Genetic Polymorphism of Interleukin-1A (IL-1A), IL-1B, and IL-1 Receptor Antagonist (IL-1RN) and Prostate Cancer Risk

Xu, Hua; Ding, Qiang; Jiang, Haowen

doi:10.7314/apjcp.2014.15.20.8741

Cited by 30 publications

(10 citation statements)

References 41 publications

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“…This included infectious diseases such as tuberculosis [44], neurodegenerative diseases such as Alzheimer’s disease [45], autoimmune and autoinflammatory diseases such as psoriasis [46] and diabetes type 2 [47], and the occurrence of tumors such as prostate cancer [48]. …”

Section: Production Of Il-1β Requires Two Distinct Signalsmentioning

confidence: 99%

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Bent

Moll

Grabbe

et al. 2018

IJMS

300

221

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Interleukin-1 beta (IL-1β) is induced by inflammatory signals in a broad number of immune cell types. IL-1β (and IL-18) are the only cytokines which are processed by caspase-1 after inflammasome-mediated activation. This review aims to summarize current knowledge about parameters of regulation of IL-1β expression and its multi-facetted role in pathophysiological conditions. IL-1 signaling activates innate immune cells including antigen presenting cells, and drives polarization of CD4+ T cells towards T helper type (Th) 1 and Th17 cells. Therefore, IL-1β has been attributed a largely beneficial role in resolving acute inflammations, and by initiating adaptive anti-tumor responses. However, IL-1β generated in the course of chronic inflammation supports tumor development. Furthermore, IL-1β generated within the tumor microenvironment predominantly by tumor-infiltrating macrophages promotes tumor growth and metastasis via different mechanisms. These include the expression of IL-1 targets which promote neoangiogenesis and of soluble mediators in cancer-associated fibroblasts that evoke antiapoptotic signaling in tumor cells. Moreover, IL-1 promotes the propagation of myeloid-derived suppressor cells. Using genetic mouse models as well as agents for pharmacological inhibition of IL-1 signaling therapeutically applied for treatment of IL-1 associated autoimmune diseases indicate that IL-1β is a driver of tumor induction and development.

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Section: Production Of Il-1β Requires Two Distinct Signalsmentioning

confidence: 99%

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Bent

Moll

Grabbe

et al. 2018

IJMS

300

221

View full text Add to dashboard Cite

show abstract

“…Lastly, intrinsic mutations and polymorphisms in IL-1 genes have been implicated as well in many cancer types as reviewed by Khazim et al [ 79 ], though results from studies are sometimes conflicting, and the association is not always clear. Single and IL-1 gene-cluster polymorphisms have been suggested to be associated with cancers such as cervical [ 80 ] and ovarian cancer [ 81 ], MM [ 82 ], esophageal [ 83 ], colorectal cancer (CRC) [ 84 ], NSCLC [ 85 ], pancreatic cancer [ 86 ], prostate cancer [ 87 ], and gastric cancer [ 88 – 90 ].…”

Section: Il-1 Dysregulation and Its Contribution To Cancer And Tumorimentioning

confidence: 99%

The Role of Interleukin-1 in the Pathogenesis of Cancer and its Potential as a Therapeutic Target in Clinical Practice

2018

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Interleukin-1 (IL-1) has long been known to be a key mediator of immunity and inflammation. Its dysregulation has been implicated in recent years in tumorigenesis and tumor progression, and its upregulation is thought to be associated with many tumors. Overexpression of the IL-1 agonists IL-1a and IL-1b has been shown to promote tumor invasiveness and metastasis by inducing the expression of angiogenic genes and growth factors. IL-1 blockers such as anakinra and canakinumab are already approved and widely used for the treatment of some autoimmune and autoinflammatory diseases and are currently being tested in preclinical and human clinical trials for cancer therapy. In this paper we review the most recent discoveries regarding the association between IL-1 dysregulation and cancer and present the novel IL-1 blockers currently being tested in cancer therapy and their corresponding clinical trials.

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“…The increase in circulating pro-inflammatory cytokines (IL-6, TNF-alpha, IL-beta) and other inflammatory markers (PCR and white blood cell counts) concentrations have been also associated with frailty syndrome in several studies [ 26 , 27 , 28 , 29 , 30 , 31 ]. Cytokines overproduction such as IL-6, TNF-alpha, IL-8 have been also involved in the PCa pathophysiology [ 32 , 33 , 34 , 35 , 36 , 37 ] and thus inflammation could be common pathophysiological framework for frailty syndrome and ADT treatment in PCa patients.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-6 and Lymphocyte Count Associated and Predicted the Progression of Frailty Syndrome in Prostate Cancer Patients Undergoing Antiandrogen Therapy

Buigues

Navarro-Martínez

Sánchez-Martínez

et al. 2020

Cancers

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Frailty syndrome is a functional state that includes a loss of ability to react to stressors, and is associated with poor outcomes, morbidity and premature mortality. The first line treatment in many men with prostate cancer (PCa) consists of an androgen-deprivation therapy (ADT) which can promote or favor frailty syndrome and ADT may therefore favor the progression of frailty over time. Among the pathophysiological bases of frailty, the presence of chronic low-grade inflammation has been associated with its adverse outcomes, but longitudinal studies are needed to validate these biomarkers. In this study, we prospectively evaluate frailty syndrome and blood inflammatory markers (IL1-beta, IL-6, IL-8, TNF alpha, C reactive protein) and leukocytes were measured at baseline and an average of 1 year later in PCa under ADT. Frailty was defined as having three or more of the following components: low lean mass, weakness, self-reported exhaustion, low activity level, and slow walking speed; prefrailty was defined as having one or two of those components. Multinomial regression analysis showed that among the inflammatory biomarkers, those significantly and repeatedly (baseline and follow-up time points) (p < 0.05) associated with frailty syndrome were high IL-6 levels and low lymphocyte counts in blood. Other biomarkers such as IL-8, monocyte counts and C reactive protein were significantly associated with frailty syndrome (p < 0.05) in cross-sectional analyses, but they do not predict frailty progression at 1 year-follow-up. Receiver operating characteristic curve analysis showed that both lymphocyte counts and IL-6 concentration significantly (p < 0.05) (although moderately) discriminate PCa patients that progressed in the severity of frailty syndrome. IL-6 and lymphocytes count are possible biomarkers, useful for identifying frail patients and predicting the progression of frailty in PCa under ADT. Our study suggests the use of these biomarkers to guide clinical decisions on prostate cancer treatment based on a multidisciplinary approach.

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Genetic Polymorphism of Interleukin-1A (IL-1A), IL-1B, and IL-1 Receptor Antagonist (IL-1RN) and Prostate Cancer Risk

Cited by 30 publications

References 41 publications

Interleukin-1 Beta—A Friend or Foe in Malignancies?

Interleukin-1 Beta—A Friend or Foe in Malignancies?

The Role of Interleukin-1 in the Pathogenesis of Cancer and its Potential as a Therapeutic Target in Clinical Practice

Interleukin-6 and Lymphocyte Count Associated and Predicted the Progression of Frailty Syndrome in Prostate Cancer Patients Undergoing Antiandrogen Therapy

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