Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare, minor salivary gland tumour of the hard palate in a middle-aged woman was presented. The small (1.0 X 0.5 cm in diameter) hemispherical tumour was well circumscribed with a fine papillomatous surface. Histopathologically, tumour cells with eosinophilic cytoplasm and a large nucleus were single-strand cuboidal and columnar cells, which showed intraductal growth exhibiting a cribriform pattern. The histological features were distinct from adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma because the tumour lacked the neurotropic infiltration, cord-like proliferation and targetoid arrangement. The tumour could not be identified as a typical salivary-duct carcinoma because Roman bridging, papillary projection, and severe cell atypia were not found. Tumour cells were negative for PAS, Alcian blue, mucicarmine, p53, c-erbB-2, CEA, S-100 protein, alpha-smooth muscle actin, lactoferrin or vimentin. About 5% of the tumour cells were positive for proliferating cell nuclear antigen. Taking these factors into account, together with the clinical features, the name low malignant intraductal carcinoma seems appropriate.
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PMID:Low malignant intraductal carcinoma on the hard palate: a variant of salivary duct carcinoma? 877 26

erbB-2 is known to be overexpressed in several human malignancies including lung cancer. Because of its role in neoplastic transformation as well as its association with poor prognosis, this oncogene has been targeted through various anti-cancer methodologies. In this regard, we have recently demonstrated that erbB-2-overexpressing ovarian tumor cell lines transfected with an endoplasmic reticulum form of an anti-erbB-2 single-chain antibody undergo a specific cytotoxicity through the induction of apoptosis. Since certain forms of lung cancer are also associated with overexpression of erbB-2, we evaluated the use of this novel therapeutic in this context. For these studies, several human lung adenocarcinoma cell lines were stably and transiently transfected with the anti-erbB-2 sFv gene. We demonstrate here that the anti-erbB-2 sFv can cause specific cytotoxicity in lung cancer cells. As a first step toward clinical translation of this strategy, we constructed a replication-deficient recombinant adenoviral vector expressing the anti-erbB-2 sFv construct. We further demonstrate that our anti-erbB-2 sFv-encoding adenoviral vector can accomplish high levels of cytotoxicity in lung cancer cells. Based on these results, it is proposed that this strategy of oncoprotein ablation may have use in the treatment of some forms of human lung cancer.
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PMID:erbB-2 knockout employing an intracellular single-chain antibody (sFv) accomplishes specific toxicity in erbB-2-expressing lung cancer cells. 881 Jun 38

The authors studied the prognostic value of EGFR and c-erbB-2 overexpression in adenocarcinoma of the uterine cervix. The aim of this research was to find a new pathway to prognosis for more adequate therapy.
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PMID:Prognostic significance of epidermal growth factor receptor (EGFR) and c-erbB-2 protein overexpression in adenocarcinoma of the uterine cervix. 885 1

A few previous studies have demonstrated the expression or mutations of oncogenes and anti-oncogenes as well as that of oncofetal antigens in intraductal papillary-mucinous neoplasm of the pancreas. In this study, we have investigated the immunohistochemical expression of oncogene (ras and c-erbB-2) and anti-oncogene (p53 and retinoblastoma [Rb]) products and oncofetal antigens (CEA, CA19-9 and DUPAN-2) in nine such tumours of the pancreas. In normal pancreas (5 cases), the Rb gene product and CA19-9 were expressed in all cases, while ras and c-erbB-2 gene products, p53 protein, CEA and DUPAN-2 were not expressed. In intraductal papillary-mucinous tumours (n = 9), ras, c-erbB-2, p53 and Rb gene products were present in 4/9 (44%), 7/9 (78%), 0.9 (0%) and 6/9 (67%) cases, respectively. CEA, CA19-9 and DUPAN-2 were expressed in 8/9 (89%), 9/9 (100%) and 2/9 (22%) cases respectively. In invasive ductal adenocarcinoma of the pancrease (7 cases), ras, c-erbB-2, p53 and Rb gene products were expressed in 3/7 (43%), 6/7 (86%), 2/7 (29%) and 3/& (43%) cases respectively. CEA, CA19-9 and DUPAN-2 were expressed in 7/7 (100%), 7/7 (100%) and 6/7 (86%) cases, respectively. The extent and intensity of the expression of these antigens was greater in invasive ductal adenocarcinomas. These data suggest that activation of ras and c-erbB-2 oncogenes and inactivation of Rb anti-oncogene may contribute to the development and progression of intraductal papillary-mucinous tumours of the pancreas and that there is neo-expression of CEA and DUPAN-2 during the development and progression of these tumours.
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PMID:Expression of oncogene products, anti-oncogene products and oncofetal antigens in intraductal papillary-mucinous neoplasm of the pancreas. 891 43

The development and progression of cancer are known to be regulated by various oncogenes and tumour suppressor genes. We analysed 63 primary malignant salivary gland tumours for the expression of p53 and c-erbB-2 proteins. Immunohistochemically, 7 of 63 tumours (11%) showed diffuse nuclear staining for p53 protein, and all 7 were also positive for c-erbB-2 protein. The overexpression of p53 protein correlated closely with the overexpression of c-erbB-2 protein (P<0.001). Overexpression of both p53 and c-erbB-2 proteins (coexpression) was found in tumours of certain histological types, such as adenocarcinoma, carcinoma in pleomorphic adenoma, and salivary duct carcinoma. Furthermore, it is noteworthy that coexpression was associated with high-grade carcinoma, advanced tumour stage, and a high Ki-67 labelling index (%) which is a marker of cell proliferation. In adenocarcinoma, we attempted to clarify the relationship between coexpression and histological grade. Coexpression was associated with histological grades showing high mitotic indices and necrotic areas, which reflected high cell-proliferative activity. These results suggest that the accumulation of genetic alterations, such as those involving p53 and c-erbB-2, plays an important part in the progression of malignant salivary gland tumours.
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PMID:Coexpression of p53 and c-erbB-2 proteins is associated with histological type, tumour stage, and cell proliferation in malignant salivary gland tumours. 892 28

I have investigated 84 endometrial specimens (from 15 cases of normal endometrium, 20 cass of hyperplasia and 49 cases of endometrial carcinoma) to determine the relationship between three proteins (proliferating cell nuclear antigen (PCNA), p53 gene product and c-erB-2 gene product) and endometrial carcinoma by immuno-histochemical staining. In 49 cases of endometrial carcinoma, the positive rates for PCNA, p53 protein (mutant type) and c-erbB-2 protein were 65.3%, 59.2% and 22.4%. I could not find the expression of p53 protein besides endometrial carcinoma. And I could find the expression of c-erbB-2 protein in 11 cases of endometrial carcinoma and 1 case of atypical hyperplasia, but not in normal endometrium. p53 protein was more common in such a case, as with lymphnode metastasis, deep myometral invasion and undifferentiated adenocarcinoma. c-erbB-2 was also more common in a case with deep myometrial invasion. In conclusion, PCNA, p53 protein and c-erbB-2 protein are related to the proliferation of endometrial carcinoma. So they can be useful factors in making the prognosis.
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PMID:[Immunohistochemical study of PCNA, p53 gene product and c-erbB-2 gene product in endometrial carcinoma]. 893 11

An androgen-repressed human prostate cancer cell line, ARCaP, was established and characterized. This cell line was derived from the ascites fluid of a patient with advanced metastatic disease. In contrast to the behavior of androgen-dependent LNCaP and its androgen-independent C4-2 subline, androgen and estrogen suppress the growth of ARCaP cells in a dose-dependent manner in vivo and in vitro. ARCaP is tumorigenic and highly metastatic. It metastasizes to the lymph node, lung, pancreas, liver, kidney, and bone, and forms ascites fluid in athymic hosts. ARCaP cells express low levels of androgen receptor mRNA and prostate-specific antigen mRNA and protein. Immunohistochemical staining shows that ARCaP cells stain intensely for epidermal growth factor receptor, c-erb B2/neu, and c-erb B3. Staining is negative for chromogranin A and positive for bombesin, serotonin, neuron-specific enolase, and the c-met protooncogene (a hepatic growth factor/scatter factor receptor). ARCaP cells also secrete high levels of gelatinase A and B and some stromelysin, which suggests that this cell line may contain markers representing invasive adenocarcinoma with selective neuronendocrine phenotypes. Along with its repression of growth, androgen is also found to repress the expression of prostate-specific antigen in ARCaP cells as detected by a prostate-specific antigen promoter-beta-galactosidase reporter assay. Our results suggest that the androgen-repressed state may be central to prostate cancer progression and that advanced prostate cancer can progress from an androgen-independent to an androgen-repressed state.
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PMID:Androgen-repressed phenotype in human prostate cancer. 898 79

Clinical data were retrieved from the hospital records of 34 patients with Paget's disease of the vulva treated from 1972 to 1990. Flow-cytometric (FCM) DNA measurements and p53 and c-erbB-2 immunostaining were performed on paraffin-embedded samples. Five patients had an underlying adenocarcinoma and 29 intraepithelial disease (IEP). Twenty-seven patients with IEP underwent surgery. The surgical margins were positive in 15 patients, negative in 10, and not evaluable in 2. The tumor was diploid in 15 patients, nondiploid in 11, and not evaluable in 1. Eight patients recurred, 6/15 (40%) with positive and 2/10 (20%) with negative margins. One patient with positive margins was never disease-free. Recurrence was seen in 6/11 (55%) patients with nondiploid tumors, 4 with positive and 2 with negative margins. Two of 15 (13%) patients with diploid tumors recurred/persisted, both with positive margins. None of the 6 patients with diploid tumors and negative margins recurred. p53 and c-erbB-2 were found negative in all but 4 patients. Tumor nondiploidy was associated with an increased risk of recurrence irrespective of surgical radicality. p53 and c-erbB-2 seemed to play no role in the pathogenesis or prognosis.
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PMID:DNA ploidy and expression of p53 and C-erbB-2 in extramammary Paget's disease of the vulva. 899 53

All-trans retinoic acid (ATRA) has been previously shown to inhibit the proliferation of some human ovarian carcinoma cell lines, and this inhibition was accompanied by cellular changes that were indicative of differentiation (Caliaro et al, 1994). In this work, a pretreatment of these adenocarcinoma cells with ATRA, for their respective doubling time, enhanced cisplatin (CDDP) cytotoxicity in the cell ines that were sensitive to its antiproliferative effect, but not in the ATRA-resistant ones. Results were assessed using median effect analysis in two ATRA-sensitive cell lines (OVCCR1 and NIHOVCAR3 cells) and in one ATRA-insensitive cell line (IGROV1 cells). Synergy between these two agents was observed only in cells sensitive to ATRA, regardless of their relative sensitivity to CDDP. Potential mechanisms for this synergy were investigated. ATRA did not increase the cellular platinum content, did not decrease the cellular glutathione and had no influence on the metallothionein IIA mRNA levels in NIHOVCAR3 cells. Moreover, the protein kinase C (PKC) activity was modulated by this differentiating agent in all cell lines tested, indicating that this activity was not directly involved in this potentiation. However, an ATRA inhibition of glutathione-S-transferase activity associated with an increase in the total DNA adducts formation could explain the potentiation of the CDDP cytotoxicity observed in NIHOVCAR3 cells. Finally, the ATRA modulation of the epidermal growth factor (EGF) receptor mRNA level could also be implicated in this synergy.
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PMID:Multifactorial mechanism for the potentiation of cisplatin (CDDP) cytotoxicity by all-trans retinoic acid (ATRA) in human ovarian carcinoma cell lines. 902 Apr 76

We compared PCR-SSCP detected mutations of k-ras (codon 12) and p53 (exons 5-8) to ERBB-2 immunostaining and clinicopathologic features in 31 pulmonary adenocarcinomas. There were nine tumors (29%) with mutations of ras, 13 tumors (42%) with mutations of p53, and three tumors (10%) with mutations of both. Neither k-ras nor p53 mutation alone was significantly correlated with stage, grade, or survival. However, tumors with k-ras mutation were more frequently associated with an invasive growth pattern, defined as > 30% tumor volume composed of infiltrative nests of cells within desmoplastic, scar-like stroma [< 30% volume invasive--1/13 (8%) with k-ras mutation vs. > 30% volume invasive--8/18 (44%) with k-ras mutation, p = 0.02]. Accordingly, k-ras mutations were observed in only 1/9 (15%) predominantly bronchoalveolar or papillary tumors versus 6/22 (28%) acinar or scar carcinoma tumors. All three patients with combined k-ras/p53 mutation had advanced stage (III/IV) at presentation and died of the disease. In contrast to k-ras, staining for ERBB-2 was more frequently observed in tumors exhibiting < 30% invasive growth pattern (12/13, 92%) than in tumors with > 30% invasive growth pattern (10/18, 56%, p = 0.03). ERBB-2 immunoreactivity was more frequent in Stage I (14/15, 93%) versus Stage II-IV (8/16, 50%) cases, but it did not correlate with survival. There was a reciprocal relationship between k-ras mutation and ERBB-2 staining; only 4/9 (44%) k-ras mutated cases were ERBB-2 positive versus 18/22 (82%) cases without k-ras mutation (p = 0.005). In contrast, 8/13 cases with p53 mutation were ERBB-2 positive. We conclude that well-differentiated and less invasive papillary and bronchoalveolar tumors are more often ERBB-2 positive/k-ras negative (i.e. at codon 12), whereas less well differentiated acinar or scar carcinomas are more often ERBB-2 negative/k-ras mutated at codon 12. These findings imply that the divergent histogenesis of pulmonary adenocarcinoma may reflect specific differences in genetic pathology.
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PMID:Clinicopathologic analysis of k-ras, p53, and ERBB-2 gene alterations in pulmonary adenocarcinoma. 902 39


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