STAT3 mutation

A significant correlation between microbiome abundance and VEGF and MMP9 was observed. This study illustrated that gut microbiomes contribute to HCC and HCV-related cirrhosis pathogenesis, opening approaches for cancer management and prevention.

This study enhances our understanding of how STAT3 mutations drive immunological dysregulation in HIES. The identified changes in immunological signature and transcriptional mechanisms offer new insights into therapeutic targets for HIES.

P1/2, N=11, Active, not recruiting, Jonathan Brammer | Recruiting --> Active, not recruiting | N=27 --> 11

Altogether, incorporation of CCL22 mutations reduced the fraction of unclassified patients, improved diagnostic sensitivity without compromising specificity, and may decrease reliance on invasive procedures. These revised international criteria represent a step toward standardized, molecularly guided NK-LGLL diagnosis.

Moreover, RA treatments such as methotrexate (MTX), Janus kinase (JAK) inhibitors, and anti-TNF therapies have complex implications, with some studies suggesting potential contributions to leukemia risk through immune suppression and hematopoietic alterations...Advances in multiomics and artificial intelligence-driven risk modeling may facilitate personalized treatment strategies, improving both RA management and leukemia prevention. Given the rising burden of RA and its associated complications, a comprehensive understanding of its link to leukemias is critical for enhancing patient outcomes and guiding clinical decision-making.

We evaluate clinical progression of breakthrough candidates such as ARV-110 for prostate cancer, ARV-471 for breast cancer, and BTK degraders, while discussing critical challenges including the "hook effect" and oral bioavailability limitations. This review provides essential foundations for rational target selection, molecular optimization, and clinical translation strategies. By integrating mechanistic insights with clinical realities, this analysis offers perspectives on PROTAC technology advancement and identifies opportunities for transforming treatment of complex diseases resistant to conventional therapies.

Underlying T-cell dysregulations, often associated with clonality and/or STAT3 gene mutation, have been a rationale for using cyclosporin and other directed immunosuppressive therapies in most of the disease subtypes, namely, thymoma-associated PRCA, large granular lymphocytic leukemia-associated PRCA, and idiopathic PRCA. Although the epidemiologic rarity of PRCA has precluded comparative clinical trials that could demonstrate the superiority of one immunosuppressive agent over another, some retrospective studies have demonstrated the significance of maintenance therapies to avoid blood transfusion dependency, a factor that may lead to poorer prognosis in patients with PRCA. This review primarily discusses clinical aspects of PRCA in line with recently updated clinical guidelines.

Despite receiving various treatments such as methotrexate, cyclosporin, cyclophosphamide, and thalidomide, the patient exhibited treatment refractoriness. This case highlights the clinical relevance of golidocitinib in developing novel therapeutic strategies for NK-LGLL. Moreover, this treatment option presents the potential as either a bridging therapy or alternative to allo-HSCT.

These results suggest that canine ILTCL is also a neoplasm of IEL with an ILC-like immunophenotype and STAT3 pathway activation, and loss-of-function mutations in NF-κB pathway inhibitors are associated with its neoplastic changes. Therefore, canine ILTCL has potential as a valuable model for investigating the pathogenesis of EATL.

We additionally provide structural analysis of the STAT3G656_M660del deletion, visualizing changes in protein architecture and potential effects on the neighboring Y705 phosphorylation site. Our model showcases the sexually dimorphic immune dysregulation caused by a STAT3 mutation and highlights that predicted gain- and loss-of-function mutations can yield unexpected phenotypes.

We propose that the STAT3 transcriptional program operating in cancer cells enforces their malignant identity, rather than providing classical features of transformation, and shapes cancer persistence following KRAS inactivation. Our findings establish STAT3 as a critical enforcer of oncogenic identity in KRAS-ablated tumors, revealing a key vulnerability.

AI-HOPE-JAK-STAT establishes a new standard for pathway-level interrogation in CRC by empowering users to generate and test clinically meaningful hypotheses without coding expertise. This system enhances access to precision oncology analyses and supports the scalable, real-time discovery of survival trends, mutational associations, and treatment-response patterns across stratified patient cohorts.