Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review of published data on the epidemiology, pathology, and molecular biology of breast cancer in African American women seeks to identify how the etiology and presentation of the disease differ from those in white women. The crossover from higher to lower age-specific incidence rates in African American women at age 45 cannot be explained by current data on the distribution of risk factors. Data from six case-control studies suggest that the relative risks associated with both established and probable breast cancer risk factors are similar in African American and white women. Lower survival in African American compared to white women is primarily attributable to diagnosis at a later stage. However, evidence from a number of studies suggests that tumors in African American women may exhibit a more aggressive phenotype, which could also contribute to the survival disparity. Tumors in African American women are more likely to occur at a younger age, to be poorly differentiated and estrogen receptor negative, and to exhibit high grade nuclear atypia, more aggressive histology (more medullary and less lobular), and higher S-phase. Overexpression of p53 and erbB-2 occurs with similar frequency in African American and white women, although limited data suggest the former may exhibit different p53 mutation spectra. One study found high risk associated with a specific CYP1A1 polymorphism in African American but not white women. Additional studies of molecular differences in African American and white women are needed, with multifactorial assessment of the independent effects of molecular and conventional risk attributes.
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PMID:Breast cancer in African American women: epidemiology and tumor biology. 888 49

The objective of this study was to evaluate molecular markers involved in mammary tumorigenesis in a canine model that mimics many essential elements of human breast cancer. Thirty mammary gland tumors and control tissues obtained from female dogs were included in the study. We analyzed changes in the expression of markers of hormone and receptor status (estradiol, estrogen receptor; ER and HER-2/neu), hormone metabolism (CYP1A1 and CYP1B1), cell proliferation and survival [proliferating cell nuclear antigen (PCNA), glutathione S-transferase-P (GST-P), nuclear factor-kappaB (NF-kappaB-p50, NF-kappaB-p65), phosphorylated-inhibitor of kappaB-alpha (p-IkappaB-alpha) and IkappaB], apoptosis (Bcl-2, Bax, caspases, Apaf-1, cytochrome-C, and PARP), invasion [matrix metalloproteinases-2 and -9 (MMP-2, MMP-9), tissue inhibitor of matrix metalloproteinase-2 (TIMP-2), and reversion-inducing cysteine-rich protein with Kazal motifs (RECK)], angiogenesis [vascular endothelial growth factor (VEGF)], and epigenetics [DNA methyltransferase (Dnmt-1), histone deacetylase (HDAC-1)] by immunohistochemical localization and Western blot analysis and correlated these with histological grade. The present study provides evidence that increased expression of ER, HER-2/neu, estradiol, and its metabolizing enzymes, as well as proteins involved in cell proliferation, apoptosis evasion, invasion, and angiogenesis may confer a selective growth advantage to canine mammary tumors. To our knowledge this is the first report on the hallmark capabilities of canine mammary tumors, which lends credence to the view that the dog is a valuable model for human breast cancer studies.
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PMID:Evaluation of molecular markers in canine mammary tumors: correlation with histological grading. 2022 57