Similar Datasets
Project description:Comparative transcriptional profiling of MYC driven HCC and MYC/Twist1 driven HCC during tumor progression, regression and recurrence.
2024-08-06 | GSE243176 | GEO
Project description:Comparative transcriptional profiling of MYC driven HCC and MYC/Twist1 driven HCC during tumor progression, regression and recurrence.
2020-01-21 | GSE135878 | GEO
Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").
2022-10-12 | PXD031478 | Pride
Project description:The suppression of oncogenic levels of MYC is sufficient to induce sustained tumor regression associated with proliferative arrest, differentiation, cellular senescence and/or apoptosis, a phenomenon known as oncogene addiction. However, after prolonged inactivation of MYC in a conditional transgenic mouse model of Em-tTA/tetO-MYC T-acute lymphomablastic lymphoma (T-ALL), some of the tumors recur, recapitulating what is frequently observed in human tumors in response to targeted therapies. Here we report that these recurring lymphomas express high levels of either transgenic or endogenous Myc suggesting that tumors continue to be addicted to oncogenic levels of MYC. Many of the recurring lymphomas (76%) harbored mutations in the tetracycline transactivator (tTA) resulting in expression of the MYC transgene even in the presence of doxycycline. Many of the remaining recurring tumors expressed high levels of endogenous Myc which was in some cases associated with a genomic rearrangement of the endogenous Myc locus or overexpression of Notch1. Gene expression profiling confirmed that the primary and recurring tumors have highly similar transcriptomes. Importantly, shRNA-mediated suppression of the high levels of MYC in recurring tumors elicited both suppression of proliferation and increased apoptosis confirming that these tumors remain oncogene addicted. These results suggest that tumors caused by MYC overexpression remain addicted to high levels of expression of this oncogene. 13 samples, no replicates included
2011-09-23 | E-GEOD-32341 | biostudies-arrayexpress
Project description:We demonstrate that there is a level of MYC expression that is required for maintaining a tumor phenotype and at this threshold there is a switch from a state of cellular proliferation to a state of proliferative arrest and apoptosis. We analyzed changes in gene expression by oligonucleotide microarray analysis and quantitative PCR and found significant changes (FDR=5%) in 2348 down regulated genes and 1573 upregulated genes. Critical changes in gene expression that occurred at or near the threshold level of MYC expression includes genes that have been implicated in G1/S, G2/M cell cycle checkpoint pathways and death receptor/apoptosis signaling. Keywords: Dose response - MYC inactivation by doxycycline treatment 11 samples, replicates not included
2010-05-25 | E-GEOD-10200 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma is generally refractory to clinical treatment. Here, we report that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers. MYC inactivation resulted en masse in tumour cells differentiating into hepatocytes and biliary cells forming bile duct structures, and this was associated with rapid loss of expression of the tumour marker alpha-fetoprotein, the increase in expression of liver cell markers cytokeratin 8 and carcinoembryonic antigen, and in some cells the liver stem cell marker cytokeratin 19. Using in vivo bioluminescence imaging we found that many of these tumour cells remained dormant as long as MYC remain inactivated; however, MYC reactivation immediately restored their neoplastic features. Using array comparative genomic hybridization we confirmed that these dormant liver cells and the restored tumour retained the identical molecular signature and hence were clonally derived from the tumour cells. Our results show how oncogene inactivation may reverse tumorigenesis in the most clinically difficult cancers. Oncogene inactivation uncovers the pluripotent capacity of tumours to differentiate into normal cellular lineages and tissue structures, while retaining their latent potential to become cancerous, and hence existing in a state of tumour dormancy. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Using regression correlation
2005-07-28 | E-GEOD-3018 | biostudies-arrayexpress
Project description:The suppression of oncogenic levels of MYC is sufficient to induce sustained tumor regression associated with proliferative arrest, differentiation, cellular senescence and/or apoptosis, a phenomenon known as oncogene addiction. However, after prolonged inactivation of MYC in a conditional transgenic mouse model of Em-tTA/tetO-MYC T-acute lymphomablastic lymphoma (T-ALL), some of the tumors recur, recapitulating what is frequently observed in human tumors in response to targeted therapies. Here we report that these recurring lymphomas express high levels of either transgenic or endogenous Myc suggesting that tumors continue to be addicted to oncogenic levels of MYC. Many of the recurring lymphomas (76%) harbored mutations in the tetracycline transactivator (tTA) resulting in expression of the MYC transgene even in the presence of doxycycline. Many of the remaining recurring tumors expressed high levels of endogenous Myc which was in some cases associated with a genomic rearrangement of the endogenous Myc locus or overexpression of Notch1. Gene expression profiling confirmed that the primary and recurring tumors have highly similar transcriptomes. Importantly, shRNA-mediated suppression of the high levels of MYC in recurring tumors elicited both suppression of proliferation and increased apoptosis confirming that these tumors remain oncogene addicted. These results suggest that tumors caused by MYC overexpression remain addicted to high levels of expression of this oncogene.
2011-09-24 | GSE32341 | GEO
Project description:We delineate the immunobiology during MYC oncogene-driven lymphomagenesis by RNA sequencing analysis followed by CIBERSORT of bulk splenic samples from healthy and SRa-tTA/tet-O-MYC mice before and after MYC inactivation. The data set also delineates global changes in signaling molecules in healthy spleens (controls) and lymphomagenic spleens in MYC ON and MYC OFF states.
2020-04-20 | GSE106078 | GEO
Project description:Residual tumor cells which remain dormant after MYC inactivation in a primary MYC-HCC derived cell line.
2024-08-06 | GSE242745 | GEO
Project description:We demonstrate that there is a level of MYC expression that is required for maintaining a tumor phenotype and at this threshold there is a switch from a state of cellular proliferation to a state of proliferative arrest and apoptosis. We analyzed changes in gene expression by oligonucleotide microarray analysis and quantitative PCR and found significant changes (FDR=5%) in 2348 down regulated genes and 1573 upregulated genes. Critical changes in gene expression that occurred at or near the threshold level of MYC expression includes genes that have been implicated in G1/S, G2/M cell cycle checkpoint pathways and death receptor/apoptosis signaling. Keywords: Dose response - MYC inactivation by doxycycline treatment
2008-07-01 | GSE10200 | GEO