT1-MMP与病理分级、淋巴结转移、临床分期和预后有关（P均〈0．0．5）。卵巢浆液性腺癌中MMP-2、MT1-MMP的表达呈正相关（L=0．61,P〈0．01）。结论卵巢浆液性腺癌中MMP-2、MT1-MMP表达上调。二者在卵巢浆液性腺癌的发生、浸润和转移中过程中协同发挥重要作用,可作为判断肿瘤恶性程度和预后的重要指标。     

Methylation profile in benign,borderline and malignant ovarian tumors

Purpose 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. Methods We examined the promoter methylation status of 9 tumor suppressor genes (RARβ2, 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. Results 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). Conclusion CM2 was an independent predictor for survival in ovarian cancer.     

卵巢恶性肿瘤组织中HLA—G、HLA—E的表达及意义

目的探讨人白细胞抗原（HLA）在卵巢恶性肿瘤发生、发展中的作用。方法采用RT—PCR和流式细胞分析技术检测60份卵巢恶性肿瘤组织（恶性组）、30份卵巢良性肿瘤组织（良性组）和10份正常卵巢组织（对照组）标本中HLA-G、HLA—E的表达。结果恶性组HLA—G、HLA-E阳性表达率显著高于良性组与对照组（P均〈0．05）;HLA—G、HLA—E表达与肿瘤组织类型无关,与临床分期、病理分级显著相关,临床期别越晚、组织分化越差,抗原表达水平越高。结论HLA-G、HIA-E参与了卵巢恶性肿瘤的发生、发展过程,可能机制为癌细胞产生免疫耐受,逃逸宿主的免疫监视。     

Influence of telomerase activity on bone and soft tissue tumors

Purpose Telomeres consisting of a repeating nucleotide sequence (TTAGGG)n are shortened in normal somatic cells. Telomerase is an enzyme that elongates the telomere sequence and is detected in most human cancers and usually not in normal somatic cells. Little is known about telomerase activity in bone and soft tissue tumors. The aim of this study was to investigate the relationship between telomerase activity and clinical factors in bone and soft tissue tumors.Methods Telomerase activity was measured using the modified telomeric repeat amplification protocol (TRAP) assay in 115 bone and soft tissue tumors obtained through open biopsy or resection.Results Telomerase activity was detected in 10% of benign tumors and 44% of malignant tumors (p<0.001). A higher incidence of telomerase activity was detected in high-grade tumors than in low-grade tumors (p=0.002). The cumulative metastasis-free and overall survival in telomerase-positive patients was significantly worse than in telomerase-negative patients (p=0.045 and p=0.048).Conclusion Our study suggests that telomerase activity is associated with tumor aggressiveness and may be a useful parameter to predict the prognosis of patients with malignant bone and soft tissue tumors.     

Arylamine N-acetyltransferase activities in human breast cancer tissues

N-Acetyltransferase activities were determined in tumor (12 malignant and 6 benign) and control (non-cancerous) breast tissues from 18 female patients. The activities of matched 12 malignant tumor and control tissue cytosols showed 6 rapid, 4 intermediate and 2 slow acetylators based on p-aminobenzoic acid (NAT1) and sulfamethazine (NAT2) as substrates. Compared to the activities of slow acetylators, the rapid acetylators exhibited mean apparent Vmax values about 5- and 50-fold greater for p-aminobenzoic acid and sulfamethazine, respectively. No correlation was observed between the blood and breast tissue N-acetyltransferase (NAT1 and NAT2) activities. When the mean apparent N-acetyltransferase activities of the malignant and benign breast tumor tissues were compared, the results showed an increased activity for both p-aminobenzoic acid (PABA) and sulfamethazine (SMZ) acetylation in the malignant tissues compared to benign ones, and also control tissues showed lower activities compared to tumor tissues. Moreover, the mean NAT2 activity was about 2-fold greater in the malignant tissues when compared to NAT1 activity.     

Morbidity and mortality after liver resection for benign and malignant hepatobiliary lesions

Aim: Although most partial liver resections are performed for malignant lesions, an increasing contingent of benign lesions is also considered for surgery. The aim was to assess post‐operative morbidity and mortality after liver resection for benign hepatobiliary lesions in comparison with outcome after resection of malignant lesions. Methods: A total of 286 liver resections were undertaken between January 1992 and December 2004. After exclusion of resection for bile duct tumours or hepatocellular carcinoma, 205 partial liver resections were retrospectively analysed. Results: Patients with benign lesions comprised 34% of the group (n=70). Benign lesions mainly consisted of focal nodular hyperplasia (n=12; 17%) and liver haemangiomas (11; 15.7%). The malignant lesions consisted of colorectal tumour metastases (n=121; 89%). Patients with benign lesions predominantly underwent minor liver resections (66 vs. 47%; P=0.013). The overall post‐operative morbidity occurred in 31% (64/205). Major morbidity occurred in 16% (22/135) in the malignant group compared with 9% (6/70) in the benign group (P=0.099). No differences were seen in major post‐operative morbidity in the earlier period compared with the later period (14 vs. 14.3%, P=0.950). In multivariate analysis, only presence of comorbidity (P=0.017), prolonged surgical procedure (P=0.021) and surgical irradicality (P=0.039) maintained significance as independent risk factors for major morbidity. Conclusion: Limited liver resections for the treatment of a wide range of benign hepatobiliary lesions are associated with low morbidity and no mortality. However, the indications must be assessed with care. The presence of comorbidity, prolonged surgical time and incomplete resections were associated with major morbidity.     

The Effect of Melatonin on TNBS-Induced Colitis

Ulcerative colitis is a multifactorial inflammatory disease of the colon and rectum with an unknown etiology. The present study was undertaken to investigate the effect of melatonin administration on oxidative damage and apoptosis in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Rats were divided into four groups as follows: Group 1 (n=8)—TNBS colitis; Group 2 (n=8)—melatonin, 10 mg/kg/day ip, for 15 days in addition to TNBS; Group 3 (n=8)—melatonin alone, 10 mg/kg/day ip, for 15 days; and Group 4 (n=8)—isotonic saline solution, 1ml/rat ip, for 15 days (sham control group). Colonic myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels, and glutathione (GSH) levels are indicators of oxidative damage, while caspase-3 activities reveal the degree of apoptosis of the colonic tissue. In all TNBS-treated rats, colonic MPO activity and MDA levels were found to be increased significantly compared to those in the sham group. Colonic MPO activity and MDA levels were significantly lower in the melatonin treatment group compared to TNBS-treated rats. GSH levels of colonic tissues were found to be significantly lower in TNBS-treated rats compared to the sham group. Treatment with melatonin significantly increased GSH levels compared to those in TNBS-treated rats. Caspas-3 activity of colonic tissues was found to be significantly higher in TNBS-treated rats compared to the sham group. Treatment with melatonin significantly decreased caspase-3 activity compared to that in TNBS-treated rats. These results imply a reduction in mucosal damage due to anti-inflammatory and anti-apoptotic effects of melatonin.     

Nuclear magnetic resonance spectroscopy of plasma to distinguish between malignant and benign diseases causing jaundice and cholestasis

The sera of 51 patients with malignant (n=25) and benign (n=26) hepatopancreatobiliary disorders were analysed by¹H magnetic resonance spectroscopy (NMR) in order to distinguish between malignant and benign diseases causing jaundice and/or cholestasis. Macromolecular linewidths were determined both manually and automatically with a computed analysis, and both methylene (CH₂) and methyl (CH₃) resonances were evaluated. The mean linewidth of the CH₃ peak was significantly narrower in the patients with malignant disease than in the patients with benign disease both in the manual and computed analyses, but no significant differences in the CH₂ peak were detected. Diagnostic sensitivity and specificity of the CH₃ peak determined in the computed analysis were 92% and 27% respectively. In the light of the current study, it seems obvious that because overlap between benign and malignant groups was too great,¹H NMR spectroscopy of plasma is not of practical value in distinguishing between benign and malignant causes of jaundice and/or cholestasis.     

Cellular localization of keratin in proliferative epithelial processes and neoplasms of the human ovary

Cytokeratins are one of the intermediate cytoplasmic filaments which contribute to the cytoskeleton. Keratins have recently been demonstrated in normal and neoplastic tissues as well as in human cell lines. It has been suggested that the cellular location of keratin may reflect tissue-specific or epithelial type differentiation. Twenty-three examples of human ovaries containing the full spectrum of epithelial proliferations from inflammatory reactive processes to malignant neoplasia were studied for the cellular distribution of cytokeratin using antisera to human keratin. Nineteen cases contained immunoreactive keratin which was limited to the epithelial cells: 2/2 inflammatory, 8/10 benign tumors, 5/7 borderline tumors, 4/4 carcinomas. There was marked regional heterogeneity in keratin expression such that adjacent morphologically-identical cells could be functionally distinguished by the immunoreactive staining. The predominant cellular localization of keratin varied between histological tumor types in the benign neoplasms: serous = apical, subciliary; endometrioid = apical; mucinous = basal. This pattern was lost in the cytological progression to borderline and malignant tumors. In borderline tumors, the most intense reactivity was noted in areas of cellular atypia and proliferation. In borderline and malignant tumors, keratin was usually present in basal cytoplasmic regions contiguous with stroma.     

Changes in antioxidant defense status in response to cisplatin and 5-FU in esophageal carcinoma

SUMMARY.  The ability of reactive oxygen species to induce cellular damage and to cause cell death opens the possibility of exploiting this property in the treatment of esophageal cancer through a free radical mediated mechanism. The present study was carried out with the aim of evaluating the changes in the antioxidant defense status in esophageal cancer patients treated without and with neoadjuvant therapy (NAT). Forty surgically resected tissue specimens from tumors, tissue adjoining the tumors and paired macroscopically normal mucosa were obtained from esophageal cancer patients treated with or without chemo-radiotherapy. An evaluation of antioxidant defense system in the normal, adjoining and tumor esophageal tissues in response to NAT revealed decreased catalase activity in tumor and adjoining tissues as compared to their respective normal tissue levels. Similarly, decreased superoxide dismutase activity was observed in tumor tissue in response to NAT. In both the treatment groups (with and without NAT), no significant change was observed in the enzyme activity of glutathione reductase in the normal, adjoining and tumor tissues. Enhanced glutathione peroxidase activity was found in tumor tissue, as compared to the adjoining and paired normal tissue of patients after NAT. Estimation of reduced glutathione (GSH) levels showed a significant decline in GSH levels in esophageal tumors after NAT. Depletion of GSH, an endogenous antioxidant, would elevate drug sensitivity and might predispose neoplastic cells to apoptosis in response to NAT. The antioxidant enzymes in the esophageal carcinoma thus may play an important role in influencing the final outcome upon NAT course.     

Prohibitin as a novel target protein of luteinizing hormone in ovarian epithelial carcinogenesis

The exact role of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in ovarian epithelial carcinoma (OEC) development has not been yet characterized. This prompted us to identify particular proteins to better understand the underlying mechanism. Total proteins from ovarian epithelial tumor (OET) cells treated with gonadotropins were analyzed by proteomics. Western blot and immunohistochemistry were used to validate the target protein (prohibitin) and to detect its expression in human ovarian tissue of serous tumors. As the results, prohibitin was found to be significantly up-regulated by LH, with a maximum of 2.5-fold increase at the concentration of 200 mIU/mL. The expression of prohibitin was steadily decreased from benign serous cystadenomas to borderline tumors and serous carcinomas (P < 0.0001). The difference between any two groups was significant (P < 0.001). Collectively, data from this study indicate that prohibitin is one LH-associated protein and it may be protective of ovarian cancer development and progression, supporting that LH may play an inhibitory role in ovarian tumorigenesis.     

Absence of human herpesvirus 8 DNA sequences in vascular tumors of the liver*

ABSTRACT— Kaposi's sarcoma-associated herpes virus (KSHV), also designated human herpesvirus 8 (HHV8), has been detected consistently in Kaposi's sarcoma, body cavity lymphoma and multicentric Castleman's disease, both in human immunodeficiency virus (HIV)-positive and -negative patients. Identification of KSHV/HHV8 DNA sequences in various benign and malignant vascular tumors in HIV-negative patients was reported in one study, but was not confirmed in several other studies. The vascular lesions, other than Kaposi's sarcoma, in which sequences could not be detected have included malignant vascular tumors of serous membranes, infantile capillary hemangiomas, and several benign and malignant vascular tumors of the spleen. We studied 30 primary benign and malignant vascular tumors of the liver; KSHV/HHV8 DNA sequences could not be detected in any. We conclude that this virus plays no role in the etiology of vascular tumors of the liver.     

On the histogenesis and morphology of ovarian carcinomas

Summary The modern classification of ovarian tumors based on histogenetic principles is clinically important in the evaluation of prognosis and differential therapy. Ninety percent of malignant ovarian tumors belong to the category of common carcinomas. All of these tumors originate from the coelomic epithelium at any of various stages of its differentiation into the derivatives of the Müllerian duct, giving rise to a large group of tumors that can be subdivided into serous papillary cystadenocarcinomas arising from surface-like epithelium, mucinous cystadenocarcinomas arising from endocervical-like epithelium, endometrioid carcinomas from endometrium-like epithelium, clear-cell carcinomas from endocervical or endometrium-like epithelium, malignant cystadenofibromas from undetermined pluripotent Müllerian epithelium, and (malignant) Brenner tumors from heterotopic epithelium resebling Wolffian differentiation, as seen in the urothelium.The well differentiated stages of these carcinomas can be readily distinguished by comparing them with the derivates of the Müllerian epithelium. The poorly differentiated types, on the other hand, may provide no criteria for comparison, but can still be classified as belonging to the group of common epithelial tumors. Adenocarcinomas of one type may also contain portions of another related type, e.g., serous papillary carcinomas may contain mucinous glands or groups of clear cells and vice versa. Serous papillary carcinomas form the largest group containing about 50% of all ovarian carcinomas. The endometrioid carcinomas comprise roughly 20%, the mucinous carcinomas 10%, and the clear-cell carcinomas roughly 10%. Five percent of all carcinomas are unclassificable and the remaining 5% constitute the group of rare ovarian carcinomas: the malignant cystadenofibromas, adenosarcomas, malignant mesenchymal mixed tumors, and malignant Brenner tumors. The three main groups can be histologically subdivided into three grades: those of high, moderate and poor differentiation. In addition, a borderline tumor representing a prestage of invasion and metastasis has been recognized.The prognosis with serous papillary carcinomas is poor, with an overall 5-year survival rate of 20%; the 5-year survival rate for mucinous carcinomas is 40%–60%, for endometrioid carcinomas 55%, and for clear-cell carcinomas 40%. Statistically significant data for predicting the prognosis for rare carcinomas are not available.Paper presented at the Annual Meeting of the Swiss Society for Oncology, Basel, March 1983