A review of canakinumab and its therapeutic potential for non-small cell lung cancer

Kara M. Schenk, Joshua E. Reuss, Karin Choquette, Alexander Spira

Research output: Contribution to journalArticle

Abstract

Inflammation is essential for our innate and adaptive immunity, but chronic inflammation can also be detrimental, playing a role in tumor development and subversion of host immunity. A multitude of proteins and cytokines are involved in chronic inflammation; interleukin-1β, in particular, has been recognized as a critical pro-inflammatory cytokine that can trigger a cascade of inflammatory mediators, promoting angiogenesis, tumor invasiveness, and metastasis. The inhibition of interleukin-1β with the antibody canakinumab was recently highlighted in a large-scale trial studying the effects of the inflammatory modulating antibody in heart disease. In this study, a marked decrease in the incidence of lung cancer (a 67% relative risk reduction) was observed in a high-risk population. Although a number of preclinical studies have demonstrated that canakinumab inhibits interleukin-1β and reduces inflammation, the question remains whether these actions positively affect both cancer incidence and recurrence. This review will summarize the role of inflammation in cancer propagation and development, discuss the biological rationale for targeting interleukin-1β in lung cancer, advocate for further investigation of the anti-inflammatory antibody canakinumab as a new attractive mechanism for future lung cancer therapy, and discuss future and ongoing trials.

Original languageEnglish (US)
Pages (from-to)879-885
Number of pages7
JournalAnti-cancer drugs
Volume30
Issue number9
DOIs
StatePublished - Oct 1 2019

Fingerprint

Non-Small Cell Lung Carcinoma
Interleukin-1
Inflammation
Lung Neoplasms
Neoplasms
Cytokines
Therapeutics
Antibodies
Incidence
Adaptive Immunity
Risk Reduction Behavior
Innate Immunity
Anti-Idiotypic Antibodies
Immunity
Heart Diseases
Anti-Inflammatory Agents
canakinumab
Neoplasm Metastasis
Recurrence
Population

ASJC Scopus subject areas

  • Oncology
  • Pharmacology
  • Pharmacology (medical)
  • Cancer Research

Cite this

A review of canakinumab and its therapeutic potential for non-small cell lung cancer. / Schenk, Kara M.; Reuss, Joshua E.; Choquette, Karin; Spira, Alexander.

In: Anti-cancer drugs, Vol. 30, No. 9, 01.10.2019, p. 879-885.

Research output: Contribution to journalArticle

Schenk, Kara M. ; Reuss, Joshua E. ; Choquette, Karin ; Spira, Alexander. / A review of canakinumab and its therapeutic potential for non-small cell lung cancer. In: Anti-cancer drugs. 2019 ; Vol. 30, No. 9. pp. 879-885.
@article{9609772d8d114096bdf308e60be98bdf,
title = "A review of canakinumab and its therapeutic potential for non-small cell lung cancer",
abstract = "Inflammation is essential for our innate and adaptive immunity, but chronic inflammation can also be detrimental, playing a role in tumor development and subversion of host immunity. A multitude of proteins and cytokines are involved in chronic inflammation; interleukin-1β, in particular, has been recognized as a critical pro-inflammatory cytokine that can trigger a cascade of inflammatory mediators, promoting angiogenesis, tumor invasiveness, and metastasis. The inhibition of interleukin-1β with the antibody canakinumab was recently highlighted in a large-scale trial studying the effects of the inflammatory modulating antibody in heart disease. In this study, a marked decrease in the incidence of lung cancer (a 67{\%} relative risk reduction) was observed in a high-risk population. Although a number of preclinical studies have demonstrated that canakinumab inhibits interleukin-1β and reduces inflammation, the question remains whether these actions positively affect both cancer incidence and recurrence. This review will summarize the role of inflammation in cancer propagation and development, discuss the biological rationale for targeting interleukin-1β in lung cancer, advocate for further investigation of the anti-inflammatory antibody canakinumab as a new attractive mechanism for future lung cancer therapy, and discuss future and ongoing trials.",
author = "Schenk, {Kara M.} and Reuss, {Joshua E.} and Karin Choquette and Alexander Spira",
year = "2019",
month = "10",
day = "1",
doi = "10.1097/CAD.0000000000000832",
language = "English (US)",
volume = "30",
pages = "879--885",
journal = "Anti-Cancer Drugs",
issn = "0959-4973",
publisher = "Lippincott Williams and Wilkins",
number = "9",

}

TY - JOUR

T1 - A review of canakinumab and its therapeutic potential for non-small cell lung cancer

AU - Schenk, Kara M.

AU - Reuss, Joshua E.

AU - Choquette, Karin

AU - Spira, Alexander

PY - 2019/10/1

Y1 - 2019/10/1

N2 - Inflammation is essential for our innate and adaptive immunity, but chronic inflammation can also be detrimental, playing a role in tumor development and subversion of host immunity. A multitude of proteins and cytokines are involved in chronic inflammation; interleukin-1β, in particular, has been recognized as a critical pro-inflammatory cytokine that can trigger a cascade of inflammatory mediators, promoting angiogenesis, tumor invasiveness, and metastasis. The inhibition of interleukin-1β with the antibody canakinumab was recently highlighted in a large-scale trial studying the effects of the inflammatory modulating antibody in heart disease. In this study, a marked decrease in the incidence of lung cancer (a 67% relative risk reduction) was observed in a high-risk population. Although a number of preclinical studies have demonstrated that canakinumab inhibits interleukin-1β and reduces inflammation, the question remains whether these actions positively affect both cancer incidence and recurrence. This review will summarize the role of inflammation in cancer propagation and development, discuss the biological rationale for targeting interleukin-1β in lung cancer, advocate for further investigation of the anti-inflammatory antibody canakinumab as a new attractive mechanism for future lung cancer therapy, and discuss future and ongoing trials.

AB - Inflammation is essential for our innate and adaptive immunity, but chronic inflammation can also be detrimental, playing a role in tumor development and subversion of host immunity. A multitude of proteins and cytokines are involved in chronic inflammation; interleukin-1β, in particular, has been recognized as a critical pro-inflammatory cytokine that can trigger a cascade of inflammatory mediators, promoting angiogenesis, tumor invasiveness, and metastasis. The inhibition of interleukin-1β with the antibody canakinumab was recently highlighted in a large-scale trial studying the effects of the inflammatory modulating antibody in heart disease. In this study, a marked decrease in the incidence of lung cancer (a 67% relative risk reduction) was observed in a high-risk population. Although a number of preclinical studies have demonstrated that canakinumab inhibits interleukin-1β and reduces inflammation, the question remains whether these actions positively affect both cancer incidence and recurrence. This review will summarize the role of inflammation in cancer propagation and development, discuss the biological rationale for targeting interleukin-1β in lung cancer, advocate for further investigation of the anti-inflammatory antibody canakinumab as a new attractive mechanism for future lung cancer therapy, and discuss future and ongoing trials.

UR - http://www.scopus.com/inward/record.url?scp=85072151690&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85072151690&partnerID=8YFLogxK

U2 - 10.1097/CAD.0000000000000832

DO - 10.1097/CAD.0000000000000832

M3 - Article

VL - 30

SP - 879

EP - 885

JO - Anti-Cancer Drugs

JF - Anti-Cancer Drugs

SN - 0959-4973

IS - 9

ER -