Non Small Cell Lung Cancer

P2, N=13, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting | N=27 --> 13

Adjuvant targeted therapy did not improve long-term survival in stage IB EGFR-mutant NSCLC with high-risk features, although it prolonged DFS in pure-solid tumors. A de-escalation strategy may be considered for postoperative management, particularly in part-solid tumors.

In addition, SGO2 compromised the cisplatin (CDDP) sensitivity of LUAD in vitro and in vivo...Silencing SGO2 with OA improved LUAD chemo sensitivity. Our work highlights the potential of SGO2 as a target for therapeutic intervention and OA as a food-bioactive compound for LUAD treatment.

Despite pembrolizumab discontinuation, both patients maintained durable systemic disease control. These cases emphasize the importance of recognizing uncommon radiological patterns such as the atoll sign in patients receiving ICIs, highlighting the need for vigilance even after prolonged therapy and underscoring the potential for sustained oncologic benefit despite treatment discontinuation.

Pan-TRK IHC has a false-positive rate of ∼4%, particularly in squamous cell carcinomas, underscoring the need for confirmatory NGS to validate IHC findings and assess fusion functionality. Functional NTRK1/2/3 fusions remain exceedingly rare in NSCLC, with a detection rate of 0.03% across our combined cohorts.

Data suggest that drugs used in the treatment of MS can modify ACE2 expression; specifically, fingolimod reduces ACE2 expression and may have a protective role against SARS-CoV-2 infection.

Subtyping based on single-cell derived marker genes and multi-level analyses provide a comprehensive understanding of LUAD biology. The distinct features of C1 and C2 subtypes highlight the need for tailored therapies. The eight-gene signature may serve as a novel prognostic, diagnostic, and therapeutic indicator.

Herein, we report the first documented case of phenotypic conversion to SCLC in a patient with advanced pulmonary sarcomatoid carcinoma (PSC) who received pemetrexed, carboplatin, and camrelizumab only, with no targeted agents administered. TP53 and RET mutations may be implicated in this phenotypic transition. This case provides new insights into the biological mechanism underlying the evolution of PSC to SCLC.

Platinum/PEM/Pembro may be a therapeutic option for TTF-1-negative non-sq NSCLC with good PS and adenocarcinoma histology, although careful management of irAE is required.

NFIC/METTL3 negative feedback loop in NSCLC cells suppresses exosomal miR-194-5p via m6A methylation; reduced miR-194-5p deepresses ZNF106 in macrophages, promoting M2 polarization and IL-6 secretion; Macrophage-derived IL-6 activates JAK2/STAT3 in NSCLC cells to upregulate METTL3, forming a positive feedback loop.

Afatinib 30 mg daily was well tolerated and demonstrated encouraging efficacy, with a 6-month PFS of 93.2%, suggesting outcomes comparable to standard dosing.

MET amplification alters the balance of EGFR/MET/ERBB3 dimerization, leading to a shift in signaling dependence from EGFR to MET. These findings provide insight into therapeutic strategies for EGFR-mutated NSCLC.