A Short-Term Study of Chimeric Monoclonal Antibody cA2 to Tumor Necrosis Factor α for Crohn's Disease

Targan, Stephan R.; Hanauer, Stephen B.; Deventer, S. J. H. Van; Mayer, Lloyd; Present, Daniel H.; Braakman, T; DeWoody, Kimberly; Schaible, T.; Rutgeerts, Paul

doi:10.1056/nejm199710093371502

Cited by 3,023 publications

(2,002 citation statements)

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“…Mitochondrial permeability is increased by Bak and Bax (proapoptotic) and maintained by Bcl-2 and Bcl-X L (antiapoptotic). Cytochrome C that has leaked out of the mitochondria forms a complex (the "apoptosome") with Apaf-1 and caspase 9, which is able to activate caspase 3. anti-inflammatory effects of 2 TNF-␣-neutralizing antibodies, infliximab and CDP571, 8,12 observed in a very similar population of patients with active Crohn's disease. Because etanercept has potent anti-inflammatory effects in rheumatoid arthritis, 13,14 the mechanisms of the therapeutic efficacy of TNF-binding molecules in Crohn's disease and rheumatoid arthritis seem to differ.…”

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confidence: 93%

“…Neutralization of tumor necrosis ␣ has potent antiinflammatory and disease-modifying effects in an expanding list of immune-mediated disease, including Crohn's disease, rheumatoid arthritis, psoriasis, and ankylosing spondylitis. [5][6][7][8][9] These results have led to a widespread echoed belief that increased production of TNF-␣, a molecule known to cause inflammation and cell death, is a common pathogenic pathway in immune-mediated diseases, and consequently the development of TNFinhibiting antibodies, proteins, peptides, and small molecules has become a cottage industry.…”

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confidence: 99%

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Transmembrane TNF-α, induction of apoptosis, and the efficacy of TNF-targeting therapies in Crohn's disease

Deventer

2001

Gastroenterology

112

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confidence: 93%

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confidence: 99%

Transmembrane TNF-α, induction of apoptosis, and the efficacy of TNF-targeting therapies in Crohn's disease

Deventer

2001

Gastroenterology

112

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“…3 That these findings were relevant to human autoimmune/inflammatory diseases is evidenced by the high efficacy of anti-TNF antibodies (Infliximab) and recombinant soluble chimeric receptor in treating rheumatoid arthritis (RA) and Crohn's disease. 4,5 More recently, their significance was further highlighted in human infectious disease, when the observation was made that in patients treated with Infliximab, reactivation and a severe course of tuberculosis is strongly over-represented 6 These latter findings indicate an important role for TNF in controlling M. tuberculosis and most probably other intracellular infections in humans.…”

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confidence: 99%

Is there a future for TNF promoter polymorphisms?

2004

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The in vitro study of TNF promoter polymorphism (SNP) function was stimulated by the numerous case-control (association) studies of the polymorphisms in relation to human disease and the appearance of several studies claiming to show a functional role for these SNPs provided a further impetus to researchers interested in the role of TNF in their disease of interest. In this review we consider case-control studies, concentrating on the autoimmune and inflammatory diseases rheumatoid arthritis, multiple sclerosis, ankylosing spondylitis, and asthma, and on infectious diseases including malaria, hepatitis B and C infection, leprosy and sepsis/septic shock. We also review the available evidence on the functional role of the various TNF promoter polymorphisms. In general, case-control studies have produced mixed results, with little consensus in most cases on whether any TNF polymorphisms are actually associated with disease, although results have been more consistent in the case of infectious diseases, particularly malaria. Functional studies have also produced mixed results but recent work suggests that the much studied À308G/A polymorphism is not functional, while the function of other TNF polymorphisms remains controversial. Studies of the TNF region are increasingly using extended haplotypes that can better capture the variation of the MHC region.

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“…A TNFα overproduction is involved in numerous chronic inflammatory diseases, such as rheumatoid arthritis [31] chronic hepatitis C [32], or Crohn's disease [33]. An increase in the TNFα level was described in diabetic patients to cause retinopathies [34], while during pancreatitis, the release of TNFα leads to inflammation and cellular damage [35].…”

Section: Tnfα α α α and Inflammationmentioning

confidence: 99%

Linking anemia to inflammation and cancer: The crucial role of TNFα

Buck

Morceau

Grigorakaki

et al. 2009

Biochemical Pharmacology

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Erythropoiesis is considered as a multistep and tightly regulated process under the control of a series of cytokines including erythropoietin (Epo). Epo activates specific signaling pathways and leads to activation of key transcription factors such as GATA-1, in order to ensure erythroid differentiation. Deregulation leads to a decreased number of red blood cells, a hemoglobin deficiency, thus a limited oxygen-carrying capacity in the blood. Anemia represents a frequent complication in various diseases such as cancer or inflammatory diseases. It reduces both quality of life and prognosis in patients. Tumor necrosis factor alpha (TNFα) was described to be involved in the pathogenesis of inflammation and cancer related anemia. Blood transfusions and erythroid stimulating agents (ESAs) including human recombinant Epo (rhuEpo) are currently used as efficient treatments. Moreover, the recently described conflicting effects of ESAs in distinct studies require further investigations on the molecular mechanisms involved in TNFα-caused anemia. The present study aims to evaluate the current knowledge and the importance of the effect of the proinflammatory cytokine TNFα on erythropoiesis in inflammatory and malignant conditions.

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A Short-Term Study of Chimeric Monoclonal Antibody cA2 to Tumor Necrosis Factor α for Crohn's Disease

Abstract: A short-term study of chimeric monoclonal antibody cA2 to tumor necrosis factor alfa for Crohn's disease Targan, S.R.; Hannauer, S.B.; van Deventer, S.J.H.; Mayer, L.; Present, D.H.; Braakman, T.; DeWoody, K.L.; Schaible, Th.F.; Rutgeerts, P.J.

Cited by 3,023 publications

References 33 publications

Transmembrane TNF-α, induction of apoptosis, and the efficacy of TNF-targeting therapies in Crohn's disease

Transmembrane TNF-α, induction of apoptosis, and the efficacy of TNF-targeting therapies in Crohn's disease

Is there a future for TNF promoter polymorphisms?

Linking anemia to inflammation and cancer: The crucial role of TNFα

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