Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04155 (pS2)
 1,234 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esophageal adenocarcinoma (EA) is increasing faster than any other cancer in the U.S. In this report, we first show that EA can be distinguished from normal esophagus (NE) and esophageal squamous cell carcinoma by plotting expression values for EpCam, TFF1, and SBEM in three-dimensional Euclidean space. For monitoring progression of Barrett's esophagus (BE) to EA, we developed a highly sensitive assay for limited quantities of tissue whereby 50 ng of RNA are first converted to cDNA using 16 gene-specific primers. Using a set of training tissues, we developed a novel quantitative three-tiered algorithm that allows for accurate (overall accuracy = 61/63, 97%) discrimination of BE versus EA tissues using only three genes. The gene used in the first tier of the algorithm is TSPAN: samples not diagnosed as BE or EA by TSPAN in the first tier are then subjected to a second-tier analysis using ECGF1, followed by a third-tier analysis using SPARC. Addition of TFF1 and SBEM to the first tier (i.e., a five-gene marker panel) increases the overall accuracy of the assay to 98% (62/63) and results in mean molecular diagnostic scores (+/- SD) that are significantly different between EA and BE samples (3.19 +/- 1.07 versus -2.74 +/- 1.73, respectively). Our results suggest that relatively few genes can be used to monitor progression of BE to EA.
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PMID:Accurate discrimination of Barrett's esophagus and esophageal adenocarcinoma using a quantitative three-tiered algorithm and multimarker real-time reverse transcription-PCR. 1578 68

The aim of this study was to identify tumor suppressor genes (TSGs) in oral squamous cell carcinoma (OSCC) using whole-genome analysis of microarray technology and real-time quantitative polymerase chain reaction (QPCR). We applied whole-genome analysis of TSGs in the specimens from 3 patients of OSCC by microarray technology. A total of 11 genes, CRISP3, SCGB3A1, AGR2, PIP, C20orf114, TFF1, STATH, AZGP1, MUC7, DMBT1 and LOC389429, were found to be down-regulated, and 2, matrix metallopeptidase (MMP) 1 and MMP3, were found to be up-regulated in the 3 OSCC patients using microarray technology. In this study, we selected the CRISP3 gene. CRISP3 belongs to the cystein-rich secretary protein gene family in chromosome 6p12.3. CRISP3 has been found in the salivary gland, spleen and prostate gland and is a prominent biomarker in the gene expression of prostate cancer. Down-regulation of this gene was previously observed in OSCC. No studies examining the DNA copy number of CRISP3 in detail exist. We analyzed the DNA copy number of CRISP3 in 5 OSCC-derived cell lines (SAS, Ca9-22, KON, HSC2 and HSC4) and 60 OSCC tissues by real-time QPCR. The DNA copy number loss of CRISP3 was observed in 2 of the 5 OSCC-derived cell lines (SAS, HSC2) and in 24 of 60 patients (40.0%) using real-time QPCR. A significant statistical correlation between the copy number loss and gender and T classification was observed. These results indicate that the inactivation of CRISP3 is an early event in OSCC, since the T1/T2 classification is correlated with DNA copy number loss of CRISP3, whereas T3/T4 classification is not. We conclude that CRISP3 may be involved in the carcinogenesis of OSCC.
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PMID:Copy number changes of CRISP3 in oral squamous cell carcinoma. 2274 Aug 59