IL2RG (Interleukin 2 Receptor Subunit Gamma)

APL mice had significantly higher levels of thrombin-antithrombin complexes compared with AML mice. These leukemia mouse models can be used to understand how the hemostatic system is dysregulated in leukemia.

Continued studies evaluating JAK inhibitors in patients with T-PLL are warranted. This trial was registered at www.clinicaltrials.gov as #NCT03989466.

The therapeutic relevance of these findings was substantiated in vivo, where DML administration significantly prolonged survival in an M-NSG mouse xenograft model engrafted with NB4 leukemia cells. These results systematically establish that DML induces apoptosis in myeloid leukemia cells directly through PERK/eIF2α/ATF4/CHOP signaling pathway in response to ER stress.

TERF2 knockdown induced apoptosis, suppressed cell proliferation, and downregulated the E2F pathway, while simultaneously enhancing cuproptosis susceptibility, as evidenced by reduced half-maximal inhibitory concentration (IC50) values of the elesclomol-copper (ES-Cu)...Downregulation of TERF2 inhibits the AML cell proliferation, induces apoptosis, and modulates cuproptosis sensitivity possibly via the E2F-mediated pathway. Targeting TERF2 not only inhibits proliferation but also unlocks cuproptosis as a therapeutic vulnerability, offering a potential strategy for AML.

This model supports consistent engraftment of SaOS-2-luc tumours with robust metastatic spread, recapitulating key human OS features. It offers a translatable preclinical platform for studying OS progression and testing chemotherapy and surgical interventions.

P2, N=56, Active, not recruiting, Center for International Blood and Marrow Transplant Research | Recruiting --> Active, not recruiting | Trial completion date: Aug 2030 --> Dec 2028 | Trial primary completion date: Aug 2029 --> Dec 2027

In HER2-positive BC, a three-gene signature (IL2RG, CD3E, CD3G) was consistently prognostic (HR 0.41, 95% CI 0.24-0.71, P = 0.0011, GEO) across independent datasets. We identified subtype-specific signatures that predict survival and immunotherapy response, providing clinically actionable biomarkers.

Additionally, a corresponding 3D organoid model (CO17) was established, which retained genetic concordance with OT17, further validating its relevance for preclinical applications. Together, the OT17 cell line and CO17 organoid system represent robust models for advancing colorectal cancer research, with potential applications in therapeutic screening, immunotherapy development, and MSS tumor biology studies.

In addition, we defined an 11-gene signature (TYK2, IL2RG, KRT17, HLA-B, NPPC, WIF1, IL32, B2M, CCND1, CRIP1, ITGB1), which characterizes cancer cells en route to metastasis and is associated with inferior outcomes. Collectively, our findings suggest that CAFs induce pro-invasive gene expression changes involved in EMT, ECM remodeling, and migration.

It also enables the evaluation of the efficacy of human-specific immunotherapies, including CART and CAR-NK therapies, immune checkpoint inhibitors, and combination therapies, along with their underlying mechanisms. This article summarizes the latest research advancements and existing challenges related to SCID mouse models and humanized immune system mouse models, as well as their applications and obstacles in immuno-oncology research.

Immune-related pathways were enriched in high-risk patients, and drug sensitivity analysis indicated that high-risk patients were more responsive to sunitinib and temsirolimus. IL2RG and its related 6-IRLs are potential biomarkers for ccRCC progression. The 6-IRLs model provides a robust tool for predicting prognosis and guiding therapeutic decisions.

Our models confirm the feasibility of achieving stable histological and molecular profiles, offering a valuable resource for precision oncology research. Ultimately, these pediatric PDXs could accelerate the discovery of targeted therapy and significantly improve treatment outcomes.