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Cytogenetic aberrations in hepatocellular carcinoma [I]

ABSTRACT: Array CGH (44K) of liver tumors and unaffected liver controls from mice conditionally deficient for Mad2 and p53 in hepatocytes aCGH of sample DNA was hybridized with sex mismatched control DNA from a different mouse. Dye swaps were performed for each sample

ORGANISM(S): Mus musculus

SUBMITTER: Lee Albacker

PROVIDER: E-GEOD-63064 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cytogenetic aberrations in hepatocellular carcinoma [II]

Project description:Array CGH (44K) of liver tumors and unaffected liver controls from mice conditionally deficient for Mad2 and p53 in hepatocytes aCGH of sample DNA was hybridized with sex mismatched control DNA from a different mouse. Tumor and unaffected liver tissues were tested for each mouse. 19 tissue samples, 10 tumors, 9 normal samples

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Cytogenetic aberrations in Hepatocellular adenoma and carcinoma [III]

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Transcriptomes of aneuploid mouse liver tumors and T-ALL

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Project description:Mad2 and p53 loss were combined in liver or T-cells specificely leading to early onset and highly aggressive aneuploid HCC and T-ALL. Tumours were characterized for (recurrrent) copy number changes with a focus on whole chromosome abnormalities. DNA content was compared to the DNA content of sex-matched uninfiltrated control liver samples from litter mates Chromosome instability (CIN) leads to aneuploidy and copy number variations (CNVs). Even though both are hallmarks of cancer cells, aneuploidy inhibits proliferation of untransformed cells, suggesting that cancer cells have adapted to cope with CIN. The spindle assembly checkpoint (SAC) prevents CIN by monitoring chromosome attachment and sister chromatid tension in mitosis. By conditionally inactivating Mad2, an essential SAC gene, we find that SAC inactivation in T-cells or hepatocytes is remarkably well tolerated and becomes tumorigenic when placed in a p53null or p53+/- predisposed background. The resulting T-ALLs and HCCs are highly aneuploid, exhibit clonal copy number changes that are tumor specific despite ongoing CIN, indicating that CIN is a powerful driver of tumor evolution.

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