Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of biliary adenofibroma in a 47-year-old woman, who presented with right upper quadrant pain for several months. Abdominal imaging revealed a 16-cm solid and cystic mass in the left hepatic lobe. Histologically, the tumor showed two distinct components: 1) cystic and tubular structures lined by low columnar to cuboidal biliary-type epithelium, and 2) a dense fibrous stroma composed of spindle-shaped cells with only mild nuclear pleomorphism and inconspicuous nucleoli. Mitoses and stromal invasion were absent. The glandular epithelium stained positively for keratin AE.3/Cam 5.2, cytokeratin 7, cytokeratin 19, carcinoembryonic antigen, and epithelial membrane antigen and had a low Ki-67 proliferative index. In addition, the epithelium was positive for D10 but did not stain for 1F6 or acid mucin with alcian blue stain. This staining pattern, similar to bile duct hamartoma (von Meyenburg complex) with which this tumor shares morphologic similarity, suggests that biliary adenofibroma originates from interlobular or larger bile ducts. Three years after a subtotal resection no metastasis or significant tumor growth was noted. However, given the marked nuclear p53 immunoreactivity and tetraploidy status observed in this tumor, we cannot exclude that biliary adenofibroma may represent a premalignant process that warrants complete resection and thorough histopathologic examination.
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PMID:Biliary adenofibroma: a rare neoplasm of bile duct origin with an indolent behavior. 1271 55

Neoplasms that are composed focally, predominantly, or exclusively of osteoclast-like giant cells admixed with variably pleomorphic mononuclear cells have been described in a wide variety of organs. In this report, we describe the case of a 76-year-old woman with an 8-cm tumor that appeared to be localized to the ovary, that was composed predominantly of diffusely distributed, bland-appearing osteoclast-like giant cells admixed with pleomorphic mononuclear cells, and that was not associated with an ovarian cystic neoplasm. Hemorrhage, large zones of necrosis, and a high mitotic index were the other characteristics of the tumor. Immunohistochemically, the mononuclear cells were strongly positive for vimentin and proliferating cell nuclear antigen and were negative for keratin AE 1/3, CAM 5.2, cytokeratin 7, epithelial membrane antigen, beta-human chorionic gonadotropin, desmin, smooth muscle actin, p53, leukocyte common antigen, S-100, inhibin, alpha-1-antichymotrypsin, and CD68. The osteoclast-like giant cells displayed immunoreactivity for CD68, vimentin, alpha-1-antichymotrypsin, and leukocyte common antigen only. Ultrastructurally, rare intercellular junctions were present between mononuclear cells, suggestive of an epithelial histogenesis. Less than a dozen ovarian lesions with the "giant cell" designation have been described, and most of these cases are thought to be analogous to the "sarcoma-like" nodules or other such lesions that have a well-known association with ovarian cystic neoplasms. Our case, in contrast, did not have an easily identifiable epithelial component and demonstrated both an infiltrative border and vascular invasion. This is, to the authors' knowledge, the first detailed clinicopathologic description of such a case as an ovarian lesion.
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PMID:A malignant ovarian tumor with osteoclast-like giant cells. 1276 94

Pure sebaceous neoplasms arising in dermoid cysts of the ovary are exceedingly rare. A 63-year-old female with abdominal swelling and pain underwent a right salpingo-oophorectomy that showed a unilocular cyst weighing 830 g and measuring 15x12x10 cm, filled with sebaceous material containing a few hair shafts. The cyst wall exhibited plaques protruding into the cavity of the cyst. Microscopy revealed a dermoid cyst with nests and lobules of atypical and infiltrating sebaceous cells surrounded by basaloid cells. The tumor cells stained diffusely for high-molecular-weight cytokeratins and focally for cytokeratin 7, cytokeratin 19, epithelial membrane antigen and carcinoembryonic antigen in the immunohistochemistry study. Low-molecular-weight cytokeratins, cytokeratin 20, vimentin, S100, p63, estrogen receptor, progesterone receptor, p53 and c-erbB-2 were negative in tumoral cells. The proliferative labeling index (Ki67 and proliferating cell nuclear antigen) was low. Basal cell carcinoma with sebaceous differentiation and sebaceoma must be considered in the differential diagnosis. However, the presence of obvious malignant sebaceous differentiation in nearly every tumor nest and lack of peripheral palisading and peri-tumoral myxoid stroma excluded these diagnoses. Some histogenetic concepts relevant to this case are discussed along with a brief review of this neoplasm. To our knowledge, this is the sixth case report of a sebaceous carcinoma arising in a mature cystic teratoma of the ovary.
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PMID:Clinicopathological and immunohistochemical features of a sebaceous carcinoma arising within a benign dermoid cyst of the ovary. 1283 22

In the previous 500 2-year chemical bioassays within the National Toxicology Program, large intestinal tumors (cecal carcinomas) related to chemical exposure have not been observed in B6C3F1 mice. The recently completed o-nitrotoluene study provided the first cecal tumor response and an opportunity to evaluate the morphology and molecular profile of oncogenes and tumor suppressor genes that are relevant to humans. Morphologically, the carcinomas were gland-forming tumors lined by tall columnar epithelial cells that were positive for cytokeratin 20 and negative for cytokeratin 7. Using immunohistochemistry beta-catenin (encoded by Catnb) protein accumulation was detected in 80% (8/10) of the cecal carcinomas, while increased cyclin D1 and p53 protein expression was detected in 73% (8/11), respectively. There was no difference in adenomatous polyposis protein expression between normal colon and cecal carcinomas. All tumors examined exhibited mutations in exon 2 (corresponds to exon 3 in humans) in the Catnb gene. Mutations in p53 were identified in nine of 11 carcinomas, and all were in exon 7. Analysis of the K-ras gene revealed mutations in 82% (9/11) of carcinomas; all had specific G --> T transversions (Gly --> Val) at codons 10 or 12. The alterations in cancer genes and proteins found in the mouse large intestinal tumors included mutations that activate signal transduction pathways (K-ras and Catnb) and changes that disrupt the cell-cycle and bypass G(1) arrest (p53, cyclin D1). These alterations, which are hallmarks of human colon cancer, probably contributed to the pathogenesis of the large intestinal carcinomas in mice following o-nitrotoluene exposure.
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PMID:o-Nitrotoluene-induced large intestinal tumors in B6C3F1 mice model human colon cancer in their molecular pathogenesis. 1468 30

The recent observation that studies of BRCA1-associated tumors contain a high proportion of medullary carcinomas and ductal carcinomas with medullary features has re-introduced pathologists to an old diagnostic problem. The term "medullary carcinoma" dates to the 19th century, but the modern entity was introduced in 1949 by Moore and Foote, who described a carcinoma with a lymphoid infiltrate, a favorable prognosis, and low frequency of metastasis. Almost three decades later, Ridolfi et al proposed specific criteria for diagnosis, resulting in an entity with an even more favorable prognosis and a lower incidence. The reproducibility and clinical relevance of the diagnosis have been questioned recently, and new criteria have been proposed and compared. The tumors typically express cytokeratin 7, often vimentin and S100-protein, but not cytokeratin 20. The usual ones are positive for p53 and negative for estrogen receptor, Her2/neu, and bcl-2. Medullary carcinomas express e-cadherin and beta-catenin more often than ordinary high-grade ductal carcinomas, and the former have genetic differences from the latter. The lymphoid infiltrate of medullary carcinomas is related to beta-actin fragments exposed by apoptotic cells. The present review discusses historical and recent developments and emphasizes diagnostic criteria.
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PMID:Medullary carcinoma, provocative now as then. 1507 61

An invasive micropapillary component has been described in tumors of several organs and is nearly always associated with aggressive biologic behavior. We present 14 cases of salivary duct carcinoma (SDC) with an invasive micropapillary component (invasive micropapillary SDC) and compare the clinicopathologic findings of these cases with those of cases of conventional SDC. The mean age of the 14 patients (10 men, 4 women) was 65.8 years (range, 26-80 years). The mean size of the tumors was 2.4 cm (range, 1.3-5 cm). The parotid gland was involved in 12 patients and the submandibular gland in 2. Histologically, all tumors had an invasive micropapillary architecture admixed with features typical for SDC. Invasive micropapillary carcinoma was characterized by morula-like small cell clusters without fibrovascular cores, surrounded by a clear space. Tumor cells exhibited moderate- to high-grade nuclear features, conspicuous nucleoli, and eosinophilic cytoplasm. This component was distributed diffusely in 9 tumors and focally in 5. Angiolymphatic and perineural invasion was seen in all tumors. A residual pleomorphic adenoma was detected in four tumors. Of the 12 tumors examined, all were diffusely positive for cytokeratin 7 and epithelial membrane antigen (with a distinctive "inside-out" pattern) but negative for cytokeratin 20. Tumors were frequently immunoreactive for BRST-2 (gross cystic disease fluid protein-15) and androgen receptor protein. Aberrant expression of HER-2/neu or p53 was detected in seven tumors each. The mean Ki-67 labeling index was 33.1% (range, 6.3%-61.6%). All 14 patients with invasive micropapillary SDC had cervical or periglandular lymph node metastasis, and this value was significantly higher than for conventional SDCs. Local recurrence developed in 4 patients and distant metastatic disease in 9. Clinical follow-up (mean, 25.5 months) was available for 13 patients: 9 died of disease within 24 months after the diagnosis (mean, 17.6 months), 1 was alive with metastatic disease at 19 months, and 3 were free of disease. Overall survival of these patients with invasive micropapillary SDC was significantly shorter than that of patients with conventional SDC (n = 49) in our series (P = 0.031). Our results suggest that invasive micropapillary SDC is a distinct, aggressive variant of SDC, with a propensity for extensive lymph node metastasis and rapid disease progression.
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PMID:Invasive micropapillary salivary duct carcinoma: a distinct histologic variant with biologic significance. 1510 94

We present a unique carcinoma of the pancreas with predominantly clear cell morphology (>95% clear cells). Mucicarmine stain revealed abundant intraluminal and intracytoplasmic mucin. Immunohistochemically, the cells were positive for the epithelial markers cytokeratin 7 and CAM 5.2, and were focally positive for cytokeratin 20. These cells also expressed monoclonal carcinoembryonic antigen. Stains for the neuroendocrine markers synaptophysin and chromogranin were negative, as were stains for vimentin, p53, HMB-45, and CD10. An additional outstanding feature was the presence of dense intraluminal and intracytoplasmic hyaline globules, which were immunohistochemically positive for alpha1-antitrypsin. Sequencing of the K-ras oncogene revealed a point mutation in codon 12, providing molecular evidence of ductal origin. In the proper morphologic context supported by immunohistochemistry, clear cell carcinoma can be regarded as a rare variant of ductal adenocarcinoma.
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PMID:Clear cell ductal adenocarcinoma of pancreas: a case report and review of the literature. 1516 26

We report a salivary duct carcinoma (SDC) of parotid gland in a 75-year-old male. Initially, it was studied by fine-needle aspiration, which disclosed features of malignancy consistent with a high-grade carcinoma. Histologically, the tumor showed typical features of SDC, predominantly with a solid and apocrine pattern. The aggressive behavior of this tumor was documented by facial palsy and the presence of 12 regional lymph node metastases. Immunohistochemical study showed positivity for cytokeratins (AE1/AE3), cytokeratin 7, GCDFP-15, C-erbB-2, Mib-1, topoisomerase II alpha, p53, and androgen receptors. Diffuse positivity with chromogranin-A, synaptophysin, and Grimelius stains was also observed, suggesting endocrine features. Phosphotungstic acid hematoxylin, antimitochondrial antigen, progesterone and estrogen receptors, cytokeratin 20, and S-100 stains were negative. To our knowledge, this is the first case reported of SDC exhibiting neuroendocrine differentiation.
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PMID:Salivary duct carcinoma with neuroendocrine features: report of a case with cytological and immunohistochemical study. 1534 92

A 63-year-old man with a history of anal fistula was admitted to our hospital because the anal pain didn't disappear after the operation. On digital examination, a hard mass measuring 3.0 cm in diameter was found at the anal canal. Biopsy of the mass showed moderately differentiated adenocarcinoma. Colonoscopy revealed another rectal cancer at 15 cm from anal verge. Biopsy of the tumor also showed moderately differentiated adenocarcinoma, resembling the anal canal tumor. Because the histological findings of both tumors were nearly identical, we considered that cancer cells from the rectal cancer had been implanted and developed the metastatic tumor in the anal fistula. The patient underwent anterior resection for the rectal cancer, and a local resection for the anal canal cancer. Immunohistochemical staining for Ki-67, p53, Muc2, CD10, CK-7, and CK-20 revealed similar patterns in both tumors. Additionally, genetic analysis for p53, K-ras, and MSI revealed similar patterns in both tumors. We may suggest from these results that cancer cells from the rectal cancer had been implanted and developed the metastatic tumor in the anal canal.
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PMID:[A case of anal fistula cancer probably developing from intraluminal dissemination of rectal cancer]. 1631 38

The presence of keratin granulomas in peritoneal cavity associated with ovarian endometrioid carcinoma, which might be related to leakage from the ovarian tumor, is rarely reported. Its clinical significance has not yet been well investigated. We report a case presenting with intermittent abdominal pain after an acute episode 1 month before a complex adnexal tumor was noted. Comprehensive cytoreductive surgery was performed. The ovarian tumor was an endometrioid adenocarcinoma with squamous differentiation. There were diffuse brownish flecks over the omental surface and pelvic peritoneum, which contained fragments of degenerated squamous cells, keratin, and numerous foreign body giant cells. Extensive multiple sections were examined for these implants. DNA flow cytometry and various immunostaining studies (HER-2/neu, p53, CK-7, and cytokeratin [AE1/AE3]) were performed. Since viable epithelial cells in the implants could be differentially identified against mesothelial or granulomatous components by CK-7 staining and DNA aneuploidy was demonstrated on primary ovarian tumor, four courses of chemotherapy were administered. The patient has been free of disease for 18 months since diagnosis.
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PMID:Ovarian endometrioid carcinoma with diffuse pigmented peritoneal keratin granulomas: a case report and review of the literature. 1644 70


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