Rearrangement and expression of myeov and hst in NIH/3T3 transfectants: A caveat for the interpretation of DNA transfection analyses

Brecht, Marcus; Steenvoorden, Agatha C.M.; Luf, Susanne; Bartram, Claus R.; Janssen, Johannes W.G.

doi:10.3892/or.17.5.1127

Cited by 4 publications

(6 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The nearest gene, MYEOV , is 67 kb away but in different haplotype block with SNP rs7931342. MYEOV is a putative oncogene that is frequently amplified in breast tumors and esophageal carcinomas (28). It often coamplifies with the cell cycle control gene CCND1 (~360 kb away from MYEOV ).…”

Section: Discussionmentioning

confidence: 99%

Association Study of Prostate Cancer Susceptibility Variants with Risks of Invasive Ovarian, Breast, and Colorectal Cancer

Song

Koessler²,

Ahmed³

et al. 2008

Cancer Research

View full text Add to dashboard Cite

Several prostate cancer susceptibility loci have recently been identified by genome-wide association studies. These loci are candidates for susceptibility to other epithelial cancers. The aim of this study was to test these tag single nucleotide polymorphisms (SNP) for association with invasive ovarian, colorectal, and breast cancer. Twelve prostate cancer-associated tag SNPs were genotyped in ovarian (2,087 cases/3,491 controls), colorectal (2,148 cases/2,265 controls) and breast (first set, 4,339 cases/4,552controls; second set, 3,800 cases/3,995 controls) case-control studies. The primary test of association was a comparison of genotype frequencies between cases and controls, and a test for trend stratified by study where appropriate. Genotype-specific odds ratios (OR) were estimated by logistic regression. SNP rs2660753 (chromosome 3p12) showed evidence of association with ovarian cancer [per minor allele OR, 1.19; 95% confidence interval (95% CI), 1.04-1.37; Ptrend = 0.012]. This association was stronger for the serous histologic subtype (OR, 1.29; 95% CI, 1.09-1.53; P = 0.003). SNP rs7931342 (chromosome 11q13) showed some evidence of association with breast cancer (per minor allele OR, 0.95; 95% CI, 0.91-0.99; Ptrend = 0.028). This association was somewhat stronger for estrogen receptor-positive tumors (OR, 0.92; 95% CI, 0.87-0.98; P = 0.011). None of these tag SNPs were associated with risk of colorectal cancer. In conclusion, loci associated with risk of prostate cancer may also be associated with ovarian and breast cancer susceptibility. However, the effects are modest and warrant replication in larger studies.

show abstract

Section: Discussionmentioning

confidence: 99%

Association Study of Prostate Cancer Susceptibility Variants with Risks of Invasive Ovarian, Breast, and Colorectal Cancer

Song

Koessler²,

Ahmed³

et al. 2008

Cancer Research

View full text Add to dashboard Cite

show abstract

“…The SNP rs1799977 present in the gene MLH1, plays a major role in mismatch repair 124 . The SNP rs10896469 present near MYEOV, a putative oncogene, as previously mentioned to be frequently amplified in a number of tumours 71,73,125 .…”

Section: Genotype and The Outcome Of Aggressive Prostate Cancer (Vs Hmentioning

confidence: 77%

“…This region houses a number of candidate oncogenes, and the amplification of this region is highly heterogeneous leading to breakpoints in and/or near the location 71,72 . MYEOV has been shown to be frequently amplified in tumours not only of the breast but also of the oesophagus 73 and head and neck squamous cell carcinoma 71 .…”

Section: Snp Genotype Analysis Of Aggressive Prostate Cancer Vs Healtmentioning

confidence: 99%

Environmental factors and risk of aggressive prostate cancer among a population of New Zealand men – a genotypic approach

et al. 2017

View full text Add to dashboard Cite

Prostate cancer is one of the most significant health concerns for men worldwide. Numerous researchers carrying out molecular diagnostics have indicated that genetic interactions with biological and behavioral factors play an important role in the overall risk and prognosis of this disease. Single nucleotide polymorphisms (SNPs) are increasingly becoming strong biomarker candidates to identify susceptibility to prostate cancer. We carried out a gene × environment interaction analysis linked to aggressive and non-aggressive prostate cancer (PCa) with a number of SNPs. By using this method, we identified the susceptible alleles in a New Zealand population, and examined the interaction with environmental factors. We have identified a number of SNPs that have risk associations both with and without environmental interaction. The results indicate that certain SNPs are associated with disease vulnerability based on behavioral factors. The list of genes with SNPs identified as being associated with the risk of PCa in a New Zealand population is provided in the graphical abstract.

show abstract

“…In fact, several candidate target genes of these common deletions and amplifications have been identified, including MYEOV as the target of gains/amplifications in 11q13 ( 7 ) and NEGR1 as a candidate tumor suppressor in 1p31 deletions. ( 8 ) Previously, MYEOV was reported as a putative transforming gene within the 11q13 amplicons in multiple myeloma, ( 9 ) whereas NEGR1 was described as a member of the IgLON (limbic system‐associated membrane protein [LAMP]/opioid‐binding cell adhesion molecule [OBCAM]/neurotrimin subgroup of the immunoglobulin superfamily) family of cell adhesion molecules. ( 8 ) However, the involvement of these genes aberrations in the pathogenesis of neuroblastoma remains unknown.…”

mentioning

confidence: 99%

“…1a). Previously, MYEOV had been identified as a putative transforming gene based on the NIH/3T3 tumorigenicity assay ( 9 ) and was shown to be highly expressed in a subset of multiple myelomas harboring t(11;14)(q13;q32). ( 7 ) We further examined the expression patterns of MYEOV in a total of 45 neuroblastoma samples using semi‐quantitative RT‐PCR analysis, in which 11 of 25 cell lines (44%) and seven of 20 fresh tumors (35%) showed higher expression levels of MYEOV compared with the median expression level ( MYEOV / β ‐ actin signal intensity = 1.4; Fig.…”

mentioning

confidence: 99%

Aberrations of NEGR1 on 1p31 and MYEOV on 11q13 in neuroblastoma

et al. 2011

View full text Add to dashboard Cite

MYEOV and NEGR1 are novel candidate gene targets in neuroblastoma that were identified by chromosomal gain in 11q13 and loss in 1p31, respectively, through single nucleotide polymorphism array analysis. In the present study, to assess the involvement of MYEOV and NEGR1 in the pathogenesis of neuroblastoma, we analyzed their mutation status and ⁄ or expression profiles in a panel of 55 neuroblastoma samples, including 25 cell lines, followed by additional functional studies. No tumor-specific mutations of MYEOV or NEGR1 were identified in our case series. Expression of MYEOV was upregulated in 11 of 25 cell lines (44%) and in seven of 20 fresh tumors (35%). The siRNA-mediated knockdown of MYEOV in NB-19 cells, which exhibit high expression of MYEOV, resulted in a significant decrease in cell proliferation (P = 0.0027). Conversely, expression studies of NEGR1 revealed significantly lower expression of this gene in neuroblastomas at an advanced stage of the disease. Exogenous NEGR1 expression in neuroblastoma cells induced significant inhibition of cell growth (P = 0.019). The results of these studies provide supporting evidence for MYEOV and NEGR1 as gene targets of 11q13 gains and 1p31 deletions in a neuroblastoma subset. In addition, the findings suggest a possible prognostic value for NEGR1 in neuroblastoma. (Cancer Sci 2011; 102: 1645-1650 N euroblastoma is one of the most common forms of solid tumors in childhood and accounts for approximately 15% of all pediatric cancer deaths.(1) Despite recent advances in chemoradiotherapy, the prognosis for advanced neuroblastoma remains poor, with an approximate 40% 5-year survival, underscoring the importance of developing novel therapeutic modalities on the basis of an understanding of the pathogenesis of neuroblastoma.(1) Conversely, knowledge of the molecular pathogenesis of neuroblastoma is largely limited in terms of targets, except for the role of MYCN amplifications in advanced neuroblastoma.(2) Thus, the recent discovery of ALK mutations ⁄ amplifications in 6-8% of neuroblastomas (3-6) represents a major development in neuroblastoma research because it not only unravels a novel molecular mechanism involved in neuroblastoma development, but could also a basis for the development of molecular-targeted therapies using ALK inhibitors.

show abstract

Rearrangement and expression of myeov and hst in NIH/3T3 transfectants: A caveat for the interpretation of DNA transfection analyses

Cited by 4 publications

References 30 publications

Association Study of Prostate Cancer Susceptibility Variants with Risks of Invasive Ovarian, Breast, and Colorectal Cancer

Association Study of Prostate Cancer Susceptibility Variants with Risks of Invasive Ovarian, Breast, and Colorectal Cancer

Environmental factors and risk of aggressive prostate cancer among a population of New Zealand men – a genotypic approach

Aberrations of NEGR1 on 1p31 and MYEOV on 11q13 in neuroblastoma

Contact Info

Product

Resources

About