Outcomes from elective colorectal cancer surgery during the SARS-CoV-2 pandemic

This study aimed to describe the change in surgical practice and the impact of SARS-CoV-2 on mortality after surgical resection of colorectal cancer during the initial phases of the SARS-CoV-2 pandemic

Histotype-specific copy-number alterations in ovarian cancer.

10.1186/1755-8794-5-47BMC medical genomics

White matter network damage mediates association between cerebrovascular disease and cognition

To determine whether white matter network disruption mediates the association between MRI markers of cerebrovascular disease (CeVD) and cognitive impairment. Participants (n = 253, aged ≥60 years) from the Epidemiology of Dementia in Singapore study underwent neuropsychological assessments and MRI. CeVD markers were defined as lacunes, white matter hyperintensities (WMH), microbleeds, cortical microinfarcts, cortical infarcts and intracranial stenosis (ICS). White matter microstructure damage was measured as fractional anisotropy and mean diffusivity by tract based spatial statistics from diffusion tensor imaging. Cognitive function was summarized as domain-specific Z-scores.Lacunar counts, WMH volume and ICS were associated with worse performance in executive function, attention, language, verbal and visual memory. These three CeVD markers were also associated with white matter microstructural damage in the projection, commissural, association, and limbic fibers. Path analyses showed that lacunar counts, higher WMH volume and ICS were associated with executive and verbal memory impairment via white matter disruption in commissural fibers whereas impairment in the attention, visual memory and language were mediated through projection fibers.Our study shows that the abnormalities in white matter connectivity may underlie the relationship between CeVD and cognition. Further longitudinal studies are needed to understand the cause-effect relationship between CeVD, white matter damage and cognition

Sox4 is a key oncogenic target in C/EBPa mutant Acute Myeloid Leukemia

Accession Number: GSE50565 Platform: GPL9185: Illumina Genome Analyzer (Mus musculus) Organism: Mus musculus Published on 2014-01-08 Summary: Mutation or epigenetic silencing of the transcription factor C/EBPa is observed in ~10% of patients with acute myeloid leukemia (AML). In both cases, a common global gene expression profile is observed, but down-stream targets relevant for leukemogenesis are not known. Here we identify Sox4 as a direct target of C/EBPa whereby its expression is inversely correlated with C/EBPa activity. Downregulation of Sox4 abrogated increased self-renewal of leukemic cells and restored their differentiation. Gene expression profiles of leukemia initiating cells (LICs) from both Sox4 overexpression and murine mutant C/EBPa AML models clustered together, but differed from other types of AML. Our data demonstrate that Sox4 overexpression resulting from C/EBPa inactivation contributes to the development of leukemias with a distinct LIC phenotype. Overall Design: A ChIP-seq sample of C/EBPa in Macrophages is used in this study Contact: Name: Salam Adli Assi Organization: University of Birmingham Deparment: Institute for Cancer and Genomic Sciences Address: IBR Birmingham United Kingdom Email: [email protected] Organization: GEO Address: US

Sox4 is a key oncogenic target in C/EBPa mutant Acute Myeloid Leukemia

Accession Number: GSE50565 Platform: GPL9185: Illumina Genome Analyzer (Mus musculus) Organism: Mus musculus Published on 2014-01-08 Summary: Mutation or epigenetic silencing of the transcription factor C/EBPa is observed in ~10% of patients with acute myeloid leukemia (AML). In both cases, a common global gene expression profile is observed, but down-stream targets relevant for leukemogenesis are not known. Here we identify Sox4 as a direct target of C/EBPa whereby its expression is inversely correlated with C/EBPa activity. Downregulation of Sox4 abrogated increased self-renewal of leukemic cells and restored their differentiation. Gene expression profiles of leukemia initiating cells (LICs) from both Sox4 overexpression and murine mutant C/EBPa AML models clustered together, but differed from other types of AML. Our data demonstrate that Sox4 overexpression resulting from C/EBPa inactivation contributes to the development of leukemias with a distinct LIC phenotype. Overall Design: A ChIP-seq sample of C/EBPa in Macrophages is used in this study Contact: Name: Salam Adli Assi Organization: University of Birmingham Deparment: Institute for Cancer and Genomic Sciences Address: IBR Birmingham United Kingdom Email: [email protected] Organization: GEO Address: US

Sox4 is a key oncogenic target in C/EBPα mutant Acute Myeloid Leukemia

Accession Number: GSE45430 Platform: GPL1261: [Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array Organism: Mus musculus Published on 2013-03-23 Summary: Mutation or epigenetic silencing of the transcription factor C/EBPα is observed in ~10% of patients with acute myeloid leukemia (AML). In both cases, a common global gene expression profile is observed, but down-stream targets relevant for leukemogenesis are not known. Here we identify Sox4 as a direct target of C/EBPα whereby its expression is inversely correlated with C/EBPα activity. Downregulation of Sox4 abrogated increased self-renewal of leukemic cells and restored their differentiation. Gene expression profiles of leukemia initiating cells (LICs) from both Sox4 overexpression and murine mutant C/EBPα AML models clustered together, but differed from other types of AML. Our data demonstrate that Sox4 overexpression resulting from C/EBPα inactivation contributes to the development of leukemias with a distinct LIC phenotype. Overall Design: K/L (bi-allelic Cebpa mutations) leukemic mice and Sox4 overexprssing leukemic mice were used for RNA extraction and hybridization on Affymetrix microarrays. We compared these microarray samples with the C57/BL6 wild type mice. Contact: Name: Henry Yang Organization: Cancer Science Institute of Singapore Address: 28 Medical Drive Singapore Singapore Email: [email protected] Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: [email protected], [email protected] Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.aff

Sox4 is a key oncogenic target in C/EBPα mutant Acute Myeloid Leukemia

Accession Number: GSE45430 Platform: GPL1261: [Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array Organism: Mus musculus Published on 2013-03-23 Summary: Mutation or epigenetic silencing of the transcription factor C/EBPα is observed in ~10% of patients with acute myeloid leukemia (AML). In both cases, a common global gene expression profile is observed, but down-stream targets relevant for leukemogenesis are not known. Here we identify Sox4 as a direct target of C/EBPα whereby its expression is inversely correlated with C/EBPα activity. Downregulation of Sox4 abrogated increased self-renewal of leukemic cells and restored their differentiation. Gene expression profiles of leukemia initiating cells (LICs) from both Sox4 overexpression and murine mutant C/EBPα AML models clustered together, but differed from other types of AML. Our data demonstrate that Sox4 overexpression resulting from C/EBPα inactivation contributes to the development of leukemias with a distinct LIC phenotype. Overall Design: K/L (bi-allelic Cebpa mutations) leukemic mice and Sox4 overexprssing leukemic mice were used for RNA extraction and hybridization on Affymetrix microarrays. We compared these microarray samples with the C57/BL6 wild type mice. Contact: Name: Henry Yang Organization: Cancer Science Institute of Singapore Address: 28 Medical Drive Singapore Singapore Email: [email protected] Organization: Affymetrix, Inc. Address: Santa Clara CA 95051 USA Email: [email protected], [email protected] Phone: 888-362-2447 Web-Link: http://www.affymetrix.com/index.aff

Additional file 2 of Breast cancer risks associated with missense variants in breast cancer susceptibility genes

Additional file 2