The association between disruption of the circadian rhythm and aggravation of colitis in mice.

Delayed recovery from ulcerative colitis is mainly due to impaired healing of the intestinal epithelium after inflammation. The circadian rhythm controls cell proliferation and energy metabolism. However, the role of circadian genes in inflammatory bowel disease is largely unknown. The purpose of this study was to investigate whether disrupting the circadian rhythm in mice can worsen colitis by altering mitochondrial energy metabolism. Mice in the experimental groups were under physiologic stress with an 8-h light shift jet-lag schedule every 3 days, whereas those in the control group were not. Subsequently, half of the mice in the control and jet-lagged groups were given dextran sodium sulfate (DSS) to induce colitis. Mice in each group were euthanized at zeitgeber time (ZT)0, ZT4, ZT8, ZT12, ZT16, and ZT20. To investigate the effects of jet lag on the mice, colon specimens were subjected to hematoxylin and eosin staining to analyse mRNA and protein expression of core circadian clock genes (Bmal1, Clock, Per1, Per2, Cry1, Cry2, and Nr1d1). We analysed the mitochondrial morphology, adenosine triphosphate (ATP) levels, and the expression of dynamin-related protein 1 (Drp1) and ser637-phosphorylated (p)-Drp1, which are closely related to ATP production. We further investigated the effect of PER2 knock-down in the colon epithelial cells (CCD 841 CoN) by measuring ATP and cell proliferation levels. Disrupting the circadian rhythm changed the oscillation of clock genes in the colon of mice, altered the mitochondrial morphology of the colon specimens, decreased the expression of p-Drp1, reduced ATP production, and exacerbated inflammatory responses in mice with DSS-induced colitis. Additionally, silencing of PER2 in the colon epithelial cells reduced ATP production and cell proliferation. Disrupting the circadian rhythm in mice decreases mitochondrial energy metabolism in the colon and exacerbates symptoms of colitis.

Multiple inhibitory effects of succinic acid on Microcystis aeruginosa: morphology, metabolomics, and gene expression.

The cell membrane permeability, morphology, metabolomics, and gene expression of Microcystis aeruginosa under various concentrations of succinic acid (SA) were evaluated to clarify the mechanism of SA inhibition of M. aeruginosa. The results showed that SA caused intracellular protein and nucleic acid extravasation by increasing the cell membrane permeability. Scanning electron microscopy suggested that a high dose of SA (60 mg L-1) could damage the cell membrane and even cause lysis in some cells. Metabolomics result demonstrated that change in intracellular lipids content was the main reason for the increase of cell membrane permeability. In addition, SA could negatively affect amino acids metabolism, inhibit the biosynthesis of nucleotides, and interfere with the tricarboxylic acid (TCA) cycle of algal cells. Furthermore, SA also affected N assimilation and caused oxidative damage to Microcystis. In conclusion, SA inhibits the growth of M. aeruginosa through multisite action.

Single-cell RNA sequencing reveals abnormal fluctuations in human eight-cell embryos associated with blastocyst formation failure.

Infertility has become a global health issue, with the number of people suffering from the disease increasing year by year, and ART offering great promise for infertility treatment. However, the regulation of early embryonic development is complicated and a series of processes takes place, including the maternal-to-zygotic transition. In addition, developmental arrest is frequently observed during human early embryonic development. In this study, we performed single-cell RNA sequencing on a biopsied blastomere from human eight-cell embryos and tracked the developmental potential of the remaining cells. To compare the sequencing results between different eight-cell embryos, we have combined the research data of this project with the data previously shared in the database and found that cells from the same embryo showed a higher correlation. Additionally, the transcriptome of embryos with blastocyst formation failure was significantly different from developed embryos, and the gene expression as well as cell signaling pathways related to embryonic development were also altered. In particular, the expression of some maternal and zygotic genes in the failed blastocyst formation group was significantly altered: the overall expression level of maternal genes was significantly higher in the failed blastocyst than the developed blastocyst group. In general, these findings provide clues for the causes of human embryonic arrest after the eight-cell stage, and they also provide new ideas for improving the success rate of ART in clinical practice.

Succinic acid inhibits photosynthesis of Microcystis aeruginosa via damaging PSII oxygen-evolving complex and reaction center.

To elucidate the mechanism of succinic acid (SA) inhibition of Microcystis aeruginosa, the chlorophyll fluorescence transients, photosynthesis, photosynthetic electron transport activity, and gene expression of M. aeruginosa were evaluated under various doses of SA. The results demonstrated that, after treatment with 60 mg L-1 SA for 1 h, the chlorophyll fluorescence transients and related parameters changed significantly, indicating that the function and structure of photosynthetic apparatuses of Microcystis were seriously damaged. The initial quantum efficiency α, maximum net photosynthetic rate Pnmax, dark respiration rate Rd, and gross photosynthetic rate decreased to 57%, 49%, 49%, and 46%, respectively, relative to the control. Furthermore, photosystem II (PSII) activity (H2O→p-BQ) and the electron transport activity of H2O→MV and DPC→MV significantly decreased. Real-time PCR analysis revealed that, following incubation with 60 mg L-1 SA for 24 h, the expression level of core protein genes (psbA, psaB, psbD, and psbO) of the photosynthesis centers photosystem I (PSI) and PSII decreased significantly. However, the transcription of gene nblA encoding phycobilisome degradation protein was elevated. The downregulation of the rbcL gene, which encodes the large subunit of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco), resulted in the suppression of CO2 fixation and assimilation. High concentration (60 mg L-1) of SA resulted in damage to oxygen-evolving complex (OEC) and reaction center of PSII, blocking photosynthetic electron transport, thereby lowering the rate photosynthesis and inhibiting the growth of Microcystis. We concluded that inhibition of photosynthesis is an important mechanism of SA inhibition in M. aeruginosa.

Role of non-inflammatory factors in intestinal fibrosis.

Intestinal fibrosis is a common complication of inflammatory bowel disease (IBD), resulting in strictures and ultimately obstruction, which is a significant clinical problem. Fibrosis is mainly triggered by local chronic inflammation and occurs when excessive extracellular matrix deposition is caused by activated mesenchymal cells. Despite the advance of anti-inflammatory therapies in IBD, the incidence and preventive strategies of intestinal fibrosis and strictures in IBD have not significantly changed over time. This shows that inflammation is necessary for fibrosis, but it does not necessarily affect the fibrotic progression. This review summarizes current knowledge about the non-inflammatory mechanisms implicated in the gut fibrotic process of IBD, which may pave the way for new mechanisms and anti-fibrotic therapies.

Functional BCL-2 rs2279115 Promoter Noncoding Variant Contributes to Glioma Predisposition, Especially in Males.

As a crucial oncogene, B cell lymphoma-2 (BCL-2) could promote cancer cell survival by inhibiting apoptosis via suppressing activation of proapoptotic proteins, such as BAX and BAK. There is a functional rs2279115 genetic polymorphism locating in BCL-2 promoter and deregulating BCL-2 expression. However, it is still largely undefined how BCL-2 rs2279115 promoter noncoding genetic variant is involved in glioma development. We examined the association between BCL-2 rs2279115 and glioma risk using a case-control approach. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression adjusted by age and sex. Our results demonstrated that BCL-2 rs2279115 was significantly associated with glioma risk. The odd of individuals harboring A allele (CA + AA genotype) was 0.50 (95% CI = 0.39-0.64, p = 1.0 × 10-7) compared with CC genotype carriers. Stratification analyses by sex elucidated that BCL-2 rs2279115 was significantly associated with glioma risk in males (OR = 0.41, 95% CI = 0.30-0.58, p = 1.0 × 10-7), but not in females (p > 0.05). In summary, our results indicate that the functional BCL-2 rs2279115 genetic variant contributes to glioma predisposition and suggest prevalent involvement of regulatory genetic variations in glioma development.

LncRNA GAS5 Indel Genetic Polymorphism Contributes to Glioma Risk Through Interfering Binding of Transcriptional Factor TFAP2A.

Long noncoding RNA (lncRNA) growth arrest-specific 5 (GAS5) accumulates in growth-arrested cells and plays a crucial role in progression of multiple cancers, including glioma. There is a functional GAS5 rs145204276 indel genetic polymorphism in the promoter region. However, it is still largely unknown how the GAS5 indel genetic polymorphism is involved in etiology of glioma. We evaluated the association between the GAS5 indel genetic polymorphism and glioma development in a Chinese population. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression adjusted by age and sex. We found that carriers of the GAS5 del allele was significantly associated with elevated risk of glioma (OR = 1.71, 95% CI = 1.34-2.18, p = 1.7 × 10-5). Compared with the GAS5 ins/ins genotype, the ins/del genotype or the del/del genotype was significantly associated with 1.57-fold or 2.61-fold increased glioma susceptibility (p = 0.001 or p = 9.0 × 10-6). When patients were stratified by disease subtypes, The GAS5 indel polymorphism was not significantly associated with risk of oligodendroglial tumor (p = 0.353). Integrated analyses indicated that the GAS5 indel polymorphism might alert the binding of transcriptional factor TFAP2A and activation of its expression based on ENCODE and REMBRANDT databases. Our results highlight the importance and potential of the biological relevance of the GAS5 indel genetic variant in glioma predisposition.

LncRNA CDKN2BAS rs2157719 genetic variant contributes to medulloblastoma predisposition.

BACKGROUND: How germline single nucleotide polymorphisms are involved in the etiology of medulloblastoma remans poorly understood. We hypothesized that CCDKN2A/B rs1063192 and rs4977756 and also the long noncoding RNA (lncRNA) CDKN2BAS rs2157719 glioma susceptibility polymorphisms identified by genome-wide association studies may contribute to medulloblastoma predisposition. METHODS: To test this hypothesis, we genotyped these genetic variants among 160 medulloblastoma patients and 443 health controls in a Chinese population. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression. RESULTS: We found that only the lncRNA CDKN2BAS rs2157719 T>C genetic polymorphism was significantly associated with an increased medulloblastoma risk (C allele: OR = 1.85, 95% CI = 1.32-2.58; p = 2.7 × 10-4 ). The stratified analyses showed an elevated risk of pediatric medulloblastoma associated with CDKN2BAS rs2157719 CC or TC genotype (both p < 0.05). Moreover, the association between the CDKN2BAS rs2157719 polymorphism and medulloblastoma risk is more pronounced in males (OR = 2.22, 95% CI = 1.36-3.62; p = 0.001). CONCLUSIONS: The findings of the present study provide important insights into the genetic complexities and predisposition of medulloblastoma in Chinese, especially at the lncRNA germline variation level.

Systemic Therapy after Radiotherapy Significantly Reduces the Risk of Mortality of Patients with 1-3 Brain Metastases: A Retrospective Study of 250 Patients.

BACKGROUND: For patients with a brain metastasis (BM), systemic therapy is usually administered after the completion of radiotherapy, especially in cases of multiple BMs. However, the role of systemic therapy in patients with a limited number of BMs is not clear. Therefore, we conducted a retrospective study to explore this question. METHODS: Consecutive patients with a pathologically confirmed malignancy and 1-3 intracranial lesions that had been documented within the last decade were selected from the databases of three hospitals in China. RESULTS: A total of 250 patients were enrolled; of them, 135 received radiotherapy alone and 115 received radiotherapy plus systemic therapy. In patients receiving whole-brain radiation therapy (WBRT) as radiotherapy, 28 received WBRT alone and 35 patients received WBRT plus systemic therapy. Of the patients treated with stereotactic radiosurgery (SRS), 107 received SRS alone and 80 received SRS plus systemic therapy. Multivariate analysis revealed that systemic therapy significantly reduced the risk of mortality compared with radiotherapy alone (hazard ratio [HR] = 0.294, 95% confidence interval [CI] = 0.158-0.548). Further, when the analysis was conducted in subgroups of WBRT (HR = 0.230, 95% CI = 0.081-0.653) or SRS (HR = 0.305, 95% CI = 0.127-0.731), systemic therapy still showed the ability to reduce the risk of mortality in patients with BMs. CONCLUSION: Systemic therapy after either SRS or WBRT radiotherapy may significantly reduce the risk of mortality of patients with 1-3 BMs.

Patterns and predictors of recurrence after radical resection of thymoma.

BACKGROUND: Recurrence of thymomas even after complete resection is common, but the relapse patterns remain controversial. This study aimed to define the patterns and predictors of relapse after complete resection of thymoma. METHODS: A single-institution retrospective study was performed with 331 patients who underwent radical resection of thymoma between 1991 and 2012. RESULTS: After a median follow-up of 59 months, the recurrence rate was 6.9% (23/331). Relapse occurred in 23 patients with the pleura (14) and tumor bed (6) as the most common sites of recurrence. According to the definitions of the International Thymic Malignancy Interest Group, 10 (43.5%) patients had local relapse, 15 (65.2%) had regional relapse, 10 (43.5%) had distant relapse. The difference in survival following relapse between lung and regional relapse was statistically significant (P=0.027) but that between lung and distant relapse was not (P=0.808). The recurrence rates correlated with the initial Masaoka stage. Further, recurrence also correlated with World Health Organization (WHO) tumor type. The recurrence-free survival rates in patients with tumor size ⩾8 cm were worse than those of patients with tumor size <8 cm (P=0.007). Tumor size was also correlated with stage (r=0.110). As tumor becomes larger, the stage is more advanced (P=0.023). Multivariate analysis showed that Masaoka stage (P=0.005), tumor size (P=0.033), and WHO histological type (P=0.046) were predictive factors of relapse. CONCLUSION: Regional recurrence is the most common relapse pattern but local and distant relapse are also common. Advanced Masaoka stage, larger tumor size, and type B3 are risk factors of recurrence. Lung relapse should be considered distant relapse. Further, tumor size was correlated with Masaoka stage and therefore should be considered in the staging system.

Long-term outcomes of adjuvant radiotherapy after surgical resection of central neurocytoma.

BACKGROUND AND PURPOSE: The role of adjuvant radiotherapy for central neurocytomas (CNs) is not clear. Therefore, we aimed to examine the clinical outcomes of treating histologically confirmed CNs with adjuvant RT after surgical resection. MATERIAL AND METHODS: Sixty-three CN patients were retrospectively evaluated: 24 patients underwent gross total resection (GTR); 28, subtotal resection (STR); 9, partial resection (PR), and 2, biopsy (Bx). They underwent adjuvant RT after surgery (median dose, 54 Gy). RESULTS: The median follow-up was 69 months (15-129 months). The 5-year overall survival (OS) and 5-year progression-free survival (PFS) were 94.4% and 95% after GTR + RT, 96.4% and 100% after STR + RT, and 100% and 90.9% after PR + RT. Only three patients had tumor recurrence: at the primary site at 30 and 24 months in two GTR + PR patients, and dissemination to the spinal cord at 75 months in one STR + RT patient. Thirty-eight (63.3%) patients experienced late neurotoxicity (28, grade 1; 7, grade 2; 3, grade 3). Short-term memory impairment was the most common toxicity. CONCLUSIONS: RT after incomplete resection (IR) led to OS and PFS comparable to those for GTR. Considering the excellent outcomes and limited late toxicity, adjuvant RT maybe a good option for CN patients who undergo IR.

A RAD52 genetic variant located in a miRNA binding site is associated with glioma risk in Han Chinese.

As a crucial homologous recombination repair gene, RAD52 participates in maintenance of genomic stability and prevention of tumorigenesis. Although several cancer susceptibility RAD52 single nucleotide polymorphisms (SNPs) have been identified previously, little was known on how the RAD52 SNPs are involved in glioma development in Han Chinese. Therefore, we examined the association between five RAD52 SNPs (rs1051669, rs10774474, rs11571378, rs7963551 and rs6489769) and glioma risk using a case-control design. Odds ratios (ORs) and 95 % confidence intervals (CIs) were estimated by logistic regression. We found that only the RAD52 rs7963551 SNP was significantly associated with glioma risk, with the odds of having the rs7963551 AC or CC genotype in patients was 0.49 (95 % CI 0.37-0.65, P = 9.2 × 10(-6)) or 0.39 (95 % CI 0.18-0.81, P = 0.012) compared with the AA genotype. These data are consistent with functional relevance of allelic regulation of RAD52 expression by the rs7963551 SNP and miRNA let-7 in cancer cells. Stratified analyses elucidated that statistically significant association between glioma and rs7963551 SNP only existed in either astrocytic tumors (P = 6.3 × 10(-6)) or oligoastrocytic tumors (P = 0.002). In conclusion, our results support the hypothesis that genetic variants influencing miRNA-mediated regulation of tumor suppressor genes or oncogenes may contribute glioma susceptibility.

1p34.2 rs621559 and 14q21 rs398652 leukocyte telomere length-related genetic variants contribute to glioma susceptibility.

Recent genome-wide association studies have identified several leukocyte telomere length (LTL)-related single nucleotide polymorphisms (SNPs). Our previous data demonstrated that two SNPs (rs398652 on 14q21 and rs621559 on 1p34.2) were associated with LTL and risk of esophageal squamous cell carcinoma in Chinese. However, the role of these genetic variants on glioma risk is still unknown. Therefore, we examined if these genetic variants have impact on the genetic susceptibility of glioma in Chinese. On the basis of analyzing 404 glioma patients and frequency-matched 820 controls, we found that subjects having the 1p34.2 rs621559 AG or GG genotype had an OR of 1.82 (95 % CI = 1.07-3.09, P = 0.026) or 2.12 (95 % CI = 1.26-3.56, P = 0.005) for developing glioma, respectively, compared with subjects having the rs621559 AA genotype. Similarly, the 14q21 rs398652 AG or GG genotype was associated with increased glioma risk (OR = 1.39, 95 % CI = 1.07-1.80, P = 0.012; OR = 1.52, 95 % CI = 1.04-2.20, P = 0.029) compared to AA genotype. In all, our results highlight the possible role of telomere in carcinogenesis.

Effect of intensity-modulated radiotherapy versus three-dimensional conformal radiotherapy on clinical outcomes in patients with glioblastoma multiforme.

BACKGROUND: Few studies were reported on the comparison of clinical outcomes between intensity-modulated radiotherapy (IMRT) and three-dimensional conformal radiotherapy (3D-CRT) in the treatment of glioblastoma multiforme (GBM). This study aimed to determine whether IMRT improves clinical outcomes compared with 3D-CRT in patients with GBM. METHODS: The records of 54 patients with newly-diagnosed GBM from July 2009 to December 2010 were reviewed. The patients underwent postoperative IMRT or 3D-CRT with concurrent and adjuvant temozolomide. Kaplan-Meier method and log rank test were used to estimate differences of patients' survival. RESULTS: The median follow-up was 13 months. Of the 54 patients, fifty (92.6%) completed the combined modality treatment. The 1-year overall survival rate (OS) was 79.6%. The pattern of failure was predominantly local. A comparative analysis revealed that no statistical difference was observed between the IMRT group (n = 21) and the 3D-CRT group (n = 33) for 1-year OS (89.6% vs. 75.8%, P = 0.795), or 1-year progression-free survival (PFS) (61.0% vs. 45.5%, P = 0.867). In dosimetric comparison, IMRT seemed to allow better sparing of organs at risk than 3D-CRT did (P = 0.050, P = 0.055). However, there was no significant difference for toxicities of irradiation between the IMRT group and the 3D-CRT group. CONCLUSIONS: Our preliminary results suggested that delivering standard radiation doses by IMRT is unlikely to improve local control or overall survival for GBM compared with 3D-CRT. Given this lack of survival benefit and increased costs of IMRT, the utilization of IMRT treatment for GBM needs to be carefully rationalized.

Functional FEN1 genetic variants and haplotypes are associated with glioma risk.

As a tumor suppressor, FEN1 plays an essential role in keeping genomic instability and preventing tumorigenesis. There are two functional genetic variants (-69G>A and 4150G>T) in the FEN1 gene, which have been associated with DNA damage levels in coke-oven workers as well as risks of lung cancer, hepatocellular carcinoma, esophageal cancer, gastric cancer and colorectal cancer in general populations. However, it is still unknown how these polymorphisms and their haplotypes are associated with glioma risk. Therefore, we investigated the role of these polymorphisms in glioma development using a case-control design in a Chinese population. The impact of the haplotypes constructed by these two polymorphisms on glioma risk was also examined. It was observed that the FEN1-69GG or 4150GG genotype were significantly associated to increased glioma risk compared with the -69AA or 4150TT genotype [Odds ratios (OR) = 1.87, 95 % confidence interval (CI) = 1.23-2.85, P = 0.003; or OR = 1.87, 95 % CI = 1.23-2.84, P = 0.003). The associations were more pronounced among female subjects (For -69AG or GG genotype: OR = 2.35, 95 % CI = 1.22-4.52; for 4150TG or GG genotype: OR = 2.33, 95 % CI = 1.21-4.48) and patients with grade 1 or 2 disease (For -69AG or GG genotype: OR = 2.21, 95 % CI = 1.20-4.05; for 4150TG or GG genotype: OR = 2.45, 95 % CI = 1.31-4.58). Additionally, the G(-69)G(4150) haplotype was also significantly associated with increased glioma risk compared with the A(-69)T(4150) haplotype. Our results suggest that FEN1 polymorphisms and haplotypes are associated with glioma risk.

A three-stage expert system based on support vector machines for thyroid disease diagnosis.

In this paper, we present a three-stage expert system based on a hybrid support vector machines (SVM) approach to diagnose thyroid disease. Focusing on feature selection, the first stage aims at constructing diverse feature subsets with different discriminative capability. Switching from feature selection to model construction, in the second stage, the obtained feature subsets are fed into the designed SVM classifier for training an optimal predictor model whose parameters are optimized by particle swarm optimization (PSO). Finally, the obtained optimal SVM model proceeds to perform the thyroid disease diagnosis tasks using the most discriminative feature subset and the optimal parameters. The effectiveness of the proposed expert system (FS-PSO-SVM) has been rigorously evaluated against the thyroid disease dataset, which is commonly used among researchers who use machine learning methods for thyroid disease diagnosis. The proposed system has been compared with two other related methods including the SVM based on the Grid search technique (Grid-SVM) and the SVM based on Grid search and principle component analysis (PCA-Grid-SVM) in terms of their classification accuracy. Experimental results demonstrate that FS-PSO-SVM significantly outperforms the other ones. In addition, Compared to the existing methods in previous studies, the proposed system has achieved the highest classification accuracy reported so far by 10-fold cross-validation (CV) method, with the mean accuracy of 97.49% and with the maximum accuracy of 98.59%. Promisingly, the proposed FS-PSO-SVM expert system might serve as a new candidate of powerful tools for diagnosing thyroid disease with excellent performance.

Endolymphatic sac papillary tumor: a case report.

Endolymphatic sac papillary tumor (ELST) is an extremely rare and aggressive tumor characterized by hearing loss and temporal bone destruction. A case with clinical, imaging, pathologic and treatment data is reported and relevant literature is reviewed. A 25-year-old woman, with ELST underwent craniotomy for tumor subtotal resection, and the diagnosis was confirmed by pathologic examination. Postoperative radiotherapy consisted of 50.4 Gy/28 f was given accordingly. The patient is currently alive with no signs of tumor recurrence locally and no radiation side-effects observed after one year follow-up. Complete resection is impossible in most cases, local resection, adjuvant radiotherapy may provide favored local control. A long-term follow-up is highly advocated in consideration of its slow development course.

Role of adjuvant radiotherapy for stage II thymoma after complete tumor resection.

PURPOSE: To determine whether patients with Masaoka stage II thymoma benefit from adjuvant radiation therapy after complete tumor resection. METHODS AND MATERIALS: A total of 107 patients with stage II thymoma who underwent complete resection of their tumors between September 1964 and October 2006 were retrospectively analyzed. Sixty-six patients were treated with adjuvant radiotherapy, and 41 patients received surgery alone. RESULTS: Eight patients (7.5%) had a relapse of their disease, including two patients (4.5%) who had surgery alone, and 6 patients (9.5%) who had adjuvant radiation therapy. Disease-free survival rates at 5 and 10 years were 92.3% and 82.6%, respectively, for the surgery-plus-radiation group, and 97.6% and 93.1%, respectively, for the group that underwent surgery alone (p = 0.265). Disease-specific survival rates at 5 and 10 years were 96.4% and 89.3%, respectively, for the surgery-plus-radiation group and 97.5% and 97.5% for the surgery group (p = 0.973). On univariate analysis, patients with type B3 thymomas had the lowest disease-free survival rates among all subtypes (p = 0.001), and patients with large thymomas (>7 cm) had lower disease-specific survival rates than those with small tumors (<7 cm) (p = 0.017). On multivariate analysis, histological type (type B3) thymoma was a significant independent prognostic factor. CONCLUSIONS: Adjuvant radiotherapy after complete tumor resection for patients with stage II thymoma did not significantly reduce recurrence rates or improve survival rates. Histological type (type B3) thymoma was a significant independent prognostic factor. Further investigation should be carried out using a multicenter randomized or controlled study.