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Literature summary for 1.14.11.27 extracted from

  • Staberg, M.; Rasmussen, R.D.; Michaelsen, S.R.; Pedersen, H.; Jensen, K.E.; Villingshoj, M.; Skjoth-Rasmussen, J.; Brennum, J.; Vitting-Seerup, K.; Poulsen, H.S.; Hamerlik, P.
    Targeting glioma stem-like cell survival and chemoresistance through inhibition of lysine-specific histone demethylase KDM2B (2018), Mol. Oncol., 12, 406-420 .
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine JmjC domain histone H3K36me2/me1 demethylase KDM2B is highly expressed in glioblastoma surgical specimens compared to normal brain. Targeting KDM2B function genetically or pharmacologically impairs the survival of patient-derived primary glioblastoma cells through the induction of DNA damage and apoptosis and sensitizes them to chemotherapy. KDM2B loss decreases the cancer stem-like cells pool, which is potentiated by coadministration of chemotherapy Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q8NHM5
-
-

Synonyms

Synonyms Comment Organism
KDM2B
-
Homo sapiens

General Information

General Information Comment Organism
physiological function JmjC domain histone H3K36me2/me1 demethylase KDM2B is highly expressed in glioblastoma surgical specimens compared to normal brain. Targeting KDM2B function genetically or pharmacologically impairs the survival of patient-derived primary glioblastoma cells through the induction of DNA damage and apoptosis and sensitizes them to chemotherapy. KDM2B loss decreases the cancer stem-like cells pool, which is potentiated by coadministration of chemotherapy Homo sapiens