[Retracted] MACC­1 antibody target therapy suppresses growth and migration of non­small cell lung cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control data in Fig. 2B and C on p. 7332, showing immunofluorescence and migration assay experiments respectively, were strikingly similar to data appearing in different form in another article which was written by different authors at different research institutes [Tian L, Shen D, Li X, Shan X, Wang X, Yan Q and Liu J: Ginsenoside Rg3 inhibits epithelial­mesenchymal transition (EMT) and invasion of lung cancer by down­regulating FUT4. Oncotarget 7: 1619­1632, 2016]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 7329­7336, 2017; DOI: 10.3892/mmr.2017.7517].

Homologous genes shared between probiotics and pathogens affect the adhesion of probiotics and exclusion of pathogens in the gut mucus of shrimp.

Clarifying mechanisms underlying the selective adhesion of probiotics and competitive exclusion of pathogens in the intestine is a central theme for shrimp health. Under experimental manipulation of probiotic strain (i.e., Lactiplantibacillus plantarum HC-2) adhesion to the shrimp mucus, this study tested the core hypothesis that homologous genes shared between probiotic and pathogen would affect the adhesion of probiotics and exclusion of pathogens by regulating the membrane proteins of probiotics. Results indicated that the reduction of FtsH protease activity, which significantly correlated with the increase of membrane proteins, could increase the adhesion ability of L. plantarum HC-2 to the mucus. These membrane proteins mainly involved in transport (glycine betaine/carnitine/choline ABC transporter choS, ABC transporter, ATP synthase subunit a atpB, amino acid permease) and regulation of cellular processes (histidine kinase). The genes encoding the membrane proteins were significantly (p < 0.05) up-regulated except those encoding ABC transporters and histidine kinases in L. plantarum HC-2 when co-cultured with Vibrio parahaemolyticus E1, indicating that these genes could help L. plantarum HC-2 to competitively exclude pathogens. Moreover, an arsenal of genes predicted to be involved in carbohydrate metabolism and bacteria-host interactions were identified in L. plantarum HC-2, indicating a clear strain adaption to host's gastrointestinal tract. This study advances our mechanistic understanding of the selective adhesion of probiotics and competitive exclusion of pathogens in the intestine, and has important implications for screening and applying new probiotics for maintaining gut stability and host health.

NETosis and thrombosis in vaccine-induced immune thrombotic thrombocytopenia.

Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare yet serious adverse effect of the adenoviral vector vaccines ChAdOx1 nCoV-19 (AstraZeneca) and Ad26.COV2.S (Janssen) against COVID-19. The mechanisms involved in clot formation and thrombocytopenia in VITT are yet to be fully determined. Here we show neutrophils undergoing NETosis and confirm expression markers of NETs in VITT patients. VITT antibodies directly stimulate neutrophils to release NETs and induce thrombus formation containing abundant platelets, neutrophils, fibrin, extracellular DNA and citrullinated histone H3 in a flow microfluidics system and in vivo. Inhibition of NETosis prevents VITT-induced thrombosis in mice but not thrombocytopenia. In contrast, in vivo blockage of FcγRIIa abrogates both thrombosis and thrombocytopenia suggesting these are distinct processes. Our findings indicate that anti-PF4 antibodies activate blood cells via FcγRIIa and are responsible for thrombosis and thrombocytopenia in VITT. Future development of NETosis and FcγRIIa inhibitors are needed to treat VITT and similar immune thrombotic thrombocytopenia conditions more effectively, leading to better patient outcomes.

Ring finger protein 180 suppresses cell proliferation and energy metabolism of non-small cell lung cancer through downregulating C-myc.

BACKGROUND: Non-small cell lung cancer (NSCLC) causes numerous deaths worldwide. however, biomarkers for NSCLC prognosis are scarce for its heterogeneity. Proteins containing the RING finger domain RING finger protein 180 (RNF180) is a key mediator for ubiquitination, which controls cell cycle and regulates progression in certain human tumors. However, the detailed function of RNF180 in NSCLC remains unclear. In the present study, we aimed to investigate the role of RNF180 and its molecule network in NSCLC. METHODS: Quantitative real-time polymerase chain reaction and immunohistochemical staining were used to analyze RNF180 levels. RNA interference and lentiviral-mediated vector transfections were performed to silence and overexpress RNF180 in NSCLC cells. Furthermore, Cell Counting Kit-8 was used for assessing biological function of RNF180 in cell proliferation and a xenograft model for examining its function in vivo. The activity of glycolysis was determined by examining the level of the extracellular acidification rate (ECAR). RESULTS: RNF180 expression decreased in NSCLC tissues, and its expression was positively correlated with the survival rate of patients with NSCLC. Moreover, RNF180 overexpression suppressed the proliferation and glycolytic activities in NSCLC cells and restricted its tumorigenicity in vivo. Furthermore, RNF180 silencing promoted the proliferation and glycolysis metabolism of NSCLC cells, whereas C-myc inhibitor disrupted these effects. The underlying anti-oncogene of RNF180 involved in C-myc downregulation via ubiquitin-dependent degradation. CONCLUSIONS: Together, these results firstly indicated the anti-tumor properties of RNF180 and its correlation with NSCLC progression, thereby endorsing the potential role of RNF180 as an efficient prognostic biomarker for tumor recurrence.

Antiplatelet antibody predicts platelet desialylation and apoptosis in immune thrombocytopenia.

Immune thrombocytopenia (ITP) is a bleeding disorder caused by dysregulated B- and T- cell functions, which lead to platelet destruction. A well-recognized mechanism of ITP pathogenesis involves anti-platelet and anti-megakaryocyte antibodies recognizing membrane glycoprotein (GP) complexes, mainly GPIb/IX and GPIIb/IIIa. In addition to the current view of phagocytosis of the opsonised platelets by splenic and hepatic macrophages via their Fc γ receptors, antibodyinduced platelet desialylation and apoptosis have also been reported to contribute to ITP pathogenesis. Nevertheless, the relationship between the specific thrombocytopenic mechanisms and various types of anti-platelet antibodies has not been established. In order to ascertain such association, we used sera from 61 ITP patients and assessed the capacity of anti-platelet antibodies to induce neuraminidase 1 (NEU1) surface expression, RCA-1 lectin binding and loss of mitochondrial inner membrane potential on donors' platelets. Sera from ITP patients with detectable antibodies caused significant platelet desialylation and apoptosis. Anti-GPIIb/IIIa antibodies appeared more capable of causing NEU1 surface translocation while anti-GPIb/IX complex antibodies resulted in a higher degree of platelet apoptosis. In ITP patients with anti-GPIIb/IIIa antibodies, both desialylation and apoptosis were dependent on FcγRIIa signaling rather than platelet activation. Finally, we confirmed in a murine model of ITP that destruction of human platelets induced by anti-GPIIb/IIIa antibodies can be prevented with the NEU1 inhibitor oseltamivir. A collaborative clinical trial is warranted to investigate the utility of oseltamivir in the treatment of ITP.

Advantages of McKeown minimally invasive oesophagectomy for the treatment of oesophageal cancer: propensity score matching analysis of 169 cases.

BACKGROUND: Oesophagectomy, the gold standard for oesophageal cancer treatment, causes significantly high morbidity and mortality. McKeown minimally invasive oesophagectomy (MIE) is preferred for treating oesophageal malignancies; however, limited studies with large sample sizes focusing on the surgical and oncological outcomes of this procedure have been reported. We aimed to compare the clinical safety and efficacy of McKeown MIE with those of open oesophagectomy (OE). PATIENTS AND METHODS: Overall, 338 oesophageal cancer patients matched by gender, age, location, size, and T and N stages (McKeown MIE: 169 vs OE: 169) were analysed. The clinicopathologic features, operational factors, postoperative complications, and prognoses were compared between the groups. RESULTS: McKeown MIE resulted in less bleeding (200 mL vs 300 mL, p<0.01), longer operation time (335.0 h vs 240.0 h, p<0.01), and higher number of harvested lymph nodes (22 vs 9, p<0.01) than OE did. Although the rate of recurrent laryngeal nerve injury in the two groups was not significantly different, incidence of anastomotic leakage (8 vs 24, p=0.003) was significantly lower in the McKeown MIE group. In addition, patients who underwent McKeown MIE had higher 5-year overall survival than those who underwent OE (69.9% vs 40.4%, p<0.001). CONCLUSION: McKeown MIE is proved to be feasible and safe to achieve better surgical and oncological outcomes for oesophageal cancer compared with OE.

Novel long non-coding RNA CYB561-5 promotes aerobic glycolysis and tumorigenesis by interacting with basigin in non-small cell lung cancer.

Abnormally expressed long non-coding RNAs (lncRNAs) have been recognized as potential diagnostic biomarkers or therapeutic targets in non-small cell lung cancer (NSCLC). The role of the novel lnc-CYB561-5 in NSCLC and its specific biological activity remain unknown. In this study, lncRNAs highly expressed in NSCLC tissue samples compared with paired adjacent normal tissue samples and atypical adenomatous hyperplasia were identified by RNA-seq analysis. Lnc-CYB561-5 is highly expressed in human NSCLC and is associated with a poor prognosis in lung adenocarcinoma. In vivo, downregulation of lnc-CYB561-5 significantly decreases tumour growth and metastasis. In vitro, lnc-CYB561-5 knockdown treatment inhibits cell migration, invasion and proliferation ability, as well as glycolysis rates. In addition, RNA pulldown and RNA immunoprecipitation (RIP) assays show that basigin (Bsg) protein interacts with lnc-CYB561-5. Overall, this study demonstrates that lnc-CYB561-5 is an oncogene in NSCLC, which is involved in the regulation of cell proliferation and metastasis. Lnc-CYB561-5 interacts with Bsg to promote the expression of Hk2 and Pfk1 and further lead to metabolic reprogramming of NSCLC cells.

HABP1 promotes proliferation and invasion of lung adenocarcinoma cells through NFκB pathway.

The aim of this research was to investigate the role of hyaluronan-binding protein 1 (HABP1) in lung adenocarcinoma. It was demonstrated by bioinformatics analysis that HABP1 was one of the differentially expressed genes in lung adenocarcinoma. Then, it was confirmed by qPCR, western blot, and immunohistochemistry analysis that HABP1 was upregulated in human tissue specimens we collected. Survival analysis showed that HABP1 was promised to serve as a new biomarker to predict the progress and prognosis of lung adenocarcinoma patients. In addition, we further studied the effects of regulating the expression of HABP1 on lung adenocarcinoma cells, indicating that altered expression of HABP1 could adjust cell proliferation and invasion through the NFκB signaling pathway.

CDK14 expression is elevated in patients with non-small cell lung cancer and correlated with poor prognosis.

OBJECTIVE: To investigate the clinical significance of cyclin-dependent kinase 14 (CDK14) expression in patients with non-small cell lung cancer (NSCLC). METHODS: The present prospective observational study included 193 patients diagnosed with NSCLC between January 2010 and December 2014. NSCLC tumor tissues and paired paracancerous normal tissues were obtained from all patients. CDK14, thyroid transcription factor 1 (TTF-1), cytokeratin 5/6 (CK5/6), and Ki67 expression was measured via immunohistochemistry (IHC). RESULTS: CDK14 staining was strong (>3) in 129 patients (66.49%) and weak (≤3) in 64 patients (33.16%). The mean IHC scores were markedly higher in tumor tissues than in paracancerous tissues. Pearson's analysis demonstrated that the IHC scores of CDK14 expression were positively correlated with TTF-1, CK5/6, and Ki67 scores. Kaplan-Meier analysis illustrated that 5-year overall survival was markedly longer in patients with weak CDK14 staining. TNM stage, pleural invasion, lymph node metastasis, CDK14 expression, and Ki67 expression were risk factors for 5-year overall survival in patients with NSCLC. CONCLUSION: CDK14 overexpression portended poor outcomes in patients with NSCLC, and CDK14 expression was correlated with TTF-1, CK5/5, and Ki67 expression.

Indirect detection of anti-platelet antibodies in immune thrombocytopenia.

Despite recent advances in the understanding and treatment of immune thrombocytopenia (ITP), its diagnosis remains clinical due to the lack of sensitive laboratory tests. The detection of anti-platelet antibodies (APA) in plasma, although highly specific, is notoriously insensitive. Specialised clinical platelet laboratories routinely perform a screening test of only one dilution for indirect APA testing by flow cytometry. We evaluated the presence of APA using several dilutions of plasma from 61 ITP patients. Herein, we report that serial dilutions can improve the diagnostic value of indirect APA assay for ITP. We show that performing just two dilutions (1:2 and 1:25) would capture over 90% of patients with detectable plasma APA. This method enables indirect testing to become a valuable tool to be incorporated into the management algorithm for ITP.

Integrative analysis of differential circular RNA and long non-coding RNA profiles and associated competing endogenous RNA networks in esophageal squamous cell carcinoma.

Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) play vital roles in the tumorigenesis of esophageal squamous cell carcinoma (ESCC). Nevertheless, the mechanism and regulatory network associated with this process remain largely unknown. In this study, we performed a comprehensive analysis of the expression of mRNAs, lncRNAs, and circRNAs by RNA-seq. A total of 3265 mRNAs, 1084 lncRNAs, and 38 circRNAs were found to be differentially expressed. Among these, 269 mRNAs were found to encode transcription factors (TFs). Functional enrichment analysis indicated that the dysregulated TFs are associated with the Hedgehog, Jak-STAT, TGF-beta, and MAPK signaling pathways. Furthermore, we constructed co-expression networks to screen the core lncRNAs and circRNAs involved in the regulation of transcription factors in these four pathways. Finally, we constructed a competing endogenous RNA (ceRNA) network of ESCC based on the abovementioned pathways. Our findings provide important insight into the role of lncRNAs and circRNAs in ESCC; the differentially expressed lncRNAs and circRNAs may represent potential targets for ESCC diagnosis and therapy.

MiR-769-5p, Which Targets HDGF, Inhibits Cell Proliferation and Invasion in Nonsmall Cell Lung Cancer.

MiR-769-5p regulates tumor correlative genes, which plays a critical role in the progression of various types of tumor. However, the precise regulatory mechanism of miR-769-5p on nonsmall cell lung cancer (NSCLC) is unknown. This study was to discover the role and underlying mechanisms of miR-769-5p in NSCLC. MiR-769-5p expression was shown to be reduced, according to our findings. MiR-769-5p overexpression inhibited NSCLC cell proliferation while promoting NSCLC cell apoptosis. Furthermore, NSCLC cell migration and invasion were reduced when miR-769-5p was overexpressed. Furthermore, HDGF was confirmed as a miR-769-5p target gene that was negatively regulated by miR-769-5p. Furthermore, more research revealed that HDGF overexpression reduced the inhibitory effect of miR-769-5p on NSCLC cell biofunction. Finally, miR-769-5p inhibited NSCLC cell proliferation and invasion by targeting HDGF, indicating that NSCLC could benefit from miR-769-5p as a diagnostic and prognostic biomarker.

Neuroepithelial Cell Transforming Gene 1 Acts as an Oncogene and Is Mediated by miR-22 in Human Non-Small-Cell Lung Cancer.

Abnormal expression of neuroepithelial cell transforming gene 1 (NET1) has been authenticated in many human cancers, including lung cancer. We have previously reported that NET1 functioned as an oncogene and promoted human non-small-cell lung cancer (NSCLC) growth and migration. However, the correlation between NET1 and its upstream miRNAs needed further illustration. Our present work demonstrated that miR-22 had a relatively low expression, and NET1 had a relatively high expression in both NSCLC samples and lung adenocarcinoma cell lines compared with corresponding normal controls. Moreover, miR-22 directly regulated NET1 and was verified to weaken cancer cell proliferation and migration, as well as enhance cell apoptosis by suppressing NET1. Furthermore, the inhibitory effect of miR-22 can be reversed via overexpressing NET1 using an ectopic expression vector in NSCLC cells. Our findings showed that miR-22/NET-1 axis may contribute to the inhibition of NSCLC growth and migration and represents a promising therapeutic target for NSCLC.

c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis.

Thrombopoietin (TPO) is a growth factor for the megakaryocytic/platelet lineage. In this study, we investigated the expression of TPO and its receptor, c-Mpl, in the human central nervous system (CNS) and their roles after a neural insult. Our results demonstrate that both TPO and c-Mpl are expressed in the neurons of the human CNS. TPO was also detected in human cerebrospinal fluid. TPO was found to be neuroprotective in hypoxic-ischemic neonatal rat brain models. In these rat models, treatment with TPO reduced brain damage and improved sensorimotor functions. In addition, TPO promoted C17.2 cell proliferation through activation of the PI3K/Akt signaling pathway. Via the Bcl-2/BAX signaling pathway, TPO exerted an antiapoptotic effect by suppressing mitochondrial membrane potentials. Taken together, our results indicate that TPO is neuroprotective in the CNS.

Low expression of long non-coding RNA ARAP1-AS1 can inhibit lung cancer proliferation by inducing G0/G1 cell cycle organization.

BACKGROUND: This paper examines the expression, function, and molecular mechanism of long non-coding ribonucleic acid (lncRNA) ARAP1 antisense RNA 1 (ARAP1-AS1) in lung cancer. Specifically, it aims to clarify the molecular mechanism of lncRNA ARAP1-AS1 that affects the occurrence and development of lung cancer, and provide a theoretical basis and molecular targets for targeted therapy or early diagnosis of lung cancer. METHODS: Fluorescence quantitative detection of lncRNA ARAP1-AS1 expression in lung cancer tissues and cell lines, and methylthiazolyldiphenyl-tetrazolium (MTT), plate cloning experiment, and flow cytometry were used to detect the effect of knockdown of lncRNA ARAP1-AS1 on cell proliferation, clone formation, and the cell cycle, respectively. Western blotting was used to detect the expression of cell cycle-related proteins as well as the effect of knockdown of lncRNA ARAP1-AS1 on lung cancer. Cell proliferation was assessed by a nude mouse subcutaneous tumor formation experiment. RESULTS: LncRNA ARAP1-AS1 is highly expressed in lung cancer tissues and cells. Knockdown of LncRNA ARAP1-AS1 can significantly inhibit the proliferation and clonal formation of lung cancer cells and induce G0/G1 cell cycle arrest. Knockdown of ARAP1-AS1 can markedly inhibit the expression of cell cycle-related protein cyclin D1, but has no significant effect on the expression of cyclin-dependent kinase (CDK)4 and CDK6. Furthermore, knockdown of ARAP1-AS1 can also notably inhibit the growth of lung cancer cells and substantially reduce the expression of Ki-67 in tumor-bearing tissues in nude mice. CONCLUSIONS: LncRNA ARAP1-AS1 is highly expressed in lung cancer. Knocking down of this gene can significantly inhibit cell proliferation in vitro and in vivo, and can also cause G0/G1 cell cycle arrest by inhibiting the expression of cyclin D1.

Acquired Glanzmann thrombasthenia associated with platelet desialylation.

BACKGROUND: The notable discrepancy between platelet count and bleeding manifestations in immune thrombocytopenia (ITP) patients with acquired Glanzmann thrombasthenia (GT) has been described. OBJECTIVES: We aimed to examine the mechanisms responsible for thrombocytopenia and the bleeding phenotype in a patient with acquired GT. PATIENT, METHODS, AND RESULTS: A patient with primary ITP underwent splenectomy due to steroid intolerance. Despite platelet count normalization, bleeding continued. Platelet aggregometry was abnormal with all agonists except for ristocetin. Flow cytometry demonstrated the presence of antiplatelet antibody, which caused dose-dependent inhibition of fibrinogen and PAC-1 binding, induction of neuraminidase-1 expression as well as platelet desialylation in donor platelets. Indirect monoclonal antibody immobilization of platelet specific antigen assay (MAIPA) confirmed specificity to αIIb ß3 only, corroborated by binding on Chinese hamster ovary (CHO) cells expressing human glycoprotein αIIb ß3 but not GP Ib/IX. Both desialylation and neuraminidase expression were observed with plasma adsorbed on Ib/IX CHO cells and with the immunoglobulin G (IgG) fraction. Desialylation was inhibited in the presence of anti-Fc-gamma receptor IIa (FcγRIIa) antibody. A nonobese diabetic/severe combined immunodeficient ITP murine model was established, which showed rapid hepatic donor platelet clearance in the presence of patient IgG. Treatment of mice with the neuraminidase inhibitor oseltamivir significantly reduced antibody-induced platelet destruction. CONCLUSIONS: We report the first case of a patient with acquired GT due to ITP with FcγRIIa mediated platelet desialylation, independent of platelet activation. Treatment with neuraminidase inhibitor may prevent platelet clearance by anti-αIIb ß3 antibodies.

Benefits of surgery in the multimodality treatment of stage IIB-IIIC small cell lung cancer.

Surgery combined with chemotherapy/radiotherapy is recommended for early stage small cell lung cancer (SCLC); however, the role of surgery in the multimodality treatment of advanced disease remains controversial. The clinical data of patients between 2000 and 2015 were obtained from the Surveillance, Epidemiology, and End Results database. The surgery group included 998 patients with stage IIB-IIIC. A matched non-surgery group (n = 2994) was generated by propensity score matching. The Kaplan-Meier method and log-rank tests were used for survival analyses. Univariate and multivariate analyses were used to identify significant prognostic factors. After matching, there were no significant differences between the two groups in race, age, sex, T classification, N classification, TNM stage, marital status, primary sites, and origin record NAACCR Hispanic Identification Algorithm (NHIA). The surgery group showed better overall survival and cancer-specific survival than the non-surgery group. Univariate and multivariate analyses showed that therapy methods, age, sex, T classification, and N classification were independent prognostic predictors for stage IIB-IIIC SCLC (all P < 0.05). Stratified analyses showed that survival outcomes favored surgery in any age groups, men and women, any T classification except T3, and N0-2 but not N3 compared with non-surgical treatment. The survival differences favored surgery in stage IIB and IIIA SCLC, although they were not significant in stage IIB and IIIC SCLC. Therefore, surgery was associated with improved survival in stage IIB and IIIA SCLC, but not in stage IIIB and IIIC SCLC.

Analysis of serum cfDNA concentration and integrity before and after surgery in patients with lung cancer.

The content and integrity of cell-free DNA (cfDNA) before and after surgery in patients with lung cancer were determined to investigate its clinical significance.   Peripheral blood was collected from 120 patients with lung cancer who were treated in our hospital from March 2016 to November 2018, including 50 cases before operation and 70 cases after operation. 60   healthy subjects served as controls. Quantitative PCR was used to determine the cfDNA level of each group. The relationship between cfDNA levels and the clinical features of lung cancer patients was determined. Receiver Operating Curves were used to determine the sensitivity and specificity of cfDNA, CEA, NSE and CYFRA21-1 in lung cancer.  The concentration and integrity of cfDNA before surgery in patients with lung cancer were significantly higher than those after surgery and those in healthy control group. The cfDNA concentration in patients with lung cancer after surgery was significantly higher than that in the control group, but there was no statistical difference in cfDNA integrity between the two groups. There was no significant correlation between cfDNA concentration/integrity and gender, age, tumor type, tumor stage, and expressions of CA199, CA125, and CA153 in patients with lung cancer before or after surgery. However, there were significant correlations between the expression levels of CEA, NSE, and CYFRA21-1 and cfDNA concentration. The expression levels of CEA and CYFRA21-1 were significantly correlated with cfDNA integrity before surgery, while the correlations were not significant after surgery.  The concentration and integrity of cfDNA increased significantly in serum of lung cancer patients. The concentration and integrity of cfDNA in patients with lung cancer after surgery were significantly lower than those before surgery. Thus, cfDNA has high application value in the diagnosis and evaluation of lung cancer.

Video-assisted thoracoscopic surgery for invasive pulmonary fungal infection in haematology patients.

BACKGROUND: Invasive pulmonary fungal infection in haematological patients sometimes was a difficult problem in diagnosis and treatments. This retrospective study was intended to assess the outcomes of video-assisted thoracoscopic surgery (VATS) in the treatments of this problem. METHODS: From January 2011 to December 2017, a total of 51 haematological patients underwent VATS for invasive pulmonary fungal infection. We collected and then analyzed potential factors including general conditions, types of haematological diseases, preoperative clinical symptoms, surgical procedures, length of postoperative hospital stay, incidence of postoperative complications and postoperative follow-ups. RESULTS: Of the 51 patients, 32 patients underwent video-assisted thoracoscopic wedge resection (62.7%), 6 patients underwent video-assisted thoracoscopic segmentectomy (11.8%) and 13 patients underwent video-assisted thoracoscopic lobectomy (25.5%). The mean operative time was 110.24±38.12 min. The average intraoperative blood loss was 112.35±87.85 mL. The mean postoperative hospital stay was 7.75±3.27 days. Prolonged air leak was found in 6 patients (11.8%), followed by excessive effusion which was found in 4 patients (7.8%). No life-threatening complications or resurgence of fungal infection occurred after surgery. Twenty-seven patients (52.9%) received postoperative antifungal therapies. No 30-day mortality and pulmonary fungal infection recurrence occurred in 6 to 24 months follow-ups. CONCLUSIONS: VATS is an effective and safe option in management of invasive pulmonary fungal infection among patients with haematological diseases.