Clinical lung cancer最新文献

Purpose: This study examines the imaging findings and malignancy suspicion associated with hydrogel lung tract sealants (h-LTS) used after CT-guided lung biopsy (CTLB).

Materials and methods: Charts of patients who underwent CTLB from 01/2016 to 01/2020 were reviewed for biopsy date, h-LTS use, resection, and imaging follow-up. Exclusion criteria included resection <3 months postbiopsy, no imaging ≥3 months, and pleural nodules. Postbiopsy imaging was analyzed for abnormalities at the biopsy tract. Out of 164 patients who underwent CTLB with h-LTS, a random subset of 64 patients (Group A) was anonymized and compared with another randomly selected, anonymized group of 64 patients who underwent CTLB without h-LTS during the study period (Group B) to assess inter-reader agreement. Two cardiothoracic radiologists reviewed the anonymized intraprocedural biopsy CT and follow-up imaging at multiple intervals (3-6, 6-12, 12-24, >24months) for abnormalities along the biopsy tract and associated malignancy suspicion (Categories 1-5 [low-high]).

Results: A serpiginous lesion was observed along the biopsy tract in 60% (99/164) of patients who received h-LTS, lasting an average of 23.3 months (Range: 3-67). Moderate inter-reader agreement was seen for abnormalities in Group A patients at all follow-up intervals. FDG-PET/CT showed mild uptake for up to 5 years in 46% of patients. At initial follow-up, 17% of h-LTS scars were rated Category 3 or higher suspicion for malignancy. Most h-LTS scars maintained or decreased in suspicion in later follow-ups.

Conclusion: h-LTS is associated with a serpiginous scar, which may be mildly hypermetabolic and last up to 5 years.

Introduction: To analyze the impact of Kirsten-Rat-Sarcoma Virus (KRAS) mutations on tumor-growth as estimated by tumor-doubling-time (TDT) among solid-dominant clinical-stage I lung adenocarcinoma. Moreover, to evaluate the prognostic role of KRAS mutations, TDT and their combination in completely-resected pathologic-stage I adenocarcinomas.

Methods: In this single-center retrospective analysis, completely resected clinical-stage I adenocarcinomas presenting as solid-dominant nodules (consolidation-to-tumor ratio > 0.5) in at least 2 preoperative computed-tomography scans were enrolled. Nodules' growth was scored as fast (TDT < 400 days) or slow (TDT > 400 days). KRAS-mutated adenocarcinomas were identified with next-generation sequencing. Logistic- and Cox-regressions were used to identify predictors of fast-growth and disease-free survival (DFS), respectively.

Results: Among 151 patients, 83 (55%) had fast-growing nodules and 64 (42.4%) were KRAS-mutated. Fast-growing nodules outnumbered in the KRAS-mutated group (n = 45; 70.3%), median TDT 95-days (interquartile range, IQR 43.5-151.5) compared to the KRAS wild-type group (38, 43.7%), median TDT 138-days (IQR 70.3-278.5). KRAS-mutations predicted faster-growth at multivariable analysis (P = .009). In a subgroup analysis including 108 pathologic-stage I adenocarcinomas, neither KRAS-mutations (P = .081) nor fast-growing pattern (P = .146) affected DFS. Nevertheless, the association of KRAS-mutations and fast-growing pattern identified a subgroup of patients with worse DFS (P = .02). The combination of fast-growing and KRAS-mutations (hazard-ratio 2.97 [95%CI 1.22-7.25]; P = .017) and average nodule diameter at diagnosis (hazard-ratio 1.08 [95%CI 1.03-1.14]; P = .004) were independent predictors of worse DFS.

Conclusion: KRAS mutations are associated to faster growth, in clinical-stage I adenocarcinoma presenting at diagnosis as solid-dominant nodules undergoing complete resection. Moreover, faster-growth identifies a subgroup of pathologic-stage I KRAS-mutated adenocarcinomas with higher recurrences.

Introduction: Brain metastases (BM) are a prevalent and severe complication of non-small cell lung cancer (NSCLC) that significantly affects quality of life. Although several predictive factors for BM have been identified, the influence of EGFR mutation subtypes remains under-explored.

Methods: We retrospectively examined patients with advanced NSCLC and EGFR mutations treated with first-line EGFR-TKIs. Our primary endpoint was intracranial progression-free survival (icPFS), defined as the time from the initiation of upfront treatment to the development of BM, the progression of existing brain lesions, or death. Additionally, we evaluated intracranial objective response rates (icORR) and disease control rates (icDCR) for patients with baseline BM. Subgroup and multivariate analyses were performed to adjust for relevant factors.

Results: Of the 324 patients analyzed, 40.7% had baseline BM. Overall, the EGFR^L858R mutation was linked to a significantly shorter median icPFS of 13.9 months, compared to 23.4 months for those with EGFR^Δ19 (HR 1.60, P < .0001) For patients without baseline BM, icPFS was 14.3 months for EGFR^L858R versus 26.2 months (HR 1.65, P = .007), while with baseline BM, it was 13.9 versus 18.5 months (HR 1.59, P = .035); icORR was lower for EGFR^L858R (31.2% vs. 58.8%). Multivariate analysis showed EGFR^L858R was independently linked to worse icPFS in patients with (HR 1.634, P = .031) and without BM (HR 1.606, P = .008), and lower icORR (OR 3.511, P = .007) and icDCR (OR 4.443, P = .006).

Conclusions: EGFR^L858R mutation significantly impacts BM development, intracranial progression, and response, emphasizing its critical role in therapy selection.

Background: Although chemoimmunotherapy is recommended for advanced nonsquamous non-small cell lung cancer (NSCLC) with low programmed cell death ligand 1 (PD-L1) expression, no head-to-head comparisons of immune checkpoint inhibitors (ICIs) have been performed. Therefore, we compared the effect and safety of regimens in these patients to guide evidence-based treatment.

Methods: This retrospective study included patients with advanced nonsquamous NSCLC with a PD-L1 tumor proportion score of 1% to 49% administered ICI combination platinum-based chemotherapy between May 2018 and May 2023 at 19 institutions in Japan. The main analysis compared survival outcomes and the incidence of grade ≥3 adverse events among regimens.

Results: Among 316 included patients (median [range] age, 69 [36-89] years; 242 males; 41 never smokers), 200 (63%), 68 (22%), and 48 (15%) received chemotherapy combined with anti-programmed cell death protein 1 (PD-1), anti-PD-L1, and anti-PD-1/cytotoxic T-lymphocyte associated protein 4 (CTLA-4) antibodies, respectively. The median overall survival times were 28.6, 23.1, and 24.4 months (P = .41), and the median progression-free survival times were 9.4, 7.2, and 8.7 months (P = .28) in the anti-PD-1/Chemo, anti-PD-L1/Chemo and anti-PD-1/CTLA-4/Chemo groups, respectively. The anti-PD-1/CTLA-4/Chemo group had the lowest incidence of hematologic toxicity (P = .13) and the highest incidence of nonhematologic toxicity (P = .07). The incidence of grade ≥3 pneumonitis was significantly lower in the anti-PD-L1/Chemo group (P = .049).

Conclusions: Despite comparable survival benefits, adverse events differed among three regimens in patients with low PD-L1 expression. Notably, anti-PD-L1 antibody combination chemotherapy may reduce the risk of severe pneumonitis.