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001     180028
005     20240229145603.0
024 7 _ |a 10.1002/ijc.34131
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024 7 _ |a 0020-7136
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100 1 _ |a von Knebel Doeberitz, Nikolaus
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245 _ _ |a Changing paradigms in oncology: toward non-cytotoxic treatments for advanced gliomas.
260 _ _ |a Bognor Regis
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500 _ _ |a #EA:E010# / 2022 Nov 1;151(9):1431-1446
520 _ _ |a Glial-lineage malignancies (gliomas) recurrently mutate and/or delete the master regulators of apoptosis p53 and/or p16/CDKN2A, undermining apoptosis-intending (cytotoxic) treatments. By contrast to disrupted p53/p16, glioma cells are live-wired with the master transcription factor circuits that specify and drive glial lineage-fates: these transcription factors activate early-glial and replication programs as expected, but fail in their other usual function of forcing onward glial lineage-maturation - late-glial genes have constitutively 'closed' chromatin requiring chromatin-remodeling for activation - glioma-genesis disrupts several epigenetic components needed to perform this work, and simultaneously amplifies repressing epigenetic machinery instead. Pharmacologic inhibition of repressing epigenetic enzymes thus allows activation of late-glial genes and terminates glioma self-replication (self-replication = replication without lineage-maturation), independent of p53/p16/apoptosis. Lineage-specifying master transcription factors therefore contrast with p53/p16 in being enriched in self-replicating glioma cells, reveal a cause-effect relationship between aberrant epigenetic repression of late-lineage programs and malignant self-replication, and point to specific epigenetic targets for non-cytotoxic glioma-therapy.
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650 _ 7 |a Cancer Epigenetics
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650 _ 7 |a Epigenetic Glioma Therapy
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650 _ 7 |a Glioma
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650 _ 7 |a Glioma Therapy
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650 _ 7 |a Neurooncology
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700 1 _ |a Paech, Daniel
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700 1 _ |a Sturm, Dominik
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700 1 _ |a Pusch, Stefan
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700 1 _ |a Turcan, Sevin
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700 1 _ |a Saunthararajah, Yogen
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773 _ _ |a 10.1002/ijc.34131
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