ROS1 positive

Nearly 7% of EGFR mutations in NSCLC patients were compound mutations, which is comparable to previous reports. The presence of multiple mutations, particularly those involving T790M , may be associated with potential resistance to first-line EGFR -TKIs. We describe a triple mutation involving del19 + G719X + S768I , which represents an uncommon scenario.

This multicentre real-world cohort describes longitudinal ROS1 management with evolving treatments. Favourable survival likely reflects reflex molecular testing, access to ROS1i, and high clinical trial enrolment.

Experimental results demonstrate that curcumin can restore cell growth and viability, scavenge ROS from cells as well as positively regulate mitochondrial function; however, the above results are regulated by the concentration of curcumin. In conclusion, these findings provide experimental support for curcumin as a preliminary intervention for Complex II deficiency and other mitochondrial diseases, further enriching the evidence for the potential application of curcumin in mitochondrial-related diseases.

The efficacy of tyrosine kinase inhibitors (TKIs) crizotinib, ceritinib, lorlatinib, entrectinib, and repotrectinib was systematically evaluated. Our findings underscore that although G2032R and L2026M mutations reside within the kinase active site, their impact extends far beyond steric hindrance, altering overall kinase domain dynamics. Collectively, these data establish a robust panel of patient-derived ROS1 cell lines that recapitulate clinical resistance patterns and, together with complementary computational modeling, provide a valuable framework to dissect ROS1 tumor biology and support rational design of next-generation inhibitors.

P=N/A, N=35, Completed, Pfizer | Active, not recruiting --> Completed

Treatment procedures are rapidly evolving, but the clinical presentations of these diseases remain unchanged. The disease profiles presented in this publication should aid in their early diagnosis and consequently in timely treatment.

NRF2 directly binds to and transcriptionally activates CARM1, thereby enhancing ferroptosis resistance and promoting TNBC progression. These findings reveal a novel molecular mechanism underlying TNBC malignancy and suggest that targeting the NRF2-CARM1 axis, particularly in combination with ferroptosis inducers, may provide a potential strategy for TNBC treatment.

Consistent with our in vitro observations, in vivo xenograft experiments verified that Cory retarded HCC tumor growth by modulating ROS and STAT3 activity. In summary, this study demonstrates Cory impedes HCC progression via a ROS-STAT3 positive feedback loop, suggesting that Cory may serve as a promising therapeutic candidate for HCC treatment.

The rate of bone metastasis was significantly higher in ROS1 rearrangement-positive than in ROS1 rearrangement-negative patients. ROS1 rearrangement plays a significant prognostic role in advanced progression of LUAD; however, the generally favorable survival outcomes of early-stage LUAD may obscure its prognostic value.

P=N/A, N=24, Recruiting, Centro de Tratamiento e Investigación sobre Cáncer, Luis Carlos Sarmiento Angulo

The silence of MIAT alleviated the inflammatory response and oxidative stress in LPS-induced RAW264.7 and alleviated the damage of AML-12 cells by adsorbing miR-942-5p.

Subsequently, the patient received furmonertinib targeted therapy. Herein, we discuss the diagnostic challenges and the potential pathogenic mechanisms of this novel mutation. How to identify rare genes and translate their identification into clinical benefits is a worthwhile avenue for exploration in our future work.