Ontology highlight
ABSTRACT:
PROVIDER: PRJNA731355 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14605700.fastq.gz | Fastqsanger.gz | |||
| SRR14605701.fastq.gz | Fastqsanger.gz | |||
| SRR14605702.fastq.gz | Fastqsanger.gz | |||
| SRR14605703.fastq.gz | Fastqsanger.gz | |||
| SRR14605704.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 57 |
Similar Datasets
Project description:MicroRNA signatures associated with basal cell carcinoma subtypes
| PRJNA1029545 | ENA
Project description:Title: CAMK1D amplification implicated in epithelial-mesenchymal transition in basal-like breast cancer Summary: Breast cancer exhibits clinical and molecular heterogeneity, where expression-profiling studies have identified five major molecular subtypes. The basal-like subtype, expressing basal epithelial markers and negative for estrogen receptor (ER), progesterone receptor (PR) and HER2, is associated with higher overall levels of DNA copy number alteration (CNA), specific CNAs (like gain on chromosome 10p), and poor prognosis. Discovering the molecular genetic basis of tumor subtypes may provide new opportunities for therapy. To identify the driver oncogene on 10p associated with basal-like tumors, we analyzed genomic profiles of 172 breast carcinomas. The smallest shared region of gain spanned just seven genes at 10p13, including calcium/calmodulin-dependent protein kinase ID (CAMK1D), functioning in intracellular signaling but not previously linked to cancer. By microarray, CAMK1D was overexpressed when amplified, and by immunohistochemistry exhibited elevated expression in invasive carcinomas compared to carcinoma in situ. Engineered overexpression of CAMK1D in non-tumorigenic breast epithelial cells led to increased cell proliferation, and molecular and phenotypic alterations indicative of epithelial-mesenchymal transition (EMT), including loss of cell-cell adhesions and increased cell migration and invasion. Our findings identify CAMK1D as a novel amplified oncogene linked to EMT in breast cancer, and as a potential therapeutic target with particular relevance to clinically unfavorable basal-like tumors.
2009-09-08 | GSE12813 | GEO
Project description:A transcriptome-based molecular census of human basal cell carcinoma subtypes at single cell resolution
| PRJNA593814 | ENA
Project description:Title: CAMK1D amplification implicated in epithelial-mesenchymal transition in basal-like breast cancer Summary: Breast cancer exhibits clinical and molecular heterogeneity, where expression-profiling studies have identified five major molecular subtypes. The basal-like subtype, expressing basal epithelial markers and negative for estrogen receptor (ER), progesterone receptor (PR) and HER2, is associated with higher overall levels of DNA copy number alteration (CNA), specific CNAs (like gain on chromosome 10p), and poor prognosis. Discovering the molecular genetic basis of tumor subtypes may provide new opportunities for therapy. To identify the driver oncogene on 10p associated with basal-like tumors, we analyzed genomic profiles of 172 breast carcinomas. The smallest shared region of gain spanned just seven genes at 10p13, including calcium/calmodulin-dependent protein kinase ID (CAMK1D), functioning in intracellular signaling but not previously linked to cancer. By microarray, CAMK1D was overexpressed when amplified, and by immunohistochemistry exhibited elevated expression in invasive carcinomas compared to carcinoma in situ. Engineered overexpression of CAMK1D in non-tumorigenic breast epithelial cells led to increased cell proliferation, and molecular and phenotypic alterations indicative of epithelial-mesenchymal transition (EMT), including loss of cell-cell adhesions and increased cell migration and invasion. Our findings identify CAMK1D as a novel amplified oncogene linked to EMT in breast cancer, and as a potential therapeutic target with particular relevance to clinically unfavorable basal-like tumors. Overall design: HEEBO oligonucleotide microarrays from the Stanford Functional Genomics Facility were used to perform gene expression profiling of four CAMK1D or control-transfected MCF10A breast epithelial cell line derivatives, in comparison to a universal RNA reference. Gene set enrichment analysis was used to identify CAMK1D-assocatied gene sets. Set of arrays that are part of repeated experiments Cell Line: CAMK1D or vector transfected MCF10A breast epithelial cell line derivatives Biological Replicate Computed
2010-06-24 | E-GEOD-12811 | biostudies-arrayexpress
Project description:Title: CAMK1D amplification implicated in epithelial-mesenchymal transition in basal-like breast cancer Summary: Breast cancer exhibits clinical and molecular heterogeneity, where expression-profiling studies have identified five major molecular subtypes. The basal-like subtype, expressing basal epithelial markers and negative for estrogen receptor (ER), progesterone receptor (PR) and HER2, is associated with higher overall levels of DNA copy number alteration (CNA), specific CNAs (like gain on chromosome 10p), and poor prognosis. Discovering the molecular genetic basis of tumor subtypes may provide new opportunities for therapy. To identify the driver oncogene on 10p associated with basal-like tumors, we analyzed genomic profiles of 172 breast carcinomas. The smallest shared region of gain spanned just seven genes at 10p13, including calcium/calmodulin-dependent protein kinase ID (CAMK1D), functioning in intracellular signaling but not previously linked to cancer. By microarray, CAMK1D was overexpressed when amplified, and by immunohistochemistry exhibited elevated expression in invasive carcinomas compared to carcinoma in situ. Engineered overexpression of CAMK1D in non-tumorigenic breast epithelial cells led to increased cell proliferation, and molecular and phenotypic alterations indicative of epithelial-mesenchymal transition (EMT), including loss of cell-cell adhesions and increased cell migration and invasion. Our findings identify CAMK1D as a novel amplified oncogene linked to EMT in breast cancer, and as a potential therapeutic target with particular relevance to clinically unfavorable basal-like tumors.
2009-09-08 | GSE12811 | GEO
Project description:We report the single cell transcriptomes of 4 basal cell carcinoma subtypes and 2 peri-tumor skin samples.
2020-08-14 | GSE141526 | GEO
Project description:Non-melanoma skin cancers (NMSC) including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are more common kinds of skin cancer. Although these tumors share common pathological and clinical features, their similarity and heterogeneity at molecular levels are not fully elaborated yet. Here, by performing comparative analysis of gene expression profiling of BCC, SCC, and normal skin tissues, we could classify the BCC into three subtypes of classical, SCC-like, and normal-like BCCs. Functional enrichment and pathway analyses revealed the molecular characteristics of each subtype. The analysis of gene expression profiling among non-melanoma skin cancer types
2014-12-13 | E-GEOD-53462 | biostudies-arrayexpress
Project description:Title: CAMK1D amplification implicated in epithelial-mesenchymal transition in basal-like breast cancer Summary: Breast cancer exhibits clinical and molecular heterogeneity, where expression-profiling studies have identified five major molecular subtypes. The basal-like subtype, expressing basal epithelial markers and negative for estrogen receptor (ER), progesterone receptor (PR) and HER2, is associated with higher overall levels of DNA copy number alteration (CNA), specific CNAs (like gain on chromosome 10p), and poor prognosis. Discovering the molecular genetic basis of tumor subtypes may provide new opportunities for therapy. To identify the driver oncogene on 10p associated with basal-like tumors, we analyzed genomic profiles of 172 breast carcinomas. The smallest shared region of gain spanned just seven genes at 10p13, including calcium/calmodulin-dependent protein kinase ID (CAMK1D), functioning in intracellular signaling but not previously linked to cancer. By microarray, CAMK1D was overexpressed when amplified, and by immunohistochemistry exhibited elevated expression in invasive carcinomas compared to carcinoma in situ. Engineered overexpression of CAMK1D in non-tumorigenic breast epithelial cells led to increased cell proliferation, and molecular and phenotypic alterations indicative of epithelial-mesenchymal transition (EMT), including loss of cell-cell adhesions and increased cell migration and invasion. Our findings identify CAMK1D as a novel amplified oncogene linked to EMT in breast cancer, and as a potential therapeutic target with particular relevance to clinically unfavorable basal-like tumors. Overall design: cDNA microarrays from the Stanford Functional Genomics Facility were used to carry out array-based Comparative Genomic Hybridization (array CGH) analysis of 172 human breast tumor specimens, in comparison to normal female DNA. Map positions for arrayed cDNA clones were assigned using the NCBI genome assembly, accessed through the UCSC genome browser database (NCBI Build 36). The CLuster Along Chromosomes (CLAC) method was used to call DNA gains and losses. Set of arrays that are part of repeated experiments Keywords: Biological Replicate Biological Replicate Computed
2010-06-24 | E-GEOD-12813 | biostudies-arrayexpress
Project description:Smoking and Obesity Related Molecular Alterations in Clear Cell Renal Cell Carcinoma
2020-09-03 | E-GEOD-46699 | ExpressionAtlas