ALK (Anaplastic lymphoma kinase)

Among two patients treated with crizotinib, PFS durations were 10.0 and 17.0 months, respectively...Although inflammatory markers did not consistently predict survival, abnormal values trended toward poorer outcomes. Larger multicenter studies are needed to clarify prognostic indicators and improve therapeutic strategies for this rare entity.

P1/2, N=37, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027

Recognition of gene fusion signatures not only enhances diagnostic precision but also opens avenues for targeted therapy in selected cases. Continued molecular investigation and case accumulation are necessary to validate the biological behavior and therapeutic implications of many of these newly recognized entities.

Genomic metrics showed tumor mutational burden (TMB) of 0.94/Mb, microsatellite stability, and CNV burden of 2.1%. He underwent near total resection followed by alectinib; to our knowledge, this is the first reported young pediatric (<10 years old) CNS IMT with this fusion.

Dirozalkib exhibited favorable safety, antitumor activity and pharmacokinetics in patients with advanced ALK-rearranged NSCLC. The recommended phase II dose was 500 mg/day.

MRD may refine prognostic evaluation beyond pCR in resectable NSCLC undergoing perioperative chemoimmunotherapy.

P3, N=1069, Recruiting, Gilead Sciences | Trial completion date: Jun 2028 --> Jan 2029

ECM gene signatures serve as robust prognostic markers across populations. This function-based approach offers a novel perspective to address genetic heterogeneity and provides a theoretical foundation for ECM-targeted combination therapies.

Moreover, in HGSOC patient-derived xenograft (PDX) models, brigatinib and PARPi combination therapy induced tumor regression and improved overall survival compared with PARPi alone, particularly in models with high FAK and EPHA2. These findings support dual targeting of FAK and EPHA2 as a strategy to achieve effective and durable PARPi responses and identify a promising biomarker-based combinatorial approach using brigatinib and PARPi for HGSOC, particularly the subset characterized by high FAK and EPHA2.

P2, N=36, Active, not recruiting, Fox Chase Cancer Center | Recruiting --> Active, not recruiting

P1, N=26, Active, not recruiting, Pfizer | Recruiting --> Active, not recruiting | N=190 --> 26

P1/2, N=12, Active, not recruiting, University of Colorado, Denver | Recruiting --> Active, not recruiting