Tafinlar (dabrafenib)

Reduced-dose dabrafenib and trametinib were initiated with prophylactic naproxen to mitigate the risk of pyrexia. Treatment has been continued for over 6 months with sustained disease stability. This case suggests that an upfront dose-attenuation strategy combined with proactive toxicity management, including pyrexia prophylaxis, may represent a practical approach to maintain treatment continuity and clinical benefit in selected very elderly or frail patients.

The cytotoxic effects of three MAPK pathway inhibitors (selumetinib, vemurafenib, dabrafenib) were assessed in ATC cell lines and xenograft models via viability assays and 18F-FDG PET/CT. Furthermore, MAPK pathway inhibitors increased radioiodine uptake in ATC cells. The MAPK pathway inhibitors enhance NIS function through two mechanisms: upregulation of NIS expression and increased ARF4-mediated NIS membrane transport.

P3, N=267, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Sep 2026 --> Dec 2026

Screening for drugs also revealed AKT1, TP53, and PIK3R4 as druggable hubs, and many drugs (e.g., Everolimus, Dabrafenib, Trabectedin) showing high-affinity interactions. The study discovers new prognostic markers (ATG4A, GABARAPL2, GAPDH) and druggable targets, which could lead to better risk stratification and smarter drug repurposing. While restricted to in silico analyses, the integrative approach provides a basis for subsequent laboratory confirmation and translational development.

P1/2, N=1000, Recruiting, Oslo University Hospital HF | N=6000 --> 1000

Whilst the link between LCH and several haematological malignancies is documented, the mechanism is still unclear. In this case, the LCH most likely developed from an already abnormal myeloid compartment and highlights the need for clinical vigilance and appropriate investigation, where effective treatments for these conditions exist.

We have recently demonstrated that a RAC1 mutation (RAC1 P34R) can induce the formation of PGCCs in aggressive thyroid cancer cells from a patient undergoing dabrafenib treatment, leading to resistance to therapy...By targeting RAC1's integrative functions, researchers may unlock new avenues for preventing PGCC-mediated recurrence and metastasis, offering a promising strategy to improve long-term outcomes in cancer treatment. This review outlines the diverse functions of RAC1 that may contribute to both the formation and sustained maintenance of PGCCs across various tumor types.

This case demonstrates that triple combination therapy may induce rapid and durable remission in PLC secondary to BRAF-mutated colorectal cancer. It underscores the importance of comprehensive molecular profiling in guiding personalized treatment for rare metastatic manifestations. Moreover, this report highlights the importance of timely, genomics-guided therapeutic decision-making and pragmatic adaptation of targeted strategies in managing aggressive BRAF V600E-mutant colorectal cancer, particularly in clinically complex and resource-constrained settings.

Furthermore, EMT-high tumors exhibited distinct drug sensitivity profiles, including reduced responsiveness to conventional chemotherapeutics and increased sensitivity to agents such as camptothecin and dabrafenib. Collectively, these findings identify PHTF2 and SNAI1 as key regulators of EMT and tumor cell proliferation in thyroid cancer, and suggest that EMT-driven TME remodeling contributes to immune evasion and therapeutic resistance, thereby revealing EMT-associated vulnerabilities as potential targets for precision therapy.

Although survival outcomes were comparable to those described in younger adults, adverse events were common and impactful in older adults.

P1/2, N=1200, Not yet recruiting, Region Hovedstaden

Genomic profiling reveals targetable alterations-IDH1/2 mutations, FGFR2 fusions, HER2 aberrations, BRAF V600E-driving the clinical success of specific inhibitors (ivosidenib, FGFR inhibitors, HER2-targeted ADCs/antibodies, dabrafenib/trametinib). However, overcoming tumor heterogeneity, resistance mechanisms, and optimizing combination strategies remain critical challenges. This paradigm shift towards molecularly guided therapies offers significant hope for improving BTC patient survival.