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)

The association between known prognostic variables such as TNM stage, histological grade and mutant p53 tumor suppressor gene product, c-erbB-2 oncoprotein, DNA ploidy and cell kinetic data, including mitoses, PCNA expression, AgNOR scores and apoptosis, was investigated in 29 transitional cell carcinoma (TCC) cases. A positive correlation between the histologic grade and all the studied parameters, except for c-erbB-2 expression, and a positive correlation between the stage and histological grade, DNA ploidy, mitoses, apoptosis and p53 expression were found. The results of this study are in accordance with some of the previous studies, except for apoptosis which had been studied for the first time in TCCs. Although we found a statistically significant correlation between the apoptosis and both tumor stage and histological grade, the predictive value of apoptosis as an independent prognostic factor remains to be established in a larger series.
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PMID:Investigation of p53, c-erbB-2, PCNA immunoreactivity, DNA content, AgNOR and apoptosis in bladder carcinoma as prognostic parameters. 958 59

The hypothetical multistep model of breast carcinogenesis suggests a transition from normal epithelium to invasive carcinoma via intraductal hyperplasia (without and with atypia) and in situ carcinoma. These presumptive precursor lesions are currently defined by their histological features, and their prognosis is imprecisely estimated from indirect epidemiological evidence. Cytogenetic and molecular-genetic analysis of these lesions give evidence for an accumulation of various genetic alterations during breast tumorigenesis. Using immuno-histochemistry overexpression of the c-erbB-2 oncogene was found in ductal carcinoma in situ (DCIS), but not in atypical intraductal hyperplasia (AIDH) and intraductal hyperplasia (IDH). An expression of mutant p53 tumor suppressor gene as well as expression of cyclin D1 was identified in DCIS. In IDH lesions loss of heterozygosity (LOH) at various loci could be identified, and comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH) studies delivered evidence for DNA amplification on chromosomal region 20q13 in the early stage of IDH.However, little is currently known about genetic alterations in those premalignant lesions, and the chronology of genetic alterations and histopathological changes during carcinogenesis is mainly undiscovered.
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PMID:Genetic alterations in presumptive precursor lesions of breast carcinomas. 1244 56