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Hedgehog pathway inhibition in chondrosarcoma using the Smoothened inhibitor IPI-926 directly inhibits sarcoma cell growth

ABSTRACT: Mice bearing primary human chondrosarcoma xenografts were treated with IPI 926, and mRNA levels of known Hh pathway genes and endpoint tumor volumes were measured. Gene expression profiling of IPI-926 treated tumors was conducted to identify potential novel Hh target genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44581 | GEO | 2014/03/18

SECONDARY ACCESSION(S): PRJNA190094

REPOSITORIES: GEO

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Hedgehog pathway inhibition in chondrosarcoma using the Smoothened inhibitor IPI-926 directly inhibits sarcoma cell growth

Project description:Mice bearing primary human chondrosarcoma xenografts were treated with IPI 926, and mRNA levels of known Hh pathway genes and endpoint tumor volumes were measured. Gene expression profiling of IPI-926 treated tumors was conducted to identify potential novel Hh target genes. 4 Control treated and 4 IPI-926 treated NSG Mice. Primary tumor was obtained from a single chondrosarcoma patient.

2014-03-18 | E-GEOD-44581 | biostudies-arrayexpress

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IPH-926 human lobular breast cancer cells

Project description:IPH-926 is an anticancer drug-resistant tumor cell line derived from a chemo-refractory human infiltrating lobular breast cancer (ILBC). IPH-926 ILBC cells were subjected to gene expression profiling using an Affymetrix HG U133 Plus 2.0 array. To characterize the global gene expression of IPH-926, cells were subjected to transcriptional profiling using the Affymetrix HG U133 Plus 2.0 technology. The correct identity of the IPH-926 cells subjected to gene expression profiling was authenticated by short tandem repeat (STR) profiling.

2011-12-21 | E-GEOD-28089 | biostudies-arrayexpress

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Project description:Hedgehog pathway inhibition in chondrosarcoma using the Smoothened inhibitor IPI-926 directly inhibits sarcoma cell growth

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EcadEGFP expression in MDA-MB-134 and IPH-926

Project description:This experiment aims to study transcriptional alterations induced by reconstitution of wild type E-cadherin expression in human lobular breast cancer cells harbouring deleterious, somatic CDH-1 mutations Two cell lines (IPH-926 and MDA-MB-134) expressing synthetic Ecad (EcadEGFP) or not (EGFP) were compared against each other. Analysis were conducted in triplicates (IPH-926) and quadruplicates (MDA-MB-134), respectively.

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Project description:Streptomyces sp. CG 926 Genome sequencing and assembly

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Hedgehog pathway inhibitor saridegib (IPI-926) increases lifespan in a mouse medulloblastoma model.

Project description:The Sonic Hedgehog (Shh) pathway drives a subset of medulloblastomas, a malignant neuroectodermal brain cancer, and other cancers. Small-molecule Shh pathway inhibitors have induced tumor regression in mice and patients with medulloblastoma; however, drug resistance rapidly emerges, in some cases via de novo mutation of the drug target. Here we assess the response and resistance mechanisms to the natural product derivative saridegib in an aggressive Shh-driven mouse medulloblastoma model. In this model, saridegib treatment induced tumor reduction and significantly prolonged survival. Furthermore, the effect of saridegib on tumor-initiating capacity was demonstrated by reduced tumor incidence, slower growth, and spontaneous tumor regression that occurred in allografts generated from previously treated autochthonous medulloblastomas compared with those from untreated donors. Saridegib, a known P-glycoprotein (Pgp) substrate, induced Pgp activity in treated tumors, which likely contributed to emergence of drug resistance. Unlike other Smoothened (Smo) inhibitors, the drug resistance was neither mutation-dependent nor Gli2 amplification-dependent, and saridegib was found to be active in cells with the D473H point mutation that rendered them resistant to another Smo inhibitor, GDC-0449. The fivefold increase in lifespan in mice treated with saridegib as a single agent compares favorably with both targeted and cytotoxic therapies. The absence of genetic mutations that confer resistance distinguishes saridegib from other Smo inhibitors.

| S-EPMC3356655 | biostudies-literature

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