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Transcriptomic characterisation of ALDH+ cells in therapy resistant breast cancer patient samples

ABSTRACT: Transcriptomic characterisation of ALDH+ cells in therapy resistant breast cancer patient samples

PROVIDER: PRJNA561838 | ENA |

REPOSITORIES: ENA

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Transcriptomic characterisation of ALDH+ cells in therapy resistant breast cancer patient samples

Project description:This study is part of a larger multidisciplinary study entitled A dormant sub-population expressing interleukin-1 receptor characterises anti-estrogen resistant ALDH+ breast cancer stem cells. In particular these data were generated to gain understanding of the development of resistance to AE therapies in ER+ breast cancer patients by comparing the gene expression pattern between ALDH+ and ALDH- cells in 9 metastatic ER+ patient samples.

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RNA-Seq of ALDH positive and ALDH negative cells from patient-derived xenograft models of colon cancer

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Transcriptomic analysis of Diffuse Intrinsic Pontine Glioma (DIPG) identifies a targetable ALDH-positive subset of highly tumorigenic cancer stem-like cells

Project description:Understanding the cancer stem-cell (CSC) landscape in diffuse intrinsic pontine glioma (DIPG) is desperately needed to address treatment resistance and identify novel therapeutic approaches. Patient derived DIPG cells demonstrated heterogeneous expression of aldehyde dehydrogenase (ALDH) and CD133 by flow cytometry. Transcriptome-level characterization identified elevated mRNA levels of MYC, E2F, DNA damage repair (DDR) genes, glycolytic metabolism and mTOR signaling in ALDH+ compared to ALDH- supporting a stem-like phenotype and indicating a druggable target. ALDH+ cells demonstrated increased proliferation and neurosphere formation and initiated tumors that resulted in decreased survival when orthotopically implanted. Pharmacological MAPK/PI3K/mTOR targeting downregulated MYC, E2F and DDR mRNAs and reduced glycolytic metabolism. In vivo PI3K/mTOR targeting inhibited tumor growth in both flank and an ALDH+ orthotopic tumor model likely by reducing cancer stemness. Characterization of DIPG CSCs coupled with targeting MAPK/PI3K/mTOR signaling provides an impetus for molecularly targeted therapy aimed at addressing the CSC phenotype in DIPG.

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