Abstract
Resistance of tumor cells to treatment often accounts for the failure of traditional forms of anti-cancer therapy. It is well known that tumors from the same histological group and stage of development are highly heterogeneous in their sensitivity to therapy. Among the factors that can influence tumor sensitivity are DNA repair capacity, distribution of cells throughout the cell cycle, proliferation potential, etc. In many cases, anti-cancer therapy eliminates tumor cells via apoptosis, an active form of cell death characterized by cell shrinkage and the removal of cells in a neat, orderly fashion. However, this process is not always efficient. In the present review, the precise role that apoptosis plays in the response of lung carcinomas to chemotherapy and radiation treatment is discussed.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use
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Apoptosis*
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Carcinoma / metabolism
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Carcinoma / pathology
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Carcinoma / physiopathology
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Carcinoma / therapy*
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Caspases / genetics
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Caspases / metabolism
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Humans
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Inhibitor of Apoptosis Proteins
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Lung Neoplasms / metabolism
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Lung Neoplasms / pathology
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Lung Neoplasms / physiopathology
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Lung Neoplasms / therapy*
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Microtubule-Associated Proteins*
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Neoplasm Proteins
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Proteins / genetics
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Proteins / metabolism
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Retinoblastoma Protein / genetics
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Retinoblastoma Protein / metabolism
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Signal Transduction / physiology
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Survivin
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
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fas Receptor / genetics
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fas Receptor / metabolism
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ras Proteins / genetics
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ras Proteins / metabolism
Substances
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Antineoplastic Agents
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BIRC5 protein, human
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Inhibitor of Apoptosis Proteins
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Microtubule-Associated Proteins
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Neoplasm Proteins
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Proteins
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Proto-Oncogene Proteins c-bcl-2
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Retinoblastoma Protein
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Survivin
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Tumor Suppressor Protein p53
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fas Receptor
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Caspases
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ras Proteins