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)

Micropapillary carcinoma (MC) has been well described in other organs, including breast, urinary bladder, lung, ovary, and salivary gland, but has not been described in the large intestine. We compared the clinicopathologic and immunohistochemical findings of MC with those of conventional adenocarcinoma in the large intestine. Fifty-five cases of adenocarcinoma with an MC component were identified among 585 consecutive cases of colorectal cancer at the Asan Medical Center between January 2003 and June 2004 and were compared with 119 cases of conventional adenocarcinoma of colorectum without an MC component. Arrayed tissue blocks were constructed and immunostained for cytokeratin 7 and 20 and CDX2. We also compared the results of MLH-1, MSH-2, p53, and carcinoembryonic antigen immunostainings between the 2 groups. The grade of both MC and conventional adenocarcinoma was mostly moderately differentiated. The proportion of MC ranged from 5% to 80%. The presence but not extent of MC in the primary tumors was associated with more frequent lymphovascular invasion and lymph node (LN) metastases, a greater mean number of positive LNs, and a higher tumor stage with more frequent distant metastases, compared with conventional adenocarcinoma (P < .05). Cytokeratin 7 staining was occasionally observed in both MC (9.1%, 5/55 cases) and conventional adenocarcinoma (13.4%, 16/119 cases). Although MLH-1 and CDX2 expression tended to be lower in conventional adenocarcinoma, none of the immunohistochemical results was significantly different between 2 groups. Recognition of MC component is important as MC appeared to be an aggressive variant of colonic adenocarcinoma and presented at a higher stage, with frequent lymphovascular invasion, LN metastasis, and distant metastasis, compared with conventional adenocarcinoma. The proportion of MC component did not impact the prognosis, and the immunoprofiles of MC were not significantly different from those of conventional adenocarcinoma.
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PMID:Invasive colorectal micropapillary carcinoma: an aggressive variant of adenocarcinoma. 1678 79

Non-mass forming, neoplastic intraepithelial proliferations (dysplasia) represent the most well-accepted precursor lesions to gallbladder adenocarcinomas. They are typically small, localized, grossly unrecognizable lesions that have been identified in the epithelium adjacent to up to 79% of gallbladder adenocarcinomas. Morphologic variants that have been reported include flat, micropapillary, papillary and cribriform. We have recently encountered a morphologically distinctive, previously unreported lesion to which we have applied the designation eosinophilic dysplasia. This lesion was identified in a gallbladder with diffuse mural fibrosis and calcification (porcelain gallbladder). The dysplastic focus was confined to one tissue section, and was comprised of a localized true papilla [i.e with a fibrovascular core], measuring approximately 1.2 mm in greatest dimension and an adjacent, flat, 7-cell epithelial segment. These foci were lined by cells displaying significant nuclear enlargement [1.5-4 times the adjacent benign cells], nuclear pleomorphism, occasional multinucleation, hyperchromasia and nuclear membrane irregularities. Nucleoli were present but inconspicuous. These cells also showed voluminous eosinophilic to granular cytoplasm, such that the overall nuclear-to-cytoplasmic ratio was generally not increased. The cells displayed diffuse and marked nuclear immunoreactivity for p53, and approximately 70% of the cells showed nuclear positivity for Ki-67. The cells were also positive for cytokeratin 7 and were entirely negative for carcinoembryonic antigen (CEA) and chromogranin A. The cells of the adjacent normal epithelium were positive for cytokeratin 7 and CEA, negative for p53 and chromogranin A and showed a Ki-67 labeling index of <10%. Marked overexpression of the p53 protein as well as its high proliferative index are strong arguments in favor of the dysplastic nature of this lesion. However, further studies are required to elucidate its true clinical significance and to determine whether or not its association with a porcelain gallbladder, as noted herein, is entirely fortuitous. However, such studies can only be performed with an increased recognition by practitioners of this distinctive variant.
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PMID:Eosinophilic dysplasia of the gallbladder: a hitherto undescribed variant identified in association with a "porcelain" gallbladder. 1687 48

Bronchioloalveolar carcinoma of mixed mucinous and nonmucinous type fulfilling the 1999 WHO criteria is rare. Here, we report a case of this type of tumor determined entirely by histological examinations. A 57-year-old man was incidentally found to have a demarcated 3cm mass in his lower lobe of the right lung. The tumor was composed of tall columnar cells containing cytoplasmic mucins, cuboidal cells without mucins, and intermediate cell types with lepidic growth patterns. Tumor cells were distributed within a region of 2cm in diameter, and no stromal, vascular, or pleural invasion was observed. Immunohistochemically, both the mucinous and nonmucinous components were positive for cytokeratin 7, TTF-1, and E-cadherin, and negative for cytokeratin 20, consistent with the results for nonmucinous bronchioloalveolar carcinoma. No mutations were detected in exons 5-8 of the p53 gene. The present tumor was composed mainly of morphologically mucinous bronchioloalveolar carcinoma, but presented different immunohistochemical profiles of ordinary mucinous bronchioloalveolar carcinoma. This case suggests that the mucinous component in bronchioloalveolar carcinoma of mixed mucinous and nonmucinous type has characters dissimilar to conventional mucinous bronchioloalveolar carcinoma, and is probably derived from the nonmucinous component.
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PMID:Bronchioloalveolar carcinoma of mixed mucinous and nonmucinous type: immunohistochemical studies and mutation analysis of the p53 gene. 1695 34

Squamous cell carcinoma is a rare thyroid neoplasm that has been described exclusively in adults. We report what appears to be the first example of a primary squamous cell carcinoma of the thyroid gland arising in a background of Hashimoto's thyroiditis in an adolescent female. The tumor was well demarcated, confined to the right thyroid lobe, and did not metastasize, although follow up has been limited. The squamous cell carcinoma was well to moderately differentiated, and the stroma contained an abundant inflammatory infiltrate rich in lymphocytes and eosinophils. The lack of goblet cells, extracellular mucin, and extensive stromal sclerosis excluded the diagnosis of sclerosing mucoepidermoid carcinoma with eosinophilia. Immunohistochemical staining revealed focal expression of cytokeratin 7 and diffuse labeling with cytokeratin AE1/AE3. The squamous cell carcinoma overexpressed p53 protein and showed increased proliferative activity, as evidenced by the high MIB-1 labeling index. In contrast, the tumor did not show immunoreactivity for thyroglobulin or thyroid transcription factor 1.
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PMID:Primary squamous cell carcinoma of the thyroid arising in Hashimoto's thyroiditis in an adolescent. 1716 93

Basal cell adenocarcinoma (BCA) is an unusual salivary gland malignancy that very rarely affects the minor glands. Here we present 2 cases of BCA arising in the minor salivary glands of the left cheek and junction of the hard and soft palate, respectively. The patients were both women aged 66 and 42 years. The tumors assumed a tubular-trabecular and a solid-membranous pattern, respectively. Both tumors showed immunopositivity for S-100, Bcl-2, and cytokeratin 7. One tumor was also immunopositive for epithelial membrane antigen and carcinoembryonic antigen, and the other tumor was reactive with p53 and vimentin. Both tumors were surgically removed. A comprehensive literature review revealed only 21 previously reported cases of BCA of oral minor salivary glands. This is an exceptionally rare salivary gland tumor, which, despite its low-grade behavior, demands complete surgical removal with adequate margins. Immunohistochemical studies may complement a thorough histopathologic analysis in discriminating BCA from other salivary gland tumors.
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PMID:Basal cell adenocarcinoma of the oral minor salivary glands: review of the literature and presentation of two cases. 1717 98

Tumor suppressor genes are often silenced in human cancer; this can occur by transcriptional repression by deacetylation in the promoter regions, mediated by histone deacetylase (HDAC). HDAC inhibitors can block cancer cell growth by restoring expression of tumor suppressor genes. In this study, we investigated the effects of a HDAC inhibitor, suberoylanilide hydroxamic acid (SAHA) on pancreatic cancer cells. SAHA inhibited the growth of 6 pancreatic cancer cell lines in a dose-dependent manner as measured by MTT and clonogenic assays (ED(50) approximately 10(-6) M) associated with induction of apoptosis, G2 cell cycle arrest and also induced differentiation as indicated by morphology and increased expression of cytokeratin 7. It increased expression of p21(WAF1) (independent of the mutational status of p53), C/EBPalpha, RARalpha and E-cadherin; these genes have been associated with decreased proliferation in other cancers. SAHA decreased cyclin B1 expression; this cyclin normally promotes progression through G2 of the cell cycle. SAHA mediated acetylation of histone H3 globally, as well as, associated with the p21(WAF1) promoter, as measured by chromatin immunoprecipitation. SAHA also decreased levels of c-myc and cyclin D1, independent of an active beta-catenin pathway. In further studies, the combination of SAHA and an inhibitor of DNA methylation, 5-Aza-2'-deoxycytidine, had an enhanced antiproliferative effect on pancreatic cancer cells. In summary, SAHA inhibited the growth of human pancreatic cancer cells by inducing apoptosis, differentiation and cell cycle arrest, as well as increase in the expression of several tumor suppressor genes. SAHA is a novel, promising therapeutic agent for human pancreatic cancers.
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PMID:Histone deacetylase inhibitor, suberoylanilide hydroxamic acid (Vorinostat, SAHA) profoundly inhibits the growth of human pancreatic cancer cells. 1741 71

Intrabiliary metastasis of colorectal carcinoma is not infrequent. We demonstrated interesting intraductal biliary epithelial lesions in two cases of colorectal carcinoma. The first case (65-year-old female) presented intrahepatic papillary adenocarcinoma with intrabiliary extension. While this biliary carcinoma was once diagnosed as intrabiliary metastasis of colon carcinoma, these carcinoma cells were positive for cytokeratin 7 (CK7, biliary cytokeratin) and negative for CK20 (intestinal cytokeratin). In addition, these carcinoma cells were oncocytic. Finally, a diagnosis of intraductal papillary cholangiocarcinoma of oncocytic variant was made. In the second case (74-year-old male), atypical biliary epithelial lesions were found near intrabiliary metastasis of colon carcinoma. The atypical lesions were immunohistochemically positive for CK7 but negative for CK20, and negative for p53. On the contrary, intraductal metastatic carcinoma was totally reversed, suggesting that atypical biliary lesions were not metastatic. Survey of such atypical biliary lesions in 6 consecutive cases with intrabiliary metastasis from colon carcinoma including this case disclosed that one third of such cases revealed such atypical biliary lesions. A variable type of biliary lesions should be carefully differentiated from intrabiliary metastatic colorectal carcinoma and a combined immunohistochemistry of CK7 and CK20 is useful for this differentiation.
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PMID:Intraductal papillary cholangiocarcinoma and atypical biliary epithelial lesions confused with intrabiliary extension of metastatic colorectal carcinoma. 1759 Oct 40

We present the surgical and pathological findings and follow-up of 5 women diagnosed with combined endometrioid and high-grade neuroendocrine carcinoma of large cell type (LCNEC) arising in the endometrium. The mean age of the women was 75 years (range, 50-88 years). Of the 5 tumors, 4 formed polypoid endometrial masses associated with extensive lymphovascular involvement of the myometrium by neoplastic cells. A single endometrial tumor was formed by LCNEC alone, and 4 tumors were composite with varying proportions formed by endometrioid (4/5) and small cell neuroendocrine carcinoma (1/5). In all 5 LCNEC tumor components, an insular growth pattern was noted, whereas a diffuse (solid) pattern was found in 4 tumors, a trabecular in 2, and rosettes/pseudorosettes in another 2. In all 5 tumors, the LCNEC tumor components were labeled with neuron-specific enolase (NSE). Four tumors were reactive for chromogranin A, CAM 5.2, and p53. Three tumors were labeled for AE1/AE3, CD56 (NCAM), p16, and cytokeratin 7. Synaptophysin was reactive in 2 tumors, and CD117 was found in only a single tumor. Of the 3 endometrioid tumor components examined, all were reactive for NSE. Two tumors were reactive for p16 and p53, 1 for CD56, but none for synaptophysin orchromogranin A. We conclude that LCNEC of the endometrium is a distinct clinicopathological entity with a poor prognosis irrespective of stage. The gross and histomorphological features are often suggestive, but confirmation requires immunoperoxidases, including NSE, synaptophysin, chromogranin A, p16, and p53. Combined endometrioid and high-grade LCNEC possess more characteristics of a type II than a type I endometrial carcinoma.
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PMID:Combined large cell neuroendocrine and endometrioid carcinoma of the endometrium. 1815 75

Carcinosarcomas are malignant tumors with a mixture of carcinomatous and differentiated sarcomatous elements. We investigate the morphology, immunohistochemistry, and comparative genomic hybridization analysis of 3 mixed squamous carcinoma and osteosarcoma of the lung. All patients were male and their ages were 72, 43, and 58 years. The sizes of the neoplasms were 7, 5, and 5 cm in maximum diameter, respectively. Two patients died of the disease 9 and 14 months after surgery; and one is alive 6 months later. By light microscopy, all cases had both squamous and osteosarcomatous structures. Immunohistochemistry was positive for AE3AE1, p63, 34 E12, CAM 5.2 (2/3 cases), CK-7 (2/3 cases), epithelial membrane antigen, E-cadherin, p53, and carcinogenic embryonic antigen in carcinomatous areas, and for vimentin and CD-68 in sarcomatous component. Areas of transition positive for both cytokeratins and vimentin were seen in all cases. A total of 55 copy number changes were detected with a median of 18 abnormalities per case: 48 gains, 6 losses, and 1 high-level amplification. Chromosome alterations in osteosarcomatous areas were similar to those found in lung metastatic osteosarcoma, comparable to those found in carcinomatous areas and to lung squamous carcinomas. Coincidences between carcinomatous areas and osteosarcomatous zones were found as gains in chromosomes 1q, 3q, 5p, 8q, and 12p. These findings provide arguments that favor a common origin for both types of cells, supported by the mixture of cells, the existence of undifferentiated cells positive to both cytokeratin and vimentin markers, and the CGH overlaps of chromosomal gains between carcinomatous and sarcomatous areas.
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PMID:Primary mixed squamous carcinoma and osteosarcoma (carcinosarcomas) of the lung have a CGH mapping similar to primitive squamous carcinomas and osteosarcomas. 1838 57

We present a 6-year-old child with intraocular and extraocular mass and high intraocular pressure. The tumor mass involved a disorganized anterior segment and extended through the medial cornea and sclera. A preliminary diagnosis of retinoblastoma with extraocular extension was made. An exenteration of the left globe and orbital tissue was performed. Histological examination showed that the lesion, which occupied the posterior chamber, involved the ciliary body, extending into the iris, sclera and cornea, projecting beyond the cornea anteriorly and extending to the retina posteriorly. The tumor cells were diffusely immunoreactive to vimentin, neuron specific enolase and CD 138. The medulloepithelioma cells were focally positive to cytokeratin (AE1/AE3), cytokeratin 18, CD56,CD57, S100, HMB-45 and bcl2 while areas of retinoblastic differentiation showed diffuse immunoreactivity to synaptophysin, neurofilament and CD138 with focal immunoreactivity to calretinin. All tumor cells showed no immunoreactivity to cytokeratin 7, cytokeratin 20, epithelial membrane antigen, carcinoembryonic antigen, desmin, GFAP, and chromogranin. Nuclear staining for P53 was seen in 80% of tumor cells. The ki-67 index was 90%. The tumor was described as malignant intraocular non-teratoid medulloepithelioma with retinoblastic differentiation arising from the ciliary body. Tumor satellites were seen in the adjacent periocular soft tissue. The treatment involved exenteration of the left globe and orbital tissue with secondary skin graft following chemotherapy. The patient is well and has no recurrence after 1 year of treatment. We report that medulloepithelioma can present as a case of infantile glaucoma, can show signs of intraocular calcifications and can show retinoblastic differentiation.
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PMID:Malignant non-teratoid medulloepithelioma of ciliary body with retinoblastic differentiation: a case report and review of literature. 1841 Feb 70


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