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)

The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local mammary production of prolactin (PRL), we have generated mice that overexpress prolactin within mammary epithelial cells under the control of a hormonally nonresponsive promoter, neu-related lipocalin (NRL). In each of the two examined NRL-PRL transgenic mouse lineages, female virgin mice display mammary developmental abnormalities, mammary intraepithelial neoplasias, and invasive neoplasms. Prolactin increases proliferation in morphologically normal alveoli and ducts, as well as in lesions. The tumors are of varied histotype, but papillary adenocarcinomas and adenosquamous neoplasms predominate. Neoplasms can be separated into two populations: one is estrogen receptor alpha (ERalpha) positive (greater than 15% of the cells stain for ERalpha), and the other is ERalpha- (<3%). ERalpha expression does not correlate with tumor histotype, or proliferative or apoptotic indices. These studies provide a mouse model of hormonally dependent breast cancer, and, perhaps most strikingly, a model in which some neoplasms retain ERalpha, as occurs in the human disease.
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PMID:Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice. 1287 11

The study of proto-oncogene Her-2/neu using the fluorescence in situ hybridization (FISH) technique in routinely paraffin-embedded formalin-fixed tissue has become commonplace over the past decade and mandatory among invasive breast cancer expressing a score 2+ by immunohistochemical analysis of c-erbB2 protein. The patient's eligibility for treatment with the biological drug trastuzumab/herceptin is based on the evidence of a Her-2/neu proto-oncogene amplification (ratio Her-2/neu/CEP-17>2.2). However, although the exclusion is declared in the absence of Her-2/neu gene amplification (ratio Her-2/neu/CEP-17 <1.8) according to the American Society of Clinical Oncology/College of American Pathologists recommendations, there are borderline cases (1.8<ratio Her-2/neu/CEP-17>2.2) that need to be investigated (eg, ductal carcinoma in situ with microinvasion, metastatic breast cancer). In such cases with Her-2/neu genetic heterogeneity it is difficult to count the nuclear signals in the areas of invasive tumor using fluorescence. The availability of a Fluorescence Immunophenotyping and Interphase Cytogenetics as a Tool for Investigation of Neoplasms technique, based on the simultaneous evaluation of immunostaining with anticytokeratins (CKAE1/AE3 and CK19), together with FISH for Her-2/neu gene status [it is therefore useful and of current applicability in breast cancer blocks (formalin-fixed and paraffin-embedded)], permits a more easy identification of even single neoplastic cells by immunofluorescence and then a better evaluation of Her-2/neu status gene by the FISH technique, as shown in our study.
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PMID:Simultaneous fluorescence immunophenotyping and Her-2/neu genotyping (FICTION) in breast carcinoma candidates to target therapy. 2241 57

Neoplasms arising in accessory lacrimal glands are rare. We describe a 33-year-old man with adenocarcinoma arising in the left lower eyelid accessory lacrimal gland. Microscopic evaluation demonstrated an infiltrative neoplasm composed of mildly to moderately pleomorphic cells with abundant eosinophilic cytoplasm and focal intracytoplasmic vacuoles, arranged predominantly in ductules. Foci of luminal and intracytoplasmic eosinophilic secretory material and occasional mucin were noted. An in situ component was identified in the gland of Wolfring. Though perineural invasion was present, high-grade nuclear features, brisk mitotic activity, and comedonecrosis were not identified. Immunohistochemical studies were notable for immunoreactivity of the tumor cells for CK7, carcinoembryonic antigen, BRST-2, androgen receptors, and HER2/neu (2+). The neoplastic cells were negative for CK20, estrogen and progesterone receptors, S-100, p63, calponin, thyroid transcription factor-1, and prostate-specific antigen. Fluorescence in situ hybridization studies for ETV6 and MAML2 rearrangements and for HER2/neu amplification were negative. Because of the absence of unifying morphologic, immunophenotypic, and molecular genetic findings, the diagnosis of adenocarcinoma, not otherwise specified, was rendered. The patient underwent comprehensive oncologic workup, which was negative for another primary tumor and metastases. He remains disease free with a follow-up of 4 years. This case illustrates the challenges encountered in applying salivary gland tumor classification to the accessory lacrimal gland neoplasm.
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PMID:Adenocarcinoma, Not Otherwise Specified, Arising in Accessory Lacrimal Gland: A Diagnostic Challenge. 3032 83