Chapter

Programmed Cell Death in Cancer Progression and Therapy

Volume 615 of the series Advances in Experimental Medicine and Biology pp 47-79

Apoptotic Pathways in Tumor Progression and Therapy

  • Armelle MeletAffiliated withDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center
  • , Keli SongAffiliated withDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center
  • , Octavian BucurAffiliated withDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center
  • , Zainab JaganiAffiliated withDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center
  • , Alexandra R. GrassianAffiliated withDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center
  • , Roya Khosravi-FarAffiliated withDepartment of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center

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Apoptosis is a cell suicide program that plays a critical role in development and tissue homeostasis. The ability of cancer cells to evade this programmed cell death (PCD) is a major characteristic that enables their uncontrolled growth. The efficiency of chemotherapy in killing such cells depends on the successful induction of apoptosis, since defects in apoptosis signaling are a major cause of drug resistance. Over the past decades, much progress has been made in our understanding of apoptotic signaling pathways and their dysregulation in cancer progression and therapy. These advances have provided new molecular targets for proapoptotic cancer therapies that have recently been used in drug development. While most of those therapies are still at the preclinical stage, some of them have shown much promise in the clinic. Here, we review our current knowledge of apoptosis regulation in cancer progression and therapy, as well as the new molecular targeted molecules that are being developed to reinstate cancer cell death.

Keywords

apoptosis cancer therapy inhibitors signal transduction oncogene intrinsic extrinsic