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)

Amplification of the Neu oncogene (c-erbB-2) has been reported by various researchers as a marker for poor clinical outcome in patients with breast cancer. We have performed immunohistochemical staining using a polyclonal antibody to the Neu oncoprotein on formalin-fixed material from normal breast, benign breast lesions, and 102 stage I node-negative breast cancers. Hybridization studies were also performed on 66 of the breast cancer cases. In the cancers 33% of cases showed positive staining of the in situ and invasive component, whereas only 25% of cases showed amplification of the Neu oncogene. The staining pattern in the tumor cells was cytoplasmic with plasma membrane accentuation. Focal positive cytoplasmic staining was noted in some cases of fibrocystic disease, fibroadenoma, and normal breast duct epithelium. Myoepithelial cells and smooth muscle of blood vessels also showed a positive reaction. This study shows that the Neu oncoprotein can be demonstrated on formalin-fixed material from normal, benign, and malignant breast lesions. In the breast cancers the differences in the number of cases showing amplification and those showing a positive immunohistochemical reaction could be due to increased transcriptional activity. It is possible that the node-negative patients whose tumors express the Neu oncogene may correspond to the group of patients who are expected to have a poor prognosis.
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PMID:Distribution and patterns of staining of Neu oncogene product in benign and malignant breast diseases. 197 59

Although over-expression of the C-erbB-2 oncogene product can be detected on formalin-fixed, paraffin-embedded sections from tumours of the human breast, fixation results in a considerable loss of immunostaining for this protein. In this study, C-erbB-2 expression was studied immunohistochemically on frozen sections in 63 infiltrating carcinomas, 3 phyllodes tumours, 15 fibroadenomas and 16 cases of fibrocystic disease. The value of C-erbB-2 expression as a prognostic indicator in ductal carcinomas was examined by seeking an association with known prognostic indicators. C-erbB-2 over-expression was confined to ductal carcinomas of the breast and was positively correlated with tumour size, grade, oestrogen receptor status and the presence of metastatic deposits in axillary lymph nodes. Only the association with lymph node and oestrogen receptor status were statistically significant. No evidence of a correlation between C-erbB-2 expression and growth fraction (as assessed with the Ki-67 antibody) was demonstrated in the cases studied. Formalin fixation was associated with the loss of immunoreactivity in all cases studied. 75% of cases which were positive on frozen sections were negative in paraffin sections. These results highlight the significance of the method of fixation used in studying C-erbB-2 expression. They confirm the association between C-erbB-2 expression and known prognostic indicators.
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PMID:C-erbB-2 oncogene product expression depends on tumour type and is related to oestrogen receptor and lymph node status in human breast carcinoma. 768 54

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

Currently, many tumor markers are routinely measured in patient serum, but none appears to adequately detect cancer-specific substances for breast cancer. Four tumor markers (CEA, CA15-3, BCA225, c-erbB-2) were compared for sensitivity and specificity to breast cancer in 393 patients with breast disease (fibrocystic disease; 40, benign tumor; 21, primary cancer; 22, recurrent or advanced cancer; 22, non-recurrent; 288), and the following results were obtained: In cases of primary breast cancer excluding stage IV cases, the positive rates of CEA, CA15-3 and BCA225 were 4.5%, 13.6% and 13.6%, respectively. These rates were not higher than the positive rates found in fibrocystic disease or benign tumor. In cases of recurrent or advanced breast cancer, the positive rates of CEA, CA15-3, BCA225 and c-erbB-2 were 31.8%, 50.0%, 40.9% and 27.3%, respectively. In the recurrent cases, the combination assay using CA15-3, BCA225 and c-erbB-2, showed more useful diagnostic value (72.7%) than other combination assays with three tumor markers. High levels of CA15-3 in eight cases, BCA225 in five and CEA in one were found during the follow up of 15 patients with initial recurrence. Serum c-erbB-2 exceeded the normal range in 6 of 7 cases with advanced breast cancer. Serum c-erbB-2 should be considered a marker of progressive breast cancer. These results suggested that CA15-3, BCA225, c-erbB-2 and combination assays are useful tumor markers for not only detecting the recurrence of breast cancer, but also diagnosing the progression of primary breast cancer.
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PMID:[Clinical usefulness of tumor markers in breast cancer]. 825 56

C-erbB-2 (Her-2 or c-neu) expression was studied by immunohistochemistry on FNA specimens of 20 breast ductal carcinomas, 20 fibroadenomas and 20 atypical fibrocystic lesions of the breast. Twelve cases of breast carcinomas, six fibroadenomas and five atypical fibrocystic lesions were found to display c-erbB-2 staining. A significant difference was found among c-erbB-2 index of breast carcinomas (mean 70,25), fibroadenomas (mean 43,83) and atypical fibrocystic disease (mean 37,4). We also found variations in c-erbB-2 expression, among individual cases of breast carcinomas, concerning the number and the intensity of carcinoma cells. It would be interesting to correlate these variations in c-erbB-2 expression with the prognosis of breast carcinomas.
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PMID:C-erbB-2: expression in patients with breast carcinoma in comparison to patients with benign breast diseases. 868 26

17 beta-hydroxysteroid dehydrogenases (17 beta-HSDs) are involved in the interconversion of biologically active and inactive sex steroids and are considered to play important roles in the in situ metabolism of estrogen in various estrogen dependent tissues. 17 beta-HSD type 1 catalyzes primarily the reduction of estrone (E1) to estradiol (E2), whereas 17 beta-HSD type 2 catalyzes primarily the oxidation of E2 to E1. However, the possible biological roles of these estrogen metabolizing isozymes in human breast cancer, especially in carcinogenesis of the human breast, have not been examined in detail. Because of the potential roles of estrogens in the early stages of human breast carcinogenesis, we have examined the immunolocalization of 17 beta-HSD type 1 and type 2 isozymes and estrogen receptor alpha(ER alpha) in both normal human breast tissue and in breast cancers, including ductal carcinoma in situ (DCIS), proliferative disease without atypia (PDWA) or fibrocystic disease and atypical ductal hyperplasia (ADH). We also correlated these findings with clinicopathological findings, Ki67 antigen, progesterone receptor (PR), c-erbB-2, and p53. 17 beta-HSD type 2 immunoreactivity was sporadically detected in non-proliferative or Ki67 negative ductal epithelia of normal breast, but rarely in breast carcinoma cells. 17 beta-HSD type 1 immunoreactivity was detected in 12/22 (54.5%) PDWA cases, 8/26 (30.8%) ADH cases, and 25/40 (62.5%) DCIS cases, respectively. 17 beta-HSD type 1 immunoreactivity was not statistically correlated with the age of the patients, Ki67 labeling index (LI), and PR LI, p-53 and c-erbB-2 immunoreactivity. There was no significant correlation between ER alpha LI and 17 beta-HSD type 1 immunoreactivity. There was a positive correlation between ER alpha and Ki67 LI in PDWA, whereas a negative correlation was detected between ER alpha and Ki67 LI in DCIS. There was no correlation between ER alpha and Ki67 LI in ADH. These results suggest that in human breast epithelial cells, development of ADH and DCIS may be associated with the loss and/or deviation of oestrogen dependent regulation of cell proliferation.
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PMID:17 beta-Hydroxysteroid dehydrogenase type 1 and type 2 in ductal carcinoma in situ and intraductal proliferative lesions of the human breast. 1081 Apr 3