Effects of the prop-1 and Ghrhr mutations in gene expression during normal aging in mice.
Gene expression profile of long-lived Ames dwarf mice and Little mice.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesGender-specific alterations in gene expression and loss of liver sexual dimorphism in the long-lived Ames dwarf mice.
Gender-specific alterations in gene expression and loss of liver sexual dimorphism in the long-lived Ames dwarf mice.
Sex, Age, Specimen part
View SamplesNewcastle disease virus (NDV) is an avian virus that selectively replicates and kills many different types of cancer cells and is being developed for cancer treatment. Our aim was to establish persistent infection in EJ28 and TCCSUP bladder cancer cells and identify the dysregulated genes and disrupted molecular pathways associated with persistent infection.
No associated publication
Sex, Age, Specimen part, Disease, Cell line
View SamplesThe RNA-Seq experiment was performed to test whether loss of CHD7 does not affect the expression of DNA double-strand break repair proteins.
No associated publication
Sex, Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Integrated genomic analysis of recurrence-associated small non-coding RNAs in oesophageal cancer.
Specimen part, Cell line, Treatment, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Comprehensive genomic analysis identifies novel subtypes and targets of triple-negative breast cancer.
Sex, Age, Specimen part, Disease stage, Race
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic analysis of hepatoblastoma identifies distinct molecular and prognostic subgroups.
Sex, Age, Specimen part, Race
View SamplesRecent meta-analyses suggest triple-negative breast cancer (TNBC) is a heterogenous disease. In this study we sought to define these TNBC subtypes and identify subtype-specific markers and targets.
Comprehensive genomic analysis identifies novel subtypes and targets of triple-negative breast cancer.
Sex, Age, Specimen part, Disease stage, Race
View SamplesTargeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC.
Integrated genomic analysis of recurrence-associated small non-coding RNAs in oesophageal cancer.
Specimen part
View SamplesObesity is thought to contribute to worse disease outcome in breast cancer as a result of increased levels of adipocyte-secreted endocrine factors, insulin, and insulin-like growth factors (IGFs) that accelerate tumor cell proliferation and impair treatment response. We examined the effects of patient obesity on primary breast tumor gene expression, by profiling transcription of a set of tumors for which the patients body mass index (BMI) was ascertained. Sample profiles were stratified according to patients obesity phenotype defined as normal (BMI <25), overweight (BMI 25-29.9), or obese (BMI>30). Widespread alterations in gene expression were evident in breast tumors from obese patients as compared to tumors from other patients, allowing us to define an obesity-associated cancer transcriptional signature of 662 genes.
A gene transcription signature of obesity in breast cancer.
Age, Disease, Disease stage, Race
View Samples