Ongoing improvements in technique and instruments for video-assisted thoracoscopic surgery (VATS) have made minimally-invasive uniportal VATS lobectomy a reality. However, the outcomes of the procedure are still under investigation, and at present, uniportal VATS lobectomy is performed infrequently at most hospitals. We have therefore reviewed our outcomes with this procedure in an attempt to validate its safety, efficacy, and feasibility. We retrospectively analyzed and compared perioperative data for patients who underwent uniportal, two-port, and traditional three-port VATS lobectomy between January 2015 and December 2015 at our hospital. Among 257 patients who had successful VATS lobectomy during the study period, 73 underwent uniportal VATS, 86 underwent two-port VATS, and 98 underwent traditional three-port VATS. There were no surgical or 30-day postoperative mortalities, and no significant differences in operative times, blood loss, number of lymph nodes retrieved and nodal stations explored, drainage times, length of hospital stay, or postoperative complications among the three groups. The visual analogue scale (VAS) pain scores were significantly lower in the uniportal VATS group after surgery (P < 0.05). Uniportal VATS lobectomy is a safe and feasible surgical procedure that is associated with decreased surgical trauma and less postoperative pain compared to traditional VATS. Further long term follow-up analyses in large numbers of patients are ongoing.

Lung cancer persistently leads as the primary cause of morbidity and mortality among malignancies. A notable increase in the prevalence of lung adenocarcinoma has become evident in recent years. Although targeted therapies have shown in treating certain subsets of non-small cell lung cancers (NSCLC), a significant proportion of patients still face suboptimal therapeutic outcomes. Neuregulin-1 (NRG1), a critical member of the NRG gene family, initially drew interest due to its distribution within the nascent ventricular endocardium, showcasing an exclusive presence in the endocardium and myocardial microvessels. Recent research has highlighted NRG1’s pivotal role in the genesis and progression across a spectrum of tumors, influencing molecular perturbations across various tumor-associated signaling pathways. This review provides a concise overview of NRG1, including its expression patterns, configuration, and fusion partners. Additionally, we explore the unique features and potential therapeutic strategies for NRG1 fusion-positive occurrences within the context of NSCLC.

Cancer signaling networks, highly dynamic with interconnected systems, regulate tumor initiation, its progression, therapeutic response and drug resistance. Rather than functioning as isolated pathways, these networks integrate extracellular and intracellular signals through coordinated interactions among membrane receptors, intracellular transducers and downstream effectors. Increasing evidence suggests that pathway crosstalk, feedback regulation and adaptive reprogramming are central to tumor phenotypic plasticity, microenvironmental adaptation and resistance to therapy. In this review, the core architecture of cancer signaling networks and the major oncogenic pathways embedded within them were summarized with a particular focus on PI3K/Akt/mTOR, MAPK/ERK and Wnt/β‑catenin signaling. The dynamic network properties that shape cancer behavior, including compensatory activation, context‑dependent signaling outputs and interactions with the tumor microenvironment, were further discussed. These features provide insights into why single‑pathway inhibition often produces only a limited and transient clinical benefit. Importantly, a network‑level understanding of cancer signaling has major translational implications. Therapeutic resistance frequently arises through pathway reactivation, bypass signaling and adaptive reprogramming, necessitating rational combination strategies and multi‑target interventions. Advances in multi‑omics, single‑cell and spatial technologies and computational modeling are crucial for characterizing signaling network dynamics and identifying clinically relevant vulnerabilities.

Assessment at progression after epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) therapy in EGFR-mutant non-small cell lung cancer requires more than identifying a single resistance mechanism. It also requires attention to lineage plasticity, tumor heterogeneity, the pattern of progression, and tissue-based findings. In a subset of patients, rebiopsy may reveal squamous histological transformation, sometimes with retention of the founder EGFR mutation. When present, retention of the founder EGFR mutation supports a shared clonal origin but does not, by itself, determine treatment. Confirmation of squamous transformation also changes the evidentiary context, because results from histologically unselected post-EGFR-TKI populations cannot always be applied directly to patients with confirmed transformation. This review focuses on squamous transformation and related basal/squamous reprogramming detected at EGFR-TKI progression, with particular emphasis on histological and molecular reassessment. We distinguish between direct clinical evidence from histologically confirmed transformed tumors and supportive translational evidence from EGFR-mutant resistance models and related lineage-transition systems. Plasma circulating tumor DNA can identify selected resistance alterations and track molecular evolution, but it cannot define morphology or lineage identity. When transformation is suspected, repeat tissue biopsy remains central, and reassessment should integrate morphology, immunohistochemistry, and paired molecular comparison with the original tumor. Integrated pathological and molecular reassessment may also uncover coexisting actionable alterations and help clarify whether progression is driven mainly by the transformed component, residual EGFR-dependent disease, or mixed resistance. Current evidence does not support a transformation-specific treatment sequence, so management remains individualized. Future studies should combine prospective rebiopsy cohorts, paired tissue–plasma profiling, and clinically annotated models to identify predictors of transformation and develop lineage-informed treatment strategies.

Histological transformation is an important mechanism of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in EGFR-mutant non-small cell lung cancer. Compared with small cell transformation, acquired squamous transformation is uncommon and remains less well characterized. We report a 52-year-old woman who underwent thoracoscopic left upper lobectomy and wedge resection of the left lower lobe for lung adenocarcinoma in April 2021. Molecular testing identified an EGFR exon 19 deletion and a TP53 c.713G>T (p.C238F) mutation. She received osimertinib, and the interval from treatment initiation to the first clinically and radiologically suspected disease progression was approximately 39 months. After this clinically suspected progression, pemetrexed plus cisplatin achieved a partial response. In August 2025, an enlarged left supraclavicular lymph node was detected, and re-biopsy confirmed squamous cell carcinoma. Systemic evaluation did not reveal evidence of a second primary malignancy. Molecular testing of the squamous lesion identified the same EGFR exon 19 deletion and TP53 mutation as those in the primary lung adenocarcinoma, providing molecular evidence consistent with a shared tumor origin and favoring acquired squamous histological transformation over a second primary squamous cell carcinoma. The patient subsequently received carboplatin, nanoparticle albumin-bound paclitaxel, and tislelizumab, achieving a radiologic partial response followed by stable disease during maintenance tislelizumab. This case highlights acquired squamous histological transformation as a rare resistance pattern after long-term osimertinib treatment. Re-biopsy and molecular comparison are important for distinguishing histological transformation from a second primary tumor. The observed response to platinum-taxane chemotherapy combined with tislelizumab should be interpreted cautiously because the relative contributions of chemotherapy and immunotherapy cannot be determined from a single case.