Disease relevance of TSPAN31

• SAS, a gene amplified in human sarcomas, encodes a new member of the transmembrane 4 superfamily of proteins [1].
• Refined mapping of 12q13-q15 amplicons in human malignant gliomas suggests CDK4/SAS and MDM2 as independent amplification targets [2].
• In comparison, amplification occurred in only 2/16 classical intramedullary osteosarcomas and involved the SAS gene [3].
• The most commonly amplified genes in glioblastomas are EGFR (in approximately 40%), CDK4, and SAS (in approximately 15%) [4].
• In addition, we used a yeast artificial chromosome (YAC) contig of several megabases covering the entire region from SAS to D12S8 for FISH to determine the pattern of amplification in the neuroblastoma cell line NGP-127 [5].

Psychiatry related information on TSPAN31

• The Brief Psychiatric Rating Scale (BPRS; Total, Positive, and Negative subscale scores) and the Simpson-Angus Scale for Extrapyramidal Symptoms (SAS) were also completed on the two occasions [6].
• Correlations between comparable ratings on the Social Adjustment Scale II (SAS II) ranged from 0.78 to 0.86 [7].
• To describe all sleep episodes and the recovery process across 4 days, and to relate adjustment to individual differences, 49 Scandinavian Airlines System (SAS) air crew were monitored for 9 days with activity monitors and sleep/wake diary before-during-after flight [8].
• Associations between the physical activity phenotypes and the polymorphisms were analyzed using the MIXED model (SAS) [9].
• The methods are illustrated on an example in Alzheimer's disease in a classical framework using SAS PROC MIXED and MLwiN, and in a Bayesian framework using BUGS [10].

High impact information on TSPAN31

• All amplicons were discontinuous between CDK4/SAS and MDM2 [2].
• These studies revealed two centers of amplification, one at CDK4/SAS and the other at MDM2 [2].
• Superoxide dismutase in SAS human tongue carcinoma cell line is a factor defining invasiveness and cell motility [11].
• This article describes an apparent inverse relationship between cell motility and intracellular Cu-Zn superoxide dismutase (SOD) activity of two human squamous carcinoma-derived clones, SAS-H1 with high invasiveness and SAS-L1 with low invasiveness [11].
• The amplified sequences are derived from chromosome 12q13-14 and encode a gene designated SAS (sarcoma amplified sequence) [12].

Chemical compound and disease context of TSPAN31

• CONCLUSIONS: Oxybuprocaine may induce a false-positive reaction in an immunochromatographic SAS Adeno Test. We recommend the use of lidocaine, instead of oxybuprocaine, for local anesthesia in taking eye swabs from patients with suspected adenovirus infection [13].
• We examined the restoration of radiation-induced p53-dependent apoptosis by a chemical chaperone (glycerol) in human head and neck cancer cells (SAS cells, showing wild-type p53 phenotype) [14].
• Analyses were performed on normalized crude ABI and on normalized residuals from multiple linear regression analyses in SAS (SAS Institute, Inc., Cary, North Carolina) that adjusted for age, sex, smoking, diabetes, hypertension, ratio of total cholesterol to high density lipoprotein cholesterol, log triglyceride level, and body mass index [15].
• MATERIALS AND METHODS: Human squamous cell carcinoma (SAS) and glioblastoma cell lines (A-172) transfected with mutant p53 (mp53) or control neo genes were used [16].
• To determine the role of the sympatho-adrenal (SAS) and hypothalamo-pituitary-adrenocortical system (HPAS) after head injury, the relationship between venous blood epinephrine (E), norepinephrine (NE), adrenocorticotropic hormone (ACTH), cortisol levels, and clinical condition was examined in 55 patients [17].

Biological context of TSPAN31

• This cosmid, previously known to contain three genes (CDK4, SAS, and OS9), was sequenced, and that information was used for computer-assisted analysis [18].
• Notably, more than 40% of all amplicons in both soft tissue and bone tumors were mapped to chromosome 12, and at least one of the previously reported recurrent amplifications in 12q13.3-14.1 and 12q15.1, including SAS and CDK4, and MDM2, respectively, were present in 85% of the soft tissue tumors and in all of the bone tumors [19].
• Four high grade intramedullary tumors had elevated mRNA expression of SAS, but did not exhibit gene amplification [3].
• One of the amplified oncogenes (SAS/CDK4) was found in a chromosomal region that was undetected by CGH [20].
• We investigated 529 subjects from 175 sibships who were originally part of the Honolulu Heart Program. Analyses included nonparametric linkage and association using SAGE (Statistical Analysis for Genetic Epidemiology) and FBAT (family-based test of association) programs and Monte Carlo simulation of Fisher's exact test in SAS [21].

Anatomical context of TSPAN31

• The activation of proMMP-2 by co-culture was also observed in other carcinoma cell lines, HSC-4 and SAS, but not in normal human keratinocytes [22].
• MATERIALS AND METHODS: Using the departmental SAS data-base we identified all patients with cervix cancer treated between 1974 and 1988 and investigated the 647 patients who received 20 fractions of external beam radiotherapy plus intracavitary therapy with a total dose to point A of at least 60Gy [23].
• METHODS: The National Hospital Discharge database for 1998 to 2001 was acquired from the Centers for Disease Control. All gallbladder disease related admissions were extracted, and the cholecystectomies (ICD-9-CM codes 51.2X) were analyzed using the SAS package [24].
• RESULTS: A procedure based on generalized estimating equations (PROC GENMOD; SAS Institute; Cary, NC) was used to fit marginal models to determine risk factors influencing the prevalence of chronic respiratory symptoms (wheeze, dyspnea, sputum, and cough) [25].
• Based on PROC CORR analysis (SAS), this correlated negatively with blood neutrophil count (r=-0.634; P=0.0009) and serum cortisol concentration (r=-0.659; P<0.0001), but showed no relationship with serum progesterone or estradiol concentrations (P > or =0.09) [26].

Associations of TSPAN31 with chemical compounds

• Oxybuprocaine induces a false-positive response in immunochromatographic SAS Adeno Test [13].
• Apoptosis in the SAS/m p53 cells was induced by X-rays with glycerol pre-treatment, but not without glycerol pre-treatment, whereas apoptosis in the SAS/ neo cells was induced in both cases [14].
• Unique pairs of dyads were used to create networks using SAS Interactive Matrix Language. PAJEK and UCINET were used to analyze the largest component from all years (1996-2000), during the epidemic (1997-1998), and after the epidemic (1999-2000) [27].
• Both the carcinogenicity and the mutagenicity of quinolone and quinoline derivatives, as determined by SAS, can be attributed to their genotoxicity potential [28].
• OBJECTIVE: To investigate whether a solution of oxybuprocaine hydrochloride, 0.4%, results in a false-positive response in an immunochromatographic SAS Adeno Test. DESIGN: Experimental study [13].

Analytical, diagnostic and therapeutic context of TSPAN31

• Sequence analysis demonstrates that SAS is a novel member of a transmembrane protein family (transmembrane 4 superfamily or TM4SF) thought to be involved in growth-related cellular processes [1].
• Southern and Northern blot analysis confirmed the coamplification of MDM2, CDK4, SAS, and CHOP [29].
• Outcome measures included the GAS, PSE, SAS, patient and relatives' satisfaction, number of admissions, and length of stay [30].
• Differential gene expression between PA and AD was analyzed in 6 female patients using human cDNA microarray slides and data analyzed using the Stanford Microarray Database. Statistical analysis for the gene expression was performed using the SAS mixed models [31].
• Beta-endorphin-like activity, measured by radioimmunoassay, was somewhat lower in patients with SAS (14.0 +/- 2.8 pmol/ml) than in control subjects (21.8 +/- 7.6 pmol/ml) (p less than 0.05) [32].

References