IDH2 mutation

This may reflect either relaxed positive selection for the mutant IDH1 locus, or negative selection for the hypermethylation phenotype later in tumor evolution. This finding highlights the challenge for therapeutic intervention by mutant IDH1 inhibitors in chondrosarcoma.

P2, N=16, Recruiting, Leland Metheny | Suspended --> Recruiting

The patient continues to be followed up for prognostic evaluation, and no recurrence or metastasis occurred until now. The case has represented a full view to gaining an improved understanding of TCCRP.

Our findings underscore the complex role of genetic factors in nTCL's clinical behaviour and emphasize the importance of ASCT. We also highlight the need for prospective clinical trials, which explore tailored therapeutic interventions, such as hypomethylating agents or IDH inhibitors, for improving survival in specific genetic contexts.

P1/2, N=84, Recruiting, M.D. Anderson Cancer Center | Trial completion date: Nov 2025 --> Nov 2027 | Trial primary completion date: Nov 2025 --> Nov 2027

Given the clinical significance of SF mutations, ongoing research is focused on developing targeted therapies that modulate aberrant RNA splicing and prevent CH-driven leukemogenesis. Understanding the mechanisms underlying mutant spliceosome-mediated CH expansion may provide novel insights into early detection, risk stratification, and therapeutic interventions in hematologic malignancies.

IDH frequently co-occurred with DNMT3A (38%), NPM1 (35%), and SRSF2 (34%). In patients treated with intensive chemotherapy, IDH mutations were not prognostic for overall survival (OS) (p=0.76), while OS was longer for patients with IDH2mut compared to IDHwt in patients treated with hypomethylating agent (HMA)-based therapy (median OS of 18.5 vs 10.2 months, p.

P1, N=4, Active, not recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Oct 2025 --> Oct 2026 | Trial primary completion date: Oct 2025 --> Oct 2026

Vorasidenib reduced tumour growth rate and improved seizure control compared with placebo, with no observed negative effects on HRQOL or neurocognition. Additional follow-up supported the robustness of progression-free survival and time to next intervention in patients with grade 2 IDH1/2-mutant diffuse glioma. These findings support the use of vorasidenib in patients with grade 2 IDH1/2-mutant gliomas who only had surgical intervention and are not in immediate need of radiotherapy or chemotherapy.

DGAT1 inhibition was strongly synergistic with metformin, while iron chelators acted antagonistically. Our results underscore the potential of leveraging metabolic vulnerabilities in AML to identify more effective and personalized therapeutic strategies.

In Grade 2 oligodendrogliomas, high cyclin D1 expression was associated with worse survival. In this cohort of oligodendroglial tumours classified by molecular criteria, the loss of p16 expression is associated with a poor prognosis, particularly in Grade 3 oligodendrogliomas.

Enasidenib plus venetoclax is safe, with no unexpected TEAEs or treatment-related deaths, and shows preliminary activity in patients with relapsed or refractory IDH2-mutated AML and MDS.