Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0001430 (adenoma)
21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although cyclin E gene amplification is reported to be an important event in various cancers, it is rarely found in human colorectal cancers. As one of the candidate factors of other mechanisms relating to cyclin E, we analyzed cyclin E-dependent kinase activity in colorectal cancer. Protein levels of cyclin E, its catalytic subunit, cyclin-dependent kinase 2 (Cdk2), and p21 and p27 were determined by western blot or immunohistochemistry in 27 colorectal cancers and 10 colorectal adenomas, and compared with adjacent normal colonic mucosa. Enzymatic activity of cyclin E-Cdk2 complex in the colorectal neoplasm was measured using in-gel kinase assay using glutathione S-transferase-retinoblastoma (GST-Rb) fusion protein as substrate, and compared with that of normal mucosa. We clearly showed that although the protein level of cyclin E in colorectal cancer and adenoma was similar to that of adjacent normal mucosa, cylin E-dependent kinase activity was increased in all the cases of colorectal cancers and 90% of colorectal adenomas. The relative kinase activity was significantly higher in colorectal cancer (3.7 +/- 1.7 -fold) than colorectal adenomas (2.0 +/- 0.8-fold) (P < 0.004). The relative expression level of Cdk2 protein in cancer was significantly higher than adenoma (4.4 +/- 2.4 vs 2.7 +/- 1.3, P < 0.04), and p21 and p27 were not detected in colorectal cancer and notably decreased in adenoma. The results of this study strongly suggest that activation of cyclin E-dependent kinase activity may play an important role in colorectal cancer, and its level appears to be related to increased Cdk2 and decreased p21 and p27 amounts rather than cyclin E protein level.
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PMID:Activation of cyclin E-dependent kinase activity in colorectal cancer. 1168 May 95

The morphologic distinction between parathyroid carcinoma and adenoma can be a difficult diagnostic problem. We analyzed nuclear immunoreactivity for the cell cycle-associated antigen Ki-67 with monoclonal antibody (MAb) MIB-1 and for retinoblastoma (RB) protein with two polyclonal antisera in 24 parathyroid carcinomas and 35 adenomas, which were formalin fixed and paraffin embedded to determine if these antibodies could assist in distinguishing between carcinomas and adenomas. In addition, 10 cases of parathyroid hyperplasia and 5 cases of normal parathyroids were examined as control tissues. The Ki-67 labeling index was significantly higher in parathyroid carcinomas compared to adenomas (7.1 +/- 1.0% vs 2.4 +/- 0.2%, p <0.001). No patient with a parathyroid adenoma, parathyroid hyperplasia, or normal parathyroid gland had a Ki-67 labeling index >5.3%. Analysis of the primary tumors from patients with recurrent carcinomas and from those with nonrecurrent carcinomas showed a higher mean Ki-67 labeling index (7.8 +/- 1.5% vs 5.2 +/- 1.1%) in the former group. Although these differences were not statistically significant, the RB protein immunoreactivity was not useful in distinguishing between parathyroid carcinomas and adenomas in paraffin-tissue sections. These results indicate that nuclear immunoreactivity for the cell cycle-associated antigen Ki-67 may be another useful method to assist in distinguishing parathyroid carcinomas from adenomas.
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PMID:Immunohistochemical Analysis of the Cell Cycle-Associated Antigens Ki-67 and Retinoblastoma Protein in Parathyroid Carcinomas and Adenomas. 1211 10

The genomic alterations in preneoplastic lesions are summarized in this review. 3p and 9p in the lung, 9p in the bladder, 8p in the prostata, 19q and 1p in oligodendroglioma, and 22q in meningioma were reported to be deleted. Somatic mutation of p53 was found in preneoplastic lesions of the esophagus, stomach, colon, thyroid, and astrocytoma. Adenoma-carcinoma sequence (Apc, ras, p53 gene alterations) in colon, LKB1 gene in Peutz-Jeghers syndrome, Smad4 in juvenile polyposis, hMSH2, hMLH1, PMS1, PMS2 genes in HNPCC, VHL gene in kidney, WT1 in Wilms tumor, RB gene in retinoblastoma, and ret gene in MEN were reportedly altered in preneoplastic lesions involved in hereditary tumors. Cervical dysplasia and papilloma of the head and neck infected by human papilloma virus and liver infected by B-type hepatitis virus are also precancerous. Genomic instability, APC gene alteration, point mutation of K-ras in preneoplastic lesions of stomach and K-ras and p16 alterations in metaplasia of pancreas were also found. Advances in research on genomic alterations in preneoplastic lesions will contribute to prevention and early detection of cancer.
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PMID:[Genomic alterations in preneoplastic lesions]. 1250 66

p130 belongs to the retinoblastoma-related gene family, and its gene product works to negatively regulate cell cycle progression in the G1 phase. In this study, we investigated p130 expression in thyroid neoplasms. p130 overexpression was observed in 33.3% of follicular adenoma and 50% of follicular carcinoma and the incidences were not significantly different. In papillary carcinoma, it was overexpressed in 36.5% of cases, but in microcarcinoma, the incidence was significantly lower (14.3%). Furthermore, in anapalstic carcinoma, p130 overexpression was less frequently seen than in papillary carcinoma except for microcarcinoma and follicular carcinoma, and only 14.3% of cases overexpressed this protein. These findings suggest that: (1) reduced p130 expression may contribute to the aggressive character of anplastic carcinoma; and (2) p130 may specify the growth characteristics of microcarcinoma.
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PMID:p130 expression in thyroid neoplasms: its linkage with tumor size and dedifferentiation. 1263 56

Although the retinoblastoma susceptibility gene RB1 is inactivated in a wide range of human tumours, overexpression in colonic carcinomas has been linked to the antiapoptotic function of the protein. In the current study we show that the Retinoblastoma susceptibility protein (Rb) protein interacts with Bag-1, an apoptotic regulator, in human colonic adenoma- and carcinoma-derived cell lines. Coimmunoprecipitation demonstrated that endogenous Rb and Bag-1 interact in both adenoma- and carcinoma-derived cell lines. The specificity of the interaction was demonstrated by expression of human Papillomavirus E7 oncoprotein, an inhibitor of Rb protein interactions, which disrupted the Rb/Bag-1 complex. We report that Bag-1 is predominantly localised in the nucleus of colorectal adenoma- and carcinoma-derived epithelial cells. Disruption of the Rb/Bag-1 complex through expression of E7 changes the subcellular distribution of Bag-1, decreasing nuclear localised Bag-1. Our work establishes that the Rb protein interacts with the Bag-1 apoptotic regulator protein, and introduces a novel function for Rb, involving modulation of the subcellular localisation of Bag-1 in human colonic epithelial cells.
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PMID:The retinoblastoma protein interacts with Bag-1 in human colonic adenoma and carcinoma derived cell lines. 1284 74

Components of cyclinD1/cyclin-dependent kinase 4 (CDK4)/p16INK4a/pRb pathway are the frequent target of many tumor types. We examined the role of retinoblastoma susceptibility gene (RB1) and the CDK4 gene in human pituitary tumorigenesis. For the RB1 gene, pRb expression and loss of heterozygosity (LOH) on 13q in pituitary adenomas were analysed. Immunostaining of pRb revealed lack of expression in 1 of 29 pituitary adenomas. In 4 of 31 pituitary adenomas, allelic imbalances including LOH of RB1 on 13q14 were detected. Three of 4 pituitary adenomas, in which one adenoma lacked pRb expression, had a common LOH region at least from D13S219 on 13q12.3-q13 to D13S265 on 13q31-32. Interphase fluorescence in situ hybridization with a probe of RB1 showed 2 copies of RB1 gene suggesting that mitotic recombination events, not deletion or chromosome loss, led to LOH in the 3 pituitary adenomas analyzed. All 27 exons, intron-exon boundaries, and essential promoter region of RB1 gene were then sequenced in genomic DNA from 4 pituitary adenomas with allelic imbalance on 13q14 including one adenoma without pRb expression and 3 adenomas with pRb expression. Any somatic mutations, insertions, or microdeletions in the RB1 gene were not detected in 4 pituitary adenomas. Methylation sensitive (MS)-polymerase chain reaction (PCR) and bisulfite sequencing analysis revealed hypomethylated status of CpG islands in the promoter region of the RB1 genes of 4 pituitary adenomas. In addition, activating mutations of CDK4 gene, which is a component of cyclinD1/CDK4/p16INK4a/pRb pathway, were not detected in 31 pituitary adenomas. Based on these results, it is concluded that somatic mutations of the RB1 gene or CDK4 gene do not appear to play a major role in pituitary tumorigenesis. This supports the presence of potential tumor suppressor gene(s) on 13q12.3-q13 to 13q31-32 in pituitary adenomas.
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PMID:Human pituitary adenomas infrequently contain inactivation of retinoblastoma 1 gene and activation of cyclin dependent kinase 4 gene. 1294 Apr 60

The expression of G1-phase cell-cycle regulators is commonly deregulated in human malignancies. In the present study, we investigate components of the retinoblastoma (RB) pathway in normal salivary glands (NSG) and in salivary gland tumours (SGT). Samples of NSG, pleomorphic adenoma (PA), adenoid cystic carcinoma (ACC), mucoepidermoid carcinoma (MEC), epithelial-myoepithelial carcinoma (EMC), malignant myoepithelioma (MEM), carcinoma ex pleomorphic adenoma (CEPA), and polymorphous, low-grade adenocarcinoma (PLGA) were examined immunohistochemically using antibodies to cyclin D1, cyclin-dependent kinase 4 (CDK-4), retinoblastoma protein (pRb), CDK inhibitor p16 and transcription factor E2F-1. In normal salivary glands, cyclin D1 and cdk-4 were not expressed in any case while p16 was positively expressed. pRb was abundant and E2F-1 moderately expressed. In tumors, cdk-4 was overexpressed in half of the cases. Most tumour cases showed decreased pRb immunoexpression compared to normal salivary glands. In contrast, expression of p16 and E2F-1 increased. pRb expression was absent in three cases of PA, two of EMC and one of CEPA. One case of MEM and one of PLGA showed no E2F-1 expression. Statistical analyses revealed positive correlations between cyclin D1 and cdk-4, cyclin D1 and E2F-1, cdk-4 and E2F-1, and p16 and E2F-1. The benign and malignant tumours expressed retinoblastoma pathway proteins differently form the normal salivary gland. Our findings suggest that, pRb pathway deregulation in salivary gland neoplasms is unrelated to their biological behaviour.
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PMID:Immunohistochemical expression of retinoblastoma pathway proteins in normal salivary glands and in salivary gland tumours. 1474 65

Various pathological disorders have been associated with primary aldosteronism, including glucagonoma, phaeochromocytoma and primary hyperparathyroidism. In this report, a case of adrenal myelolipoma (a rare non-functioning tumour composed of mature adipose tissue and normal haematopoietic elements similar to bone marrow cells), aldosterone-producing adenoma and a pituitary microadenoma coexisting in a 62-year-old man with a 15-year history of arterial hypertension, previous ablation of an autonomously-functioning thyroid adenoma, multiple lipomas and an heterozygosity of the retinoblastoma (RB) susceptibility gene is reported. We believe that this case probably represents another variant of the multiple neoplasia syndrome and we speculate that structural alteration of the RB gene may play a role in the tumorogenesis.
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PMID:A rare combination consisting of aldosterone-producing adenoma and adrenal myelolipoma in a patient with heterozygosity for retinoblastoma (RB) gene. 1513 74

Cyclin D1 encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the retinoblastoma protein and promotes progression through the G1-S phase of the cell cycle. Amplification or overexpression of cyclin D1 plays pivotal roles in the development of a subset of human cancers including parathyroid adenoma, breast cancer, colon cancer, lymphoma, melanoma, and prostate cancer. Of the three D-type cyclins, each of which binds cyclin-dependent kinase (CDK), it is cyclin D1 overexpression that is predominantly associated with human tumorigenesis and cellular metastases. In recent years accumulating evidence suggests that in addition to its original description as a CDK-dependent regulator of the cell cycle, cyclin D1 also conveys cell cycle or CDK-independent functions. Cyclin D1 associates with, and regulates activity of, transcription factors, coactivators and corepressors that govern histone acetylation and chromatin remodeling proteins. The recent findings that cyclin D1 regulates cellular metabolism, fat cell differentiation and cellular migration have refocused attention on novel functions of cyclin D1 and their possible role in tumorigenesis. In this review, both the classic and novel functions of cyclin D1 are discussed with emphasis on the CDK-independent functions of cyclin D1.
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PMID:Minireview: Cyclin D1: normal and abnormal functions. 1533 80

We describe the clinical and pathologic features of 14 cases of high-grade neuroendocrine carcinoma (HGNEC) of the ampulla of Vater classified according to WHO classification of lung tumors into small cell carcinoma (SCC, 6 cases) and large cell neuroendocrine carcinoma (LCNEC, 8 cases) types. The immunohistochemical findings were compared with those of 13 cases of primary poorly differentiated ampullary adenocarcinomas (PDACA) lacking neuroendocrine morphology. The mean age of 10 males and 4 females was 70 years. The mean tumor size was 2.5 cm. Ten of 13 patients had lymph node metastases (mean, 2.3 nodes involved). Documented sites of distant metastases included brain and liver. Overall, 64% of patients with ampullary HGNEC died of disease (mean follow-up, 14.5 months). Four patients had no evidence of disease after resection (mean, 20 months). Half of the tumors were associated with adenomas of the adjacent mucosa, 2 with high-grade dysplasia. Two HGNECs were combined with a conventional adenocarcinoma and another with a squamous cell carcinoma component. By immunohistochemistry, the HGNECs were positive for cytokeratins (AE1/AE3, 100%; Cam5.2, 67%; CK7, 87%; CK20, 38%), similar to the pattern found in PDACAs. p27 expression was lost in 1 case of HGNEC and in all PDACAs. Retinoblastoma (Rb) protein expression was lost in 60% of HGNECs and in none of the PDACA cases. In conclusion, HGNECs of the ampulla are rare (2%-3% of ampullary tumors in our material). The clinical course parallels that of their pulmonary counterparts and appears to be worse than that of locally advanced ampullary adenocarcinomas. The association with adenoma and or conventional adenocarcinoma components may suggest a common pathway in the initial carcinogenesis of these two types of tumors. Loss of Rb expression, a characteristic finding in pulmonary SCCs, is present in almost half of ampullary HGNECs. In contrast, p27 expression is lost in PDACAs and retained in most HGNECs. Thus, there are differences in the molecular phenotypes of these two types of ampullary carcinoma, supporting the distinction of poorly differentiated carcinomas with a neuroendocrine phenotype from those without.
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PMID:High-grade neuroendocrine carcinoma of the ampulla of vater: a clinicopathologic and immunohistochemical analysis of 14 cases. 1583 81


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