P24_STVI_colorectal_cancer_GEX
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Jean-Charles Soria
PROVIDER: E-MTAB-2864 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2013-12-11 | E-MTAB-1132 | biostudies-arrayexpress
Project description:Previous reports have described the use of microarrays to assess the molecular classification of human breast cancers and defined new subgroups based on gene expression that are relevant to patient management through their ability to predict metastatic relapse and survival relapse. However, different mechanisms may be associated with the development of early and late distant metastases. With the hypothesis that tumors may lead to early or distant metastases based on their intrinsic biological initial features. We aimed at defining molecular profiles for several subgroups of patients based on their outcome over time. Breast primary tumors were selected from retrospective series of patients with frozen material available. These series include patients of all ages, LN- and LN+; Estrogen or Progesteron-receptor positive, Her2-negative, no adjuvant treatment, with a follow-up of more than 10 years (y) for the control group or distant metastatic relapse as first event (DM) for the study group. Patients tumors were classified in 3 groups: no relapse at 10y (M0), DM before 5 y (M0-5), DM between 5 and 15 y (M5-15).Gene expression analysis of breast tumor samples was performed using custom-made Agilent 4x44K high-density microarrays and hybridized against the Mammaprint reference pool (MRP). MRP=MammaReference Pool (The reference sample consisted of pooled and amplified RNA of 105 primary breast tumors, see Glas AM, BMC Genomics, 2006). The design of this study consists to 20 hybridizations in dual color with Agilent Human Genome 4x44K (design 014850) of breast tumors with a MRP reference with an addition as controls of 2 dye swaps and two self-self of the MRP and HMG (Human normal mammary Gland , Clontech).
2013-08-01 | E-MTAB-949 | biostudies-arrayexpress
Project description:S78454 (Abexinostat, PCI-24781) is a pan histone deacetylase inhibitor (HDACi) that demonstrates efficacy in malignancy treatment. Like other HDACi, this drug induces a profound thrombocytopenia, whose mechanism is partially understood. We have tested its effect at doses reached in patients plasma on in vitro megakaryopoiesis derived from human CD34+ cells. When added at day 0 in culture, S78454 inhibited CFU-MK growth, megakaryocyte (MK) proliferation and differentiation. This effect only required a short incubation period. When added later on (day 8), the compound induced a dose-dependent decrease (up to 10-fold) in proplatelet formation. Decreased proliferation was due to induction of apoptosis and was not related to a defect in TPO/MPL/JAK2 signaling. MK gene profiling revealed a silencing in the expression of DNA repair genes with a marked RAD51 decrease at protein level. Double DNA strand breaks were increased as attested by elevated gH2AX phosphorylation level. Consequently, ATM was phosphorylated leading to p53 stabilization and increased BAX and p21 expression. The use of a p53 shRNA rescued apoptosis, but only partially the defect in proplatelet formation. These results suggest that HDACi induces a thrombocytopenia by a p53 dependent mechanism along MK differentiation and a p53 independent mechanism for proplatelet formation.
2013-06-30 | E-MTAB-1180 | biostudies-arrayexpress
Project description:Non-small cell lung cancer (NSCLC), a leading cause of cancer deaths, represents a heterogeneous group of neoplasms, mostly comprising squamous cell carcinoma (Squamous cell carcinoma), aC (AC) and large-cell carcinoma (Large cell carcinoma). The aim of this study was to gain a systems biology insight into the current clinical classification. Patients and Methods: Comparative genomic hybridization followed by mutational analysis, gene expression and miRNA microarray profiling were performed on 123 paired tumor and non-tumor tissue samples from patients with NSCLC. Using integrated systems biology approches, we sought to find out if combining data types from different levels of biology would improve clinical assessment of NSCLC. Results: At both DNA, RNA and miRNA levels we could identify molecular markers that discriminated significantly between the various clinicopathological entities of NSCLC. Conclusions: We report proofs of distinct molecular profiles that contribute to distinguishing NSCLC tumor subtypes even in small biopsies. The246 miRNA experiments have been made in single color with Agilent Human Genome miRNA 15K arrays v3 (design 021827).
2013-12-11 | E-MTAB-1134 | biostudies-arrayexpress
Project description:Carcinomas of unknown primary (CUP) are characterized by early metastatic dissemination in the absence of a detectable primary tumor. This disease accounts for about 3% of all malignant tumors. Most CUPs are poorly responsive to chemotherapy and have a rapid fatal evolution. The biological mechanisms supporting metastatic growth in various sites combined with regression or absence of growth in the primary site are still poorly understood. The aim of this project was to investigate characteristics of gene expression profile specific of CUPs with special attention to genes overexpressed or silenced in CUPs but not in classical secondary metastases. Three series of experiments were performed in 2006 and 2007. In all experiments, the mRNA used as a reference was obtained from diploid untransformed human fibroblasts (MRC5). The CUP samples were 2 xenografted CUP tumors (Capi1 and Capi3) and 4 CUP biopsies including a squamous carcinoma (Aud) and 3 adenocarcinomas (Gal, Pro, Gag). Samples representative of secondary metastases were xenografted tumors derived from metastases of nasopharyngeal carcinoma (C17), lung adenocarcinoma (IC14) and pancreatic adenocarcinoma (xenografted Capan 1 cell line) and one biopsy from a breast carcinoma (Vuc).
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Project description:Non-small cell lung cancer (NSCLC) with activating mutations in the epidermal growth factor receptor (EGFR) responds to EGFR tyrosine kinase inhibitors such as erlotinib. However, secondary somatic EGFR mutations (e.g. T790M) confer resistance to erlotinib. BMS-690514, a novel panHER/VEGFR inhibitor described here, exerted antiproliferative and pro-apoptotic effects on NSCLC cell lines, with prominent efficacy on H1975 cells expressing the T790M mutation. In this model, BMS-690514 induced a G1 cell cycle arrest, as well as ultrastructural hallmarks of apoptosis, mitochondrial release of cytochrome c, and activation of caspases involved in the intrinsic (e.g. caspase -2, -3, -7 and -9), but not in the extrinsic (e.g. caspase-8) pathway. Caspase inhibition conferred partial protection against BMS-690514 cytotoxicity, pointing to the involvement of both caspase-dependent and -independent effector mechanisms. Transcriptome analyses revealed the upregulation of pro-apoptotic (e.g. Bim, Puma) and cell cycle inhibitory (e.g. p27Kip1, p57Kip2) factors, as well as the downregulation of anti-apoptotic (e.g. Mcl1), heat shock (e.g. HSP40, HSP70, HSP90) and cell cycle promoting (e.g. cyclins B1, D1 and D3, CDK1, MCM family proteins, PCNA) proteins. BMS-690514-induced death of H1975 cells was modified in a unique fashion by a panel of siRNAs targeting apoptosis modulators. Downregulation of components of the NF-kappaB survival pathway (e.g. p65, Nemo/IKK, TAB2) sensitized cells to BMS-690514, whereas knockdown of pro-apoptotic factors (e.g. Puma, Bax, Bak, caspase-2, etc) and DNA damage-related proteins (e.g. ERCC1, hTERT) exerted cytoprotective effects. BMS-690514 is a new pan-HER/VEGFR inhibitor that may become an alternative to erlotinib for the treatment of NSCLC.
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