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)

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

To clarify whether p53 protein expression is involved in multistep carcinogenesis or the progression of mammary ductal carcinoma, we investigated p53 protein expression in 83 invasive ductal carcinomas (IDC), 10 IDC with a predominant intraductal component, 13 non-invasive ductal carcinoma (NIDC), 16 atypical ductal hyperplasia (ADH) and 39 benign epithelial hyperplasia (EH), using immunohistochemistry. Expression of p53 protein was detected in 24 (28.9%) cases of IDC, 5 (50%) cases of IDC with a predominant intraductal component and 1 (7.6%) case of NIDC. No expression was observed in either ADH or EH. In IDC, including cases with a predominant intraductal component, p53 protein expression was associated with a higher histological grade (P < 0.0001) or mitotic index (P < 0.0005). Although overexpression of c-erbB-2 protein has also shown a similar association with these prognostic indicators, expression of p53 protein correlated regardless of the status of c-erbB-2 overexpression. Completely coordinated expression of p53 protein was seen in both intraductal and invasive components. The intraductal component in IDC including cases with a predominant intraductal component which expresses p53 protein had significantly higher histological grade (P < 0.0005) or more comedo-subtypes (P < 0.0001). These results suggested that p53 protein expression occurs at a stage of NIDC with high histological grade or in comedo-subtypes. Its expression is maintained throughout invasion.
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PMID:Expression of p53 protein in benign epithelial hyperplasia, atypical ductal hyperplasia, non-invasive and invasive mammary carcinoma: an immunohistochemical study. 791 68

The expression of mRNA for epidermal growth factor (EGF), transforming growth factor-alpha (TGF-alpha), EGF receptor (EGFR) and c-erbB-2 genes and the immunoreactivity to these gene products were examined in 3 newly established human pancreatic carcinoma cell lines and their corresponding in vivo tumor lines using the Northern blot technique and the immunohistochemical method. All 3 cell lines expressed TGF-alpha, EGFR and 2 of the 3 lines expressed EGF and c-erbB-2 mRNAs. The immunohistochemical study showed immunoreactivity to EGF, TGF-alpha and EGFR in all these 3 cell lines and their corresponding in vivo tumor lines. These results indicate that the autocrine loop of EGF and/or TGF-alpha/EGFR in pancreatic carcinoma cells may be one of the important reasons for the uncontrolled growth of the pancreatic carcinoma. The c-erbB-2 overexpression in some of the cell lines may also contribute to the carcinogenesis or progression of this cancer.
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PMID:Expression of EGF, TGF-alpha, EGFR and c-erbB2 genes and their gene products in human pancreatic carcinoma cell lines. 794 34

Experimental data and clinical observations indicate that an increased expression of oncogenes or their point mutations play an essential role in the process of carcinogenesis. It was important to find out that environmental and occupational carcinogens activate cellular oncogenes and contribute to increased amounts or occurrence of mutated oncoproteins. The latter are responsible for activating mechanisms which further the neoplastic transformation of cells. The researches are mainly concerned about two oncoproteins: oncoprotein coded by the ras oncogene--called p21 protein and oncoprotein coded by the erbB-2 oncogene--called p185 protein. Investigations performed on neoplastic cells show that the neoplastic transformation process involves not only the afore-said oncogenes and their oncoproteins but also other oncogenes, and that the process itself required activating of more than one oncogene. At present, it is possible to use measurements of oncoproteins in the biological material which is easily available. Due to this fact, a number of works in which measurements of oncoproteins in blood serum were used to assess cancer risk in persons exposed to carcinogens present at the work place, have been published.
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PMID:Oncoproteins as biomarkers of a preclinical form of cancer of the respiratory tract induced by environmental carcinogens. 801 97

Gene amplification in stomach and oesophageal cancers was reviewed. In stomach cancers, two receptor type tyrosine kinases, c-erbB-2 and K-sam, are frequently amplified and overexpressed. c-erbB-2 seems to be preferentially amplified in well-differentiated, and K-sam in poorly-differentiated, gastric adenocarcinomas. 11q13 genes are amplified in about 50% of the oesophageal cancers. These genes include hst-1, int-2 and cyclin D/prad1, all of which are mapped to chromosome 11 at band q13. Although hst-1 and int-2 are usually not expressed despite amplification, elevated transcription of the cyclin D gene is accompanied by its amplification, suggesting a role of a G1 cyclin in oesophageal carcinogenesis.
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PMID:Amplified genes in cancer in upper digestive tract. 809 12

Thirty-five patients with ovarian tumors operated on between December, 1989 and June, 1991 were studied to detect K-ras codon 12 point mutation (PM). (1) Five of 35 ovarian tumors (14.3%) disclosed K-ras PM at codon 12 and all the PM cases were in transition from GGT to GAT. On the other hand only one case (5.3%) with K-ras oncogene amplification was found and no C-myc or erbB-2 amplification was detected. (2) The incidence of PM according to clinical stages was seen in 3 of 11 stage I cases (27.3%), in 1 of 3 stage II cases (33.3%), in 1 of 14 stage III cases (7.1%) and in neither of 2 stage IV cases. PM was therefore seen in relatively early stages. (3) The occurrence of PM according to the histologic type was found in 3 of 16 serous tumors (18.8%), in 2 of 5 mucinous tumors (40.0%) and in none of 7 clear cell carcinomas or 2 endometrioid carcinomas. (4) Concerning the relation of PM to the involvement of serosal surface of ovarian tumors and to the ascitic cytology, no particular correlation was observed in our study. (5) Regarding the cytologic findings in imprint smears of the tumors in reference to PM, such as nuclear size, shape, N/C ratio, chromatin pattern, nucleolar size and number, the cases with PM tended to have more multiple nucleoli than PM negative cases. No other findings seemed to indicate the clinical progress of cancer. In conclusion, our study indicated that PM in ovarian cancers was a relatively early event in carcinogenesis.
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PMID:[Studies on the point mutation of ras oncogene in ovarian tumor]. 825 28

Recent progress in the field of oncogenes has produced valuable information concerning the molecular and cellular biology of the cancer cell and provided a tool to investigate the process of carcinogenesis. Some oncogenes such as the ras, myc, erbB-2 and abl have been extensively investigated in the progression of carcinogenesis in several types of human tumors. The p53 tumor suppressor gene has recently been shown to play the role of "molecular policeman," and is obviously important in the development of many tumors, as mutations in this gene are the most common genetic abnormalities found in all neoplasias. In certain cases the incidence of aberrant gene expression and genetic alterations of oncogenes and tumor suppressor genes have been shown to be important in the progression of these cancers and may be of use as prognostic indicators and form the basis for a successful therapy.
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PMID:Prognostic significance of oncogenes and tumor suppressor genes in human malignancy. 831 5

Non-small cell lung carcinoma specimens of 173 previously untreated patients were analyzed for the expression of proteins encoded by the oncogenes c-myc, c-fos, c-jun, c-erbB-1, c-erbB-2, c-H-ras, c-K-ras and c-N-ras. Forty-six per cent of the tumors were positive for the c-MYC protein, 60% for c-FOS, 50% for c-JUN, 80% for c-ERBB-1, 55% for c-ERBB-2, 12% for c-H-RAS, 5% for c-K-RAS and 71% for c-N-RAS. Proteins encoded by c-fos and c-jun are overexpressed more frequently in carcinomas of smokers (c-fos: P < 0.005; c-jun: P < 0.01). When we grouped the patients according to their tumor histology the results became more evident. Squamous cell lung carcinomas of smokers showed a higher incidence of c-FOS (P = 0.01), c-JUN (P < 0.01) and c-ERBB-1 (P = 0.01) proteins than squamous cell lung carcinomas of non-smokers. The expression rate and the intensity of staining proved not to be influenced either by the number of cigarettes smoked daily or by cessation of smoking. In adenocarcinomas, however, we only found a trend for a more frequent overexpression of c-fos (P = 0.07) and c-jun (P = 0.14) encoded proteins in carcinomas of smokers and no correlation between the expression of c-erbB-1 products and smoking. No correlation was found between the expression of c-MYC, c-ERBB-2, c-H-RAS, c-K-RAS and c-N-RAS proteins and the smoking habits of the patients, neither in squamous cell carcinomas nor in adenocarcinomas of the lung.
Carcinogenesis 1993 Jun
PMID:Overexpression of oncoproteins in non-small cell lung carcinomas of smokers. 838 72

The c-erbB-2 proto-oncogene (HER-2/neu) codes for a transmembrane, tyrosine kinase, 185 kD oncoprotein (p185erbB2), which is related to the epidermal growth factor receptor. p185erbB2 overexpression occurs in carcinomas at many sites, including the uterine cervix, and predicts poor clinical outcome. The authors hypothesize that p185erbB2 immunohistochemistry will provide additional information in the evaluation of uterine cervix carcinomas with glandular differentiation (CCGD), a difficult and more frequent clinical problem. Paraffin sections from 82 CCGDs including 41 pure adenocarcinomas and 41 adenosquamous carcinomas (7 glassy cell predominant and 34 exhibiting a gland forming component) are immunostained with anti-p185erbB2 (CB11 monoclonal, Novacastra Laboratories, Newcastle upon Tyne, UK). Seventy-seven percent of CCGDs exhibit p185erbB2 immunoreactivity with distinct plasma membrane localization (M) in 50%, the remaining 27% show cytoplasmic staining only. Adjacent benign tissue is negative. The p185erbB2 staining intensity and distribution is as follows: 54.9% strong diffuse (SD, > or = 50% cells positive) with 40.2% M, 17.1% strong focal (SF, < 50% cells positive) with 9.8% M, and 4.9% weak with no M. Immunoreactivity occurs in both squamous and glandular areas of adenosquamous carcinomas. Endometrioid histology is associated with absence of p185erbB2 (P < .01); all other histopathologic features show no association. Follow-up information is available in 77 patients: 37 exhibit recurrent disease (8 pelvic, 15 distant and 14 both) at 1 to 144 months (mean 34, median 16) and 40 were disease free at 12 to 216 months (mean 75, median 64). Strong p185erbB2 immunoreactivity predicts recurrence at 24 months (P < .05) but not overall recurrence at longer follow-up periods. Recurrent disease is associated with nuclear grade (P < .00001); high clinical stage (P < .001); vascular space invasion (P < .001); large size on clinical exam or pathologic evaluation (P < .005); and pelvic lymph node involvement (P < .05). Considering only patients in good prognosis groups, p185erbB2 immunoreactivity does not predict recurrence. Strong p185erbB2 immunoreactivity is associated with stage 3,4 disease (P < .01). p185erbB2 expression is associated with CCGD carcinogenesis but occurs late in the disease, in patients who present at late stage, hindering its prognostic predictive value. p185erbB2 immunolocalization may have a diagnostic role in confirming CCGD in histologically challenging cases, predicting high stage at initial biopsy, and defining therapeutic strategies.
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PMID:c-erbB-2 oncoprotein overexpression in uterine cervix carcinoma with glandular differentiation. A frequent event but not an independent prognostic marker because it occurs late in the disease. 885 48

Amplification of the HER-2/neu oncogene was assessed in 80 cases of epithelial ovarian tumors using differential polymerase chain reaction. HER-2/neu gene was amplified in 22 of 46 invasive cancers (48%) and in 5 of 34 borderline cancers (15%), but none of the 20 specimens of normal ovaries showed amplification. THis difference is statistically significant (p = 0.00004). The incidence of HER-2/neu amplification in late stage (III-IV, 77%) was significantly higher than that in early stage (I-II, 21%) in invasive epithelial carcinoma (p = 0.0004). There was no correlation between HER-2/neu amplification and cell type or grade of tumor. In cases of ovarian tumors of borderline malignant potential, the amplification of HER-2/neu was not correlated with clinicopathologic features. Follow-up with a mean of 22 months (6-50 months) was available for 39 cases of invasive ovarian cancers and all 34 borderline ovarian cancers. The incidence of HER-2/neu amplification in the invasive cancer and borderline cancer patients who were alive with disease was 50 and 50%, and is not statistically different from that in the patients who were alive with no evidence of disease (p = 0.662 and 0.345, respectively). The incidence of amplification in the invasive cancers of patients who died of the disease (86%) was higher than that in the patients who were still alive (44%), but the difference is not statistically significant (p = 0.175). This study supports the association of HER-2/neu amplification with progression of invasive ovarian cancer. It also suggests that HER-2/neu amplification may be an adjunctive prognostic factor of invasive epithelial ovarian cancer, shown to be associated with an unfavorable clinical course. In addition, HER-2/neu amplification occurs relatively infrequently in early invasive and borderline ovarian cancers, making it unlikely that such amplification is a general early event in ovarian carcinogenesis.
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PMID:Prevalence and significance of HER-2/neu amplification in epithelial ovarian cancer. 852 57


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