Ask about this productRelated genes to: IL32 antibody
- Gene:
- IL32 NIH gene
- Name:
- interleukin 32
- Previous symbol:
- -
- Synonyms:
- NK4, TAIF, TAIFb, TAIFd
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-08
- Date modifiied:
- 2014-11-18
Related products to: IL32 antibody
Related articles to: IL32 antibody
- Ovarian cancer is the most lethal gynecological malignancy worldwide, largely due to late diagnosis and lack of effective population-level screening tools. Inflammatory cytokines regulate proliferation, apoptosis, angiogenesis, and immune surveillance, making inherited variation in cytokine pathways biologically plausible determinants of ovarian cancer susceptibility and progression. Since the early 2000s, numerous candidate-gene studies have evaluated polymorphisms of genes such as the interleukin () families, tumor necrosis factor alpha (), transforming growth factor beta 1 (), and components of the nuclear factor kappa B () signaling pathway and adhesion pathways, across diverse populations. In this review, we summarize these potential markers to give readers an overview showing accumulated evidence supports a coherent model in which genetically modulated inflammation is an integral driver of epithelial ovarian carcinogenesis. Collectively, studies reveal recurrent patterns of risk-increasing and risk-protective variants. Risky genotypes predicted to enhance pro-inflammatory, pro-angiogenic, or immunosuppressive signaling include rs16944 CC, rs1800795, rs2227306 TT, rs1126647 TT, rs11556218 GT/GG, rs4778889 CT/CC, rs10889677 AC/CC, rs4758680 CA/AA, rs28372698 TT, rs1800629 GA/AA, and peroxisome proliferator-activated receptor gamma () rs1801282 CG genotypes. Conversely, protective variants tend to dampen inflammatory tone or rebalance cytokine networks, including rs17561 GT/TT, rs4848300 CT/CC, rs3783553 insertion/insertion, rs7596684 CT/CC, rs1880242 GT/TT, rs7977932 CG/GG, rs1800469 CT/TT, selectin E () rs5361 AC, intercellular adhesion molecule 1 () rs5498 AG genotypes and specific haplotypes. Beyond risk , several polymorphisms appear predictive of clinical features, including tumor stage, cytoreductive resectability and recurrence, highlighting potential prognostic relevance. Notably, associations are often population-specific, reflecting differences in allelic frequencies and linkage disequilibrium across ethnic groups, underscoring the need for cross-ethnic replication. Further investigations may ultimately enable further improved the prevention, early detection, and personalized management of ovarian cancer. - Source: PubMed
Chang Wen-ShinTsai Chia-WenChen Jaw-ChyunWang Yun-ChiBau DA-Tian - An increasing body of evidence suggests an association between metabolic syndrome and gastric cancer. However, the shared genetic signatures and underlying molecular mechanisms between them remain to be elucidated. - Source: PubMed
Publication date: 2026/04/20
Kong WeihaoWang JiawenZhang KangjieWang XingyuZhang Jianlin - Refractory pneumonia (RMPP) presents a major clinical challenge in children, largely due to the absence of reliable early diagnostic markers, which contributes to delayed intervention and an increased risk of severe complications. This study aimed to identify early diagnostic biomarkers based on peripheral blood mononuclear cell (PBMC) gene expression profiles and to develop and validate a model capable of distinguishing RMPP from general MPP (GMPP) and healthy controls (Normal). - Source: PubMed
Publication date: 2026/04/07
Wu QiutingLu ZhiweiHe XuehuiWang HepingZhang XiaoliWu XiangtaoLu WeihongFeng QiSu QiruZhang Xingliang - - Source: PubMed
- Atherosclerosis is characterized by chronic vascular inflammation involving endothelial dysfunction and macrophage-mediated inflammatory responses. However, the molecular mechanisms linking these processes remain incompletely understood. This study investigates the role of interleukin-32γ (IL-32γ) in mediating endothelial-macrophage interactions during atherosclerosis progression. IL-32 isoform expression was analyzed in peripheral blood samples from atherosclerosis patients and healthy controls. Human endothelial cells were treated with oxidized low-density lipoprotein (Ox-LDL) with or without NF-κB inhibitor. Endothelial-macrophage interactions were studied using Transwell co-culture systems with THP-1-derived macrophages. Macrophage polarization was assessed by flow cytometry, qRT-PCR, and ELISA. The direct effects of IL-32γ were evaluated using recombinant protein with or without p38 MAPK inhibitor. In vivo studies employed ApoE-/- mice fed a Western diet and administered with IL-32γ alone or with p38 inhibitor. IL-32γ was significantly upregulated in atherosclerosis patients. Ox-LDL induced IL-32γ expression in endothelial cells through NF-κB activation, concurrent with endothelial dysfunction. Ox-LDL-treated endothelial cells promoted M1 macrophage polarization and migration, effects attenuated by either NF-κB inhibition or IL-32γ neutralization. Treatment with recombinant IL-32γ induced M1 polarization through p38 MAPK signaling. In ApoE-/- mouse model, IL-32γ administration accelerated atherosclerotic plaque formation and macrophage infiltration, while p38 inhibition reversed these effects. IL-32γ serves as a crucial mediator between Ox-LDL-induced endothelial dysfunction and macrophage-mediated inflammatory responses in atherosclerosis. Endothelial-derived IL-32γ promotes M1 macrophage polarization through p38 MAPK signaling, accelerating disease progression. These findings identify IL-32γ as a potential therapeutic target for atherosclerotic cardiovascular disease. - Source: PubMed
Publication date: 2026/02/27
Yang ZicongLiu MengzhenShi YinLu ZhengdeLu ZhaoLin YingzhongJi QingweiLiu Ling