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Historical perspectives on tumor necrosis factor and its superfamily: 25 years later, a golden journey
Open accessAbstract
Although activity that induced tumor regression was observed and termed tumor necrosis factor (TNF) as early as the 1960s, the true identity of TNF was not clear until 1984, when Aggarwal and coworkers reported, for the first time, the isolation of 2 cytotoxic factors: one, derived from macrophages (molecular mass 17 kDa), was named TNF, and the second, derived from lymphocytes (20 kDa), was named lymphotoxin. Because the 2 cytotoxic factors exhibited 50% amino acid sequence homology and bound to the same receptor, they came to be called TNF-α and TNF-β. Identification of the protein sequences led to cloning of their cDNA. Based on sequence homology to TNF-α, now a total of 19 members of the TNF superfamily have been identified, along with 29 interacting receptors, and several molecules that interact with the cytoplasmic domain of these receptors. The roles of the TNF superfamily in inflammation, apoptosis, proliferation, invasion, angiogenesis, metastasis, and morphogenesis have been documented. Their roles in immunologic, cardiovascular, neurologic, pulmonary, and metabolic diseases are becoming apparent. TNF superfamily members are active targets for drug development, as indicated by the recent approval and expanding market of TNF blockers used to treat rheumatoid arthritis, psoriasis, Crohns disease, and osteoporosis, with a total market of more than US $20 billion. As we learn more about this family, more therapeutics will probably emerge. In this review, we summarize the initial discovery of TNF-α, and the insights gained regarding the roles of this molecule and its related family members in normal physiology and disease.
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“death receptors, whose activation depends on the binding of the cognate ligand(s)”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [269]
In the citing paper
“Extrinsic apoptosis is mostly driven by either of two types of plasma membrane receptors: (1) death receptors, whose activation depends on the binding of the cognate ligand(s), and (2) dependence receptors, whose activation occurs when the levels of their specific ligand drop below a specific threshold [267 269–271].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [269]
In the citing paper
“dependence receptors, whose activation occurs when the levels of their specific ligand drop below a specific threshold [267 269–271].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [269]
In the citing paper
“Death receptors include (but are not limited to): Fas cell surface death receptor (FAS; also known as CD95 or APO-1), and TNF receptor superfamily member 1A (TNFRSF1A; best known as TNFR1), 10a (TNFRSF10A; best known as TRAILR1 or DR4), and 10b (TNFRSF10B; best known as TRAILR2 or DR5) [269, 270, 272, 273].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [269]
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Metadata
- Authors
- Aggarwal, B. B., Gupta, S. C., & Kim, J. H.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2012-01-19
- Volume
- 119
- Issue
- 3
- Pages
- 651-665
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC3265196
- OpenAlex
- W1989219560
- Cited by
- 877
- References
- 144
- Citations by year
- 2026: 35 · 2025: 76 · 2024: 72 · 2023: 82 · 2022: 57 · 2021: 74 · 2020: 76 · 2019: 62 · 2018: 45 · 2017: 59 · 2016: 62 · 2015: 70 · 2014: 49 · 2013: 41 · 2012: 13
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (CA-16 672, 16672, CA-124787-01A2)
- Genentech
- University of California, San Francisco
- National Cancer Institute (CA-16672, P01CA124787, CA-124787-01A2, P30CA016672)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- TNF-α, TNF superfamily, lymphotoxin, TNF receptor, TNF-alpha inhibitors, apoptosis, inflammation, angiogenesis, metastasis, drug development, rheumatoid arthritis, psoriasis, Crohn's disease, osteoporosis
- MeSH terms
- Humans, Neoplasms, Tumor Necrosis Factor-alpha, History, 20th Century, History, 21st Century
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