Genetic Variations in Inflammatory Response Genes and Their Association with the Risk of Prostate Cancer

Cui, Xin; Hu, Yan; Ou, Tongwen; Jia, Chenguang; Wang, Qi; Xu, Jianjun

doi:10.1155/2015/674039

Cited by 8 publications

(3 citation statements)

References 28 publications

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“…Prostate cancer (Zhang et al 2009, Kopp et al 2013, Cui et al 2015, Han et al 2015 rs28362491, rs2233406, rs3138053, rs28362491 Susceptibility 24:7 the rs28362491 insertion/deletion polymorphism in NFKB1 and has identified this polymorphism as a susceptibility factor for PTC (Wang et al 2015). We hypothesize that NF-κB-related genetic variants could represent important risk factors in development or clinical progression of NMTC and could improve our understanding of the mechanisms responsible for the effects of NF-κB on RAI responsiveness.…”

Section: Susceptibilitymentioning

confidence: 89%

Association of NF-κB polymorphisms with clinical outcome of non-medullary thyroid carcinoma

Plantinga¹,

Petrulea

Oosting³

et al. 2017

Endocrine-Related Cancer

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The NF-κB inflammatory pathway plays a major role in cancer development and clinical progression. Activation of NF-κB signaling is promoted by NFKB1 and inhibited by NFKBIA. The present study aimed to determine the relevance of rs4648068 and rs2233406 genetic variants for non-medullary thyroid cancer (NMTC) susceptibility, progression and clinical outcome. This case-control and cohort study consists of a Romanian discovery cohort (157 patients and 258 controls) and a Dutch validation cohort (138 patients and 188 controls). In addition, patient cohorts were analyzed further for the association of genetic variants with clinical parameters. Functional studies were performed on human peripheral blood mononuclear cells. No associations were observed between the studied genetic variants and TC susceptibility. Although no statistically significant associations with clinical parameters were observed for rs4648068, the heterozygous genotype of rs2233406 was correlated with decreased radioactive iodide sensitivity requiring higher cumulative dosages to achieve clinical response. These findings were discovered in the Romanian cohort ( < 0.001) and confirmed in the Dutch cohort ( = 0.01). Functional studies revealed that this rs2233406 genotype was associated with elevated TLR4-mediated IL-1β production. In conclusion, genetic variation in, an inhibitor of NF-κB signaling, is associated with clinical response to RAI therapy and with increased production of the pro-inflammatory cytokine IL-1β, providing a potential mechanism for the observed clinical associations. These data suggest that NF-κB signaling is involved in NMTC pathogenesis and that the inflammatory tumor microenvironment could contribute to RAI resistance.

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Section: Susceptibilitymentioning

confidence: 89%

Association of NF-κB polymorphisms with clinical outcome of non-medullary thyroid carcinoma

Plantinga¹,

Petrulea

Oosting³

et al. 2017

Endocrine-Related Cancer

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show abstract

“…Prostate cancer (PC) is a form of cancer that starts in the prostate gland of the male reproductive system and emerges as the result of a mutation in tumor suppressor genes or oncogenes, which deregulates the homeostatic functions and causes the transformation of normal cells into malignant cells [98,99]. PC is considered the leading non-cutaneous cancer or most commonly diagnosed cancer in men worldwide, even though the incidence and mortality rates fluctuate substantially by population and geographic location [100].…”

Section: Gene-environment Interactions In the Development Of Prostate Cancermentioning

confidence: 99%

Impact of Gene–Environment Interactions on Cancer Development

Mbemi

Khanna

Njiki

et al. 2020

IJERPH

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Several epidemiological and experimental studies have demonstrated that many human diseases are not only caused by specific genetic and environmental factors but also by gene–environment interactions. Although it has been widely reported that genetic polymorphisms play a critical role in human susceptibility to cancer and other chronic disease conditions, many single nucleotide polymorphisms (SNPs) are caused by somatic mutations resulting from human exposure to environmental stressors. Scientific evidence suggests that the etiology of many chronic illnesses is caused by the joint effect between genetics and the environment. Research has also pointed out that the interactions of environmental factors with specific allelic variants highly modulate the susceptibility to diseases. Hence, many scientific discoveries on gene–environment interactions have elucidated the impact of their combined effect on the incidence and/or prevalence rate of human diseases. In this review, we provide an overview of the nature of gene–environment interactions, and discuss their role in human cancers, with special emphases on lung, colorectal, bladder, breast, ovarian, and prostate cancers.

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“…Activation of NF-κB results in the induction of a variety of genes influencing cellular proliferation, inflammation, and adhesion [20,21]. A genome-wide association study and other gene expression studies have linked NF-κB-associated pathways to prostate cancer progression [22]. Within NF-κB itself, p100 and p105 can mediate interactions with NF-κB subunits that can also function as IκB proteins, activating or contributing to deregulation of the pathway (Figure S2) [20].…”

Section: Introductionmentioning

confidence: 99%

Complex Systems Biology Approach in Connecting PI3K-Akt and NF-κB Pathways in Prostate Cancer

Shankar

Weis

Avva

et al. 2019

Cells

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Phosphatidylinositol 3′-OH kinase (PI3K)-Akt and transcription factor NF-κB are important molecules involved in the regulation of cell proliferation, apoptosis, and oncogenesis. Both PI3K-Akt and Nuclear Factor-kappaB (NF-κB) are involved in the development and progression of prostate cancer, however, the crosstalk and molecules connecting these pathway remains unclear. A multilevel system representation of the PI3K-Akt and NF-κB pathways was constructed to determine which signaling components contribute to adaptive behavior and coordination. In silico experiments conducted using PI3K-Akt and NF-κB, mathematical models were modularized using biological functionality and were validated using a cell culture system. Our analysis demonstrates that a component representing the IκB kinase (IKK) complex can coordinate these two pathways. It is expected that interruption of this molecule could represent a potential therapeutic target for prostate cancer.

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Genetic Variations in Inflammatory Response Genes and Their Association with the Risk of Prostate Cancer

Cited by 8 publications

References 28 publications

Association of NF-κB polymorphisms with clinical outcome of non-medullary thyroid carcinoma

Association of NF-κB polymorphisms with clinical outcome of non-medullary thyroid carcinoma

Impact of Gene–Environment Interactions on Cancer Development

Complex Systems Biology Approach in Connecting PI3K-Akt and NF-κB Pathways in Prostate Cancer

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