We are analyzing https://link.springer.com/article/10.1007/s00262-003-0474-8.

Title:
Apoptosis pathways in cancer and cancer therapy | Cancer Immunology, Immunotherapy
Description:
Activation of apoptosis pathways is a key mechanism by which cytotoxic drugs kill tumor cells. Also immunotherapy of tumors requires an apoptosis sensitive phenotype of target cells. Defects in apoptosis signalling contribute to resistance of tumors. Activation of apoptosis signalling following treatment with cytotoxic drugs has been shown to lead to activation of the mitochondrial (intrinsic) pathway of apoptosis. In addition, signalling through the death receptor (extrinsic) pathways, contributes to sensitivity of tumor cells towards cytotoxic treatment. Both pathways converge finally at the level of activation of caspases, the effector molecules in most forms of cell death. In addition to classical apoptosis, non-apoptotic modes of cell death have recently been identified. Mechanisms to overcome apoptosis resistance include direct targeting of antiapoptotic molecules expressed in tumors as well as re-sensitization of previously resistant tumor cells by re-expression of caspases and counteracting apoptotis inhibitory molecules such as Bcl-2 and molecules of the IAP family of endogenous caspase inhibitors. Molecular insights into regulation of apoptosis and defects in apoptosis signalling in tumor cells will provide novel approaches to define sensitivity or resistance of tumor cells towards antitumor therapy and provide new targets for rational therapeutic interventions for future therapeutic strategies.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

google, scholar, pubmed, cas, apoptosis, article, cell, cancer, debatin, death, cells, activation, caspase, res, fulda, pathways, resistance, drugs, caspases, leukemia, signaling, apofas, expression, tumor, signalling, mitochondrial, herr, krammer, therapy, cytotoxic, system, blood, anticancer, druginduced, nat, dna, oncogene, mol, biol, receptor, molecules, natl, exp, nature, differ, friesen, reed, kroemer, med, angel,

Topics {✒️}

klaus-michael debatin month download article/chapter transcription factor nf-kb apoptosis signalling contribute γ-irradiation-induced apoptosis cellular stress response anticancer drug-induced apoptosis rational therapeutic interventions future therapeutic strategies cancer therapy resistance translational view iap family proteins-suppressors article cancer immunology fas/fas ligand interactions activation-induced cell death apoptosis-inducing factor apoptosis signalling jnk/sapk activity contributes bak-mediated mitochondrial apoptosis full article pdf immunotherapy summer school low bax-alpha expression etoposide-induced apoptosis cytotoxic anticancer drugs privacy choices/manage cookies drug-induced apoptosis drug resistance updates human ovarian cancer ifn γ sensitizes negative prognostic factor multidrug resistance phenotype author correspondence independent mechanisms stress-induced apoptosis receptor/ligand system stat-1-independent upregulation involves activation malignant breast tissue doxorubicin-induced apoptosis endogenous caspase inhibitors colon carcinoma cells hepatocellular carcinoma cells jnk/sapk activity solid tumor cells tumor cells correlates cancer cells treated chemotherapy-induced apoptosis anti-apoptosis gene kaufmann sh apoptosis sensitive phenotype

Questions {❓}

Borner C, Monney L (1999) Apoptosis without caspases: an inefficient molecular guillotine?
Finkel E (1999) Does cancer therapy trigger cell suicide?

Schema {🗺️}

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