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BET

BET pathway activity expressed on a tumor cell diagram

Bromodomain and extraterminal domain (BET) proteins recognize acetylated histones to regulate gene transcription through the recruitment of transcriptional factors. Inhibition of BET proteins has been shown to have an antitumor activity.

  • BET is a family of 4 epigenetic reader proteins (BRD2, BRD3, BRD4, and BRDT) that recognize acetyl groups in the histone tail and are involved in recruiting transcriptional factors to activate gene transcription1-3
  • BET proteins are widely expressed and under normal conditions are responsible for regulating a variety of cellular processes2,4
  • Inhibition of BET can lead to a reduction in cell proliferation and have been evaluated in several preclinical studies1
    • BET inhibition was found to be effective in several cancer cell lines1
    • Preclinical studies demonstrate that inhibition of BET can suppress expression of PD-L1, which may lead to increased activity of cytotoxic T cells3,6
  • Preclinical studies also show that inhibition of BET in combination with checkpoint pathways may enhance antitumor activity greater than blockade of BET alone6

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REFERENCES–BET

1. PĂ©rez-Salvia M, Esteller M. Bromodomain inhibitors and cancer therapy: from structures to applications. Epigenetics. 2017;12(5):323-339. 2. Fu L-L, Tian M, Li X, et al. Inhibition of BET bromodomains as a therapeutic strategy for cancer drug discovery. Oncotarget. 2015;6(8):5501-5516. 3. Zhu H, Bengsch F, Svoronos N, et al. BET bromodomain inhibition promotes anti-tumor immunity by suppressing PD-L1 expression. Cell Rep. 2016;16(11):2829-2837. 4. Sahai V, Redig AJ, Collier KA, et al. Targeting BET bromodomain proteins in solid tumors. Oncotarget. 2016;7(33):53997-54009. 5. Delmore JE, Issa GC, Lemieux ME, et al. BET bromodomain inhibition as a therapeutic strategy to target c-Myc. Cell. 2011;146(6):904-917. 6. Hogg SJ, Vervoort SJ, Deswal S, et al. BET-Bromodomain inhibitors engage the host immune system and regulate expression of the immune checkpoint ligand PD-L1. Cell Rep. 2017;18(9):2162-2174.