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https://www.selleckchem.com/products/gsk467.html Pediatric high-grade gliomas (pHGGs), including glioblastoma multiforme (GBM) and diffuse intrinsic pontine glioma (DIPG), are morbid brain tumors. Even with treatment survival is poor, making pHGG the number one cause of cancer death in children. Up to 80% of DIPGs harbor a somatic missense mutation in genes encoding histone H3. To investigate whether H3K27M is associated with distinct chromatin structure that alters transcription regulation, we generated the first high-resolution Hi-C maps of pHGG cell lines and tumor tissue. By integrating transcriptome (RNA-seq), enhancer landscape (ChIP-seq), genome structure (Hi-C), and chromatin accessibility (ATAC-seq) datasets from H3K27M and wild-type specimens, we identified tumor-specific enhancers and regulatory networks for known oncogenes. We identified genomic structural variations that lead to potential enhancer hijacking and gene coamplification, including A2M, JAG2, and FLRT1 Together, our results imply three-dimensional genome alterations may play a critical role in the pHGG epigenetic landscape and contribute to tumorigenesis.Several North Pacific studies of the last deglaciation show hypoxia throughout the ocean margins and attribute this phenomenon to the effects of abrupt warming and meltwater inputs. Yet, because of the lack of long records spanning multiple glacial cycles and deglaciation events, it is unclear whether deoxygenation was a regular occurrence of warming events and whether deglaciation and/or other conditions promoted hypoxia throughout time. Here, subarctic Pacific laminated sediments from the past 1.2 million years demonstrate that hypoxic events recurred throughout the Pleistocene as episodes of highly productive phytoplankton growth and were generally associated with interglacial climates, high sea levels, and enhanced nitrate utilization-but not with deglaciations. We suggest that hypoxia was typically stimulated by high productivity from ir

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