Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy
Abstract
Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death mostly by apoptosis is crucially involved in the regulation of tumor formation and also critically determines treatment response. Killing of tumor cells by most anticancer strategies currently used in clinical oncology, for example, chemotherapy, gamma-irradiation, suicide gene therapy or immunotherapy, has been linked to activation of apoptosis signal transduction pathways in cancer cells such as the intrinsic and/or extrinsic pathway. Thus, failure to undergo apoptosis may result in treatment resistance. Understanding the molecular events that regulate apoptosis in response to anticancer chemotherapy, and how cancer cells evade apoptotic death, provides novel opportunities for a more rational approach to develop molecular-targeted therapies for combating cancer.
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Endogenous protein inhibitors of the XIAP-caspase-9 interaction are present in the form of Smac (second mitochondrial-derived caspase activator).
“Endogenous protein inhibitors of the XIAP-caspase-9 interaction are present in the form of Smac (second mitochondrial-derived caspase activator).457”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [457]
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- Authors
- Fulda, S., & Debatin, K.-M.
- Affiliations
- University Hospital Ulm (DE)
- Corresponding author
- Fulda, S
- ORCID
- Venue
- Oncogene
- Published
- 2006-08-07
- Volume
- 25
- Issue
- 34
- Pages
- 4798-4811
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2009183786
- Cited by
- 2,312
- References
- 152
- Citations by year
- 2026: 50 · 2025: 84 · 2024: 78 · 2023: 106 · 2022: 134 · 2021: 134 · 2020: 137 · 2019: 133 · 2018: 157 · 2017: 151 · 2016: 186 · 2015: 170 · 2014: 136 · 2013: 135 · 2012: 140
- FWCI
- 5.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Deutsche Krebshilfe
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- apoptosis, extrinsic apoptotic pathway, mitochondrial apoptosis, cancer chemotherapy, apoptosis signaling, treatment resistance, cancer cell death
- MeSH terms
- Animals, Antineoplastic Agents, Humans, Neoplasms, Signal Transduction, Apoptosis
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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