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Sorafenib maintenance improves outcomes after hematopoietic cell transplant (HCT) for patients with FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) acute myeloid leukemia (AML). Although promising outcomes have been reported for sorafenib plus intensive chemotherapy, randomized data are limited. This placebo-controlled, phase 2 study (ACTRN12611001112954) randomized 102 patients (aged 18-65 years) 2:1 to sorafenib vs placebo (days 4-10) combined with intensive induction: idarubicin 12 mg/m2 on days 1 to 3 plus either cytarabine 1.5 g/m2 twice daily on days 1, 3, 5, and 7 (18-55 years) or 100 mg/m2 on days 1 to 7 (56-65 years), followed by consolidation and maintenance therapy for 12 months (post-HCT excluded) in newly diagnosed patients with FLT3-ITD AML. Four patients were excluded in a modified intention-to-treat final analysis (3 not commencing therapy and 1 was FLT3-ITD negative). Rates of complete remission (CR)/CR with incomplete hematologic recovery were high in both arms (sorafenib, 78%/9%; placebo, 70%/24%). With 49.1-months median follow-up, the primary end point of event-free survival (EFS) was not improved by sorafenib (2-year EFS 47.9% vs 45.4%; hazard ratio [HR], 0.87; 95% confidence interval [CI], 0.51-1.51; P = .61). Two-year overall survival (OS) was 67% in the sorafenib arm and 58% in the placebo arm (HR, 0.76; 95% CI, 0.42-1.39). For patients who received HCT in first remission, the 2-year OS rates were 84% and 67% in the sorafenib and placebo arms, respectively (HR, 0.45; 95% CI, 0.18-1.12; P = .08). In exploratory analyses, FLT3-ITD measurable residual disease (MRD) negative status (<0.001%) after induction was associated with improved 2-year OS (83% vs 60%; HR, 0.4; 95% CI, 0.17-0.93; P = .028). In conclusion, routine use of pretransplant sorafenib plus chemotherapy in unselected patients with FLT3-ITD AML is not supported by this study.
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http://dx.doi.org/10.1182/blood.2023020301 | DOI Listing |
BMJ Open
September 2025
Department of Gastroenterology, Hepatology, Infectious Diseases and Intoxication, University Hospital Heidelberg, Heidelberg, Germany.
Introduction: Combined vascular endothelial growth factor/programmed death-ligand 1 blockade through atezolizumab/bevacizumab (A/B) is the current standard of care in advanced hepatocellular carcinoma (HCC). A/B substantially improved objective response rates compared with tyrosine kinase inhibitor sorafenib; however, a majority of patients will still not respond to A/B. Strong scientific rationale and emerging clinical data suggest that faecal microbiota transfer (FMT) may improve antitumour immune response on PD-(L)1 blockade.
View Article and Find Full Text PDFPathol Res Pract
September 2025
Department of Biotechnology, Delhi Technological University, India. Electronic address:
The intricate interplay between cancer and autoimmune diseases (ADs) is rooted in immune dysregulation, where genetic susceptibility, chronic inflammation, epigenetic modifications, and immunosuppressive therapies contribute to tumorigenesis. The dualistic nature of immune activation complicates therapeutic strategies, as immune checkpoint inhibitors and other immune-stimulatory therapies may exacerbate underlying ADs, leading to immune-related adverse events (irAEs), including organ toxicity, dermatologic reactions, and disease flares. Conversely, immunosuppressive treatments aimed at controlling ADs can compromise anti-tumor immunity and reduce the efficacy of cancer therapies.
View Article and Find Full Text PDFFASEB J
September 2025
Department of Obstetrics, Obstetrics and Gynecology Center, The First Hospital of Jilin University, Changchun, Jilin, China.
Tumor-associated macrophages (TAMs) act as a vital player in the immunosuppressive tumor microenvironment (TME) and have received widespread attention in the treatment of cancer in recent times. Nevertheless, simultaneously inducing TAM repolarization and strengthening their phagocytic ability on cancer cells is still a significant challenge. Ferroptosis has received widespread attention due to its lethal effects on tumor cells, but its role in TAMs and its impact on tumor progression have not yet been defined.
View Article and Find Full Text PDFJ Cancer Res Clin Oncol
September 2025
Drug Inspection Laboratory, Jingzhou Institute for Food and Drug Control, Jingzhou, 434000, China.
Objective: Dipeptidyl peptidase 9 (DPP9) not only regulates tumor progression and drug sensitivity, but also modifies oxidative stress mediated ferroptosis. This study aimed to investigate the effect of DPP9 inhibition on sorafenib sensitivity and its interaction with ferroptosis in hepatocellular carcinoma (HCC).
Methods: Two HCC cell lines (Huh7 and MHCC-97H) were transfected with DPP9 siRNA, followed by detection of reactive oxygen species (ROS), ferrous iron (Fe), malondialdehyde (MDA), and ferroptosis-related proteins, and treated by 0-16 μM sorafenib to calculate half-maximal inhibitory concentration (IC) for sensitivity assessment.
Nano Lett
September 2025
KU-KIST Graduate School of Converging Science and Technology, Korea University, Seoul 02841, Republic of Korea.
Sorafenib, a clinically approved multityrosine kinase inhibitor, exhibits poor aqueous solubility, which limits its bioavailability and therapeutic efficacy. In this study, we introduce a solvent-directed self-assembly strategy to modulate the nanostructure of sorafenib without the use of external carriers or complex formulation techniques. In pure water, sorafenib forms large lamellar aggregates, whereas in 30% methanol-water mixtures, it self-assembles into uniform spherical particles approximately 450 nm in diameter.
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