In order to characterize the differences between the co-receptors LRP5 and LRP6, we have analyzed the transcriptome of HCC38 cells - a triple negative breast cancer cell line - 24, 48 and 72 hours following the depletion of LRP5 or LRP6 using siRNAs.
LRP5 regulates the expression of STK40, a new potential target in triple-negative breast cancers.
Disease, Disease stage, Cell line, Time
View SamplesThe aim of this study was to characterize the stroma displayed by different models of breast cancer tumors in mice. For this purpose, transcriptomic and flow cytometry analyses on murine populations were performed in a series of 25 PDXs and 2 most commonly used GEMs (MMTV-PyMT and MMTV-erBb2). Specifically, macrophages from 5 models were sorted and profiled by gene expression and phenotypically characterized by flow cytometry.
Characterization of Breast Cancer Preclinical Models Reveals a Specific Pattern of Macrophage Polarization.
Specimen part, Subject
View SamplesWe compare the genetic profiles of the primary tumors of uveal melanoma or metastasis to their corresponding xenografts that have been passaged over time.
Patient-derived xenografts recapitulate molecular features of human uveal melanomas.
Disease
View SamplesAcquired resistance to endocrine therapy occurs with high frequency in patients with luminal breast cancer (LBC). We report here the establishment of four patient-derived xenograft models of LBC with acquired resistance in vivo to tamoxifen and estrogen deprivation.
Acquired resistance to endocrine treatments is associated with tumor-specific molecular changes in patient-derived luminal breast cancer xenografts.
Specimen part
View SamplesLong intergenic non-coding RNAs (lincRNAs) are emerging as integral components of signaling pathways in various cancer types. In neuroblastoma, only a handful of lincRNAs are known as upstream regulators or downstream effectors of oncogenes. Here, we exploit RNA sequencing data of primary neuroblastoma tumors, neuroblast precursor cells, neuroblastoma cell lines and various cellular perturbation model systems to define the neuroblastoma lincRNome and map lincRNAs up- and downstream of neuroblastoma driver genes MYCN, ALK and PHOX2B. Each of these driver genes controls the expression of a particular subset of lincRNAs, several of which are associated with poor survival and are differentially expressed in neuroblastoma tumors compared to neuroblasts. By integrating RNA sequencing data from both primary tumor tissue and cancer cell lines, we demonstrate that several of these lincRNAs are expressed in stromal cells. Deconvolution of primary tumor gene expression data revealed a strong association between stromal cell composition and driver gene status, resulting in differential expression of these lincRNAs. We also explored lincRNAs that putatively act upstream of neuroblastoma driver genes, either as presumed modulators of driver gene activity, or as modulators of effectors regulating driver gene expression. This analysis revealed strong associations between the neuroblastoma lincRNAs MIAT and MEG3 and MYCN and PHOX2B activity or expression. Together, our results provide a comprehensive catalogue of the neuroblastoma lincRNome, highlighting lincRNAs up- and downstream of key neuroblastoma driver genes. This catalogue forms a solid basis for further functional validation of candidate neuroblastoma lincRNAs. Overall design: CLB-GA was transduced with control or inducible shPHOX2B. The cells were treated with doxycycline for 5 days.
Integrative analysis identifies lincRNAs up- and downstream of neuroblastoma driver genes.
Cell line, Treatment, Subject
View SamplesRNA-Sequencing analysis of 18 papillary thyroid carcinoma biopsies and of 4 healthy donors'' thyroids. In this analysis we assessed differential gene expression and investigated the mutational landscape in this tumor type. Analysis of gene fusion was also performed, leading to the identification of a novel chimeric transcript, potential driver in tumor initiation. Overall design: Total RNA isolated from 18 papillary thyroid carcinoma biopsies and 4 healthy donors'' thyroids.
New somatic mutations and WNK1-B4GALNT3 gene fusion in papillary thyroid carcinoma.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cell growth in aggregates determines gene expression, proliferation, survival, chemoresistance, and sensitivity to immune effectors in follicular lymphoma.
No sample metadata fields
View SamplesFollicular Lymphomas are blood tumors growing as spheres in patients. Before this study, there was no experimental model mimicking the 3D organization of these in vivo tumors. We develop such a model, called MALC, and observed a progressive enrichment in quiescent cells in these with time of culture; these cells were sorted, as their cycling counterparts, and their transcriptomes were compared. We used microarrays to detail the differential global gene expression profile between quiescent and cycling cells isolated from MALC.
Cell growth in aggregates determines gene expression, proliferation, survival, chemoresistance, and sensitivity to immune effectors in follicular lymphoma.
No sample metadata fields
View SamplesFollicular Lymphomas are blood tumors growing as spheres in patients. Before this study, there was no experimental model mimicking the 3D organization of these in vivo tumors. We develop such a model, called MALC, and performed a pan-genomic comparative analysis between MALC and classical suspension cultures. We used microarrays to detail the global gene expression profile induced by aggregated growth of lymphoma cells.
Cell growth in aggregates determines gene expression, proliferation, survival, chemoresistance, and sensitivity to immune effectors in follicular lymphoma.
No sample metadata fields
View SamplesT-cell acute lymphoblastic leukemia (T-ALL) is an aggressive type of blood cancer resulting from malignant transformation of T-cell precursors. Several oncogenes, including the 'T-cell leukemia homeobox 1' TLX1 (HOX11) transcription factor, have been identified as early driver events that cooperate with other genetic aberrations in leukemic transformation of progenitor T-cells. The TLX1 controlled transcriptome in T-ALL has been investigated extensively in the past in terms of protein-coding genes, but remains unexplored thus far at the level of long non-coding RNAs (lncRNAs), the latter renown as well-established versatile and key players implicated in various cancer hallmarks. In this study, we present the first extensive analysis of the TLX1 regulated transcriptome focusing on lncRNA expression patterns. We present an integrative analysis of polyA and total RNA sequencing of ALL-SIL lymphoblasts with perturbed TLX1 expression and a primary T-ALL patient cohort (including 5 TLX1+ and 12 TLX3+ cases). We expanded our initially presented dataset of TLX1 and H3K27ac ChIP data in ALL-SIL cells (Durinck et al., Leukemia, 2015) with H3K4me1, H3K4me3, and ATAC-seq data to accurately define (super-) enhancer marked lncRNAs and assigned potential functional annotations to candidate TLX1-controlled lncRNAs through an in silico guilt-by-association approach. Our study paves the way for further functional analysis of selected lncRNAs as potential novel therapeutic targets for a precision medicine approach in the context of T-ALL. Overall design: polyA+ RNA-seq data was generated for a primary T-ALL patient cohort
A comprehensive inventory of TLX1 controlled long non-coding RNAs in T-cell acute lymphoblastic leukemia through polyA+ and total RNA sequencing.
Subject
View Samples