Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcriptomes of triple negative breast cancer enriched breast cancer cohort

ABSTRACT: Breast cancers enriched for the triple negative breast cancer phenotype with extensive clinico-pathological features were profiled to establish their comprehensive transcriptional profiles

ORGANISM(S): Homo sapiens

SUBMITTER: Anita Grigoriadis

PROVIDER: E-MTAB-5270 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

PIM1 kinase regulates cell death, tumor growth and chemotherapy response in triple-negative breast cancer.

Brasó-Maristany Fara F Filosto Simone S Catchpole Steven S Marlow Rebecca R Quist Jelmar J Francesch-Domenech Erika E Plumb Darren A DA Zakka Leila L Gazinska Patrycja P Liccardi Gianmaria G Meier Pascal P Gris-Oliver Albert A Cheang Maggie Chon U MC Perdrix-Rosell Anna A Shafat Manar M Noël Elodie E Patel Nirmesh N McEachern Kristen K Scaltriti Maurizio M Castel Pau P Noor Farzana F Buus Richard R Mathew Sumi S Watkins Johnathan J Serra Violeta V Marra Pierfrancesco P Grigoriadis Anita A Tutt Andrew N AN

Nature medicine 20161024 11

Triple-negative breast cancers (TNBCs) have poor prognosis and lack targeted therapies. Here we identified increased copy number and expression of the PIM1 proto-oncogene in genomic data sets of patients with TNBC. TNBC cells, but not nonmalignant mammary epithelial cells, were dependent on PIM1 for proliferation and protection from apoptosis. PIM1 knockdown reduced expression of the anti-apoptotic factor BCL2, and dynamic BH3 profiling of apoptotic priming revealed that PIM1 prevents mitochondr ...[more]

PMID: 27775704

Publication: 1/4

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Project description:The microarray data presented here relate to a study on TEL-AML1 associated childhood leukemia (Hong et al, 2008) the abstract of which is as follows: "Understanding cancer pathogenesis requires knowledge of not only the specific contributory genetic mutations but also the cellular framework in which they arise and function. Here we explore the clonal evolution of childhood precursor B-cell acute lymphoblastic leukemia characterised by a chromosomal translocation generating a TEL-AML1 fusion gene. We identify a cell compartment in leukemic children which can propagate leukemia when transplanted in mice. By studying a monochorionic twin pair, one pre-leukemic and one with frank leukemia, we establish the lineal relationship between these "tumor-propagating" cells and the pre-leukemic cell in which the TEL-AML1 fusion first arises or has functional impact. Analysis of TEL-AML1 transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this pre-leukemic cell with altered self-renewal and survival properties." The cells used to generate the microarray data were obtained as follows: We prospectively isolated CD34+CD38-/lowCD19+ cells from NOD/SCID mice transplanted with TEL-AML1-transduced human cord blood cells and compared their gene expression profiles, ascertained by affymetrix microarray analysis (see methods), to control 'hematopoietic stem cells' (HSCs immunophenotypically-defined as CD34+CD38-/lowCD19-) and pro-B cells (immunophenotypically-defined as CD34+CD38+CD19+) isolated from NOD/SCID animals transplanted with control vector transduced cord blood cells. While these different populations were obtained from three independent transduction and transplantation experiments, the data were generated from small numbers of cells and have not been validated by independent analyses such as RQ-PCR or protein analysis. They should therefore be regarded as preliminary in nature and we would therefore caution against detailed analysis of individual gene expression profiles based on these particular datasets. This caveat aside, the data may provide a broad overview of gene expression profiles in these cell types and such analyses suggest that TEL-AML1 generates a novel population of cells that contain features of both stem cells and committed B progenitors (Hong et al 2008). We are currently repeating the analyses using larger numbers of cells and more replicates together with appropriate cell populations from ALL patients and will post these data online when they become available.

Dataset Information

Transcriptomes of triple negative breast cancer enriched breast cancer cohort

Publications

PIM1 kinase regulates cell death, tumor growth and chemotherapy response in triple-negative breast cancer.

Similar Datasets

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