EGFR mutation + KRAS mutation

TMS analysis reveals that smoking is associated with LUAD with KRAS mutations. Defective DNA mismatch repair and endogenous cytidine deamination are associated with LUAD with EGFR mutations, especially for the EGFR 19Del. The endogenous mutational process is stronger in Asian LUAD patients than Western LUAD patients.

PSC exhibits high KRAS and EGFR mutation rates, and spindle cell carcinoma has a worse prognosis. Immunotherapy shows potential as a treatment for advanced PSC.

Finally, we found that targeting PRMT1 to reduce persistence is more effective in lung cancer models with intact vs. deleted chromosome 5q31.1, a region enriched with JAK-STAT pathway genes, suggesting a potential stratification criterion. Together, our study pinpoints the PRMT1 isoform as a critical vulnerability of cancer persistence in EGFR- or KRASG12C-targeted therapies.

The major translational relevance of this study is to exploit new targets for the development of innovative and improved therapeutic strategies with NOA drugs, over combinations including target genes within the oncogene pathway, to overcome resistance to TKI therapies in patients with NSCLC who are oncogene-addicted.

Our results confirm cancer-kidney crosstalk in specific cancer types. In the era of precision medicine, further research is essential to identify at-risk oncology populations, enabling early detection and management of renal complications.

We report a new RIT1 M90I -mutant autochthonous lung tumor model The most common oncogenic variant of RIT1, RIT1 M90I , weakly promotes lung tumor development RIT1 M90I drives the formation of lethal lung tumors in cooperation with p53 and Nf2 tumor suppressor gene loss RIT1 M90I and YAP cooperatively regulate cJUN expression Therapeutic MEK and TEAD targeting suppresses RIT1 M90I -driven tumorigenesis.

Our results regarding the proportion of samples with actionable mutations demonstrate the value of NGS testing for NSCLC patients in a real-world clinical diagnostic setting.

P=N/A, N=0, Not yet recruiting, The First Affiliated Hospital, Jinan University; The First Affiliated Hospital, Jinan University

Similar to the West, KRAS G12 mutations are the most common, with KRAS G12C nearly twice as common in men than in women. Furthermore, co-existence of EGFR and KRAS mutations occurs approximately 18% KRAS cases representing a diagnostic and therapeutic challenge worthy of further study.

The present series demonstrates the presence of EGFR and KRAS mutations and documents the presence of HPV strains in several patients with SIP, alterations associated with squamous carcinomas of the nasal cavity (CNC). However, the low prevalence of the documented alterations in the present series prevents the establishment of a solid causality between these alterations and the development of SIP. New prospective series with larger sample sizes are needed to better understand the clinicopathological implications of the underlying molecular alterations.

Erlotinib or osimertinib with selinexor in EGFR-mutant cells and trametinib plus selinexor in KRAS mutant abolish tumor cell proliferation. Selinexor with a PD-1 inhibitor with or without trametinib abrogates the tumor growth in the murine Lewis lung cancer model. An in-depth exploration of the functions of HMGB1 mRNA and protein is expected to uncover new potential targets and provide a basis for treating metastatic NSCLC in combination with ICI.

The first U.S. food and drug administration (US FDA) approval of the imatinib tyrosine kinase inhibitor in 2001 paved the way for nearly 100 small-molecule anti-cancer drugs approved by the US FDA and the national medical products administration (NMPA)...Accumulating evidence has enabled scientists and clinicians to strategize the therapeutic approaches of targeting cancer cells and to navigate the development of drug resistance through the continuous monitoring of tumor evolution and oncogenic adaptations. In this review, we highlight the emerging aspects of Hippo signaling in cross-talk with other oncogenic drivers and how this information can be translated into combination therapy to target a broad range of aggressive tumors and the development of drug resistance.