ALK positive

P1/2, N=85, Active, not recruiting, Bristol-Myers Squibb | Recruiting --> Active, not recruiting

P=N/A, N=240, Recruiting, Institut für Klinische Krebsforschung IKF GmbH at Krankenhaus Nordwest

After about 20 years of exciting improvements in treatment efficacy outcomes of advanced epidermal growth factor receptor (EGFR) mutant and anaplastic lymphoma kinase (ALK) rearranged non-small cell lung cancer (NSCLC), also combined with a progressively better safety profile, from chemotherapy to new generation tyrosine kinase inhibitors (TKIs) (osimertinib, alectinib, brigatinib), the recent MARIPOSA and CROWN trials have changed this trend. The story would be easy and totally positive if these two innovative, amazing treatments were not associated with new peculiar features in safety profiles that must be discussed with patients, because they potentially affect their quality of life. When treating these patient populations, the peculiar safety profiles of amivantamab plu lazertinib and lorlatinib require a well-structured shared decision making, "where and when", both the high probability of a longer survival and the risk of worse quality of life must be well announced and explained to our patients before the shared final treatment choice.

P=N/A, N=9, Recruiting, Fudan University | Trial completion date: Sep 2025 --> Dec 2026 | Trial primary completion date: Sep 2025 --> Dec 2026

Multidisciplinary collaboration is needed to determine the necessity and timing of intervention for pericardial effusions causing hemodynamic compromise in pregnancy. Sanguineous effusions should prompt evaluation for both aortic dissection and malignancy.

Small-molecule ALK inhibitors, including crizotinib, have demonstrated high overall response rates (67%-88%) and complete remission rates (~60%-80%) in relapsed or refractory ALK-positive ALCL, often with rapid clinical responses...In addition, it explores emerging strategies for integrating ALK inhibitors into precision-based management of T-cell lymphomas, including combination approaches with chemotherapy, immunotherapy or antibody-drug conjugates. Collectively, these developments highlight a paradigm shift towards biology-driven, personalized therapy in ALK-positive ALCL.

This case highlights the importance of genetic profiling and rapid and substantial efficacy of alectinib in treating ALK-positive PLADC, reinforcing the role of ALK inhibitors in managing severe cases and offering valuable insights for clinical strategies.

P1, N=135, Active, not recruiting, AbbVie | Recruiting --> Active, not recruiting | N=225 --> 135

This case highlights distinctive CT features of ALK-RCC that may raise suspicion in young patients and guide molecular testing. The identification of the DCTN1::ALK fusion expands the molecular landscape of ALK-RCC and supports the potential utility of ALK inhibitors.

In vivo, STAT3 knockdown suppressed tumor formation and hepatosplenomegaly in mice inoculated with Ba/F3 cells expressing NPM-ALK, and these phenotypes were rescued by wild-type STAT3, but not by the T714A mutant. These findings indicate that STAT3 phosphorylation at T714 is required for subsequent Y705 phosphorylation, nuclear translocation, and transcriptional activation specifically within the context of NPM-ALK-mediated signaling.