open access

Cytokines Regulation and Role in Modulating Cancer Related Pain

A Brief Overview

  • Anbreen Faisal Department of Biochemistry and Biotechnology, Institute of life Sciences, University of Gujrat, Pakistan
  • Muhammad Asad Ullah Department of Biotechnology, Quaid-i-Azam University 45320, Islamabad, Pakistan
  • Ayesha Bajwa Department of Biochemistry and Biotechnology, Institute of life Sciences, University of Gujrat, Pakistan
  • Rizwan Nasir Department of Biochemistry and Biotechnology, Institute of life Sciences, University of Gujrat, Pakistan
  • Muhammad Javed Iqbal Department of Biotechnology, University of Gujrat, Sialkot Sub Campus, Pakistan
  • Muzamil Shah Department of Biotechnology, Quaid-i-Azam University 45320, Islamabad, Pakistan
  • Wali Muhammad Department of Biotechnology, Quaid-i-Azam University 45320, Islamabad, Pakistan

Abstract

Cancer linked mechanism of inflammatory and neuropathic pain came out as complex pathologic process and a formidable clinical impasse. Over the decades significant headway has been made to unravel etiology of cancer pain and prime pathological maneuver tie with its microenvironment by models incited approaches. The cross talk between the cancer cell and their dynamic interaction decipher some of the cancer-induced inflammatory mediators which act in primary efferent neurons in absolute diversified way. Cytokines are the key inflammatory mediator in the microenvironment parole by cancerous cell and immune system cells that exert malicious autocrine and paracrine activity particular relevance to pain. To date very few strategies have been contemplated to modulate the release of cytokines that seems allied to cancer pain. In this scenario, the present review analyzes the main cytokines produced with peripheral and central mechanism analysis for better understanding their clinical traits. While treatment strategies are detailed with novel mechanistic insights that can have considerably cut down the pattern of neuropathic pain linked with tumorigenic estate.