Deregulated inflammatory response plays a pivotal role in the initiation, development and progression of tumours. Potential molecular mechanism(s) that drive the establishment of an inflammatory-tumour microenvironment is not entirely understood owing to the complex cross-talk between pro-inflammatory and tumorigenic mediators such as cytokines, chemokines, oncogenes, enzymes, transcription factors and immune cells. These molecular mediators are critical linchpins between inflammation and cancer, and their activation and/or deactivation are influenced by both extrinsic (i.e. environmental and lifestyle) and intrinsic (i.e. hereditary) factors. At present, the research pertaining to inflammation-associated cancers is accumulating at an exponential rate. Interest stems from hope that new therapeutic strategies against molecular mediators can be identified to assist in cancer treatment and patient management. The present review outlines the various molecular and cellular inflammatory mediators responsible for tumour initiation, progression and development, and discusses the critical role of chronic inflammation in tumorigenesis.

Download full-text PDF

Source
http://dx.doi.org/10.1042/BJ20141337DOI Listing

Publication Analysis

Top Keywords

chronic inflammation
8
inflammation cancer
8
molecular mediators
8
analysis intricate
4
intricate relationship
4
relationship chronic
4
cancer deregulated
4
deregulated inflammatory
4
inflammatory response
4
response plays
4

Similar Publications

Establishment of a Mouse Model with Cough Hypersensitivity via Inhalation of Citric Acid.

J Vis Exp

January 2025

State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University;

Cough is one of the most common symptoms of many respiratory diseases. Chronic cough significantly impacts quality of life and imposes a considerable economic burden. Increased cough sensitivity is a pathophysiological hallmark of chronic cough.

View Article and Find Full Text PDF

Nitric oxide synthase inhibitors reduce the formation of neutrophil extracellular traps and alleviate airway inflammation in the mice model of asthma.

Naunyn Schmiedebergs Arch Pharmacol

January 2025

Department of Pulmonary and Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, 200240, China.

Asthma, a widespread chronic inflammatory disease can contribute to different degrees of lung function damage. The objective of this study is to explore the potential effects of nitric oxide synthase (NOS) inhibitors in asthma using mice model induced by ovalbumin (OVA). BALB/c mice were treated with OVA to establish an asthma model.

View Article and Find Full Text PDF

Objectives: Due to the increasingly faster pace of life and responsibilities, stress has become an integral part of daily life. Every year, numerous social campaigns in the media raise the issue of increasing alcohol consumption. Endometriosis is a chronic, causally incurable, estrogen-dependent and inflammatory gynecological disorder, described as presence of ectopic endometrial tissue outside the uterine cavity.

View Article and Find Full Text PDF

Background: There are little available data about the impact of geriatric nutritional risk index (GNRI) on clinical outcomes following endovascular therapy (EVT) in chronic limb-threatening ischemia (CLTI) regarding the severities of renal dysfunction (RD).

Aims: The aim of this study is to evaluate the impact of GNRI on clinical outcomes following EVT in CLTI regarding the severities of RD.

Methods: We enrolled 705 consecutive CLTI cases treated with EVT between January 2010 and December 2019 at our hospital.

View Article and Find Full Text PDF

Background: Intervertebral disc degeneration (IVDD) is one of the main causes of chronic low back pain. The degenerative process is often initiated by an imbalance between catabolic and anabolic pathways. Despite the large socio-economic impact, the initiation and progress of disc degeneration are poorly understood.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!