The Association of Compact Groups of Galaxies with Large-scale Structures

We use various samples of compact groups (CGs) to examine the types of association CGs have with rich and poor clusters of galaxies at low (z~0.04) and intermediate (z~0.1) redshifts. We find that ~10-20 % of CGs are associated with rich clusters and a much larger fraction with poorer clusters or loose groups. Considering the incompleteness of catalogs of poorer systems at intermediate redshift, our result is consistent with all CGs at intermediate redshift being associated with larger-scale systems. The richness of the clusters associated with CGs significantly increases from z~0.04 to z~0.1, while their Bautz-Morgan type changes from early to late type for the same range in z. Neither trend is compatible with a selection effect in the cluster catalogs used. We find earlier morphological types of galaxies to be more frequent in CGs associated with larger-scale structures, compared to those in CGs not associated to such structures. We consider this as new evidence that CGs are part of the large-scale structure formation process and that they may play an important role in the evolution of galaxies in these structures.Comment: 5 pages, no figures, Proc. ESO Workshop "Groups of galaxies in the nearby Universe", Santiago, Chile, 5-9 Dec. 2005, ESO Astrophysics Symposia, eds. I. Saviane, V. Ivanov & J. Borissova, Springer-Verlag; very minor revision of text on 15 Mar 2006, added one referenc

Mapping the evolution of pure CO2 ices irradiated by ions, UV, and electrons using the upgraded PROCODA code (employing an effective rate constant ordering by thermochemistry data)

Laboratory astrophysics and astrochemistr

NMD inhibition fails to identify tumour suppressor genes in microsatellite stable gastric cancer cell lines

BACKGROUND: Gastric cancers frequently show chromosomal alterations which can cause activation of oncogenes, and/or inactivation of tumour suppressor genes. In gastric cancer several chromosomal regions are described to be frequently lost, but for most of the regions, no tumour suppressor genes have been identified yet. The present study aimed to identify tumour suppressor genes inactivated by nonsense mutation and deletion in gastric cancer by means of GINI (gene identification by nonsense mediated decay inhibition) and whole genome copy number analysis. METHODS: Two non-commercial gastric cancer cell lines, GP202 and IPA220, were transfected with siRNA directed against UPF1, to specifically inhibit the nonsense mediated decay (NMD) pathway, and with siRNA directed against non-specific siRNA duplexes (CVII) as a control. Microarray expression experiments were performed in triplicate on 4 × 44 K Agilent arrays by hybridizing RNA from UPF1-transfected cells against non-specific CVII-transfected cells. In addition, array CGH of the two cell lines was performed on 4 × 44K agilent arrays to obtain the DNA copy number profiles. Mutation analysis of GINI candidates was performed by sequencing. RESULTS: UPF1 expression was reduced for >70% and >80% in the GP202 and IPA220 gastric cancer cell lines, respectively. Integration of array CGH and microarray expression data provided a list of 134 and 50 candidate genes inactivated by nonsense mutation and deletion for GP202 and IPA220, respectively. We selected 12 candidate genes for mutation analysis. Of these, sequence analysis was performed on 11 genes. One gene, PLA2G4A, showed a silent mutation, and in two genes, CTSA and PTPRJ, missense mutations were detected. No nonsense mutations were detected in any of the 11 genes tested. CONCLUSION: Although UPF1 was substantially repressed, thus resulting in the inhibition of the NMD system, we did not find genes inactivated by nonsense mutations. Our results show that the GINI strategy leads to a high number of false positives

Overexpression of the miR-17-92 cluster in colorectal adenoma organoids causes a carcinoma-like gene expression signature

Gain of chromosome arm 13q is one of the most prevalent DNA copy number alterations associated with colorectal adenoma-tocarcinoma progression. The oncogenic miR-17-92 cluster, located at 13q, was found to be overexpressed in colorectal cancer and in adenomas harboring 13q gain. However, to what extent overexpression of this group of microRNAs actually drives progression to cancer remains to be resolved. Therefore, we aimed to clarify the role of miR-17-92 cluster in the progression from colorectal adenoma to carcinoma.The miR-17-92 cluster was overexpressed in human colorectal adenoma organoids without 13q gain and downstream effects on mRNA expression were investigated, along with functional consequences in vitro and in vivo.Comparison of mRNA sequencing results of organoids overexpressing miR-17-92 and cultures transduced with control vector revealed a miR-17-92 expression signature. This signature appeared to be enriched in an independent series of colorectal cancers and adenomas with 13q gain, confirming that miR-17-92 expression is associated with malignant progression. However, tumor-associated characteristics, such as increased proliferation rate, were not observed in miR-17-92 overexpressing adenoma organoids in vitro. In addition, subcutaneous injection of these organoids in immunodeficient mice was insufficient to cause tumor outgrowth.In conclusion, this study showed that miR-17-92 expression contributes to 13q gain-associated adenoma-to-carcinoma progression, however, this is insufficient to cause malignancy.Cellular mechanisms in basic and clinical gastroenterology and hepatolog

IBD-associated dysplastic lesions show more chromosomal instability than sporadic adenomas

Inflammatory bowel disease (IBD) patients are at increased risk of developing colorectal cancer. However, histologically, it is challenging to distinguish between IBD-associated dysplasia from sporadic adenomas. We have molecularly characterized these precursor lesions and show that IBD-associated dysplasia lesions are genomically much more unstable