KMT2D suppresses Sonic Hedgehog-driven medulloblastoma progression and metastasis [ATAC-seq]
UID: 11005
- Description
- Summary from GEO:
"The major cause for treatment failure, morbidity and mortality amongst medulloblastoma patients is metastasis intracranially or along the spinal cord. The molecular mechanisms driving tumor metastasis in SHH-driven medulloblastoma (SHH-MB) patients remain largely unknown. In this study we used mouse models of SHH-MB to define a tumor suppressive role of KMT2D (MLL4), a gene frequently mutated in the most metastatic β-subtype. Strikingly, heterozygous loss of Kmt2d in conjunction with aberrant activation of the SHH pathway causes highly penetrant disease with decreased survival, hindbrain invasion and spinal cord metastasis. Loss of Kmt2d shifts the transcriptional and chromatin landscape of primary and metastatic tumor cells to preferentially upregulate pathways and genes associated with advanced stage cancer and metastasis including TGFβ, Notch, Atoh1, Sox2/9 and Myc. Our study provides strong evidence that secondary mutations in KMT2D will have prognostic value for identifying SHH-MB patients that are likely to develop metastasis."
Overall design from GEO:
"ATAC-seq of a mouse model of Sonic Hedgehog-driven medulloblastoma."
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Access via GEO
Accession #: GSE211029Access via BioProject
Accession #: PRJNA868710 - Access Restrictions
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Free to All
- Access Instructions
- The NCBI Gene Expression Omnibus and BioProject databases provide open access to these files.
- Associated Publications
- Equipment Used
- Dataset Format(s)
- TAR, BW
- Dataset Size
- 5.2 GB
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