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

TLDR
In this article, the authors dissect literature from the patient perspective, the tumor biology perspective, therapy-induced metastasis, and cell data generated in the laboratory to discover and investigate more targeted therapy with more efficacy.
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.

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Linking the future of anticancer metal-complexes to the therapy of tumour metastases

TL;DR: The capacity of NAMI-A to modulate the relationship established between metastatic cells and their microenvironment suggests that metal-based drugs shall be viewed as an opportunity for the treatment of tumour metastases.
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Curcumin as an anti-inflammatory agent: Implications to radiotherapy and chemotherapy.

TL;DR: Evidence from clinical trials suggesting the potential utility of curcumin for acute inflammatory reactions during radiotherapy such as dermatitis and mucositis and low toxicity ofCurcumin is linked to its cytoprotective effects in normal tissues makes it a potential candidate for use as an adjuvant in cancer therapy.
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Off to the organelles - killing cancer cells with targeted gold nanoparticles.

TL;DR: This review summarizes the impact of AuNPs on selected subcellular organelles that are relevant to cancer therapy and focuses on the nucleus, its subcompartments, and mitochondria, because they are intimately linked to cancer cell survival, growth, proliferation and death.
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Chemoresistance and the Self-Maintaining Tumor Microenvironment.

TL;DR: This review discusses how the properties of the tumor microenvironment promote chemoresistance in cancer cells, and the interplay between these external stimuli, and how a chemoresistant phenotype emerges from the complex signaling network present.
References
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5-Fluorouracil: mechanisms of action and clinical strategies

TL;DR: This work has shown that novel genes identified in DNA microarray profiling have the potential to identify novel genes that are involved in mediating resistance to 5-FU, and these genes might prove to be therapeutically valuable as new targets for chemotherapy, or as predictive biomarkers of response to5-FU-based chemotherapy.
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STATs in cancer inflammation and immunity: a leading role for STAT3

TL;DR: Signal transducer and activator of transcription proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer, and STAT3 is a promising target to redirect inflammation for cancer therapy.
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Promotion of microtubule assembly in vitro by taxol

TL;DR: It is reported here that taxol acts as a promoter of calf brain microtubule assembly in vitro, in contrast to plant products such as colchicine and podophyllotoxin, which inhibit assembly.
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TLR4 links innate immunity and fatty acid–induced insulin resistance

TL;DR: It is suggested that TLR4 is a molecular link among nutrition, lipids, and inflammation and that the innate immune system participates in the regulation of energy balance and insulin resistance in response to changes in the nutritional environment.
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Risk factors for doxorubicin-induced congestive heart failure.

TL;DR: There was a continuum of increasing risk as the cumulative amount of administered drug increased, and a weekly dose schedule of doxorubicin was associated with a significantly lower incidence of congestive heart failure than was the usually employed every 3-week schedule.
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Trending Questions (1)
Does chemotherapy-enhanced inflammation lead to the failure of therapy and metastasis?

Yes, chemotherapy-enhanced inflammation may lead to the failure of therapy and metastasis.