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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAYgpm9_030AvcqXeDtLrbemgJxJ-U-rPL_asjxIMvcII#_4 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAYgpm9_030AvcqXeDtLrbemgJxJ-U-rPL_asjxIMvcII#_3 http://www.w3.org/ns/prov#value Enforced expression of Bcl-2 protein from plasmid vectors, in contrast, abrogates sensitivity to the apoptosis promoting effects of antiestrogens in breast cancer lines, while antisense BCL-2 prevents estrogen-mediated apoptosis suppression, thus establishing a direct functional connection between ER, Bcl-2, and suppression of apoptosis (Teixeira et al., 1995). expression of Bcl-2 or Bcl-XL can be downregulated in specific types of cancer and leukemia cells by smallmolecule drugs that modulate the activity of retinoic acid receptors (RAR), retinoid X receptors (RXR), PPAR?, vitamin D receptors (VDR), and certain other members of the SRTF superfamily. RAR and RXR ligands are already approved for treatment of some types of leukemia and lymphoma, and are in advanced clinical testing for solid tumors. 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