Ask about this productRelated genes to: STAT6 Blocking Peptide
- Gene:
- STAT6 NIH gene
- Name:
- signal transducer and activator of transcription 6
- Previous symbol:
- -
- Synonyms:
- D12S1644, IL-4-STAT
- Chromosome:
- 12q13
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2019-04-23
Related products to: STAT6 Blocking Peptide
Related articles to: STAT6 Blocking Peptide
- Pelvic solitary fibrous tumor (SFT) is a rare mesenchymal neoplasm with marked clinical and radiological heterogeneity, posing significant diagnostic challenges. Standardized management strategies remain lacking for special clinical scenarios, including paraneoplastic syndromes, synchronous primary malignancies, and pregnancy-associated incidental diagnosis. - Source: PubMed
Publication date: 2026/07/31
Yang XinjiLiu LeiHou Xiaofei - The urethral caruncle is the most common lesion arising from the posterior lip of the urethral meatus in women; however, various benign and malignant tumours may mimic this condition. We report a case of a solitary fibrous tumour (SFT) presenting as a urethral caruncle. A woman in her late 60s presented with a progressively enlarging urethral mass that was accompanied by urinary spraying. Physical examination revealed a smooth spherical mass measuring 1.2 cm at the posterior urethral meatus. The lesion was completely excised under local anaesthesia. Histologically, the tumour consisted of spindle cells within collagenous stroma. Immunohistochemically, the tumour cells showed nuclear expression of STAT6 with focal CD34 positivity, supporting the diagnosis of SFT. No recurrence was observed during the 9-month follow-up period. This case highlights that lesions clinically resembling urethral caruncle may include mesenchymal tumours such as SFT, underscoring the importance of histopathological evaluation. - Source: PubMed
Publication date: 2026/08/13
Ono YoshihiroMiyazawa YoshiyukiArai SeijiSekine YoshitakaSugita Keisuke - In recent years, immunotherapy has shown obvious advantages in treating cancers. The close interaction between cancer cells and immune cells in the tumor microenvironment (TME) underlies the progression of glioblastoma multiforme (GBM). However, there are no effective immune-related targets against GBM. Here, analyses and experimental data showed that Interferon Gamma Inducible Protein 30 (IFI30), modulated by histone modifications both H3K4me3 and H3K27ac, was up-regulated in GBM and had a potential role in the antitumor immune responses. and experiments further revealed that IFI30 modulated the infiltration of tumor-associated macrophages (TAMs) and reduced the proportion of CD8 T cells. Mechanistically, IFI30 induced PGE2 expression in GBM cells the MAFF/PTGS2 pathway, and PGE2 bound to macrophage EP2/EP4, activating the downstream ERK1/2 and KLF4/STAT6 pathways, stimulating the infiltration of TAMs. Taken together, we characterized the role and mechanisms of IFI30 in the malignant progression of GBM by regulating TAMs, highlighting that IFI30 may benefit GBM patients as a therapeutic target. - Source: PubMed
Publication date: 2026/06/08
Zhang SenChen WenlinRen LiwenYi JieZheng XiangjinYang YihuiYang HongDu GuanhuaLi WanWang YuWang Jinhua - Oral squamous cell carcinoma (OSCC) is an aggressive malignancy with a profoundly immunosuppressive tumor microenvironment and persistently poor responses to immune checkpoint inhibitors. Recent evidence highlights dysregulated iron metabolism as a critical yet underrecognized driver of this immunosuppressive state. Excess intratumoral iron perturbs macrophage polarization toward pro-tumoral M2-like phenotypes through iron-sensing pathways, including HIF-1α stabilization, IL-10/STAT6 signaling, and NF-κB-mediated redox programs, driving T-cell suppression, angiogenesis, and extracellular matrix remodeling that collectively reinforce resistance to PD-1/PD-L1 checkpoint blockade. Concurrently, iron-dependent regulated cell death via ferroptosis - governed by the GPX4-glutathione- axis - represents an emerging immunological vulnerability, as ferroptotic tumor cells release damage-associated molecular patterns that potentiate anti-tumor CD8 T-cell responses and synergize with checkpoint inhibitor activity. This review synthesizes current findings on the mechanistic interplay between iron homeostasis, macrophage phenotypic switching, and ferroptosis in OSCC and evaluates emerging therapeutic strategies targeting this axis, including iron chelators, ferroportin modulators, ferroptosis inducers, pathway inhibitors, exosome-mimetic delivery systems, and iron-based nanoplatforms. While these approaches show promise, challenges remain regarding TME specificity, off-target iron depletion, and the absence of validated biomarkers for patient stratification. By integrating mechanistic insights with translational advances, this review underscores the therapeutic potential of targeting the iron-macrophage-ferroptosis axis and outlines how precision medicine-based interventions may overcome immune evasion and improve immunotherapy outcomes in OSCC. - Source: PubMed
Publication date: 2026/07/29
Bashah AhmedGhaleb EslamAl-Waqeerah AliChen Gang - Hypertensive cerebral hemorrhage (HCH) accounts for the majority of spontaneous intracerebral hemorrhage (ICH) cases. Cognitive impairment (CI) is a major contributor to long-term disability following ICH, yet the molecular mechanisms underlying CI in hypertensive ICH remain poorly understood. Therefore, identifying biomarkers capable of effectively diagnosing or predicting CI in HCH is particularly critical for managing patients with hypertensive cerebral hemorrhage with cognitive impairment (HCHwCI). - Source: PubMed
Publication date: 2026/07/29
Tang YaoYang BoyinLuo Xingmei