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BAC-microarrays aCGH data from 67 Ewing's Sarcoma tumor samples and 16 Ewing's Sarcoma cell lines

ABSTRACT: 67 tumor samples were aCGH profiled in order to obtain frequencies of recurrent copy number alterations intended to posterior correlations with clinical data. 16 cell lines were characterized as well. Whole genomic DNA from all samples was Cy5 labeled and co-hybridized onto BAC-microarrays along with a Cy3-labeled pool of 100 healthy donors' DNA

ORGANISM(S): Homo sapiens

SUBMITTER: Carlos Mackintosh

PROVIDER: E-GEOD-20355 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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1q gain clinical impact in Ewing's Sarcoma: role of DTL

Project description:This SuperSeries is composed of the following subset Series: GSE20355: BAC-microarrays aCGH data from 67 Ewing's Sarcoma tumor samples and 16 Ewing's Sarcoma cell lines GSE20356: Evaluation of copy number alterations in the Ewing's Sarcoma cell line SKES1 with Affymetrix 500k SNP microarray GSE20357: Expression data from DTL silenced-Ewing Sarcoma's cell lines along with their controls Refer to individual Series

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BAC-microarrays aCGH data from 67 Ewing's Sarcoma tumor samples and 16 Ewing's Sarcoma cell lines

Project description:67 tumor samples were aCGH profiled in order to obtain frequencies of recurrent copy number alterations intended to posterior correlations with clinical data. 16 cell lines were characterized as well.

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Project description: Not available

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Project description:The hallmark of Ewing's sarcoma (EWS) is a translocation--t(11;22)(q24;q12)--that most frequently results in the EWS/FLI1 aberrant chimeric gene. Because EWS afflicts young patients, it stands out among the diverse sarcoma subtypes. The frontline, standard-of-care cytotoxic chemotherapy regimens produce minimal benefit in patients with metastases at presentation or those with relapsed disease. While the outcomes of chemorefractory EWS patients are generally poor, recent developments have led to the promising use of targeted therapy. Specifically, inhibition of insulin-like growth factor 1 receptor (IGF1R) signaling and the mammalian target of rapamycin (mTOR) pathways has emerged as a targeted therapy in EWS, with select patients experiencing dramatic therapeutic responses. However, targeted therapies in general, and these responders in particular, are faced with the ultimate conundrum of eventual resistance. To optimize response, combining IGF1R and mTOR inhibitor-based regimens with chemotherapy in the upfront setting in newly diagnosed high-risk EWS may clarify the true benefit of IGF1R inhibitors in these patients. Another option is to explore novel targeted multikinase inhibitors and poly(ADP-ribose) polymerase (PARP) inhibitors, which have experienced a surge in supporting preclinical data. Drugs inhibiting the downstream targets of EWS/FLI1 are also in preclinical development. However, ultimately, the underlying biomarker correlates of resistance and response must be delineated along with ways to overcome them. Novel agents, together with integration of advances in multimodal approaches (including surgery and radiation), as well as offering targeted therapies early in the disease course represent new strategies for confronting the challenges of EWS.

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