Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 64-year-old woman (gravida 0, para 0) had a unilateral ovarian mass measuring 14 cm in its greatest diameter, which was mostly solid. Microscopically, the tumour was characterized by two predominant proliferating patterns: a carcinoid-like pattern with trabecular, tubular, glandular, or insular arrangements and a closely packed nesting pattern with central coagulation necrosis and occasional glandular arrangements. These two patterns were intermingled, and numerous mitotic figures were present. Electron microscopy showed neurosecretory granules in the cells, which were argyrophilic and positive for neuroendocrine markers (chromogranin, leu 7, neuron-specific enolase, and synaptophysin). The tumour was aneuploid by flow cytometry. The patient received chemotherapy postoperatively, developed brain and multiple bone metastases and died of disease 10 months after surgery. This tumour must be distinguished from other small cell neoplasms, especially ovarian small cell carcinoma of the hypercalcaemic type.
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PMID:Small cell neuroendocrine carcinoma of the ovary. 913 47

Breast cancer is the most frequent malignant tumor in women, whereas it is rare in men. In our own case series the ratio is 175:1. The present paper deals with an evaluation of clinical and morphological findings from a series of 54 de novo male breast cancers observed in our institution from 1978 to 1996 and a comparative discussion of 528 female breast cancers from the same geographic area. We should like to focus on the following observations: At the time of histopathological diagnosis, male patients with breast cancer were on average 67 (34-87) years old and thus 5 years older than women. Below the age of 40, breast cancer is very rare in men. The lag time between first symptoms and surgery was on average 42 weeks, i.e. twice as long as in women. In the vast majority of cases palpation of a retromamillary nodule was the leading diagnostic symptom. Mamillary secretion appeared to be an early symptom with favorable relation to prognosis by tumor size whereas diffuse breast swelling was an unfavorable late symptom. Bilateral carcinoma and double cancer (breast and prostatic cancer) was observed in one case each. Three patients (3/51 = 6%) had a positive family history (breast cancer in 1st and 2nd degree relatives). The average invasive tumor size was nearly identical with 23 mm (s11.02) in men and 25 mm (s13.48) in women. Men presented more frequently with regional lymph node metastases (53% versus 45%), which tended to develop earlier. pT4 cancers were twice as frequent in men compared to women. In situ cancers were found in 2% (1/54) in men and 4% in women. Similar to females, male breast cancers are predominantly of ductal histological type (NOS-cancers), classical lobular carcinoma with LCIS-components were not observed; special forms (tubular, papillary, mucinous) are slightly more common in men. When reviewing our series, need for revision of the origin of tumor was not found in any of the cases. Metastases of prostatic cancer were never misinterpreted as primary breast cancer. In case of isolated NSE-reaction, cancers with carinoid differentiation pattern are to be found in nearly every second tumor. However, when multiple markers were used (chromogranin A or synaptophysin) only 10% displayed such pattern, which corresponded to a positive hormone receptor status in each case. Quantitative (enzyme immunoassay) and semiquantitative (immunohistochemistry) analysis of steroid hormone receptor status was positive in 86% of 35 cases in men and in 75% in women. In contrast to female breast cancer, hormone status proved to be independent of age in males. The average levels of estrogen and progesterone were higher in men. Overlapping results were found only when cases were compared with postmenopausal women. The Nottingham prognostic index, a product of primary tumor size, axillary lymph node status and grading allows an approximative estimate of the course of the disease; its predictive value is higher than that of isolated tumor markers.
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PMID:[Breast carcinoma in the man. Current results from the viewpoint of clinic and pathology]. 915 4

We report three cases of intrathyroidal paraganglioma. The patients were adult women without significant personal or family histories that presented with an asymptomatic thyroid nodule. The tumors were single, well-circumscribed solid masses, 2 cm in greatest diameter, located within one thyroid lobe. Microscopically, they were encapsulated and showed the typical nesting (Zellballen) pattern of paraganglioma in other sites. Two of the tumors were composed of small- to medium-sized cells with granular amphophilic cytoplasm, and the third consisted of relatively large cells having a similar staining quality. Immunohistochemically, all tumors showed positivity for neuron-specific enolase, chromogranin A, and synaptophysin. S-100 protein-positive sustentacular cells were demonstrated in each case. Negative staining for epithelial markers, thyroglobulin, carcinoembryonic antigen, calcitonin, calcitonin gene-related peptide, serotonin, vimentin, and Congo red excluded other tumors that were considered in the differential diagnosis, such as medullary carcinoma, hyalinizing trabecular adenoma, atypical follicular adenoma, Hurthle-cell neoplasm, and metastatic carcinoid tumor. The patients were alive and well without evidence of recurrent disease at the time of the last follow-up. The previous literature on these tumors is discussed. We conclude that intrathyroidal paraganglioma exists and that this tumor can be distinguished from other similar-appearing neoplasms in this organ.
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PMID:Thyroid paraganglioma: a clinicopathologic and immunohistochemical study of three cases. 923 30

High-grade prostatic intraepithelial neoplasia (HGPIN) is the most likely precursor proliferation of peripheral zone, moderately to poorly differentiated prostatic adenocarcinomas. The usual cell type of the epithelial lining of HGPIN is a glandular epithelial cell with characteristic nuclear abnormalities. Here we report nine cases of unusual types of HGPIN, including three cases of signet-ring cell HGPIN, one case of small cell neuroendocrine HGPIN, and five cases of HGPIN with distinctive mucinous features. The three examples of signet-ring cell PIN were all associated with an invasive primary signet-ring cell carcinoma of the prostate. The HGPIN assumed a classical tufted and micropapillary architectural growth pattern, with the constituent cells exhibiting a morphologic appearance identical to that of the invasive signet-ring cells. The intraepithelial and invasive signet-ring cells were mucin negative and were immunoreactive for prostate-specific antigen (PSA). A fourth case displayed a mixed intraepithelial glandular-small cell neoplastic proliferation, where intraepithelial small cells were histologically identical to surrounding invasive small cell carcinoma cells. The small cell HGPIN and invasive small cell carcinoma cells were positive for the neuroendocrine markers chromogranin, synaptophysin, and neuron-specific enolase. In five cases, mucinous distension of HGPIN glands, producing a flat pattern of the epithelial lining layer, comprised the third unusual pattern of HGPIN. These blue mucinous secretions were readily detected by hematoxylin and eosin staining and were composed of both neutral (periodic acid-Schiff-positive) and acidic (alcian blue-positive) mucins. Herein we document the existence of an intraepithelial proliferation of neoplastic cell types-small cell neuroendocrine and signet-ring cell-that are usually considered as stromal-invasive cells in the prostate. The presence of these rare prostatic cell types in both HGPIN and invasive carcinoma provides further support for a close relationship between HGPIN and invasive carcinoma of the prostate. All three unusual types of HGPIN-signet-ring cell, small cell neuroendocrine, and mucinous-are important to diagnostically recognize because of the strength of association of HGPIN with invasive carcinoma.
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PMID:Unusual histologic types of high-grade prostatic intraepithelial neoplasia. 933 Dec 95

Thirty-five chordomas and more than 100 other tumors that have to be considered in the differential diagnosis, were immunohistochemically analyzed using a panel of antibodies including those to subsets of keratins (K), HBME-1, a monoclonal antibody recognizing an unknown antigen on mesothelial cells, and neuroendocrine markers. The patterns of immunoreactivities in chordoma were compared with those in renal cell carcinoma, colorectal mucinous adenocarcinoma, pituitary adenoma, skeletal chondrosarcoma, and extraskeletal myxoid chondrosarcoma (ESMC). Chordomas were consistently positive for keratin cocktail AE1/AE3, and for the individual keratins K8 and K19, and nearly always positive for K5, but they showed negative or only sporadic reactivity for K7 and K20. The keratin K8 and K19 reactivity was retained in those chordomas showing solid sheets of epithelioid, spindle cells, or cartilaginous metaplasia, and in one of two cases showing overtly sarcomatous transformation. In comparison, keratins were never present in skeletal chondrosarcoma, although K8 and to a lesser extent K19 were seen in occasional cases of ESMC with chordoid features. HBME-1 reacted strongly with chordoma and skeletal chondrosarcoma but was almost never positive in renal or colorectal carcinoma. These carcinomas lacked K5-reactivity, in contrast to chordoma. Chordomas were also consistently positive for neuron-specific enolase and occasionally focally for synaptophysin, but never for chromogranin. In contrast, pituitary adenomas regularly expressed the full spectrum of neuroendocrine markers and differed from chordoma by having a narrower repertoire of keratins, often showing negative or focal keratin 8- or AE1/AE3 reactivity and being almost always K19-negative. These findings indicate that chordoma can be immunohistochemically separated from tumors that can resemble it. Immunohistochemistry is especially useful in the diagnosis of small biopsy specimens that offer limited material for morphological observation.
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PMID:Keratin subsets and monoclonal antibody HBME-1 in chordoma: immunohistochemical differential diagnosis between tumors simulating chordoma. 949 Feb 69

The presence and distribution of S100 protein (alpha and beta subunits), cytokeratin polypeptides, glial fibrillary acidic protein, neurofilaments, vimentin, neuron specific enolase, synaptophysin, HLA class II DR antigen, and pituitary hormones (prolactin, adrenocorticotropic hormone and human chorionic gonadotrophin) in stellate cells were studied immunohistochemically in four normal canine pituitary glands, five canine pituitary adenomas, two canine pituitary carcinomas and two equine pituitary adenomas (with surrounding normal glandular tissue). Stellate cells of the pars distalis and pars intermedia of canine and equine adenohypophyses showed a strong reaction with antibodies against S100 protein subunits alpha and beta. They also reacted with antibody against high and low molecular weight cytokeratins, but not with those against other intermediate filament proteins, neuroendocrine markers, the HLA-class II DR antigen or the pituitary hormones. Other populations of cells expressing both subunits of the S100 protein were polygonal cells of the pars distalis of the adenohypophysis (horse) and marginal epithelial cells of the pars intermedia of the adenohypophysis (dog and horse). Some pituitary tumours had S100-immunoreactive cells with a distribution of alpha and beta subunits that differed between the two species. Some canine tumours (one adenoma and one carcinoma) expressed only the alpha subunit, but both of the equine adenomas expressed alpha and beta protein subunits. Some of the S100-immunoreactive tumour cells reacted with RCK-102 (cytokeratins 5+8) antibody in the dog but not in the horse. The results suggested that canine and equine stellate cells of the adenohypophysis are more closely related to epithelial than to glial cells, as is the case in cattle, sheep and goats but not human beings or mice. No subpopulation of cells of bone marrow origin could be identified among canine stellate cells, as they lack MHC class II antigen. The results also suggested that the presence of S100-immunoreactive cells is more striking in canine and equine tumours than in human tumours.
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PMID:Comparative immunohistochemical study of stellate cells in normal canine and equine adenohypophyses and in pituitary tumours. 950 Feb 36

We present 14 patients with primary sinonasal melanomas (SM) identified from 1984-1997 in our archives (11/14 lateral nose, 1/14 nasal septum, 2/14 paranasal sinuses; 8M/6F, mean age 67.7 years, range 39-88 years). Survival was poor (median 9 months) with death related to extensive local disease and/or widespread hematogenous metastases. The following histological subtypes were identified in descending order: amelanotic small blue cell, pleomorphic, epithelioid, spindle cell and myxoid. High mitotic rate and vascular invasion, absence of tumor-infiltrating lymphocytes and regression were features shared by all SM. Negative staining of B- and T-cell markers, LCA, neuroendocrine markers such as NSE, chromogranin and synaptophysin, and CK-negativity excluded olfactory neuroblastoma, small cell undifferentiated carcinoma, and lymphoma. S-100 protein was expressed in all SM, but demonstrated variable staining intensity with areas of complete negativity. HMB45 was strongly and uniformly (>80%) expressed in all undifferentiated small blue cell SM. The pigmented SM were predominantly HMB45-negative. The strong HMB45 staining in amelanotic small blue cell SM is explained by the reaction of HMB45 antibody with an oncofetal antigen found in immature melanosomes. In these poorly differentiated amelanotic malignant melanomas, antibody to HMB45 proved to be a superb diagnostic marker. We therefore strongly advocate the inclusion of HMB45 antibody in the panel of antibodies for initial work-up of undifferentiated mucosal neoplasms, since a negative S-100 stain in small biopsy material may result in incorrect classification of these neoplasms.
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PMID:Primary mucosal melanomas of the nasal cavity and paranasal sinuses. A clinicopathological analysis of 14 cases. 954 30

Cancer registration statistics of economically advanced countries indicate that bladder carcinoma incidence ranks fourth in men and eighth in women, but a reliable tumor marker for predicting the disease course is still lacking. We designed an immunohistochemical study to comprehensively assess the trophoblastic hormone production profile of transitional cell carcinoma (TCC) of the bladder. Moreover, we correlated histological differentiation and tumor stages with marker expression and, finally, evaluated a potential tumor origin of hCGbeta core-fragment (hCGbetacf). To this end, formalin-fixed, paraffin-embedded tumor tissues from 104 patients with urothelial neoplasms of various histological grades (23 GI, 24 GII, and 38 GIII) and stage (19pTis, 21pTa, 29pT1, and 35pT2-T4) were analyzed by the immunoperoxidase technique using our own well-characterized monoclonal antibodies against the glycoprotein hormones human chorionic gonadotropin (hCG) and its derivatives hCGalpha, hCGbeta, hCGbetacf, luteinizing hormone (LH, LHbeta), follicle-stimulating hormone (FSH, FSHbeta), and the protein hormones placental lactogen (hPL) and growth hormone (hGH-V/N). Overall, trophoblastic hormone immunoreactivity was found in 36% of TCC. Detailed analysis showed 35% hCGbeta, 17% hCGbetacf, 9% hCGalpha, 4% hCG, and 2% hPL-positive cases. The tumors produced neither GH-N, placental GH-V, nor the pituitary gonadotropins FSH/FSHbeta and LH/LHbeta. Marker positivity significantly increased with high-grade lesions (26% GI- v 55% GIII-TCC) and advanced tumor stages (24% pTa v 63% > or = pT2). Hormone immunoreactivity was frequently observed in highly proliferating areas. Our findings, together with recent structural and clinical studies, strongly suggest that these hormones, or derivates thereof, might act as local tumor growth factors. Normal urothelium, urothelial papillomas, and carcinoma in situ showed no positive reactions. All tumors producing hCG-derived molecules were negative for the concommitantly analyzed neuroendocrine markers chromogranin A, synaptophysin, and neuron-specific enolase (NSE). In summary, one third of TCC ectopically produce trophoblastic hormones, which is specifically correlated with stage and grade. Apart from hCGbeta (97% of the marker-positive cases), the intracellular occurrence of hCGbetacf, apparently the second most frequently produced marker, was surprising, and there was also a lesser degree free hCGalpha and intact holo-hormone expression. The placental protein hormones PL and GH-V are not appropriate tumor marker candidates. Finally, our histogenetic findings support a metaplastic origin of the hCG producing choriocarcinomatous phenotype of some TCC.
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PMID:Production of trophoblastic hormones by transitional cell carcinoma of the bladder: association to tumor stage and grade. 956 88

Pancreatic ductal adenocarcinoma is one of the major causes of cancer mortality in the industrialized world, having among the poorest prognosis of any malignancy. Mutations or alterations in the p53 tumor suppressor gene/protein are observed in 50-70% of these cancers, yet little information is available regarding the phenotypic effects of restoration of wild-type (wt) p53 function in pancreatic ductal carcinoma cells. The consequences of stable reintroduction of wt p53 on apoptosis and differentiation was examined in a poorly differentiated pancreatic carcinoma cell line (Panc-1), possessing only mutant (mt) p53 (codon 273 mutation). Cells were transfected with a temperature-sensitive mouse p53val135 (tsp53) vector under additional control of a genetically-modified metallothionein promoter. This tsp53 has a 'mt' phenotype at 37.5 degrees C, and a 'wt' phenotype at 32.5 degrees C and the presence of 100 microM ZnCl2. Stable expression of wt p53 caused upregulation of the p21/WAF1 gene, and G1 growth arrest as shown by flow cytometry and BrdU labeling. Additionally, apoptosis was induced 8-12 post-induction in the majority of the cells (60-70%), as demonstrated by morphological changes, in situ TdT labeling and internucleosomal laddering. However, a subpopulation (30%) of the transfectants survived this apoptotic fate. Unlike the epithelial parental Panc-1 cells, these cells exhibited the appearance of a neuroendocrine-like phenotype with extensive branch-like processes, and marked cytoplasmic and cytoskeletal immunostaining for tau-2, synaptophysin, and chromogranin A. These studies suggest that stable and regulated expression of wt p53 can have multiple phenotypic consequences (apoptosis and altered differentiation to a neuroendocrine-like phenotype) in poorly-differentiated pancreatic carcinoma cells.
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PMID:Stable reintroduction of wild-type P53 (MTmp53ts) causes the induction of apoptosis and neuroendocrine-like differentiation in human ductal pancreatic carcinoma cells. 956 27

Oncocytic neoplasms of the adrenal gland are rare. We describe the clinicopathologic and immunohistochemical findings of seven oncocytic adrenocortical neoplasms, five oncocytomas, and two oncocytic neoplasms of uncertain malignant potential. Three tumors were studied using electron microscopy. These neoplasms occurred in five women and two men (median age, 55 years) with no clinical evidence that the neoplasms were functional. The size of the neoplasms varied from 5.0 cm to 13.5 cm. Histologically, each neoplasm was composed exclusively of oncocytes. The oncocytomas had very low or absent mitotic activity and no evidence of necrosis. The two oncocytic neoplasms of uncertain malignant potential had increased mitotic activity and necrosis but no evidence of invasion or metastases. Nuclear atypia, either focal or generalized, was found in all neoplasms. Immunohistochemical studies performed using fixed, paraffin-embedded sections showed strong reactivity with the mitochondrial antibody mES-13 in all neoplasms. Four of five oncocytomas and one oncocytic neoplasm of uncertain malignant potential expressed keratin, predominantly keratin 18, as shown using the CAM 5.2 and AE3 antibodies. Two neuroendocrine-associated markers, neuron specific enolase and synaptophysin, were positive in seven and five neoplasms, respectively. However, all neoplasms were negative for the other neuroendocrine markers tested, including chromogranin A, tyrosine hydroxylase, and dopamine beta-hydroxylase, as well as for epithelial membrane antigen, S100, and p53. Using the MIB-1 (Ki-67) antibody, proliferative activity was increased in both oncocytic neoplasms of uncertain malignant potential. All six patients with available clinical follow-up data are alive without evidence disease, although the follow-up interval is relatively short (< 2 years) for the two patients with oncocytic neoplasms of uncertain malignant potential. We conclude that oncocytic adrenocortical neoplasms are nonfunctional tumors that can become large before they are detected by radiologic studies. The majority of neoplasms are benign and should not be misdiagnosed as carcinoma.
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PMID:Oncocytic adrenocortical neoplasms: a report of seven cases and review of the literature. 959 31


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