Abstract
Programmed cell death (also known as apoptosis) plays an essential role in tissue homeostasis, where it ensures that new cell production in the body is offset by a commensurate rate of cell loss. Defects in the genetic pathway that regulate the cell death process can figure prominently in the origins of cancer and also in problems with cancer treatment. Eventually, it may be possible to develop novel treatments for cancer that specifically seek to modulate the physiologic cell death pathway as opposed to nearly all currently available drugs, which are intended to interfere with some aspect of the cell division cycle.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology*
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Antineoplastic Agents / therapeutic use
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Apoptosis / genetics
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Apoptosis / physiology*
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Drug Resistance / physiology*
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Forecasting
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Gene Expression Regulation, Neoplastic*
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Humans
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Leukemia / genetics
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Leukemia / pathology
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Lymphoma, Non-Hodgkin / genetics
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Lymphoma, Non-Hodgkin / pathology
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Mice
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Mice, Knockout
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics
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Neoplasm Proteins / physiology*
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Neoplasms / drug therapy*
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Neoplasms / metabolism
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Neoplasms / pathology
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Protein Binding
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Proto-Oncogene Proteins / biosynthesis
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / physiology*
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Proto-Oncogene Proteins c-bcl-2
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Radiation Tolerance / physiology
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Recombinant Fusion Proteins / biosynthesis
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Recombinant Fusion Proteins / genetics
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Structure-Activity Relationship
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Translocation, Genetic
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Treatment Outcome
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Tumor Suppressor Protein p53 / biosynthesis
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / physiology
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bcl-2-Associated X Protein
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bcl-X Protein
Substances
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Antineoplastic Agents
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BCL2L1 protein, human
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Bcl2l1 protein, mouse
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Neoplasm Proteins
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Recombinant Fusion Proteins
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Tumor Suppressor Protein p53
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bcl-2-Associated X Protein
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bcl-X Protein