This analysis demonstrates continued efficacy of entrectinib in Asian patients with advanced ROS1-fp NSCLC, both overall and in the 1L setting. No new safety signals emerged.

This case highlights the significant efficacy and safety of alectinib in the management of advanced, recurrent, and aggressive UIMT, while also emphasizing the essential role of multidisciplinary management. It provides valuable insights and serves as a reference for the management of similar rare cases.

Together, these findings provide a multidimensional understanding of DILI risks associated with ceritinib combination therapies. By integrating pharmacovigilance signals with physiologically relevant in vitro validation, this study highlights the utility of the human liver organoids for elucidating the mechanisms of hepatotoxicity insights and supporting safer prescribing practices, especially when ceritinib is co-administered with non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen in real-world clinical settings.

Although NTRK-associated fusions are significant in various cancers and have led to the development of targeted therapies, such as larotrectinib and entrectinib, the specific molecular impact of atypical PRUNE2::NTRK2 fusion remains unclear. The PRUNE2::NTRK2 gene fusions described here express a non-functional TrkB protein, and it is unclear whether the PRUNE2 function is intact or affected.

This presentation aligns with a case reported in Japan, describing severe hemolytic anemia with morphological changes in erythrocytes under alectinib treatment. This is the first report describing a rapid increase in hemoglobin after pausing alectinib and no relapse of hemolysis after switching to lorlatinib, while the lung cancer remained stable (stable disease).

The mechanism of lorlatinib-induced hyperglycemia is unclear but may involve reduced insulin secretion. This case underscores the importance of monitoring for hyperglycemia in patients receiving lorlatinib, even in the absence of pre-existing diabetes, to enable early detection and prevent life-threatening complications like DKA.

These patients also showed heightened sensitivity to several chemotherapeutic and targeted agents, including Cisplatin and Crizotinib. Integrating single-cell sequencing, MR-based causality, clinical validation, and functional experiments, we identified ASPH and PTTG1 as key regulators of LUAD angiogenesis and immune evasion. These findings substantiate ASPH/PTTG1 as promising biomarkers and therapeutic targets, offering new insights into precision therapies integrating anti-angiogenic and immunomodulatory strategies.

This case report identifies a novel SNX25-ROS1 fusion mutation in NSCLC, showing strong sensitivity to ROS1-targeted therapy. It highlights the importance of molecular profiling in detecting rare genetic alterations and underscores the therapeutic potential of targeted treatments for NSCLC with unique molecular subtypes.

Our study reveals a novel mechanism by which the NOTCH2-NTRK1 fusion confers resistance to osimertinib through its interaction with EGFR in NSCLC.

P3, N=200, Active, not recruiting, Hoffmann-La Roche | Trial completion date: Oct 2025 --> May 2026 | Trial primary completion date: Oct 2025 --> May 2026

The safety profile of crizotinib remained consistent with previous reports, with most adverse events being grade 1 or 2 and no new safety concerns identified. This analysis supports the efficacy of crizotinib in patients with advanced NSCLC and ROS1 rearrangements, although its activity in patients with BM remains limited, highlighting the need for brain-penetrant tyrosine kinase inhibitors to improve outcomes in this patient group.

Our results confirm that cell surface NCL is a biomarker and a potential target for NB, paving the way for further investigations aimed at the future clinical translation of innovative combination strategies against NB.