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Molecular diversity of breast cancers at the time of endocrine resistance

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE54497 | GEO | 2014/12/01

SECONDARY ACCESSION(S): PRJNA236645

REPOSITORIES: GEO

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Molecular diversity of breast cancers at the time of endocrine resistance [mRNA]

Project description:Dataset containing whole-genome expression profiles of breast cancers at the time of endocrine resistance. It has been used to identify five distinctive phenotypes with different expression of gene clusters associated with ER-signalling, stromal rearrangement and cytokine-signalling. Pathway-focused analysis suggested individual tumours with active ER-signalling (24/55, 44%), PIK3CA-signalling (18/55, 32%), RAS (12/55, 22%) and MYC-signalling (11/55, 20%). 3 or 4 of the above pathways were simultaneously active in 6/55 (11%) cases. Results provide important information about prevalence of different mechanisms of endocrine resistance in clinical samples of breast cancer. Please note that the tumor samples are clinically quite homogeneous: all are post-menopausal ER+ve breast cancers, endocrine treated and growing on treatment. The main purpose of collecting these data was not to compare transcriptional profiles with clinical parameters, but rather to use the transcriptional profiles of these clinically homogeneous tumours for identifying intrinsic subgroups within endocrine resistance. However, the relevant clinical data was also provided as Series supplementary file (ClinicalData_AL28Jan2014.xlsx).

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Project description:Dataset containing micro-RNA expression profiles of breast cancers at the time of endocrine resistance. It has been used to correlate micro-RNA and mRNA expressions and to identify two distinctive phenotypes with different expression of micro-RNA gens. Please note that the tumor samples are clinically quite homogeneous: all are post-menopausal ER+ve breast cancers, endocrine treated and growing on treatment. The main purpose of collecting these data was not to compare transcriptional profiles with clinical parameters, but rather to use the micro-RNA expression profiles of these clinically homogeneous tumours for (i) identifying intrinsic subgroups within endocrine resistance and (ii) for relating micro-RNA and mRNA expressions. However, the relevant clinical data was also provided as Series supplementary file (ClinicalData_AL28Jan2014.xlsx).

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