Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:O76050 (neu)
 3,969 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, there has been an increased interest in saliva as a diagnostic tool. Diagnosis of many diseases, including gastric cancer and immunodeficiency, has been made using saliva. The purpose of this study was to determine whether Her2/neu antibody, made in response to certain carcinomas of the breast, could be detected in saliva when experimentally placed at a remote site. This study was conducted using two male SD rats, each weighing between 300 g and 500 g. One experimental animal received 200 microliters, and the other, 500 microliters, of encapsulated c-erbB-2 monoclonal antibody (Signet, Dedham, MA) intraperitoneally. Prior to capsule placement, baseline serum and saliva samples were taken. Samples were also taken twenty, sixty-eight, 140, 188, 308 and 356 hours post-placement. Saliva flow was induced by administration of ophthalmic pilocarpine prior to sampling. All samples were kept at -20 degrees C. Antibody detection was performed using a modified double capture ELISA system. Tissue samples from various organs were evaluated using standard laboratory staining and immunostaining techniques. The animal receiving the higher antibody concentration showed a markedly greater salivary level of the antibody than the other (peak 24.158 hnu/ml vs. 18.313 hnu/ml at 308 and 188 hours post-implantation, respectively). These results seem to indicate that Her2/neu antibody saliva levels may serve as a useful, non-invasive method in the early detection of some breast cancers.
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PMID:Sustained delivery of Her-2/neu antibody by TCPL delivery device using adult male rats as a model. 1272 14

Proteins can be efficiently introduced into cells when fused to a protein transduction domain, such as Tat from the human immunodeficiency virus. We recently reported that dendritic cells transduced with a Tat fusion protein containing the extracellular domain of Her2/neu (Tat-Her2/neu) induced CD8 cytotoxic T lymphocytes (CTL) that specifically lysed Her2/neu-expressing breast and ovarian cancer cells. In the current study we further investigated the mechanism of protein transduction, utilizing the breast cancer-associated protein, mammaglobin-A, which is expressed in about 80% of breast cancers. Using a Tat-mammaglobin fusion protein, we tested the ability of Tat-mammaglobin transduced dendritic cells to stimulate antigen-specific CD4 and CD8 T cells. Low levels of serum considerably improved protein transduction as determined by Western blot, and also improved presentation of antigenic peptide as evidenced by functional studies using antigen-specific T cells. Confocal microscope analyses of antigen-presenting cells (APC) incubated with Tat-mammaglobin showed localized distribution in addition to diffuse distribution in the cytosol. In contrast, mammaglobin lacking Tat showed only a localized distribution. Simultaneous incubation with both proteins resulted in overlapping localized distributions, suggesting Tat fusion proteins are processed through both the MHC class I and class II pathways. Indeed, stimulation of T cells with Tat-mammaglobin transduced dendritic cells led to an expansion of mammaglobin-specific CD4 T helper-1 lymphocytes along with CD8 CTL. We conclude that Tat-mammaglobin transduced dendritic cells can induce both CD4 and CD8 mammaglobin-specific T cells. These findings could be further exploited for the development of a mammaglobin-based vaccine for breast cancer.
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PMID:Tat mammaglobin fusion protein transduced dendritic cells stimulate mammaglobin-specific CD4 and CD8 T cells. 1595 60

High prevalence of squamous anal lesions is linked to oncogenic human papillomavirus (HPV). Human immunodeficiency virus (HIV) promotes anal carcinogenesis. Epidermal growth factor receptor (EGFR), HER2/neu, c-Met, and vascular endothelial growth factor receptor-1 (VEGFR1) (tyrosine kinase growth factor receptors) are implicated in tumor progression, but little is known about their role in anal lesions. We investigated their expression and distribution in normal, dysplastic, and carcinomatous anal epithelium and then tried to analyze the effects on these variables of HPV and the HIV-positive status. Seventy-one HIV-positive and 47 HIV-negative patients were selected. We studied growth factor receptors, p16 and Ki67 expression, by in situ hybridization, fluorescent in situ hybridization (FISH) and chromogen in situ hybridization (CISH), immunocytochemistry, and morphological quantification in 226 lesions, either infected by HPV6 and 11 (31 condylomas acuminata) or infected with oncogenic HPVs (48 invasive cancers, 147 anal intraepithelial neoplasias). No HER2/neu was detected. Strong EGFR immunolabeling was not accompanied by gene amplification. The number and intensity of EGFR- and c-Met-immunoreactive cells increased significantly during lesion progression, highlighting the effects of oncogenic HPVs. EGFR, c-Met, VEGFR1, and p16 were coexpressed in 96% of invasive cancers. HIV-modified c-Met expression in condyloma acuminata (P < .008) and invasive cancers (P < .02). Strong HIV-related immunodeficiency and an absence of antiretroviral therapy increased c-Met and/or EGFR expression. HIV-positive anal cancers showed correlated c-Met and VEGFR1 (P < .003), strong p16 labeling, and an increased Ki67 proliferation. The finding that EGFR, c-Met, and VEGFR1 involved in carcinogenesis are well-represented and coexpressed in anal cancers, especially in HIV-positive population, suggests possible novel targeted treatments for anal diseases.
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PMID:Growth factor receptor expression in anal squamous lesions: modifications associated with oncogenic human papillomavirus and human immunodeficiency virus. 1971 55