Conmana (icotinib)

This molecular event consequently activates downstream RAF/MAPK signaling, attenuating apoptosis while promoting cellular proliferation and drug resistance. Collectively, this study reveals the pivotal involvement of the circ_0097112/UPF1/NRAS axis in driving EGFR-TKI resistance in LUAD and offers a new theoretical basis for targeting circ_0097112 to reverse EGFR-TKI resistance.

She was initially treated with icotinib for an EGFR exon 21 L858R mutation but the disease progressed after 4 months. CONCLUSIONS As a single case with multiple confounders, this study generates hypotheses but does not confirm efficacy. Further investigation is required to validate high-dose furmonertinib for NSCLC with EGFR exon 14 missense mutations.

Following resection of a right lung nodule, molecular testing identified an EGFR exon 19 deletion, and icotinib was subsequently administered for contralateral ground-glass nodules...In published reports, these two conditions generally have different driving gene changes, and their potential biological relationship is still unclear. This case shows that when new lesions are found after lung cancer surgery, besides tumor recurrence, other diagnoses, namely PLCH, should be considered, and the diagnosis should be confirmed by histopathological examination.

VS biology reflects integrated genetic and epigenomic dysregulation. Advancing care will require multi-omic classification, biomarker-driven trials, and combination therapies targeting both signaling and epigenetic vulnerabilities. Future management is expected to shift toward personalized, mechanism-based strategies aimed at durable tumor control while preserving hearing and quality of life.

The patient was managed with a combination therapy of icotinib (an EGFR-TKI) and Pirfenidone (an anti-fibrotic agent). Tumor molecular testing is also important in patients with NSCLC concurrent with IPF. Furthermore, it provides preliminary clinical evidence suggesting that, with careful monitoring and concomitant anti-fibrotic therapy, EGFR-TKIs like Icotinib may represent a viable treatment option for patients co-existing with IPF and EGFR-mutated NSCLC.

P1, N=94, Not yet recruiting, Fuzhou General Hospital

Since 1997, EGFR tyrosine kinase inhibitors (EGFR-TKIs) have evolved from first-generation agents, such as gefitinib, erlotinib, and icotinib, to second-generation agents like afatinib and dacomitinib, now to third-generation agents, including osimertinib, aumolertinib, furmonertinib, befotertinib, rezivertinib, rilertinib, limertinib, lazertinib, mifanertinib for EGFR L858R, sunvozertinib for EGFR exon 20 insertion (20ins), and zorifertinib for EGFR-sensitive mutation with brain metastases. Over the past 30 years, substantial advancements have been made in the comprehensive management of EGFR-mutant NSCLC. This systemic review provides the history of the development of EGFR-TKI therapy for NSCLC from 1997 to 2026, highlighting clinical milestones, emerging therapies, and future directions in this rapidly evolving field.

The combination of aumolertinib and icotinib shows encouraging efficacy and a tolerable safety profile in patients with EGFR-mutant NSCLC and BMs, supporting its potential as a therapeutic option warranting further investigation.

Adjuvant immunotherapies for lung cancer deliver meaningful clinical benefits, but their economic value and affordability are highly context-specific. While several strategies are cost-effective at the individual patient level, health system affordability is strongly influenced by the pace and scale of adoption. Scenario-based budget impact analyses demonstrate that accelerated uptake can impose substantial short-term fiscal pressure, whereas phased or restricted implementation markedly improves affordability without altering cost-effectiveness conclusions. These findings underscore the importance of integrating cost-effectiveness evidence with explicit consideration of budget impact, adoption strategies, and managed entry mechanisms to support sustainable and equitable scale-up of adjuvant immunotherapies in routine clinical practice.

The patient showed no meaningful response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), including the first-generation (Icotinib), the second-generation (Afatinib) and the third-generation (Aumolertinib). Trophoblast cell surface antigen 2-antibody-drug conjugate (TROP2-ADC) and immune checkpoint inhibitors (ICIs) combined with Bevacizumab also resulted in limited efficacy. Based on the clinical features and treatment response of this case, we reviewed the published literature about the pathological characteristics, mutational landscape, and current therapeutic approaches for PEAC, with a particular focus on the therapeutic challenges and future research directions for EGFR-mutant PEAC, aiming to provide insights for clinical practice and further studies..

P=N/A, N=88, Not yet recruiting, Beijing Hospital; Beijing Hospital

P=N/A, N=200, Not yet recruiting, Beijing Chest Hospital Capital Medical University; Beijing Chest Hospital Capital Medical University