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)

c-erbB-2 protein expression was investigated immunohistochemically in frozen thyroid tissue specimens from 42 patients using a polyclonal sheep antibody. c-erbB-2 immunoreactivity was detected in 12 out of 17 papillary carcinomas, while no c-erbB-2 protein immunostaining was seen in cases of follicular adenoma (five cases), follicular carcinoma (five cases) or medullary carcinoma (one case), nor in cases of non-neoplastic tissue, including normal thyroid tissue from tumour-bearing glands. RNA was extracted from 51 thyroid tissue samples from 34 of the above patients, and c-erbB-2 mRNA was analysed by slot-blot hybridisation. c-erbB-2 mRNA was detectable in all samples, but papillary carcinomas and lymph node metastases showed significantly higher levels of c-erbB-2 mRNA compared to non-neoplastic tissue. The present demonstration of positive c-erbB-2 immunostaining in papillary thyroid carcinomas is contradictory to previous findings on formalin-fixed, paraffin-embedded material, and emphasises the importance of tissue quality for c-erbB-2 protein detection.
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PMID:Expression of c-erbB-2 protein in papillary thyroid carcinomas. 135 25

In order to analyze the correlation between immunohistochemical positivity for c-erbB-2 oncoprotein and prognosis in patients with malignant salivary gland tumors, 59 cases of malignant tumors of the major salivary glands, including 35 parotid gland, 20 submaxillary gland and 4 sublingual gland tumors, were studied immunohistochemically using a polyclonal antibody against c-erbB-2 oncoprotein. Positive staining was observed in 13 (22%) of the 59 cases. Interestingly, positive results were obtained only in adenocarcinoma (6/20) and carcinoma in pleomorphic adenoma (7/15), and not in any other histological types such as adenoid cystic carcinoma, mucoepidermoid tumor, and squamous cell carcinoma. There was no correlation between the degree of differentiation of adenocarcinoma and c-erbB-2 positivity. Since the carcinoma in pleomorphic adenoma positive for c-erbB-2 oncoprotein was adenocarcinoma, adenocarcinoma and adenocarcinoma in pleomorphic adenoma were placed together (n = 33), and the presence or absence of c-erbB-2 oncoprotein in this group was examined for correlation with patients' survival and other clinicopathological features, including clinical stage, tumor size, surgical margins, and lymph node status. The c-erbB-2-positive tumors tended to be more advanced and larger than negative tumors. Similarly, c-erbB-2-positive tumors were difficult to resect completely, were associated with lymph node metastasis more frequently, and showed lower disease-free survival than negative cases (P less than .05). We conclude that immunohistochemical positivity for c-erbB-2 is an indicator of aggressiveness in both adenocarcinoma and adenocarcinoma in pleomorphic adenoma of the major salivary glands.
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PMID:Immunohistochemical study of c-erbB-2 oncoprotein overexpression in human major salivary gland carcinoma: an indicator of aggressiveness. 135 53

An immunohistochemical study of c-erbB-2 oncoprotein expression was carried out on 201 cases of primary salivary gland tumors, using a polyclonal antibody, raised to the intracytoplasmic domain of the c-erbB-2 oncogene product. An intense membrane reactivity was observed in one case of sialocarcinoma transformed from pleomorphic adenoma (n = 8) and one case of mucoepidermoid carcinoma (n = 22). A comparative histopathologic evaluation of c-erbB-2 positive tumors showed marked variation in cell size, nuclear pleomorphism, multinucleation, a high mitotic rate and increased lymphoid cell infiltration and an aggressive clinical course with poor survival. The results indicate that c-erbB-2 oncoprotein is rarely expressed in malignant salivary gland tumors. However, the overexpression appears to have a distinct histopathologic feature, but a larger study incorporating histopathology and clinical data would be necessary to correlate the significance of c-erbB-2 oncogene product in salivary malignant tumors.
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PMID:Rare expression of the c-erbB-2 oncoprotein in salivary gland tumors: an immunohistochemical study. 136 Oct 5

The immunohistochemical detection of the c-erbB-2 oncopeptide (p185erbB2) has been shown to be a valid marker for over-expression of this oncogene. To evaluate the possible relevance of gene expression to the proliferation of hepatocytes and bile ducts in human disease, the authors applied a monoclonal anti-p185 antibody to formalin-fixed, paraffin-embedded tissues from 67 examples of benign proliferative and neoplastic hepatic lesions and fetal liver. Focal membrane-based reactivity for the oncopeptide was detected on tumor cells in two of eight hepatocellular carcinomas and on tumor cells and adjacent bile ducts and hepatocytes in four of six cholangiocarcinomas. Each of the latter four lesions were in patients with primary sclerosing cholangitis. No reactivity was obtained in examples of hepatoblastoma, mixed cholangiocarcinoma-hepatocellular carcinoma, bile duct adenoma, or hepatocellular adenoma. Weak staining for p185erbB2 also was seen in two of seven cases of (sub)massive hepatic necrosis and two examples of postnecrotic cirrhosis, all of which were secondary to either hepatitis B or C virus infection. No other benign proliferative lesions were labeled by the anti-p185 antibody, including cases of chronic allograft rejection, necrosis secondary to hepatic artery thrombosis, metabolic-associated and nonmetabolic-associated cirrhosis, focal nodular hyperplasia, and nodular regenerative hyperplasia. The authors' results indicate that c-erbB-2 may be amplified in specific neoplastic and hepatitis B virus and hepatitis C virus infectious lesions of liver. The authors postulate that: (1) c-erbB-2 immunoreactivity may be a marker for malignant transformation in primary sclerosing cholangitis; and 2) overproduction of p185erbB2 may be an epiphenomenon of hepatitis B virus or hepatitis C virus infection.
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PMID:Immunoreactivity for c-erbB-2 oncopeptide in benign and malignant diseases of the liver. 137 19

Sections of formalin-fixed, paraffin-embedded primary salivary gland tumours were stained with a monoclonal antibody to the c-erbB-2 oncoprotein to determine the incidence and significance of expression of this protein. The series of 131 tumours comprised 33 cases of pleomorphic adenoma, 2 of malignant mixed tumour, 1 oxyphil adenoma, 31 Warthin's tumours, 4 basal cell adenomas, 6 mucoepidermoid carcinomas, 14 acinic cell carcinomas, 19 adenoid cystic carcinomas, 3 squamous carcinomas, and 18 poorly differentiated adenocarcinomas. Positive staining, as defined in previous studies, was present in five tumours (three cases of poorly differentiated adenocarcinoma, one mucoepidermoid carcinoma, and one adenoid cystic carcinoma). A review of the medical records of all patients did not disclose any clear difference between the clinical behaviour of positive and negative cases over a period of follow-up that ranged from 18 to 120 months. The findings of this study indicate that the protein product of the c-erbB-2 proto-oncogene is infrequently expressed in salivary gland tumours, and when it is localized on the tumour cell surface membrane, there is no clear evidence that this determines the biological behaviour of the tumour.
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PMID:Expression of c-erbB-2 oncoprotein in salivary gland tumours: an immunohistochemical study. 167 54

The c-erbB-2 proto-oncogene is known to encode a 185,000 molecular weight glycoprotein. This protein has been detected immunohistochemically in several human adenocarcinomas, suggesting that it may play a role in the development of these malignancies. In the otolaryngological field none of the adenocarcinomas expressing c-erbB-2 protein has yet been described. In this article we presented a case of parotid adenocarcinoma expressing the c-erbB-2 protein. In this case the adenocarcinoma was thought to have originated from pleomorphic adenoma. Immunohistochemically, the adenocarcinoma cells were stained and the remaining pleomorphic adenoma cells were not stained by polyclonal antibody against the c-erbB-2 protein. The expression of c-erbB-2 protein may have been related to the malignant development of the pleomorphic adenoma.
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PMID:Expression of c-erbB-2 protein detected in adenocarcinoma arising from parotid pleomorphic adenoma. 197 76

Malignant Balb/c mouse lung cell clones related to alveologenic carcinoma exhibited low levels of epidermal growth factor (EGF) receptor activity compared to nonmalignant cell clones. Immunoprecipitation of cell homogenates and immunohistochemistry on urethane-induced lung tumors suggest that the absence of activity reflects decreased amounts of EGF receptor protein. Low levels of EGF receptor alone cannot cause neoplastic transformation, since a nonneoplastic cell cone, B5D3, exhibited low levels of EGF receptor despite its nontransformed phenotype. The reduced levels of EGF receptor in malignant clones have been mimicked by long-term (12 h) treatment of a nontransformed cell clone with 200 nM phorbol dibutyrate. The detection of mutated ras oncogene in the transformed cell lines, taken together with the EGF receptor findings, suggests that more than one alteration in the signal transduction pathway may be necessary for transformation in alveologenic adenoma and carcinoma cell systems. A further phenotypic feature of transformation, reduced expression of the extracellular matrix proteins fibronectin and laminin, may be mediated at the transcriptional level.
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PMID:EGF-receptor and extracellular matrix changes in mouse pulmonary carcinogenesis. 205 35

Multi-autocrine loops of the epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), platelet-derived growth factor (PDGF) and TGF beta system are expressed in human gastrointestinal carcinomas. In esophageal and gastric carcinomas, they evidently play an important role in tumor progression. Gastrin, one of the major gut hormones, may also act as an autocrine growth factor for gastric and colonic carcinomas. The HST1 and INT-2 genes, belonging to the fibroblast growth factor gene family, are coamplified in approximately 50% of primary tumors and in all the metastatic tumors of esophageal carcinoma. TGF alpha and EGF are the ligands of the tumor cells that overexpress EGF receptor in esophageal carcinomas. The synchronous expression of EGF and its receptor, as well as TGF alpha and ras p21, is evidently correlated with the depth of tumor invasion, metastasis and prognosis of gastric carcinomas. Amplification of c-erbB-2 and EGF receptor genes has been observed in many metastatic sites of gastric carcinomas regardless of histological type. In addition to TGF alpha and EGF, TGF beta and PDGF A chain produced by tumor cells may stimulate collagen synthesis not only by fibroblasts but also by tumor cells themselves, resulting in extensive progression and diffuse fibrosis of scirrhous gastric carcinomas. Moreover, TGF alpha or EGF and estrogen may also play a cooperative role in the development of scirrhous gastric carcinoma. In colorectal carcinoma, it has been shown that the accumulation of several alterations in ras genes and p53 genes is most important for the conversion of adenoma to carcinoma. Critical genetic changes, including activation of oncogenes, mutation and deletion of tumor suppressor genes and disturbances in transcriptional regulatory sequences, may bring about aberrant expression of growth factors and their receptors in gastrointestinal carcinomas. The understanding of the significance of EGF-related growth factors in tumor progression provides a framework for a biological approach to the therapy of human gastrointestinal carcinomas. 8-Cl-cAMP, which inhibits expression of oncogenes and TGF alpha, may be useful not only for cancer therapy but also for the study of cell differentiation.
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PMID:Growth factors and oncogenes in human gastrointestinal carcinomas. 215 13

To determine the frequency and clinical significance of oncogene abnormalities in colon cancer, deoxyribonucleic acids from 45 colon carcinomas and 15 benign adenomas were hybridized with 14 different protooncogene probes. Abnormalities of oncogenes were found in 22% of cancers at the time of resection. Amplification of c-myc or c-erbB-2 and allelic deletion of c-ras-Ha or c-myb were the most frequent abnormalities. The presence of altered oncogenes did not correlate with Dukes' stage, tumor progression, or patient survival after resection. One adenoma had an allelic deletion of the c-myb oncogene which was not seen in either the normal colon or an adjacent carcinoma. These data indicate that the spectrum of altered protooncogenes in colon carcinoma is similar to that of other adenocarcinomas, and that unstable oncogenes can be found before overt malignancy develops.
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PMID:Protooncogene abnormalities in colon cancers and adenomatous polyps. 355 13

Clear cell carcinoma of salivary gland is a rare neoplasm. We report a third case of clear cell carcinoma arising in a pleomorphic adenoma and also in an extraparotid location. We document the immunohistochemical profile of the tumour including reactivity with a marker for the c-erbB-2 oncoprotein and suggest a myoepithelial origin for these lesions. The presence of a tetraploid stemline may account for the rapid tumour progression in this case.
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PMID:Clear cell carcinoma arising in a pleomorphic adenoma of the submandibular gland. 751 88


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