Targeting the inflammatory pathways to enhance chemotherapy of cancer

Cancer Biol Ther. 2011 Jul 15;12(2):95-105. doi: 10.4161/cbt.12.2.15952. Epub 2011 Jul 15.

Abstract

Epidemiological and experimental evidence has emerged that a dysregulated inflammation is associated with most of the tumors. Recent studies have begun to unravel molecular pathways linking inflammation and cancer. The identification of transcription factors such as NF-kappaB, STAT3, HIF-1 alpha and their gene products such as COX-2, cytokines, chemokines and chemokine receptors have laid molecular foundation for the decisive role of inflammation in carcinogenesis. Inflammation contributes to survival and proliferation of malignant cells, tumor angiogenesis, metastasis and reduced response to chemotherapy. In view of their involvement at different stages of tumor development, inflammatory pathways represent attractive targets for cancer prevention and therapy. However, advances in this field have not been fully realized, and challenge remains to obtain clinical data from patients and then to utilize this information for optimal and personalized therapy. We present evidence that targeting inflammatory pathways have a potential role to improve chemotherapy of cancer.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Cell Transformation, Neoplastic / genetics*
  • Chemokines / metabolism
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Cytokines / metabolism
  • Humans
  • Inflammation / genetics*
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Neoplasms / drug therapy*
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism
  • Transcription Factors / antagonists & inhibitors*
  • Transcription Factors / metabolism

Substances

  • Antineoplastic Agents
  • Chemokines
  • Cytokines
  • NF-kappa B
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Transcription Factors
  • Cyclooxygenase 2
  • PTGS2 protein, human