Expression of p160erbB-3 and p185erbB-2 in Prostatic Intraepithelial Neoplasia and Prostatic Adenocarcinoma

Myers, Richard S.; Srivastava, Sudhir; Oelschlager, Denise K.; Grizzle, William E.

doi:10.1093/jnci/86.15.1140

Cited by 146 publications

(89 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…26,33 Moderate-tostrong immunoreactivity for HER-2/neu was detected in 27 of 29 localized adenocarcinomas (93%) and in 15 of 16 metastatic prostatic adenocarcinomas (94%). 12 Cohen et al noted expression of HER-2/neu in 7 of 23 patients with organ-confined prostate carcinoma and in 9 of 44 samples from metastatic deposits, resulting in an overall expression rate of 24%. 27 Sadasivan et al found that 9 of 25 prostate carcinoma samples (36%) showed HER-2/neu overexpression, and such overexpression was correlated with tumor grade, stage, and high S-phase and DNA aneuploidy.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of HER‐2/neu expression in prostatic adenocarcinoma

Sanchez

Sweeney

Mass³

et al. 2002

Cancer

View full text Add to dashboard Cite

BACKGROUNDSome evidence suggests a role for HER‐2/neu overexpression in prostate carcinoma progression. Reported rates of HER‐2/neu overexpression in patients with prostate carcinoma vary greatly.METHODSThe authors studied radical prostatectomy specimens from 38 patients who had biochemical failure after undergoing radical prostatectomy for prostate carcinoma. Immunohistochemistry for HER‐2/neu overexpression using the HercepTest kit (Dako Corporation, Carpenteria, CA) was employed. Two different antigen‐retrieval techniques were used: 1) the standard U.S. Food and Drug Administration (FDA)‐approved HercepTest assay and 2) a modified HercepTest, which employed an alkaline citrate buffer, pH 9.0, for antigen retrieval and a 1‐hour primary antibody incubation time. The level of HER‐2/neu expression was evaluated on a scale from 0 (no staining) to 3+ according to the published guidelines. Fluorescent in situ hybridization for gene amplification was performed on all specimens.RESULTSWith the standard technique, only one specimen had 2+ staining, and no specimens had 3+ staining. With the modified technique, 10 specimens (26%) had 2+ staining, and 9 specimens (24%) had 3+ staining. There was a significant association between the level of HER‐2/neu expression shown with the modified technique and tumor stage (P = 0.03) as well as Gleason grade (P = 0.01). None of the specimens had HER‐2/neu gene amplification.CONCLUSIONSThe authors report a simple modification of the HercepTest that resulted in an increased rate of HER‐2/neu expression, which was correlated with poor‐risk pathologic findings. The findings suggest that adenocarcinoma of the prostate should be evaluated for HER‐2/neu expression with a prostate specific immunohistochemical procedure that differs from the FDA‐approved standard procedure. Cancer 2002;95:1650–5. © 2002 American Cancer Society.DOI 10.1002/cncr.10839

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of HER‐2/neu expression in prostatic adenocarcinoma

Sanchez

Sweeney

Mass³

et al. 2002

Cancer

View full text Add to dashboard Cite

show abstract

“…[248][249][250] Furthermore, ERBB2/ERBB3 complexes caused AKT-independent phosphorylation of the androgen receptor that stabilized the protein and enhanced its transcriptional activity. 248 Increased expression of ERBB3 in prostate cancers, compared with normal prostate, has been demonstrated by immunohistochemistry in several studies 79,[251][252][253][254] and was associated with poor prognosis. 252 Microarray analyses have likewise shown an increase in ERBB3 mRNA in these cancers.…”

Section: Prostate Cancermentioning

confidence: 99%

The ERBB3 receptor in cancer and cancer gene therapy

2008

View full text Add to dashboard Cite

ERBB3, a member of the epidermal growth factor receptor (EGFR) family, is unique in that its tyrosine kinase domain is functionally defective. It is activated by neuregulins, by other ERBB and nonERBB receptors as well as by other kinases, and by novel mechanisms. Downstream it interacts prominently with the phosphoinositol 3-kinase/AKT survival/mitogenic pathway, but also with GRB, SHC, SRC, ABL, rasGAP, SYK and the transcription regulator EBP1. There are likely important but poorly understood roles for nuclear localization and for secreted isoforms. Studies of ERBB3 expression in primary cancers and of its mechanistic contributions in cultured cells have implicated it, with varying degrees of certainty, with causation or sustenance of cancers of the breast, ovary, prostate, certain brain cells, retina, melanocytes, colon, pancreas, stomach, oral cavity and lung. Recent results link high ERBB3 activity with escape from therapy targeting other ERBBs in lung and breast cancers. Thus a wide and centrally important role for ERBB3 in cancer is becoming increasingly apparent. Several approaches for targeting ERBB3 in cancers have been tested or proposed. Small inhibitory RNA (siRNA) to ERBB3 or AKT is showing promise as a therapeutic approach to treatment of lung adenocarcinoma.

show abstract

“…113 A member of the CIP/KIP family of cyclin-dependent kinase inhibitory proteins, p27KIP1, also showed significant reduction in expression in PIN, cancer, and metastatic cancer when compared with benign prostatic epithelium. 114 Other markers show progressive increase, including including human glandular kallikrein 2 (hK2), 115 c-erbB-2 (Her-2/neu) and c-erbB-3 oncoproteins, 108,116 c-met proto-oncogene, 41 bcl-2 oncoprotein, 117,118 mutator (RER( þ )) phenotype, 104 epidermal growth factor and epidermal growth factor receptor, 108,119 type IV Collagenase, Lewis Y antigen, TGF-alpha, apoptotic bodies, 71,73,104 mitotic figures, 71 PCNA expression, Ki-67 expression, MIB-1 expression, 111 tenascin-C, 120 aneuploidy and genetic abnormalities, 62,111,121-127 microvessel density, Ep-Cam transmembrane glycoprotein, 128 Insulin-like growth factor binding protein IGFBP-rP1, and p53 mutations, 129 although one group found no p53 expression immunohistochemically in PIN. 130 Prostate-specific membrane antigen, an abundant transmembrane glycoprotein, shows increased expression in PIN and cancer when compared with benign epithelium, 131,132 and this expression was unaffected by short-term androgen deprivation therapy.…”

Section: Genetic and Molecular Changesmentioning

confidence: 99%

High-grade prostatic intraepithelial neoplasia

2004

View full text Add to dashboard Cite

High-grade prostatic intraepithelial neoplasia (PIN) is now accepted as the most likely preinvasive stage of adenocarcinoma, almost two decades after its first formal description. PIN has a high predictive value as a marker for adenocarcinoma, and its identification warrants repeat biopsy for concurrent or subsequent invasive carcinoma. The only method of detection is biopsy; PIN does not significantly elevate serum prostate-specific antigen (PSA) concentration or its derivatives and cannot be detected by current imaging techniques, including ultrasound. Most patients with PIN will develop carcinoma within 10 years. PIN is associated with progressive abnormalities of phenotype and genotype, which are similar to cancer rather than normal prostatic epithelium, indicating impairment of cell differentiation with advancing stages of prostatic carcinogenesis. Androgen deprivation therapy decreases the prevalence and extent of PIN, suggesting that this form of treatment may play a role in chemoprevention.

show abstract

Expression of p160erbB-3 and p185erbB-2 in Prostatic Intraepithelial Neoplasia and Prostatic Adenocarcinoma

Cited by 146 publications

References 0 publications

Evaluation of HER‐2/neu expression in prostatic adenocarcinoma

Evaluation of HER‐2/neu expression in prostatic adenocarcinoma

The ERBB3 receptor in cancer and cancer gene therapy

High-grade prostatic intraepithelial neoplasia

Contact Info

Product

Resources

About