Thoracic Cancer最新文献

Background: The relationship between the combination of platelet count and neutrophil-lymphocyte ratio (COP-NLR) and prognosis in patients with advanced non-small cell lung cancer (NSCLC) treated with immune checkpoint inhibitor (ICI) combination therapy with chemotherapy remains unclear. Thus, we investigated prognostic factors, including the COP-NLR, to identify patients who could benefit from the therapeutic efficacy of ICI combination therapy for advanced NSCLC. Furthermore, we evaluated the relationship between the COP-NLR score during ICI combination therapy and treatment response.

Methods: We conducted a retrospective cohort study of 88 patients with NSCLC who initially received ICI combination therapy. The primary outcome was overall survival (OS). The prognostic factors were extracted using the Cox proportional hazards model. The relationship between COP-NLR score at 3 weeks after starting ICI combination therapy and a good response (complete response [CR] and partial response [PR]) to treatment was analyzed using the chi-square test.

Results: The median OS was 15.7 months. In the multivariable analysis, Eastern Cooperative Oncology Group Performance Status (ECOG PS) 2, distant metastatic sites ≥2, and baseline COP-NLR scores of 1, 2 were extracted as significant poor prognostic factors. The proportion of patients with CR and PR in the 3-week COP-NLR score of 0 group was significantly higher than that in scores of 1, 2 group.

Conclusions: Baseline COP-NLR, ECOG PS, and number of distant metastatic sites were prognostic factors in patients with NSCLC with ICI combination therapy. A lower 3-week COP-NLR was associated with a good response to treatment.

Background: Patients with programmed cell death-ligand 1 (PD-L1) ≥50% metastatic non-small cell lung cancer (NSCLC) treated with first-line immunotherapy showed heterogeneous tumor responses. In this study, we investigated the clinical and immune-inflammatory markers distinguishing patients with metastatic NSCLC achieving high depth of tumor response (HDPR) from those with non-high depth of response (NHDPR). The impact of clinical features on the prognosis of patients with PD-L1 ≥50% were further clarified.

Methods: The clinical characteristics and immune-inflammatory markers of 17 patients with PD-L1 ≥50% metastatic NSCLC at Beijing Tiantan Hospital between July 2020 and December 2023 were retrospectively analyzed.

Results: Among the 17 patients, seven (41.2%) patients achieved HDPR (range: -50%, -72%) and 10 (58.8%) patients achieved NHDPR (range: -13%, -45%). Below normal CD4 + T lymphocytes/CD8 + T lymphocytes (CD4/CD8) ratio (p = 0.01) and oncogenes and/or tumor suppressor gene mutations (TP53/KRAS/EGFR) (p = 0.001) were found enriched for NHDPR compared with HDPR. With a median follow-up of 26.0 months (range: 17.2-34.8 months), the median progression-free survival (PFS) following first-line immunotherapy and overall survival (OS) were 9.0 months (95% CI: 5.0-13.0) and not reached (NR), respectively. The neutrophil-to-lymphocyte ratio (NLR) was identified as an independent prognostic factor on first-line PFS. Patients with an NLR ≥4 exhibited a shorter median PFS (7.0 months vs. NR; p = 0.033; 95% CI: 1.2-80.2) than those with an NLR <4 following first-line immunotherapy.

Conclusions: Among patients with PD-L1 ≥50% metastatic NSCLC who received first-line immunotherapy, a lower CD4/CD8 ratio and the presence of genes mutations showed a diminished tumor response and a higher NLR ratio exhibited a worse median PFS.

Objectives: The influence of lung resection on cardiac function has been reported, and previous studies have mainly focused on right ventricular (RV) dysfunction. As few studies have analyzed changes in left ventricular hemodynamic variables caused by lung resection, we aimed to investigate the perioperative changes in left ventricular stroke volume (LVSV) caused by anatomical lung resection.

Methods: We enrolled 61 patients who underwent anatomical lung resection and perioperative LVSV monitoring. The Flo Trac system was used for dynamic monitoring. We investigated changes in LVSV after lung resection and the factors that affected these changes. The operative procedures that contributed to these changes were also investigated.

Results: LVSV decreased after anatomical lung resection in the majority of patients (n = 38, 62.2%). Operative procedures affecting this change were (a) taping the superior pulmonary vein (SPV; right: V1-3) before dorsal part procedure (e.g., major fissure division of right upper lobectomy, A1 + 2c, and A4 + 5 division of left upper lobectomy); (b) division of the SPV (right: V1-3, V4 + 5); (c) division of A6-10 (in lower lobectomy); and (d) finish division of all vessels.

Conclusions: LVSV decrease was caused by anatomical lung resection in the majority of patients owing to the intraoperative procedures described above.

Background: Awareness of age-related features of carcinogenesis and the importance of cellular immunity is crucial for developing effective antitumor therapies for specific patient groups.

Methods: In this study, we examined different populations of cancer stem cells (CSCs) and circulating tumor cells (CTCs) in "young" (8-10 weeks) and "aged" (80-82 weeks) C57BL/6 male mice. We used an orthotopic model of Lewis lung carcinoma (LLC) to evaluate the effectiveness of cell therapy targeting lung cancer through reprogrammed CD8-positive T cells (rCD8+ T cells) in mice from two different ages.

Results: The findings revealed that tumor progression with age is primarily caused by impaired recruitment of T cells to the lungs. Additionally, a lower number of CTCs and CSCs were observed in younger mice compared to the older mice. The antitumor effect of rCD8+ T cells in aged mice was found to be inferior to that in young mice, which can be attributed to the reduced impact of therapy on specific CSCs populations.

Conclusions: These results offer new insights into the treatment of lung cancer using rCD8+ T cells. Considering the age-related characteristics influencing disease progression, this therapy has the potential to significantly enhance the effectiveness of treatment methods.

Bronchiolar adenoma (BA)/ciliated muconodular papillary tumor (CMPT) is a rare pulmonary neoplasm, with less than 150 cases documented in the literature. We report a unique case of BA/CMPT complicated by lymphoid interstitial pneumonia (LIP) in a 55-year-old male with Sjögren's disease. This is the first documented instance of such a comorbidity. Through a systematic review of PubMed, we also summarize the demographic, clinical, radiological, histopathological, and treatment characteristics of CMPT.

Background: To evaluate the safety and efficacy of percutaneous biopsy and microwave ablation (B + MWA) in patients with pulmonary nodules (PNs) who are receiving antithrombotic therapy by rivaroxaban as bridging therapy.

Methods: The study comprised 187 patients with PNs who underwent 187 B + MWA sessions from January 1, 2020, to December 31, 2021. The enrolled patients were divided into two groups: Group A, who received antithrombotic therapy five days before the procedure and received rivaroxaban as a bridging drug during hospitalization, and group B, who had no antithrombotic treatment. Information about the technical success rate, positive biopsy rate, complete ablative rate, and major complications were collected and analyzed.

Results: Group A comprised 53 patients and group B comprised 134 patients. The technical success rate was 100% in both groups. The positive biopsy rates were 88.68% and 91.04%, respectively (p = 0.6211, X² = 0.2443). In groups A and B, the complete ablative rates at 6, 12, and 24 months were 100.0% versus 99.25%, 96.23% versus 96.27%, and 88.68% versus 89.55%, respectively. There were no significant differences in bleeding and thrombotic complications between the two groups. No grade 5 complications occurred.

Conclusions: It is generally considered safe and effective that patients who are on antithrombotic therapy by rivaroxaban as bridging to undergo B + MWA for treating PNs.

Background: Lymph node (LN) metastasis is a significant prognostic factor for esophageal squamous cell carcinoma (ESCC), and there are no satisfactory methods for accurately predicting metastatic LNs. The present study aimed to assess the efficacy of ^99mTc-3PRGD₂ single-photon emission computed tomography (SPECT)/computed tomography (CT) for diagnosing metastatic LNs in ESCC.

Methods: A total of 15 enrolled patients with ESCC underwent ^99mTc-3PRGD₂ SPECT/CT and 18F-fluorodeoxyglucose positron emission tomography-computed tomography (¹⁸F-FDG PET/CT) examinations preoperatively. High-definition bone carving reconstruction technology (HD-xSPECT Bone) was applied to quantitatively assess the LN's SUV_max via SPECT/CT. The two methods were compared for diagnosing metastatic LNs with pathology as the gold standard.

Results: Among 15 patients, 23 metastatic lymph node stations (mLNSs) were predicted by SPECT/CT, with a mean SUV_max of 2.71 ± 1.34, of which 15 were pathologically confirmed; 32 mLNSs were predicted by PET/CT with a mean SUV_max of 4.41 ± 4.02, of which 17 were pathologically confirmed. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of SPECT/CT for diagnosing metastatic LNs were 62.50%, 91.30%, 85.34%, 65.22%, and 90.32%, respectively, and those of PET/CT were 70.83%, 83.70%, 81.03%, 53.13%, and 91.67%, respectively. There was no significant difference in sensitivity (p = 0.061) or specificity (p = 0.058) between the two methods. The AUC_SPECT/CT was 0.816 and the SUV_max threshold was 2.5.

Conclusion: ^99mTc-3PRGD₂ SPECT/CT might be an effective method for diagnosing metastatic LNs in ESCC, especially in combination with HD-xSPECT Bone. The diagnostic efficiency of this method was noninferior to that of ¹⁸F-FDG PET/CT. The SUV_max threshold of 2.5 showed the highest agreement with the pathology findings.

Background: Circular RNAs (circRNAs), produced by reverse splicing, act as important players in human cancers. We aimed to assess the biological functions of circRNA pituitary homeobox 1 (circ-PITX1) in non-small-cell lung cancer (NSCLC).

Methods: qRT-PCR was employed to determine RNA expression. Biological behaviors of NSCLC cells were assessed by CCK-8, colony formation, EdU assay, flow cytometry, wound healing, and transwell assays. Glutamine catabolism was examined via the measurement of glutamine consumption, α-ketoglutarate levels, as well as ATP levels. Protein levels were detected by western blot assays. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to reveal the mechanism responsible for circ-PITX1 regulating NSCLC cell malignancy. The murine xenograft model was established to investigate circ-PITX1's effect on tumor formation.

Results: Circ-PITX1 was overexpressed in NSCLC tissue samples and cells. Its low expression repressed NSCLC cell proliferation and motility. Moreover, our data revealed its downregulation inhibited glutamine catabolism and tumor formation and promoted cell apoptosis. In addition, circ-PITX1 bound to miR-615-5p, and its inhibitory effect on tumor cellular behaviors could be reversed after decreasing miR-615-5p expression. The miRNA targeted E26 transformation specific-1 (ETS1), whose upregulation abolished miR-615-5p overexpression-induced effects in NSCLC cells. Furthermore, circ-PITX1 positively modulated ETS1 production through interaction with miR-615-5p.

Conclusion: Circ-PITX1 facilitated NSCLC progression via modulating miR-615-5p/ETS1 pathway.

The distinction between separate primary lung carcinomas (SPLCs) and intrapulmonary metastases (IPMs) is crucial to accurate cancer staging. Histopathology-based classification cannot always determine the relatedness of multiple tumors taken from the lung. Recently, next-generation sequencing (NGS) has been used for biomarker determination, but it also has the potential to inform clonality determination among multiple tumors. Here we present a patient with three lung tumors, each diagnosed as adenocarcinoma by histopathology with a differential diagnosis of SPLC versus IPM. We pursued molecular profiling by NGS, which revealed three unique mutational patterns ruling out the possibility of clonal relatedness among the cancers. Our case supports the utility of NGS in supplementing histopathological methods to distinguish between SPLCs and IPMs and to guide treatment decisions.

Background: The aim of the present study was to investigate the function of novel circular RNA hsa_circ_0036683 (circ-36683) in non-small cell lung cancer (NSCLC).

Methods: RNA sequencing was used to screen out differentially expressed miRNAs. Expression levels of miR-4664-3p and circ-36683 were evaluated in lung carcinoma cells and tissues by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The effects of miR-4664-3p and circ-36683 on proliferation and migration were assessed using cell counting kit-8 (CCK-8), wound healing and transwell migration assays and xenograft experiments. The targeting relationship of circ-36683/miR-4664-3p/CDK2AP2 was assessed by luciferase reporter assays, western blot, qRT-PCR and argonaute2-RNA immunoprecipitation (AGO2 RIP). Co-immunoprecipitation (Co-IP), 5-ethynyl-2'-deoxyuridine (EdU) staining and CCK-8 were used to validate the indispensable role of CDK2AP2 in suppressing cell proliferation as a result of CDK2AP1 overexpression.

Results: By RNA sequencing, miR-4664-3p was screened out as an abnormally elevated miRNA in NSCLC tissues. Transfection of miR-4664-3p could promote cell proliferation, migration and xenograft tumor growth. As a target of miR-4664-3p, CDK2AP2 expression was downregulated by miR-4664-3p transfection and CDK2AP2 overexpression could abolish the proliferation promotion resulting from miR-4664-3p elevation. Circ-36683, derived from back splicing of ABHD2 pre-mRNA, was attenuated in NSCLC tissue and identified as a sponge of miR-4664-3p. The functional study revealed that circ-36683 overexpression suppressed cell proliferation, migration and resulted in G0/G1 phase arrest. More importantly, the antioncogenic function of circ-36683 was largely dependent on the miR-4664-3p/CDK2AP2 axis, through which circ-36683 could upregulate the expression of p53/p21/p27 and downregulate the expression of CDK2/cyclin E1.

Conclusion: The present study revealed the antioncogenic role of circ-36683 in suppressing cell proliferation and migration and highlighted that targeting the circ-36683/miR-4664-3p/CDK2AP2 axis is a promising strategy for the intervention of NSCLC.