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- W2231660138 abstract "ND-1 The genetic instability inherent to cancer gives rise to defects in both cell growth and cell death pathways that facilitate tumor initiation and progression. Apoptosis is an evolutionarily conserved and highly regulated process that is the primary mechanism for the removal of damaged and unnecessary cells. One of the fundamental hallmarks of cancer is the ability to evade physiologic cues that would initiate this form of cellular suicide in normal cells. This is often accomplished through dysregulation of apoptotic signaling pathways. The Bcl-2 protein family regulates the intrinsic or mitochondrial apoptotic pathway through an array of interactions between pro-apoptotic (pro-death) and anti-apoptotic (pro-survival) family members. The anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, act as checkpoints in this signaling cascade by binding and sequestering pro-apoptotic proteins thereby protecting cells from apoptosis. Cancer cells frequently over-express Bcl-2 and/or Bcl-xL in order to promote survival or confer resistance to chemotherapy. Inhibition of these anti-apoptotic Bcl-2 family members should specifically target the abnormal cell death pathway found in these cancer cells and offers an attractive approach to antitumor therapy. Using structure based drug design we have discovered small molecule BH-3 mimetics that effectively antagonize the function of anti-apoptotic Bcl-2 family proteins by competing for binding to their hydrophobic surface groove. ABT-263 is an orally bioavailable inhibitor with high affinity (Ki" @default.
- W2231660138 created "2016-06-24" @default.
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- W2231660138 date "2007-05-01" @default.
- W2231660138 modified "2023-09-24" @default.
- W2231660138 title "ABT-263: An orally bioavailable Bcl-2 family protein inhibitor" @default.
- W2231660138 hasPublicationYear "2007" @default.
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