Background: In studies of stage IV epidermal growth factor receptor (EGFR)-mutant nonsmall-cell lung cancer (NSCLC), <10% of patients underwent surgery; thus, the effect of surgery in these patients remains unclear. We investigated whether primary lung tumor resection could improve the survival of patients with stage IV EGFR-mutant NSCLC without progression after first-line EGFR-tyrosine kinase inhibitor (EGFR-TKI) treatment.
Methods: This retrospective case-control study included patients treated with first-line EGFR-TKIs without progression on follow-up imaging. Patients in the surgery group (n = 56) underwent primary tumor resection, followed by TKI maintenance therapy. Patients in the control group (n = 224; matched for age, metastatic status, and Eastern Cooperative Oncology Group performance status) received only TKI maintenance therapy. Local ablative therapy for distant metastasis was allowed in both groups. The primary endpoint was progression-free survival. The secondary endpoints were overall survival, failure patterns, and complications/adverse events.
Results: The median time from TKI treatment to surgery was 5.1 months. For the surgery and control groups, the median follow-up periods were 34.0 and 38.5 months, respectively, with a median (95% confidence interval) progression-free survival of 29.6 (18.9-40.3) and 13.0 (11.8-14.2) months, respectively (P < 0.001). Progression occurred in 29/56 (51.8%) and 207/224 (92.4%) patients, respectively. The median overall survival in the surgery group was not reached. The rate of surgical complications of grade ≥2 was 12.5%; complications were treated conservatively.
Conclusions: Primary tumor resection is feasible for patients with EGFR-mutant nonprogressed NSCLC during first-line EGFR-TKI treatment and may improve survival better than maintenance EGFR-TKI therapy alone.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1245/s10434-022-11483-7 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Durvalumab as consolidation therapy in patients who received chemoradiotherapy for unresectable stage III NSCLC: Real-world data from an expanded access program in Brazil (LACOG 0120).
J Bras Pneumol
January 2025
. Centro de Pesquisa em Oncologia, Hospital São Lucas, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre (RS), Brasil.
Objective: The PACIFIC trial established standard therapy for patients with unresectable stage III NSCLC who did not progress after platinum-based concurrent chemoradiation therapy. However, real-world data, particularly from Latin America, remain limited. The LACOG 0120 study aimed to evaluate the efficacy and safety of consolidation therapy with durvalumab in a real-world setting in Brazil.
View Article and Find Full Text PDFAntiproliferative effect of hydroalcoholic brown propolis extract on tumor and non-tumor cells.
Braz J Biol
January 2025
Universidade Tecnológica Federal do Paraná - UTFPR, Departmeno de Química e Ciências Biológicas, Francisco Beltrão, PR, Brasil.
Studies show that propolis has antimicrobial, antifungal, antiviral, anti-inflammatory, antioxidant, antitumor, and immunomodulatory properties, and may protect against diseases such as diabetes, cardiovascular disease, and cancer. We aimed to extract compounds of brown propolis with hydroalcoholic solvents and evaluate their cytotoxic activity on tumor and non-tumor cells by MTT test. We tested the solute:solvent ratio (ethanol:water) and extraction time in a Shaker incubator (710 rpm) before conducting a central composite rotational design (CCRD) to optimize time and solvent mixture.
View Article and Find Full Text PDFSMARCA4 regulates the NK-mediated killing of senescent cells.
Sci Adv
January 2025
MRC Laboratory of Medical Sciences (LMS), Du Cane Road, London W12 0NN, UK.
Induction of senescence by chemotherapeutic agents arrests cancer cells and activates immune surveillance responses to contribute to therapy outcomes. In this investigation, we searched for ways to enhance the NK-mediated elimination of senescent cells. We used a staggered screen approach, first identifying siRNAs potentiating the secretion of immunomodulatory cytokines to later test for their ability to enhance NK-mediated killing of senescent cells.
View Article and Find Full Text PDFA histochemical approach to activity-based copper sensing reveals cuproplasia-dependent vulnerabilities in cancer.
Proc Natl Acad Sci U S A
January 2025
Department of Chemistry, University of California, Berkeley, CA 94720.
Copper is an essential nutrient for sustaining vital cellular processes spanning respiration, metabolism, and proliferation. However, loss of copper homeostasis, particularly misregulation of loosely bound copper ions which are defined as the labile copper pool, occurs in major diseases such as cancer, where tumor growth and metastasis have a heightened requirement for this metal. To help decipher the role of copper in the etiology of cancer, we report a histochemical activity-based sensing approach that enables systematic, high-throughput profiling of labile copper status across many cell lines in parallel.
View Article and Find Full Text PDFIncreased Systemic Immune-Inflammatory Index and Association with Occult Nodal Disease in Non-Small Cell Lung Cancer.
J Am Coll Surg
November 2024
Department of Cardiovascular and Thoracic Surgery, Rush University Medical Center, Chicago, Illinois, USA.
Background: It has been proposed that more aggressive tumors trigger a stronger inflammatory response than less aggressive types. We hypothesize that systemic immune inflammatory index (SII) is associated with occult nodal disease (OND) in clinically node negative (cN0) patients undergoing lung resection for non-small cell lung cancer (NSCLC).
Study Design: The study included patients who underwent lung resection with nodal dissection, according to current guidelines, at a single center between 2010-2021 for NSCLC.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!