ALK fusion

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.

This includes work that led to the FDA approvals of immune checkpoint inhibitors in multiple rare pediatric tumor types, the NTRK inhibitors larotrectinib, entrectinib, and repotrectinib for children and adults with solid tumors with NTRK fusions, the ALK inhibitor crizotinib in children and adults with ALK-positive inflammatory myofibroblastic tumors, and the radioligand LUATHERA for adolescents and adults with somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors. Despite these advances, the study of rare pediatric cancers faces multiple challenges including a limited number of patients for efficient and well-powered clinical trials and a dearth of financial incentives. Ongoing, coordinated efforts are needed to continue the advancement of novel treatments and improve survival and minimize late effects.

These alterations were mutually exclusive with common drivers such as EGFR or KRAS. Detection of rare fusions highlights the therapeutic potential of comprehensive NGS profiling in Romanian NSCLC patients.

Atypical-location AFH (e.g., adrenal) exhibits divergent pathologic phenotypes. Diagnosis requires integrated IHC/molecular analysis (e.g., EWSR1 status). Prognostic implications of genetic alterations (e.g., ALK expression) highlight the need for molecular profiling to guide therapy and prognosis.

Initial treatment with chemoimmunotherapy was complicated by hypersensitivity reactions to nivolumab and paclitaxel, leading to a brief hospitalization...This case demonstrates the efficacy of neoadjuvant alectinib in managing ALK-mutant stage III lung adenocarcinoma, highlighting the potential benefits of targeted therapy in the neoadjuvant setting. Further studies are needed to establish optimal treatment protocols for patients with ALK-positive lung cancer.

By synthesizing current evidence, this review aims to provide insights into the diagnostic, prognostic, and therapeutic landscape of TPM3-related gene fusions, fostering advancements in precision oncology.

The study confirms the marked efficacy of ALK inhibitors in ALK-positive PMP, but highlights the need to monitor neurotoxicity in adolescent patients. Through analysis of the FN1(Fibronectin 1)-ALK fusion mechanism and literature review, this study emphasizes the importance of pathological differentiation, individualized treatment, and dynamic cognitive monitoring, providing insights for precision therapy in rare diseases.

This case underscores the importance of molecular profiling in diagnosing metastatic tumors and confirms lorlatinib as a highly effective first-line therapy for ALK-positive non-small cell lung cancer with atypical metastases.

P2, N=12, Terminated, Oncology Institute of Southern Switzerland | Trial completion date: Dec 2024 --> May 2025 | Active, not recruiting --> Terminated; Terminated for futility, as determined by an interim data analysis.

Nonreciprocal/reciprocal ALK translocations represent an independent adverse prognostic factor for ALK-positive NSCLC patients compared with solitary 3'-ALK fusions. However, their poorer prognosis does not appear to be directly associated with TP53 co-mutations.

This report describes the first case of gastric adenocarcinoma harboring a DCTN1-ALK fusion that was successfully treated with the ALK-targeted agent alectinib after first- and second-line chemotherapy-based regimens had failed...The other documented cases with DCTN1-ALK fusion treated with the first or second generation of ALK inhibitors indicated this rare fusion as an actionable driver gene mutation. This successful personalized anti-tumor strategy highlights the clinical utility of comprehensive genomic profiling and liquid biopsy in detecting and monitoring actionable ALK fusions in solid tumors.

Here, we present a patient diagnosed with high grade metastatic inflammatory myofibroblastic tumor driven by a RANBP2::ALK fusion, who later developed an ALK G1202R resistance mutation in the setting of treatment with crizotinib. The patient remains without evidence of disease now 18 months after discontinuing adjuvant lorlatinib. This case illustrates the importance of serial molecular profiling to guide selection of the optimal ALK inhibitor for the best clinical outcomes.