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Although there is no evidence from prospective randomized controlled trials to support this practice, pulmonary metastases of sarcomas are often treated surgically if they are resectable. The purpose of this retrospective study was to evaluate the prognostic factors and outcome of pulmonary metastasectomy (PM) for soft tissue sarcomas (STSs) arising in the trunk wall and extremities in 66 consecutive patients. Prognostic factors associated with disease-specific survival after PM were evaluated using univariate and multivariate analyses. The patients included 38 men and 28 women, with a median age of 49 years. The median disease-specific survival after PM was 48 months, and the 5-year survival rate was 45%. No major perioperative complications occurred. Disease-free interval (<12 months), size of largest lung lesion (≥20 mm), and non-curative resection were independent prognostic factors in multivariate analysis. PM was effective in selected patients with pulmonary metastases from STSs arising in the trunk wall and extremities. Disease-free interval, maximum size of metastases, and resectability were identified as prognostic factors.

Surfactant protein D (SP-D) is a member of the collectin family of proteins, which is secreted by airway epithelial cells. SP-D serves an important role in the immune system and in the inflammatory regulation of the lung. SP-D was recently found to suppress lung cancer progression by downregulating epidermal growth factor signaling. However, the relationship between SP-D and pulmonary metastases from colon cancer remains unknown. The present study aimed to determine whether SP-D may suppress the development of the mouse rectal carcinoma cell line, CMT93, in vitro. The present study investigated the effect of SP-D on pulmonary metastases from colon cancer in vivo using SP-D knockout mice. A wound healing assay and cell invasion assay revealed that SP-D suppressed the proliferation, migration and invasion of CMT-93 cells. After injection of CMT-93 cells into the tail vein, SP-D knockout mice were significantly more susceptible to developing pulmonary metastases than C57/BL6 mice (control). Moreover, a novel cell line (CMT-93 pulmonary metastasis; CMT-93 PM) was established from the lesions of pulmonary metastases in C57/BL6 mice following injection of CMT93 into the tail vein. CMT-93 PM exhibited more robust invasion and proliferation compared to CMT93, which was unaffected by exposure to SP-D. A higher incidence of pulmonary metastases was detected following injection of CMT93 PM into the tail vein of C57/BL6 mice compared with CMT-93. Consequently, SP-D may be involved in the pathogenesis of pulmonary metastases from colon cancer.

[This corrects the article DOI: 10.3389/fimmu.2025.1645909.].

Giant cell tumor (GCT) of bone is an intermittent and locally aggressive tumor with increasing pulmonary metastatic potential. In this study, we evaluated the interim clinical outcome of denosumab in patients with pulmonary metastatic GCT. We retrospectively reviewed seven patients with pulmonary metastatic GCT who received denosumab treatment after local tumor surgery during January 2014 and July 2016. Denosumab treatment for all patients lasted for at least 12 months. Serial chest computerized tomography scan was used to monitor the drug response and RECIST 1.1 standard was used to evaluate the therapeutic efficacy. All patients experienced chest pain relief in the first month of treatment. Three patients showed partial response. Four patients got stable disease after denosumab treatment. Adverse events included one patient with hypocalcemia and two patients with fever. No treatment-related deaths were reported. No patient with metastatic disease progression was found during an average of 28.6 months follow-up period. We presented a promising interim clinical outcome using denosumab to treat patients with pulmonary metastatic GCT. Denosumab might be considered as the first-line treatment for patients with inoperable metastatic pulmonary GCT. However, Phase II clinical study with larger number of patients and longer follow-up period is needed to detect the further efficacy and safety of this drug for lung metastatic GCT.

Colorectal cancer (CRC) is the third most common malignancy and the second most common cause of cancer-related mortality worldwide. A total of 20% of CRC patients present with distant metastases, most frequently to the liver and lung. In the primary tumor, as well as at each metastatic site, the cellular components of the tumor microenvironment (TME) contribute to tumor engraftment and metastasis. These include immune cells (macrophages, neutrophils, T lymphocytes, and dendritic cells) and stromal cells (cancer-associated fibroblasts and endothelial cells). In this review, we highlight how the TME influences tumor progression and invasion at the primary site and its function in fostering metastatic niches in the liver and lungs. We also discuss emerging clinical strategies to target the CRC TME.

Background The regulatory role of N6-methyladenosine (m6A) modification in the onset and progression of cancer has garnered increasing attention in recent years. However, the specific role of m6A modification in pulmonary metastasis of colorectal cancer remains unclear. Methods This study identified differential m6A gene expression between  primary colorectal cancer and its pulmonary metastases using transcriptome sequencing and immunohistochemistry. We investigated the biological function of METTL3 gene both in vitro and in vivo using assays such as CCK-8, colony formation, wound healing, EDU, transwell, and apoptosis, along with a BALB/c nude mouse model. The regulatory mechanisms of METTL3 in colorectal cancer pulmonary metastasis were studied using methods like methylated RNA immunoprecipitation quantitative reverse transcription PCR, RNA stability analysis, luciferase reporter gene assay, Enzyme-Linked Immunosorbent Assay, and quantitative reverse transcription PCR. Results The study revealed high expression of METTL3 and YTHDF1 in the tumors of patients with pulmonary metastasis of colorectal cancer. METTL3 promotes epithelial-mesenchymal transition in colorectal cancer by m6A modification of SNAIL mRNA, where SNAIL enhances the secretion of CXCL2 through the NF-κB pathway. Additionally, colorectal cancer cells expressing METTL3 recruit M2-type macrophages by secreting CXCL2. Conclusion METTL3 facilitates pulmonary metastasis of colorectal cancer by targeting the m6A-Snail-CXCL2 axis to recruit M2-type immunosuppressive macrophages. This finding offers new research directions and potential therapeutic targets for colorectal cancer treatment.

Bronchopneumonia is defined as an acute infection of the lung parenchyma involving the alveolar territory, associating an inflammation at the level of the bronchioles, most often grafting on a weakened area. The symptoms can be very variable, depending on the severity of the condition. Imaging, the chest X-ray shows multiple nodular or reticulonodular opacities that tend to be irregular and/or confluent. The distribution is often bilateral and asymmetric, predominantly involving the lung bases. The differential diagnosis of bronchopneumonia or the multiple pulmonary nodules described in the presented case is mainly made with pulmonary metastases, due to the increased frequency of diagnosis of pulmonary metastases in the case of multiple pulmonary nodules detected by chest CT; the lung being one of the main sites of metastasis of neoplasms.

BackgroundRadiofrequency ablation (RFA) and chemotherapy are used to treat lung cancer or pulmonary metastases, but no direct comparison of overall survival (OS) has been published. The present study aimed to assess the OS of RFA and/or chemotherapy in patients with lung cancer or pulmonary metastases who were not candidates for surgical resection.MethodsTo identify relevant studies, the following databases were electronically searched from their inception to 31 March 2023: PubMed, Embase, Web of Science, Cochrane Library, Scopus, Ovid, ScienceDirect, SinoMed, China National Knowledge Infrastructure Database, Chongqing VIP Chinese Science and Technology Periodical Database, Wanfang Database, LILACS,ClinicalTrials.gov, andChictr.org. Manual retrieval was also conducted. We used published hazard ratios (HRs) if available or estimates from other survival data.ResultsA total of 1,387 participants from 14 trials were included in the final analysis. Patients treated with RFA combined with chemotherapy significantly improved OS compared with those treated with chemotherapy alone [HR 0.50, 95% confidence interval (CI) 0.41–0.61; p < 0.00001], with an absolute difference at 12 months of 29.6% (95% CI 23.7–35.5), at 24 months of 19.2% (95% CI 10.1–28.2), and at 36 months of 22.9% (95% CI 12.0–33.7). No statistically significant difference was observed in the subgroups of case type, cancer type, chemotherapy drugs, and tumor size. The HR for OS with RFA plus chemotherapy vs. RFA alone was 0.53 (95% CI 0.41–0.70; p < 0.00001), corresponding to a 27.1% (95% CI 18.3–35.8), 31.0% (95% CI 19.9–41.9), and 24.9% (95% CI 15.0–34.7) absolute difference in survival at 12 months, 24 months, and 36 months, respectively. Subgroup analysis by geographic region and TNM stage showed that RFA combined with chemotherapy still significantly improved OS compared to RFA. The HR of RFA vs. chemotherapy was 0.98 (95% CI 0.60–1.60; p = 0.94), with an absolute difference at 12 months of 1.4% (95% CI -19.2 to 22.1), at 24 months of 7.8% (95% CI -11.3 to 26.8), and at 36 months of 0.3% (95% CI -13.2 to 13.8). The overall indirect comparison of OS for RFA vs. chemotherapy was 0.95 (95% CI 0.72–1.26; p = 0.74). Data on progression-free survival were not sufficiently reported.ConclusionRFA combined with chemotherapy might be a better treatment option for patients with lung cancer or pulmonary metastases than chemotherapy alone or RFA alone. The comparison between RFA and/or chemotherapy remains to be specifically tested.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=335032, identifier CRD42022335032.

Recurrence after pulmonary metastasectomy (PM) is frequent, but it is unclear to whom repeated pulmonary metastasectomy (RPM) offers highest benefits. Retrospective analysis of oncological and post-operative outcomes of consecutive patients who underwent PM from 2003 to 2018. Overall survival (OS) and disease-free interval (DFI) were calculated. Cox regression was used to identify variables influencing OS and DFI. In total, 264 patients (female/male: 114/150; median age: 62 years) underwent PM for colorectal cancer (32%), sarcoma (19%), melanoma (16%) and other primary tumors (33%). Pulmonary metastasectomy was approached by video-assisted thoracic surgery (VATS) in 73% and pulmonary resection was realized by non-anatomical resection in 76% of cases. The overall median follow-up time was 33 months (IQR 16–56 months) and overall 5-year survival rate was 62%. Local or distant recurrences were observed in 172 patients (65%) and RPM could be performed in 66 patients (25%) for a total of 116 procedures. RPM was realized by VATS in 49% and pulmonary resection by wedge in 77% of cases. In RPM patients, the 5-year survival rate after first PM was 79%. Post-operative cardio-pulmonary complication rate (13% vs. 12%; p = 0.8) and median length of stay (4 vs. 5 days; p = 0.2) were not statistically different between first PM and RPM. Colorectal cancer (HR 0.56), metachronous metastasis (HR 0.48) and RPM (HR 0.5) were associated with better survival. In conclusion, our results suggest that RPM offers favorable survival rates without increasing post-operative morbidity.

ContextFew studies have explored radioactive iodine–refractory (RAIR) disease in children, adolescents, and young adults with papillary thyroid cancer (CAYA-PTC). ObjectiveThis study systematically investigated the clinicopathologic characteristics and prognosis of CAYA-PTC with RAIR disease. MethodsSixty-five patients with PTC aged ≤20 years were enrolled in this study, and all patients were confirmed to have pulmonary metastases. Clinicopathologic profiles were compared between the radioactive iodine–avid (RAIA) and RAIR groups. Univariate and multivariate regression analyses were performed to identify risk factors for RAIR status and progressive disease (PD). Gene alterations were detected in 17 patients. ResultsOverall, 20 patients were included in the RAIR group, accounting for 30.8% (20/65) of all patients. No significant difference in pathologic characteristics was observed between patients aged <15 years and patients aged 15-20 years, but younger patients were more likely to develop RAIR disease (hazard ratio [HR] 3.500, 95% CI 1.134-10.803, P = .023). RET fusions were the most common genetic alterations in CAYA-PTC, but an association with RAIR disease was not detected (P = .210). RAIR disease (HR 10.008, 95% CI 2.427-41.268, P = .001) was identified as an independent predictor of PD. The Kaplan–Meier curve revealed a lower progression-free survival (PFS) and disease-specific survival (DSS) rate in the RAIR group than in the RAIA group (P < .001 and P = .039). Likewise, RAIR disease was a risk factor for unfavorable PFS in patients aged <15 years (P < .001). ConclusionRAIR disease occurs in one-third of CAYA-PTC with pulmonary metastases. Younger patients (aged < 15 years) are more susceptible to RAIR status, which leads to unfavorable PFS and DSS.