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Chemotherapy-enhanced inflammation may lead to the failure of therapy and metastasis.

Vyas D, Laput G, Vyas AK - Onco Targets Ther (2014)

Bottom Line: The lack of therapy and the failure of existing therapy has been a challenge for clinicians in treating various cancers.Doxorubicin, 5-fluorouracil, cisplatin, and paclitaxel are the first-line therapy in various cancers; however, toxicity, resistance, and treatment failure limit their clinical use.In this article, we dissect literature from the patient perspective, the tumor biology perspective, therapy-induced metastasis, and cell data generated in the laboratory.

View Article: PubMed Central - PubMed

Affiliation: College of Human Medicine, Michigan State University, East Lansing, MI, USA.

ABSTRACT
The lack of therapy and the failure of existing therapy has been a challenge for clinicians in treating various cancers. Doxorubicin, 5-fluorouracil, cisplatin, and paclitaxel are the first-line therapy in various cancers; however, toxicity, resistance, and treatment failure limit their clinical use. Their status leads us to discover and investigate more targeted therapy with more efficacy. In this article, we dissect literature from the patient perspective, the tumor biology perspective, therapy-induced metastasis, and cell data generated in the laboratory.

No MeSH data available.


Related in: MedlinePlus

Cisplatin-induced inflammation is mediated through multiple effectors including activation of NFkB, TNF-α, and PARP. NFkB is a focal point for downstream cell survival and proliferation signaling that involves IL-6 and IL-8 upregulation. Cisplatin also induces the MAPK/ERK pathway and EMT acquisition. The ERK signaling cascade is suggested as an upstream signal for TNF-α activation.Abbreviations: ADP-ribose, poly; COX-2, cyclooxygenase; EMT, epithelial–mesenchymal transition; ERK, mitogen-activated protein kinase; HGF, hepatocyte growth factor; HIF-α, hypoxia-inducible factor; ICAM-1, intercellular adhesion molecule; IL, interleukin; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; NFκB, nuclear factor kappa B; PARP, polymerase; STAT-3, signal transducer and activator of transcription; TNF-α, tumor necrosis factor alpha; VCAM-1, vascular cell adhesion molecule; VEGF, vascular endothelial growth factor.
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f1-ott-7-1015: Cisplatin-induced inflammation is mediated through multiple effectors including activation of NFkB, TNF-α, and PARP. NFkB is a focal point for downstream cell survival and proliferation signaling that involves IL-6 and IL-8 upregulation. Cisplatin also induces the MAPK/ERK pathway and EMT acquisition. The ERK signaling cascade is suggested as an upstream signal for TNF-α activation.Abbreviations: ADP-ribose, poly; COX-2, cyclooxygenase; EMT, epithelial–mesenchymal transition; ERK, mitogen-activated protein kinase; HGF, hepatocyte growth factor; HIF-α, hypoxia-inducible factor; ICAM-1, intercellular adhesion molecule; IL, interleukin; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; NFκB, nuclear factor kappa B; PARP, polymerase; STAT-3, signal transducer and activator of transcription; TNF-α, tumor necrosis factor alpha; VCAM-1, vascular cell adhesion molecule; VEGF, vascular endothelial growth factor.

Mentions: (Figure 1). Although there is evidence of the association between inflammation and metastasis as a result of cisplatin treatment,37 the underlying mechanism remains to be elucidated. Several reports suggest that ERK is an upstream signal for the expression of TNF-α, prostaglandin, interleukin, and COX-2. Inhibition of ERK pathway reduces gene expression of TNF-α in mouse kidney tissue.38 In sertoli cells, an ERK inhibitor reduced the cisplatin induction of prostaglandin, interleukin, and COX-2.39


Chemotherapy-enhanced inflammation may lead to the failure of therapy and metastasis.

Vyas D, Laput G, Vyas AK - Onco Targets Ther (2014)

Cisplatin-induced inflammation is mediated through multiple effectors including activation of NFkB, TNF-α, and PARP. NFkB is a focal point for downstream cell survival and proliferation signaling that involves IL-6 and IL-8 upregulation. Cisplatin also induces the MAPK/ERK pathway and EMT acquisition. The ERK signaling cascade is suggested as an upstream signal for TNF-α activation.Abbreviations: ADP-ribose, poly; COX-2, cyclooxygenase; EMT, epithelial–mesenchymal transition; ERK, mitogen-activated protein kinase; HGF, hepatocyte growth factor; HIF-α, hypoxia-inducible factor; ICAM-1, intercellular adhesion molecule; IL, interleukin; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; NFκB, nuclear factor kappa B; PARP, polymerase; STAT-3, signal transducer and activator of transcription; TNF-α, tumor necrosis factor alpha; VCAM-1, vascular cell adhesion molecule; VEGF, vascular endothelial growth factor.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061164&req=5

f1-ott-7-1015: Cisplatin-induced inflammation is mediated through multiple effectors including activation of NFkB, TNF-α, and PARP. NFkB is a focal point for downstream cell survival and proliferation signaling that involves IL-6 and IL-8 upregulation. Cisplatin also induces the MAPK/ERK pathway and EMT acquisition. The ERK signaling cascade is suggested as an upstream signal for TNF-α activation.Abbreviations: ADP-ribose, poly; COX-2, cyclooxygenase; EMT, epithelial–mesenchymal transition; ERK, mitogen-activated protein kinase; HGF, hepatocyte growth factor; HIF-α, hypoxia-inducible factor; ICAM-1, intercellular adhesion molecule; IL, interleukin; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; NFκB, nuclear factor kappa B; PARP, polymerase; STAT-3, signal transducer and activator of transcription; TNF-α, tumor necrosis factor alpha; VCAM-1, vascular cell adhesion molecule; VEGF, vascular endothelial growth factor.
Mentions: (Figure 1). Although there is evidence of the association between inflammation and metastasis as a result of cisplatin treatment,37 the underlying mechanism remains to be elucidated. Several reports suggest that ERK is an upstream signal for the expression of TNF-α, prostaglandin, interleukin, and COX-2. Inhibition of ERK pathway reduces gene expression of TNF-α in mouse kidney tissue.38 In sertoli cells, an ERK inhibitor reduced the cisplatin induction of prostaglandin, interleukin, and COX-2.39

Bottom Line: The lack of therapy and the failure of existing therapy has been a challenge for clinicians in treating various cancers.Doxorubicin, 5-fluorouracil, cisplatin, and paclitaxel are the first-line therapy in various cancers; however, toxicity, resistance, and treatment failure limit their clinical use.In this article, we dissect literature from the patient perspective, the tumor biology perspective, therapy-induced metastasis, and cell data generated in the laboratory.

View Article: PubMed Central - PubMed

Affiliation: College of Human Medicine, Michigan State University, East Lansing, MI, USA.

ABSTRACT
The lack of therapy and the failure of existing therapy has been a challenge for clinicians in treating various cancers. Doxorubicin, 5-fluorouracil, cisplatin, and paclitaxel are the first-line therapy in various cancers; however, toxicity, resistance, and treatment failure limit their clinical use. Their status leads us to discover and investigate more targeted therapy with more efficacy. In this article, we dissect literature from the patient perspective, the tumor biology perspective, therapy-induced metastasis, and cell data generated in the laboratory.

No MeSH data available.


Related in: MedlinePlus