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Unknown,Transcriptomics,Genomics,Proteomics

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EIF4F is a nexus of resistance to anti-BRAF and anti-MEK cancer therapies

ABSTRACT: The amounts of eIF4G and eIF4B were decreased in the vemurafenib-treated sensitive A375 cell line. To find mechanisms behind this decrease, we sought to identify the genes whose expression changes after vemurafenib treatment in A375 cells as compared to Mel624 cells by using microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Caroline Robert

PROVIDER: E-MTAB-2607 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of human colorectal cancer samples with CpG island methylator phenotype (CIMP)

Project description:The CpG island methylator phenotype (CIMP) in colorectal tumors can be recognized by an increased frequency of aberrant methylation in a specific set of genomic loci. Because of the strong association of CIMP with high microsatellite instability (MSI-H), the identification of CIMP+ tumors within microsatellite stable (MSS) colorectal cancers may not be straightforward. To overcome this potential limitation, we have built an improved 7-loci set of methylation markers that includes CACNA1G, IGF2, RUNX3, HTR6, RIZ1, MINT31 and MAP1B. This new set of CIMP markers revealed a bimodal distribution of methylation frequencies in a group of 95 MSS colorectal cancers, which allowed a clearer separation between CIMP classes. Correlation of CIMP+ tumors with bio-pathological traits revealed significant associations with location to the proximal colon, mucinous histology and chromosomal stability. Although not statistically significant, a trend toward an adverse prognosis for CIMP+ cases was observed. Microarray analysis revealed that CIMP+ tumors are characterized by a unique expression profile, a result that confirms that CIMP+ tumors represent a distinct molecular class within MSS colorectal cancers. Moreover, our results suggest that this expression pattern may represent the molecular background for the development of CIMP+ tumors that, in turn, develop MSI when aberrant methylation occurs at the MLH1 gene promoter.

2008-01-01 | E-TABM-328 | biostudies-arrayexpress

Genes induced by HERV-K virus retroviral envelop

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Transcription profiling of non-small cell lung carcinoma cell line H1975 treated with cisplatin or BMS-69014 a novel panHER/VEGFR inhibitor

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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Transcription profiling of cohort of human cutaneous primary melanomas associated with a distant metastasis free survival

Project description:Identification of genomic characteristics in a cohorte of human cutaneous primary melanoma associated with a distant metastasis free survival.

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Transcription profiling of 9 pairs of human metastasis/primary melanoma (each from the same patient)

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2007-04-01 | E-TABM-4 | biostudies-arrayexpress

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Transcription profiling of human T cell lines isolated from tumor infiltrating lymphocytes or peripheral blood lymphocytes of a patient with large cell carcinoma of the lung

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