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)

Monoclonal antibody PAb3 to c-erbB-2/neu protein was utilized in the immunoperoxidase staining of 86 human specimens from oral mucosa. These tissue specimens represented a spectrum from 7 normal to 9 simple hyperplasia, 15 mild dysplasia, 14 moderate dysplasia, 20 severe dysplasia and 21 squamous cell carcinoma. Our study indicated that as the cells acquire a more malignant phenotype, there was a progressive increase in neu expression. It also suggested that neu may be involved in the development of oral cancers and that its evaluation in the early stages may assist in the diagnosis and management of oral cancers.
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PMID:Oral cancer progression and c-erbB-2/neu proto-oncogene expression. 135 5

Gene amplification (overexpression) of c-erb B-2 was tested in a variety of cystic renal diseases, renal cell neoplasms (adenomas and carcinomas) and end stage kidneys without cysts. C-erb B-2 encodes a receptor-like protein that shares homology with, but is distinct from the epidermal growth factor (EGF) receptor. A monoclonal antibody that immunoprecipitates a protein of approximately 185 kD from a lysate of NIH/3T3 cells transfected with the c-erb B-2 gene was utilized for testing. Simple renal cysts, cystic renal dysplasia, autosomal recessive polycystic kidney disease (ARPKD), and non-cystic, essentially normal kidneys failed to show c-erb B-2 overexpression. In contrast, autosomal-dominant polycystic kidney disease (ADPKD), acquired (dialysis-associated) cystic disease (ACD), non-cystic end stage kidneys and renal cell neoplasms revealed overexpression of c-erb B-2 with some frequency (40% or more of cases tested). Three cystic disorders revealing c-erb B-2 overexpression also showed platelet-derived growth factors (PDGFs) expression in similar locations (cyst lining and adjacent tubules). Other growth factors [insulin-like growth factor (IGF-I), fibroblast growth factor (FGF) and beta transforming growth factor (TGF beta)] were not noted to be overexpressed in either c-erb B-2 positive or negative cystic diseases. C-erb B-2 may be a marker related to the proliferative/growth capabilities of selected cystic diseases, including potential for associated genesis of benign and malignant renal cell tumors.
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PMID:C-erb B-2 amplification in cystic renal disease. 168 89

Frequent recurrences and multicentricity of bladder cancer suggest that alterations of the urothelium distant from the tumor may be relevant to prognosis. In this study immunohistochemistry and fluorescence in situ hybridization (FISH) were used to examine expression of p53, erbB-2, and epidermal growth factor receptor (EGF-r), genomic aberrations, and tumor cell proliferation (Ki67 LI) in normal and dysplastic urothelium. Biopsy specimens examined included normal urothelium (n = 40), mild dysplasia (n = 34), moderate dysplasia (n = 18) and carcinoma in situ (CIS; n = 20). Several different oncogene expression patterns were found, only some of which were associated with dysplasia. EGF-r expression was equally frequent in normal and dysplastic urothelium and showed a strong association with Ki67 LI (P < .0001). A purely superficial erbB-2 positivity was present in both normal and dysplastic biopsies. However, diffuse erbB-2 positivity and p53 overexpression were both associated with advanced dysplasia (P < .0001 each). FISH analysis showed erbB-2 gene amplification and p53 deletions in selected CIS, as well as a marked chromosome 17 copy number heterogeneity in all six CIS examined. These findings indicate a considerable genomic instability in bladder CIS. They show that both erbB-2 and p53 are altered during malignant transformation. Detectable oncogene expression alone, however, is not diagnostic of malignancy in bladder urothelium.
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PMID:Patterns of p53, erbB-2, and EGF-r expression in premalignant lesions of the urinary bladder. 767 97

AIMS--To investigate overexpression of the oncoprotein c-erbB-2 in the dysplasia/carcinoma sequence of Barrett's columnar-lined oesophagus (CLO). METHODS--Immunohistochemical staining was performed using the monoclonal antibody NCL-CB-11 on formalin fixed tissue from 31 cases of Barrett's carcinoma, 20 cases of cancer associated dysplastic CLO, seven cases of dysplastic CLO without cancer, and 20 cases of non-dysplastic CLO. Membranous staining was regarded as positive for c-erbB-2 overexpression; cytoplasmic staining was recorded separately as its significance is uncertain. RESULTS--Membranous c-erbB-2 overexpression was observed in eight of 31 (26%) carcinomas and in none of the cases of dysplastic CLO. Variable cytoplasmic staining was seen in four of 31 (13%) tumours and seven of 27 (26%) cases of dysplastic CLO. No staining was observed in non-dysplastic CLO. CONCLUSIONS--C-erbB-2 overexpression is a relatively late event in the development of some Barrett's carcinomas and is unlikely to be involved in the early stages of neoplastic transformation of CLO.
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PMID:c-erbB-2 overexpression in the dysplasia/carcinoma sequence of Barrett's oesophagus. 774 11

The prognosis of gastric carcinoma remains unfavorable despite a greater understanding of its molecular pathology. This retrospective study of primary gastric carcinomas was collected from one of the highest risk regions of China and examined for the oncogenetic expression of p53, c-erbB-2, and PCNA using immunohistochemistry and DNA contents by flow cytometry and image analysis. These products are reported to influence the tumor behavior. The p53 nuclear and c-erbB-2 membrane-bound stainings were seen in 58% and 34% of cases, respectively. A high PCNA index was found in 90% of the tumors. The p53 expression did not correlate with the histological differentiation, gross morphology, and depth of tumor invasion. Additionally, p53 and c-erbB-2 reactivity did not correlate with the proliferative index (PI) or S-phase DNA content. However, the mutant p53 expression was detected in the dysplastic cells adjacent to the tumor, suggesting a possible role of the oncogene in tumor pathogenesis. Mutant p53 expression can also be helpful in early detection of cases with dysplasia in well-differentiated adenocarcinomas.
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PMID:Gastric carcinoma: recent issues in prognostic factors. 777 39

The expressions of c-erbB-2 oncogene and epidermal growth factor receptor (EGFR) were investigated immunohistochemically in specimens from 184 cases of hepatitis B, cirrhosis and hepatocellular carcinoma (HCC) and 29 normal liver specimens. EGFR was expressed in 36% (48/134) of the hepatocellular carcinoma and chronic liver disorder specimens and it was immunolocalized mainly in the sinusoidal endothelial cells. No significant difference was found between EGFR expression in HCC and in benign chronic liver disorders. These results indicate that EGFR may have some role in the proliferation of the sinusoidal epithelial cells in chronic liver disease. Low level c-erbB-2 expression was observed in 5/29 (17%) of normal liver specimens. In chronic hepatitis B and liver cirrhosis, its expression was found in all specimens. c-erbB-2 protein was immunolocalized mainly in small polygonal liver cells (SPLCs) and hepatocytes in small-cell dysplasia (SCD) and in ductular metaplasia (DM); c-erbB-2 expression in HCC cells was found to be weaker than in SPLCs, the hepatocytes in SCD and in DM. These results indicate that activated c-erbB-2 oncogene may have a role in human HCC genesis through promoting the development of SCD from SPLC proliferation and the progression of SCD. The close relation between the expression of c-erbB-2 and HBxAg imply that the activation of c-erbB-2 in human liver tissues may be related to HBV X gene.
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PMID:[Expression of c-erbB-2 protein and EGF receptor in hepatitis B, cirrhosis and hepatocellular carcinoma]. 778 35

Intraductal papillary growth of mucin producing hypersecreting, columnar cells characterizes a group of rare pancreatic exocrine neoplasms which we propose to call intraductal papillary-mucinous tumors (IPMT). We analysed the histopathology of 26 IPMT in relation to gastro-enteropancreatic marker expression, genetic changes and biology. Four IPMT showing only mild dysplasia were considered to be adenomas. Nine tumours displayed moderate dysplasia and were regarded as borderline. Severe dysplasia-carcinoma in situ changes were found in 13 IPMT which were therefore classified as intraductal carcinomas. Six of these carcinomas were frankly invasive and two of these had lymph node metastases. The invasive component resembled mucinous non-cystic carcinoma in all but one tumour which showed a ductal invasion pattern. Immunohistochemically, an intestinal marker type was found in most carcinomas, while gastric type differentiation prevailed among adenomas or borderline tumours. K-ras mutations (seven at codon 12 and one at codon 13) were found in 31% of IPMT (2 adenomas, 1 borderline, 5 carcinomas). Nuclear p53 overexpression was detected in 31% of IPMT (6 carcinomas and 2 borderline IPMT) and correlated with p53 mutations (one at exon 8 and the other at exon 5) in two carcinomas. p53 abnormalities were unrelated to K-ras mutation. c-erbB-2 overexpression was observed in 65% of IPMT, with various grades of dysplasia. Twenty-two of 24 patients are alive and well after a mean post-operative follow-up of 41 months. Only two patients, both with invasive cancer at the time of surgery, died of tumour disease. It is concluded that pancreatic IPMT encompass neoplasms which, in general, have a favorable prognosis, but are heterogeneous in regard to grade of dysplasia and marker expression. Adenoma, borderline tumour, intraductal carcinoma and invasive carcinoma can be differentiated. p53 changes but not K-ras mutation or c-erbB-2 overexpression are related to the grade of malignancy. Most IPMT differ in histological structure, marker expression and behaviour from ductal adenocarcinoma.
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PMID:Intraductal papillary-mucinous tumours represent a distinct group of pancreatic neoplasms: an investigation of tumour cell differentiation and K-ras, p53 and c-erbB-2 abnormalities in 26 patients. 782 Mar

Among the tissue, cellular, and molecular changes which take place during the development of squamous cell carcinoma (SCC) of the upper aerodigestive tract, only a limited number can be used as surrogate endpoint biomarkers (SEBs) in cancer chemoprevention trials. Molecular SEBs will be genes or gene products which can be measured accurately and reliably, are altered in intraepithelial neoplasia (dysplasia), correlate strongly with the true outcome (invasive cancer), and are modulated by a chemoprevention agent(s). To identify and modulate molecular SEBs in intraepithelial neoplasia of the upper aerodigestive tract, we studied expression of the epidermal growth factor receptor (EGFR), transforming growth factor-alpha (TGF-alpha), and HER-2/neu genes in oral leukoplakia before, during, and after treatment with 13-cis-retinoic acid, a vitamin A derivative. Four of nine patients treated for 3 months with 1 mg/kg/day of 13-cis-retinoic acid had complete resolution of their leukoplakia. Biopsies were taken of leukoplakia and adjacent normal-appearing mucosa before, during, and after treatment. Immunohistochemistry was performed using the BioGenex Super Sensitive Biotin-Streptavidin horseradish peroxidase detection system. Pretreatment expression of EGFR, TGF-alpha, and HER-2/neu in leukoplakia was increased when compared to normal-appearing mucosa. TGF-alpha expression decreased during treatment in leukoplakia, but not in normal-appearing mucosa, suggesting that TGF-alpha may serve as an intermediate endpoint in cancer chemoprevention trials.
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PMID:Retinoid modulation of biomarkers in oral leukoplakia/dysplasia. 782

Molecular biologic studies have shown that human papillomavirus (HPV), some oncogenes and tumor suppressor genes are associated with uterine cervical carcinogenesis. We examined HPV DNA typing and its gene expression, oncogenes (c-myc, EGF-R, c-erb B2) and p53 in cervical dysplasia and cancer with molecular biologic, immunohistochemical technique and binding assay to establish a gene diagnosis of uterine cervical cancer. The HPV study revealed that HPV DNA was detected at a high frequency at a higher grade of dysplasia and in the early stage of cervical cancer; especially HPV type 16 was associated with cervical carcinogenesis. In the oncogene study, c-myc gene overexpression was recognized in the advanced stage of cervical cancer. The other oncogene and p53 were found in a low frequency and were non-specific genes in cervical cancer. These findings indicated that HPV DNA diagnosis is a useful tool for screening the high risk group of cervical precancerous lesions and that oncogene detection might be useful in determining the biological behavior of a malignant tumor.
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PMID:[Gene diagnosis of uterine cervical cancer]. 790 55

Fine needle aspirates (FNA) from 106 high-risk women and 25 low-risk women were evaluated for overexpression of estrogen receptor (ER), epidermal growth factor receptor (EGFR), mutant p53, and HER-2/neu by immunocytochemistry, and for aneuploidy by image analysis. Aspirates were also classified cytologically as normal, apocrine metaplasia, epithelial hyperplasia (EH), or dysplasia. High-risk women were those with a first-degree relative with breast cancer (76%), precancerous breast disease (26%), prior cancer of the contralateral breast (9%), or multiple abnormalities (11%). Low-risk women had none of the above risk factors, nor a prior breast biopsy or clinical evidence of fibrocystic disease. The median 10-year Gail risk for the high-risk group was 4%, compared to 0.7% for the low-risk group. There were significant differences (p < 0.01) between high- and low-risk women in the prevalences of hyperplasia (55% versus 12%), dysplasia (19% versus 0%), aneuploidy (32% versus 0%), overexpressed EGFR (32% versus 4%), and overexpressed p53 (29% versus 4%). The prevalence of multiple biomarker abnormalities was also greater in high-risk than in low-risk women (28% versus 0%; p < 0.01). Four percent (4%) of FNAs from high-risk women with normal cytology, 29% of aspirates with hyperplastic cytology, and 60% of those with dysplasia were associated with two or more biomarker abnormalities. The differences in the prevalence of multiple biomarker abnormalities among various cytologic categories were statistically significant (p = 0.02, normal versus EH; p = 0.02, EH versus dysplasia; p < 0.01, normal versus dysplasia).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biomarker and cytologic abnormalities in women at high and low risk for breast cancer. 791 61


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