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PubMed2007

Basal-like grade III invasive ductal carcinoma of the breast: patterns of metastasis and long-term survival.

INTRODUCTION: Cytokeratin (CK) 14, one of several markers expressed in normal myoepithelial/basal cells, is also expressed in a proportion of breast carcinomas. Previous studies have suggested that expression of such 'basal' markers predicts different biological behaviour, with more frequent lung and brain metastases and poorer prognosis than other carcinomas. METHODS: We performed CK14 immunohistochemistry on 443 grade III invasive ductal carcinomas with extended clinical follow-up (mean 116 months), and we correlated CK14 immunopositivity (basal-like phenotype) with clinicopathological criteria. RESULTS: Eighty-eight of 443 (20%) tumours showed CK14 expression. CK14-positive tumours were more likely to be oestrogen receptor-negative (p < 0.0001) and axillary node-negative (p = 0.001) than were CK14-negative cases. CK14-positive cases developed less bone and liver metastases (hazard ratio [HR] 0.49, p = 0.01, and HR 0.53, p = 0.035, respectively) but more frequent brain metastases (HR 1.92, p = 0.051). In patients without metastatic disease, disease-free survival in CK14-positive cases was significantly better than in CK14-negative cases (HR 0.65, p = 0.005). In patients with metastatic disease, however, CK14 positivity was associated with a poorer prognosis (HR 1.84, p = 0.001). The overall survival in CK14-positive and -negative patients was similar at 5 years (60% and 59%, respectively), but the long-term survival was better in CK14-positive patients (HR 0.69, p = 0.02). CONCLUSION: These results demonstrate that basal-like tumours differ in their biological behaviour from other tumours, with a distinct pattern of metastatic spread. Compared to other grade III tumours, basal-like tumours appear to have a relatively good long-term survival but survival after metastases is poor.

Adult↗

PubMed1999

Prognostic significance of DNA ploidy pattern in osteosarcomas in association with chemotherapy.

In this study, we analysed the DNA ploidy of osteosarcomas at biopsy and attempted to clarify the relationship between DNA ploidy pattern and prognosis. Thirty patients with non-metastatic osteosarcoma of an extremity were studied. All underwent intensive chemotherapy with doxorubicin, cisplatin and methotrexate, in addition to wide tumor resection. DNA ploidy was detected by DNA cytofluorometry, using isolated and smeared cells of biopsied tumor tissue. Twelve tumors showed a diploid ploidy pattern and 18 showed a non-diploid pattern such as aneuploidy (15 tumors) and euploid-polyploidy (3 tumors). The event-free survival rate at 9 years was 63.5% in non-diploid osteosarcoma patients and 13.3% in diploid osteosarcoma patients. There was a statistically significant difference between the two groups (P = 0.0278). These results lead us to conclude that a non-diploid osteosarcoma may be more sensitive to chemotherapy than a diploid tumor.

Adolescent↗

PubMed1996

99mTc-MIBI scintigraphy in metastatic renal cell carcinoma: clinical validation of the relationship between 99mTc-MIBI uptake and P-glycoprotein expression in tumour tissue.

Technetium-99m hexakis-2-methoxyisobutylisonitrile (MIBI) and thallium-201 imaging was performed in a patient with metastatic renal cell carcinoma (RCC), which is a well-known tumour type demonstrating P1-glycoprotein (PGP) overexpression. Two scintigraphic patterns - Tl(+)/MIBI(-) in primary tumour and Tl(+)/MIBI(+) in metastatic tumour - were observed, suggesting high- and low-level PGP expression, respectively. Immunochemical study for PGP revealed strong staining of the primary tumour cells. This case clinically validates the previously suggested relationship between 99mTc-MIBI uptake and PGP expression.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1987

DNA clonal heterogeneity of hepatocellular carcinoma demonstrated by Feulgen-DNA analysis.

To demonstrate DNA clonal heterogeneity of hepatocellular carcinomas (HCC), the DNA histographic pattern of both primary HCCs and their recurrent or metastatic lesions were studied among 36 patients (33 men and 3 women). Thirty-six paired aspirations or imprints taken from primary, recurrent or metastatic lesions were stained, using the modified Feulgen method, and the DNA content was measured with a scanning microdensitometer at a wavelength of 550 nm. Paired aspirations or imprints taken from different parts of the same HCC were examined in 17 cases; the DNA distribution patterns were similar in 15 (88%) and differed in only two (12%). A similar DNA histogram was also shown among different tumors in 10 (71%) of 14 patients with multiple HCCs, with a DNA ploidy discrepancy in only four (29%). Two of two subcutaneous metastases and two of three recurrent tumors showed DNA distribution patterns similar to those in their primary HCCs. In summary, a DNA clonal heterogeneity of HCC was found in 19% (7/36). In contrast, the similar DNA histographic patterns found in most instances among different parts of the HCC and between the primary and recurrent or metastatic lesions suggest that HCC may derive from a single cell clone in the majority of cases.

Adult↗

PubMed1986

Patterns of DNA distribution and neurohormone immunoreactivity in the tumour cells: tools for the histopathological assessment of gastro-intestinal carcinoids.

Modern immunohistochemical and DNA cytochemical analyses of gastro-intestinal carcinoids have yielded results that have increased our knowledge of the biological properties and the histogenesis of these theoretically and practically so fascinating kinds of neoplasm. Carcinoids in different anatomical localisations were found to show marked differences with regard to their neurohormone peptide immunoreactivity pattern and their ability to evoke clinical signs and symptoms of hormone overproduction. This can be of great help to the practising pathologist when he tries to predict the anatomical site of an unknown primary tumour from the results of this histopathological assessment of a metastatic nodule of a carcinoid. The DNA distribution pattern in the nuclei of carcinoid tumour cells is a tool in the histopathological assessment of the neoplasm that seems to be of some value in predicting the subsequent clinical course of the disease. This conclusion is based on the results of a pilot study of 8 cases of ileal carcinoids with liver and lymph node metastases. It was found that 4 cases with a rapidly progressive fatal disease had a higher proportion on non-diploid tumour cell nuclei than 4 cases still alive and at full work 5 years after the diagnosis of liver metastases. However, the number of aneuploid tumour cell nuclei was negligible in both groups.

Adult↗

PubMed1995

Significance of endothelium in the fine-needle aspiration biopsy diagnosis of hepatocellular carcinoma.

We reviewed fine-needle aspiration biopsies (FNAB) of hepatocellular carcinoma (HCC) (n = 35), benign hepatic processes (n = 35), cholangiocarcinoma (CC) (n = 6), and metastatic tumors (n = 100) to evaluate the significance of endothelium present either peripherally-wrapping around groups of cells, (peripheral endothelium (PE)), or transgressing sheets of cells (transgressing endothelium (TE)), in distinguishing these lesions. These patterns were assessed as absent, focal, or prominent. Thirty-three of 35 (94%) HCCs contained either focal or prominent PE or TE, compared to only 3 of 35 (9%) benign hepatocytic lesions. Only one benign lesion contained a prominent endothelial component (TE only). Two cases of HCC failed to contain endothelium, one fibrolamellar variant and one well-differentiated HCC. These differences were statistically significant (P < 10(-5), sensitivity 94%, specificity 91%, and positive predictive value [PPV] 92%). Neither pattern of endothelium was present in any CC or metastatic tumor. These differences were also statistically significant (P < 10(-5), sensitivity 94%, and specificity and PVP 100%). We conclude that the presence of endothelium, at least focally in either one or both distinctive patterns, is highly sensitive and specific for HCC and aides in distinguishing it from benign hepatocytic lesions, CC, and metastases.

Adenoma, Bile Duct↗

PubMed2004

The pattern of gene copy number changes in bilateral breast cancer surveyed by cDNA microarray-based comparative genomic hybridization.

The nature of genetic alterations in bilateral breast cancer (BBC) associated with the distinctive development of a second primary tumor or a metastatic lesion is not clearly established. In this study, patterns of promoter methylation and gene copy number changes were assessed for their utility in the distinction of two types of BBC (synchronous and metachronous). Seven cases of synchronous and five cases of metachronous breast cancer tissues were used in X chromosome inactivation assay to assess the methylation pattern of human androgen receptor gene. X chromosome inactivation assay alone did not provide enough information to distinguish the genetic origins of synchronous and metachronous BBC. When four pairs of paraffin-embedded BBC tissues were used in cDNA array-based CGH with placenta DNA as a reference, higher DNA copy number changes were observed from metachronous pairs (9.0%) than from synchronous pairs (3.1%). From the two cases of metachronous pairs tested, 44 genes were found to be commonly modulated in gene copy numbers in a cancer detected later.

Breast Neoplasms↗

PubMed1995

Early metastasis of human solid tumours: expression of cell adhesion molecules.

Loss and gain of cell surface molecules determines the mobilization, emigration and invasiveness of epithelial cancer cells. As a first approach to gain further insight into these processes, we have followed two strategies: (1) to identify tumour cells which have disseminated early from primary carcinomas and to obtain information about the phenotype and prognostic significance of these cells; and (2) to identify molecular changes occurring in primary tumour cells at the time they develop their metastatic potential. Our analyses indicate that changes in the adhesive properties of solid tumour cells, such as down-regulation of desmosomal proteins (e.g. plakoglobin) and neo-expression of ICAM-1 or MUC18, are important determinants of the metastatic capability of individual malignant cells. The expression pattern of these cell adhesion molecules during tumour progression appears to reflect a disturbance at the level of the molecular elements normally responsible for controlling their expression. The outlined current strategies for detection, characterization and antibody therapy of cancer micrometastasis can be applied to the secondary prevention of metastatic disease in patients with minimal residual cancer.

Antigens, CD↗

PubMed2000

Methylation patterns of the E-cadherin 5' CpG island are unstable and reflect the dynamic, heterogeneous loss of E-cadherin expression during metastatic progression.

Metastatic progression of most common epithelial tumors involves a heterogeneous, transient loss of expression of the homotypic cell adhesion protein, E-cadherin, rather than the uniform loss of a functional protein resulting from coding region mutation. Indeed, whereas E-cadherin loss may promote invasion, reexpression may facilitate cell survival within metastatic deposits. The mechanisms underlying such plasticity are unclear. We now show that the heterogeneous loss of E-cadherin expression in primary human breast cancers reflects a heterogeneous pattern of promoter region methylation, which begins early prior to invasion. In cultured human tumor cells, such heterogeneous methylation is dynamic, varying from allele to allele and shifting in relation to the tumor microenvironment. Following invasion in vitro, which favors diminished E-cadherin expression, the density of promoter methylation markedly increased. When these cells were cultured as spheroids, which requires homotypic cell adhesion, promoter methylation decreased dramatically, and E-cadherin was reexpressed. These data show that the methylation associated with E-cadherin loss in human breast cancer is heterogeneous and unstable and suggest that such epigenetic plasticity may contribute to the dynamic, phenotypic heterogeneity that drives metastatic progression.

Alleles↗

PubMed1998

Immunohistopathological characterizatin of spontaneous metastases in a human lung mucoepidermoid adenocarcinoma (HLMC) xenograft.

The most common clinical form of lung cancer is a disseminated disease with distant metastases; several years of cancer progression precede presentation, and this ultimately limits the efficacy of curative therapy. In this immunohistochemical study, we examined a mucinous adenocarcinoma cell line, maintained by xenogeneic transplantation, and a spontaneous metastatic variant which produces distant tumors (in liver, spleen and kidney). The aim was to investigate possible parameters which characterize the metastatic process. Histopathological comparison between the two subcutaneous transplanted tumor lines showed that both lines presented a similar cellular morphology, a different pattern of cellular growth and an increased vascularization in the metastatic line with respect to its parent. All the tumor sections expressed differential immune reactivity with monoclonal antibodies against Lewis y (MAb C14), sialyl-Lewis x (MAb SNH3) and Lewis x (MAb FH2) determinants. Neither expressed MUC 1 mucins detectable with monoclonal antibodies reactive with the mucin protein core (MAbs C595 and SM3) nor was carcinoembryonic antigen (MAb C365) expressed. Neoplastic cells were reactive with an anti-pan cytokeratin monoclonal antibody confirming their epithelial histogenesis. Our findings have been evaluated with respect to defining metastatic phenotypes in lung cancer by examination of distinct histopathological and immunological parameters.

Adenocarcinoma, Mucinous↗

PubMed1998

A unique allogenic model of metastatic pheochromocytoma: PC12 rat pheochromocytoma xenografts to nude mice and establishment of metastases-derived PC12 variants.

Local invasion and metastatic spread to distant sites are major causes of death in patients with malignant pheochromocytoma. Since appropriate in vivo models do not exist, little is known about the underlying mechanisms of tumor growth and invasion. We, therefore, developed an animal model of malignant pheochromocytoma and established organotropic metastatic variants of PC12 rat pheochromocytoma cells. PC12 cells were established as xenografts to BALB/c NCR-NU mice. Subsequent to development of tumors or metastases, primary cultures from local tumors, metastases to lymph nodes, lungs and liver were established. These were subcultured in vitro and reinjected for up to five successive in vivo/in vitro cycles. Xenografted PC12 cells grew tumors with a doubling time of 6.78 +/- 0.58 days during log phase of tumor growth, killing hosts within 5-12 weeks depending on the experimental conditions. Tumors reproducibly metastasized to lymph nodes and the lung. Spontaneous metastases to the liver were not observed, but were achieved by intrasplenic injection of parent PC12 cells. In vitro, the metastatic cell lines displayed striking differences in morphology, overall growth patterns and nutritional requirements as well as binding to purified extracellular matrix proteins compared to the parent cell line. In vivo, the metastatic variants showed marked enhancement of metastatic ability. This is the first report of PC12 rat pheochromocytoma cells to exhibit the malignant phenotype in vivo. We also established variant PC12 cell lines that preferentially metastasized to specific sites and that had acquired different in vitro behavior and ability to metastasize. This unique model system should be useful for further studies relating to the invasion and metastases of pheochromocytoma and may prove valuable for investigations of novel antineoplastic therapies in vitro and in vivo.

Animals↗

PubMed1989

Endometrial adenocarcinoma: therapeutic impact of preoperative histopathologic examination of endometrial tissue.

Adenocarcinoma of the endometrium is diagnosed by the histologic evaluation of endometrial tissue. In stage I disease, five-year survival depends upon a number of prognostic factors. Histologic grade and type of carcinoma are most important. The need for pelvic and para-aortic lymphadenectomy is often based on the preoperative histologic grade and type of tumor. The purpose of this study was: 1) to compare preoperative histology of endometrial carcinoma to that found at hysterectomy, 2) to determine if preoperative histology can accurately predict depth of myometrial invasion or extra-uterine spread, 3) to determine whether para-aortic lymphadenectomy could be deleted based only on the preoperative finding of well differentiated carcinoma. In 19 (28%) of the 68 patients studied, the histologic grade or pattern at hysterectomy was different from that found preoperatively. In seven (13%) of the 52 "good prognosis" patients with grades 1 and 2 preoperative histology, hysterectomy revealed a more serious histologic type. Three of the seven (43%) had extrauterine spread. In the 16 "poor prognosis" patients with preoperative grade 3 or papillary serous/clear cell carcinoma, 14 (88%) had a similar histologic pattern at hysterectomy. Three of these patients had metastatic disease. Depth of myometrial invasion could not be predicted by preoperative histology even though the data suggested that extrauterine spread could. Clinical stage I endometrial carcinoma, grade 1 or 2, should not be treated without para-aortic nodal sampling based only on a supposedly favorable preoperative histologic pattern. Confirmed para-aortic nodal disease will alter the fields of post-operative radiation therapy should that become necessary. In these patients, however, pelvic lymphadenectomy is not justified.2 +

Adenocarcinoma↗

PubMed2006

Expression of S-100 protein in renal cell neoplasms.

Polyclonal antibody to S-100 protein has been routinely applied for initial screening of various types of tumors, including, melanocytic tumors and neurogenic tumors. S-100 protein has been shown to have a broad distribution in human tissues, including renal tubules. The potential utility of S-100 protein in renal cell neoplasms has not been extensively investigated. Using an EnVision-Horseradish Peroxidase (HRP; Dako, Carpinteria, Calif) kit, we evaluated the diagnostic value of S-100 protein on tissue microarray sections from 175 cases of renal epithelial neoplasm (145 primary renal neoplasms and 30 metastatic renal cell carcinomas) and 24 non-neoplastic renal tissues. Immunohistochemical stains for pancytokeratin, HMB-45, and Mart-1 were also performed. Western blot using the same antibody (anti-S-100 protein) was performed on 10 cases of renal cell neoplasm. The results demonstrated that nuclear and cytoplasmic staining pattern for S-100 protein was observed in 56 (69%) of 81 conventional (clear cell) renal cell carcinomas (RCCs), 10 (30%) of 33 papillary RCCs, 1 (6%) of 16 ChRCCs, and 13 (87%) of 15 oncocytomas. Among the 81 cases of CRCC, positivity for S-100 protein was seen in 41 (71%) of 58 and 15 (65%) of 23 cases with Furhman nuclear grade I/II and III/IV, respectively. Focal immunostaining was present in 22 (92%) of 24 normal renal tubules. Similar staining pattern was observed in 21 (70%) of 30 metastatic RCCs. Western blotting demonstrated the S-100 protein expression in both renal cell neoplasm and normal renal tissue. Overexpression of S-100 in oncocytomas compared with ChRCCs was confirmed by the data of Western blot and cDNA microarray analysis. Importantly, 14.8% (12/81) of clear cell RCC and 13.3% (4/30) of metastatic RCC revealed an immunostaining profile of pancytokeratin (-)/S-100 protein (+). These data indicate that caution should be taken in interpreting an unknown primary with S-100 positivity and cytokeratin negativity. In addition, it suggests that S-100 has a diagnostic value in differentiating oncocytoma from ChRCC.

Adenoma, Oxyphilic↗

PubMedDate not supplied

Proteinases and proteinase inhibition by cytotoxic and antimetastatic drugs in transplantable solid metastasizing tumors in mice.

The tissue levels of two proteolytic enzymes, plasminogen activator and cathepsin B - like cysteine proteinase, which were found to be increased in malignant tumors and to be proportional to tumor metastatic potential in some instances, have been determined in a panel of solid metastasizing tumors in mice. The examination of B16 melanoma, MCa mammary carcinoma and of two lines of Lewis lung carcinoma with widely different potential to spontaneously metastasize, showed no correlation between metastatic potential and the tissue content of the proteinases considered. The treatment of the animals with cytotoxic antitumor drugs (CCNU, GANU, cisplatin, and cyclophosphamide) or with antimetastatic drugs acting with a mechanism unrelated with cytotoxicity (ICRF 159 and DM-COOK) caused only marginal inhibition in some instances, whereas no meaningful pattern of inhibition either based in terms of metastatic potential of the tumor or on drug mechanism of action was recognizable. A direct involvement of the two proteinases examined in the process of metastasis in the tumor panel used is thus not apparent, although a more complex interaction with other latent proteinases and inhibitors might be operative.

Animals↗

PubMed2005

Gene expression profiles correlate with the morphology and metastasis characteristics of renal cell carcinoma cells.

Renal cell carcinoma (RCC) shows various clinical behaviors, and currently surgical modalities are the only effective therapy against this cancer. To discern the genomic background affecting clinical characteristics such as metastasis, we analyzed the gene expression profiles of the RCCs by DNA microarray using cell lines originating from primary or metastatic lesions. RNA was extracted from ten SKRC RCC cell lines and gene expression profiling was performed using a cDNA microarray of nearly 4,000 human cDNA clones. We compared the gene expression profiles between these SKRC cell lines and the normal renal proximal tubular cell line and among SKRC cell lines that showed different characteristics. The clustering of the selected 62 genes revealed similar profiling patterns between SKRC-17 and SKRC-29 cells that were derived from metastatic RCC lesions. Another cell line from a metastatic lesion, SKRC-52, with a unique spindle-shaped morphology, had a different pattern of expression profiling from the other cell lines. We found several genes up-regulated in the cell lines from metastatic lesions; transgelin, which is reportedly involved in cell proliferation and migration, was up-regulated in SKRC-52. The unique profiling pattern of gene expression clearly correlated with cell morphology and metastatic potential. Such profiling might contribute to identifying the genes involved in the clinical characteristics of RCC.

Carcinoma, Renal Cell↗

PubMed1992

Helix pomatia lectin binding pattern of brain metastases originating from breast cancers.

The glycosylation pattern of brain metastases originating from primary breast carcinomas was investigated using Helix pomatia agglutinin (HPA), a lectin which recognises N-acetyl-galactosamine (GalNac) residues of glycoconjugates. In a previous retrospective study this lectin was shown to label only those primary breast cancers that metastasised. To explore this as a clinical marker of metastatic breast cancer behaviour it is necessary to analyse the HPA binding pattern of metastases to see if this differs from primary cancers. To test the question if brain metastases commitently retain this trait of metastatic primary tumors, we studied Helix pomatia binding pattern of brain metastases removed by surgical excision and immediately fixed and processed. Brain metastases from 16 patients with breast cancer were obtained, 13/16 metastases showed binding to the cytoplasm in the majority of cancer cells, 3/16 did not show binding to cancer cells. Normal adjacent brain showed binding to red blood cells, to capillary endothelium of several biopsies and to rare neurones; this binding did not relate to cancer cell binding. Therefore we conclude that HPA is a relatively stable marker for metastasizing breast cancer cells.

Animals↗

PubMed1994

A correlation between mutation of the p53 gene and histological heterogeneity in differentiated adenocarcinomas of the lung, with reference to stepwise progression and metastatic ability.

I examined 15 cases of differentiated adenocarcinoma of the lung which showed mutation of the p53 gene and whose primary lesions could be divided into three components (peripheral component, intermediate component and central component). Mutation of the p53 gene in each component was examined by an immunohistochemical method and polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) analysis in order to elucidate the correlation between histological types in the adenocarcinoma and mutation of the p53 gene. Furthermore, immunohistochemical detection of Ki-67 antigen and the ploidy pattern were examined for each component of the primary lesions and metastatic lesions. As a result, mutation of the p53 gene was detected mainly in the intermediate and central components, that is, in 13 cases in the intermediate component and in all cases in the central component. Higher proliferative activity as well as a DNA aneuploidy pattern were seen in these areas. In contrast, the peripheral component showed mutation of the p53 genes in only 4 cases. Lower proliferative activity and a normal diploidy pattern were seen in this area. As for the metastatic lesions, mutations of the p53 gene were detected in the metastasis of the lymph nodes and brain, as well as in the intermediate and central components of the primary lesions. Moreover, these metastatic lesions showed a higher proliferative activity which was similar index to the central or intermediate one. In 2 cases the metastasis of the lymph node showed an aneuploidy pattern as well as the intermediate and central components.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed1993

New and unusual aspects of ovarian germ cell tumors.

Ovarian germ cell tumors are reviewed with emphasis on recent developments. In the primitive germ cell tumor group the recently recognized subtypes of yolk sac tumor, the hepatoid and glandular variants are described. Hepatoid tumors, which resemble hepatocellular carcinomas, are usually admixed with other patterns of yolk sac neoplasia but when the hepatoid component predominates, distinction from metastatic hepatocellular carcinoma may be difficult. Glandular yolk sac tumors include those with a cribriform pattern as well as tumors that may be confused with endometrioid carcinoma. Within the teratoma category, a recent paper exploring the occasional relation between immature teratomas and dermoid cysts is reviewed. Problems caused by some of the monodermal teratomas are also highlighted. Struma ovarii may be the source of many diagnostic problems. It may be cystic and microscopic examination may reveal inconspicuous numbers of clearly recognizable thyroid follicles, resulting in confusion with other cystic ovarian tumors. In noncystic strumas many patterns, such as solid or pseudotubular, may be seen and the presence of cells with abundant clear or eosinophilic cytoplasm may add to the diagnostic difficulty, particularly if other teratomatous elements are lacking. Immunohistochemical staining for thyroglobulin may be crucial in establishing the diagnosis of a struma in these situations. The problem of identifying reliable criteria for malignancy of struma ovarii is explored on the basis of recent information. The two most recently recognized subtypes of carcinoid tumor, strumal and mucinous, are reviewed as are primary neuroectodermal and sebaceous tumors of the ovary. Unusual clinical features of germ cell tumors are discussed under three main categories: endocrine syndromes, paraendocrine and paraneoplastic syndromes, and miscellaneous. Included in these categories are disorders such as sexual precocity in association with germ cell tumors containing syncytiotrophoblast cells, endocrine abnormalities associated with the recently described functioning ovarian tumors with peripheral steroid cell proliferation, hyperthyroidism with struma ovarii, the carcinoid syndrome, autoimmune hemolytic anemia associated with dermoid cysts, complications of dermoid cyst rupture, which may simulate disseminated carcinomatosis, and ascites and Meigs' syndrome associated with struma ovarii.

Carcinoid Tumor↗