Objective To propose a lung artery segmentation method that integrates shape and position prior knowledge, aiming to solve the issues of inaccurate segmentation caused by the high similarity and small size differences between the lung arteries and surrounding tissues in CT images. Methods Based on the three-dimensional U-Net network architecture and relying on the PARSE 2022 database image data, shape and position prior knowledge was introduced to design feature extraction and fusion strategies to enhance the ability of lung artery segmentation. The data of the patients were divided into three groups: a training set, a validation set, and a test set. The performance metrics for evaluating the model included Dice Similarity Coefficient (DSC), sensitivity, accuracy, and Hausdorff distance (HD95). Results The study included lung artery imaging data from 203 patients, including 100 patients in the training set, 30 patients in the validation set, and 73 patients in the test set. Through the backbone network, a rough segmentation of the lung arteries was performed to obtain a complete vascular structure; the branch network integrating shape and position information was used to extract features of small pulmonary arteries, reducing interference from the pulmonary artery trunk and left and right pulmonary arteries. Experimental results showed that the segmentation model based on shape and position prior knowledge had a higher DSC (82.81%±3.20% vs. 80.47%±3.17% vs. 80.36%±3.43%), sensitivity (85.30%±8.04% vs. 80.95%±6.89% vs. 82.82%±7.29%), and accuracy (81.63%±7.53% vs. 81.19%±8.35% vs. 79.36%±8.98%) compared to traditional three-dimensional U-Net and V-Net methods. HD95 could reach (9.52±4.29) mm, which was 6.05 mm shorter than traditional methods, showing excellent performance in segmentation boundaries. Conclusion The lung artery segmentation method based on shape and position prior knowledge can achieve precise segmentation of lung artery vessels and has potential application value in tasks such as bronchoscopy or percutaneous puncture surgery navigation.

ObjectiveTo investigate the mechanism of Huangqin Tang （HQT） in regulating metabolic reprogramming during the inflammation-cancer transformation in colitis-associated colorectal cancer （CAC）. MethodsCAC mouse model was established using the carcinogen azoxymethane （AOM） combined with the inflammatory agent dextran sulfate sodium （DSS）. HQT treatment was adopted. Serum metabolomics analysis was performed at three stages （inflammation， proliferation， and tumor formation） using liquid chromatography-tandem mass spectrometry （LC-MS/MS） untargeted metabolomics coupled with multivariate statistical analysis to explore the mechanism of HQT intervention in metabolism in CAC. ResultsThe results revealed that HQT significantly reversed the disturbance of key metabolites in CAC mice. A total of 52， 67， and 45 differential metabolites were identified in the model group， compared to the normal group， during inflammation， proliferation， and tumor stages， respectively. Lactate， linoleic acid， oleic acid， elaidic acid， and betaine were characteristic metabolites persistently enriched throughout colitis-cancer transformation. Pathway enrichment analysis of differential metabolites showed that linoleic acid metabolism and arachidonic acid metabolism were the most significantly disturbed in CAC pathogenesis. The proliferation stage featured expanded amino acid metabolic networks， while the tumor stage uniquely exhibited two new pathways of nicotinate and nicotinamide metabolism and phosphoinositide metabolism. HQT exerted stage-specific regulatory effects： targeting arachidonic acid metabolism in the inflammation stage， correcting the dysregulation of choline-carnitine metabolism in the proliferation stage， and rescuing nicotinamide and tryptophan metabolic collapse in the tumor stage. ConclusionHQT exerts regulatory effects on metabolic disorders at various stages of the colitis-cancer transformation process， thereby effectively slowing the progression from colitis to cancer. The study also reveals the dynamic metabolic characteristics of colorectal "inflammation-cancer transformation，"providing new insights for research on the targeted mechanisms of traditional Chinese medicine in anti-tumor therapy based on metabolic reprogramming.

ObjectiveTo induce the rat model of ulcerative colitis （UC） with spleen-kidney Yang deficiency and liver depression， and explore the efficacy and mechanism of Sishenwan combined with Tongxie Yaofang （SSW&TXYF） based on the therapeutic principles of tonifying spleen， soothing liver， warming kidney， and astringing intestine. MethodSixty male SD rats were randomized into normal， model， mesalazine， and high-， medium-， and low-dose SSW&TXYF groups. The rats in other groups except the normal group were administrated with Sennae Folium decoction and hydrocortisone and received tail clamping for 14 days. On day 14， rats received enema with TNBS-ethanol solution to induce UC. The rats were administrated with corresponding drugs from day 15 of modeling， and the body weight and mental state were observed and recorded. The sucrose preference test was performed from day 25. On day 28， the rectal temperature was measured， and the rats were administrated with 3% D-xylose solution at a dose of 10 mL·kg^-1 by gavage. Blood was sampled 1 h later， from which the serum was collected for measurement of the D-xylose content. The serum， hippocampus， and colorectum samples of rats were collected on day 29. The levels of gastrin （GAS）， adrenocorticotropic hormone （ACTH）， corticosterone （CORT）， cyclic adenosine monophosphate （cAMP）， cyclic guanosine monophosphate （cGMP）， interleukin （IL）-4， tumor necrosis factor （TNF）-α， and interferon （IFN）-γ in the serum and 5-hydroxytryptamine （5-HT） in the hippocampus were determined by enzyme-linked immunosorbent assay. Hematoxylin-eosin staining was employed to reveal the colonic lesions. The mRNA and protein levels of p38 mitogen-activated protein kinase （MAPK）， extracellular signal-regulated kinase （ERK）， and c-Jun N-terminal kinase （JNK） in the colon tissue were determined by Real-time PCR and Western blot， respectively. ResultCompared with the normal group， the model group showed decreased body weight， anal temperature， and D-xylose content in the serum and increased GAS content （P<0.01）. The modeling led to cAMP/cGMP unbalance and decreased the ACTH and CORT content in the serum （P<0.01）， the preference for sucrose water， and the 5-HT content in the hippocampus （P<0.01）. Moreover， it shortened the colorectal length and caused massive infiltration of inflammatory cells and severe structural damage in the colon tissue. High， medium， and low doses of SSW&TXYF improved above indicators （P<0.05， P<0.01）， reduced inflammatory infiltration， and repaired the pathological damage of the tissue. Compared with the normal group， the model group showed lowered IL-4 level （P<0.01） and elevated TNF-α and IFN-γ levels （P<0.05， P<0.01） in the serum， as well as up-regulated expression of p38 MAPK， ERK， and JNK （P<0.05， P<0.01）. Compared with the model group， SSW&TXYF elevated the IL-4 level （P<0.01）， lowered the TNF-α and IFN-γ levels （P<0.05， P<0.01）， and down-regulated the mRNA and protein levels of p38 MAPK， ERK， and JNK （P<0.05， P<0.01）. ConclusionA rat model of UC with spleen-kidney Yang deficiency and liver depression was successfully established. SSW&TXYF can significantly mitigate this syndrome by reducing the inflammatory response in the colon and inhibiting the MAPK pathway.

Objective To optimize the method of combining azomethane oxide(AOM)and dextran sodium sulfate(DSS)to create a colitis-associated colon cancer(CAC)model,and to explore the pathogenesis of the intestinal flora in CAC.Methods Model groups A and B were established by one and two injections of AOM,respectively,combined with free drinking of DSS,and a normal control group was injected intraperitoneally with normal saline combined with purified water(n=10 mice per group).The better modeling scheme was selected by comprehensive evaluation of the disease activity index score,colon length,tumor rate,and mortality.Serum levels of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),and tumor markers CA199,CEA,and CA724 were detected by enzyme-linked immunosorbent assay.Colon lesions were evaluated by hematoxylin and eosin(HE)staining.Changes in the intestinal microbiota in CAC mice were detected by 16S rDNA high-throughput gene sequencing analysis of mouse feces.Results Both single and enhanced AOM injections combined with DSS induced CAC mice;however,colon growths were larger,more closely arranged,and their morphological size was more consistent in group B compared with group A,with a tumor-formation rate of 100％.IL-6 levels were increased in the model group compared with the normal group(P＜0.05).TNF-α levels were increased in the model group compared with the normal group(P＞0.05).The CA199 and CEA levels were also significantly increased(P＜0.05),but CA724 levels were not.Infiltration of inflammatory cells in the colon detected by HE pathology was accompanied by high-grade intraepithelial tumor-like changes on the surface of the lumen.The diversity and abundance of intestinal bacteria were decreased in CAC mice compared with normal mice:phyla Verrucomicrobiota and Actinobacteriota were significantly increased(P＜0.05),Bacteroidota and Campilobacterota were significantly decreased(P＜0.05).Akkermansia,Prevotellaceae,Ruminococcus,and Bifidobacterium were significantly increased(P＜0.05),and Roseburia,Rikenellaceae_RC9_gut_group,Anaeroplasma,and Muribaculaceae were significantly decreased(P＜0.05).Conclusions Two injections of AOM combined with 1.5％(1.5 g/100 mL)DSS induced CAC model mice with a high colon-tumorigenesis rate,uniform tumor morphology,and low mortality,and may thus be the preferred modeling scheme for pharmacodynamic experiments.Disorders or dysfunction of the intestinal flora may lead to increased permeability,loss of intestinal mucosal barrier function,and the release of enterogenic endotoxins,Resultsing in a sustained inflammatory response,as an indirect or direct cause of CAC pathogenesis.

ObjectiveTo construct a mouse model of inflammation-associated colorectal cancer （CAC） by using azoxymethane （AOM）/dextran sulfate sodium （DSS） and investigate the effect of Huangqintang on the gut microbiota structure of mice during the occurrence and development of CAC by 16S rRNA gene high-throughput sequencing. MethodA total of 225 C57BL/6J mice were randomized into 5 groups （n=45）： Normal， model， positive drug （mesalazine）， and high （18 g·kg^-1） and low （9 g·kg^-1）-dose Huangqintang. Except those in the normal group， each mouse was injected with 10 mg·kg^-1 AOM on day 1 and day 5 within 1 week and then given 1.5% DSS solution for 7 days， which was then changed to sterile water for 14 days. This process referred to as one cycle， and mice were treated for a total of 3 cycles. On the first day of DSS treatment， mice were administrated with corresponding drugs by gavage， and the normal group and the model group were administrated with pure water by gavage， once a day until the end of the third cycle. The progression of CAC was divided into inflammation， proliferation， and tumorigenesis stages. At the end of each cycle， the body weight and colon length were measured for mice in each group， and the number of colon tumors in mice was recorded. Meanwhile， the disease activity index （DAI） was determined. The serum levels of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and carbohydrate antigen-199 （CA199）， a tumor marker in the gastrointestinal tract of mice， were measured by ELISA. Hematoxylin-eosin staining was employed to observe colon lesions. At the same time， 3-5 pellets of fresh feces of mice in the normal group， model group， and high-dose Huangqintang group were collected， from which the fecal DNA of mice was extracted for 16S rRNA gene high-throughput sequencing. ResultCompared with the normal group， the model group showed decreased body weight （P<0.01）， increased DAI， and shortened colon length （P<0.05） at the three stages. Compared with the normal group， the model group showed elevated levels of IL-1β， IL-6， and TNF-α （P<0.05） at the proliferation stage and elevated levels of CA199 at the inflammation， proliferation， and tumorigenesis （P<0.01） stages. Compared with the normal group， the model group presented obvious infiltration of inflammatory cells at the inflammation stage， thickening of the muscle layer and abnormal proliferation of mucosal layer cells at the proliferation and tumorigenesis stages， and final formation of advanced intraepithelial tumor lesions. Compared with the model group， the Huangqintang groups showed no significant improvement in the body weight， decreased DAI score， and increased colon length at the three stages， and the increase of colon length in the tumorigenesis stage was significant （P<0.01）. At the tumorigenesis stage， the administration of Huangqintang inhibited tumor formation and growth， reduced the number of tumors （P<0.01）， lowered the levels of IL-6 （P<0.05， P<0.01）， TNF-α （P<0.05， P<0.01）， and IL-1β at the three stages， and decreased CA199 at the inflammation stage as well as at the proliferation and tumorigenesis stages （P<0.01， P<0.05）. Compared with the model group， the administration of Huangqintang reduced inflammation and abnormal cell proliferation， delaying the occurrence of tumors. Compared with the normal group， the model group showcased decreased alpha and beta diversity and altered structure of gut microbiota at the inflammation， proliferation， and tumorigenesis stages. The administration of Huangqintang adjusted the abundance and diversity of gut microbiota to the normal levels. At the inflammation stage， Huangqintang positively regulated two differential phyla （Firmicutes and Bacteroidetes） and three differential genera （Muribaculaceae， Rikenellaceae_RC9_gut_group， and Flavonifractor） in mice. At the proliferation stage， Huangqintang positively regulated two differential phyla （Bacteroidetes and Patescibacteria） and five differential genera （Muribaculaceae， Rikenellaceae_RC9_gut_group， Candidatus_Saccharimonas， norank_f__UCG-010， and Allobaculum）. At the tumorigenesis stage， Huangqintang positively regulated two differential phyla （Proteobacteria and Patescibacteria） and eight differential genera （Muribaculaceae， Candidatus_Saccharimonas， norank_f_UCG-010， Lachnospiraceae_UCG-006， Allobaculum， Bacteroides， Lachnospiraceae_NK4A136_group， and Flavonifractor） in mice. ConclusionHuangqintang can intervene in the AOM/DSS-induced transformation of inflammation to CAC in mice by correcting inflammation and short-chain fatty acid-related microbiota disorders.

Objective:To retrospectively analyze the surgical treatment of isolated pulmonary mucormycosis, explore the timing and effect of operation.Methods:Clinical data of patients with isolated pulmonary mucormycosis who underwent surgical treatment from April 2019 to April 2024 were collected and retrospectively analyzed, combined with literature review.Results:The clinical data of 13 patients with pulmonary mucormycosis who underwent operation were collected, including 9 males and 4 females, aged 22~64(45.4±15.4)years old. The basic diseases included diabetes mellitus in 10 cases and hematological malignancy in 3 cases. Seven patients had hemoptysis during the course of the disease. All 13 patients received adequate antifungal therapy before surgery, and 12 patients received bronchoscopic interventional therapy. Ten patients underwent lobectomy, two underwent pneumonectomy, and one underwent a right sleeve pneumonectomy. All patients were cured except one patient with bronchopleural fistula after operation. All patients achieved complete elimination of mucor and also discontinuation of antifungal drug.Conclusion:For isolated pulmonary mucormycosis, on the basis of systemic antifungal treatment, actively seek the opportunity of surgical intervention, can shorten the course of the disease and achieve good therapeutic results.

Objective:Immune checkpoint inhibitors have a high remission rate in the preoperative application of resectable and potentially resectable non-small cell lung cancer when combined with chemotherapy. For the unresectable stage Ⅲ non-small cell lung cancer, whether the transformation can be achieved through this regimen to provide opportunities for surgical resection is controversial. In this study, we evaluated the pattern of transformation therapy by reviewing the efficacy and safety of preoperative therapy and surgery of this group.Methods:A review of 23 patients undergoing surgical resection after transformation therapy by preoperative immunotherapy combined chemotherapy between November 2019 and November 2021 was performed. All patients must clarify the pathological diagnosis of non-small cell lung cancer by biopsy. After the multi-disciplinary treatment team and preoperative imaging assessment, the diagnosis should be consistent with unresectable stage III as described in the Expert Consensus on Multidisciplinary Management of Stage Ⅲ Non-Small Cell Lung Cancer, 2019 Edition. After 2 to 4 cycles of preoperative anti-PD-1 monoclonal antibody combined with chemotherapy, the surgical team assessed the chance of resection and performed surgery. Important indicators such as surgical resection rate, R0 resection rate, MPR, pCR, incidence of grade 3-5 adverse reactions and various other perioperative data were counted.Results:In the whole group, initial imaging evaluation was 10 of stage cⅢA and 13 of stage cⅢB.15 cases had multiple stations N2 lymph nodes metastasis, 9 had enlarged fused N2 lymph nodes metastasis, 6 had large vessel invasion(T4), and 1 had contralateral mediastinal lymph node metastasis(N3). After preoperative neoadjuvant therapy, 17 cases achieved PR, 3 achieved SD and 3 achieved PD. The surgical resection rate of the whole group was 91.3%(21/23, 1 lobectomy combined with superior vena cava reconstruction, 2 sleeve lobectomy, 5 pneumonectomy, 12 lobectomy/combined lobectomy, 1 wedge resection and 2 unresectable cases), R0 resection rate was 95.2%(20/21). MPR was achieved in 13 cases, 8 of them reached pCR. There were no perioperative deaths, median surgical time was 260(190-460) min, median bleeding volume was 100(50-750) ml, median drainage time was 5(3-9) days, and median hospitalization was 7(5-11) days. Two cases got immunotherapy-related grade 3 adverse reactions, one was interstitial pneumonia and the other was immune-related injury involving the eye, oral and genital mucosa. Two cases got surgical complications and one was persistent lung leakage, which stopped after 46 days of conservative treatment; The other was pleural effusion, which was relieved after drainage.Conclusion:For the unresectable stage Ⅲ NSCLC, immunotherapy combined chemotherapy is an effective preoperative downstage method. It can convert 91.3% cases to resectable ones while achieving a good degree of pathological remission. Its side reactions are generally controllable and safety.

ObjectiveTo investigate the efficacy of Huangqintang on mouse models of colitis-associated colon cancer （CAC） and explore the mechanism of Huangqintang in regulating immune function and inflammatory response， inhibiting abnormal cell proliferation， and delaying or inhibiting CAC formation in CAC. MethodC57BL/6J mice were randomly divided into a normal group， model group， mesalazine group， and high- and low-dose Huangqintang groups according to body weight， with 12 mice in each group. Except for the normal group， the rest of the mice were given two intraperitoneal injections of 10 mg·kg^-1 azomethane （AOM） and allowed to drink 1.5% dextran sodium sulfate （DSS） freely for seven days and water normally for two weeks. Then， two cycles of ''DSS-drinking water'' were repeated. During the administration of DSS， mice in the normal group and model group were given gavage in equal doses of pure water. Mice in the mesalazine group were given 150 mg·kg^-1·d^-1 mesalamine suspension for gavage， and mice in the high- and low-dose Huangqintang groups were given 18 and 9 g·kg^-1·d^-1 Huangqintang for gavage， respectively. Each group was given one dose daily until the end of three cycles. After the intervention， the body weight， colon length， and number of colon tumors in each group were measured， and disease activity index （DAI） scores were performed. The serum contents of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-4 （IL-4）， interleukin-10 （IL-10）， and gastrointestinal tumor marker carbohydrate antigen-199 （CA199） were detected by enzyme linked immunosorbent assay （ELISA）. The colonic lesions were observed by hematoxylin-eosin （HE） staining. The expression of proliferative cell-associated antigen （Ki67） was observed by immunohistochemistry. The expression of T lymphocyte subsets （CD3⁺， CD4⁺， CD8⁺， and CD49b⁺） in mouse plasma was detected by flow cytometry. Fluorescein isothiocyanate-D （FITC-D） content in mouse serum was detected by fluorescent labeling method. The Western blot method was used to detect the expression of Cyclin D₁， cyclin-dependent kinase 2 （CDK2）， cyclin-dependent kinase 4 （CDK4）， and tightly junction-related Occludin and Claudin-1. ResultCompared with the normal group， the body weight of mice in the model group decreased. DAI score increased significantly， and the colon became shorter. Pro-inflammatory factors such as IL-6， TNF-α， and IL-1β increased， and IL-6 and TNF-α were significantly increased （P<0.05）. The inflammatory factor IL-4 （P<0.05） and IL-10 were significantly reduced， and the tumor marker CA199 was significantly increased （P<0.01）. HE staining showed that colon lesions， intestinal mucosal epithelial defects with a large number of inflammatory infiltrates， serious crypt structure damage， and glandular arrangement disorder were observed in the model group. Ki67 positive granules were expressed in large areas of colonic tissue. The serum CD4⁺ and CD4⁺/CD8⁺ of mice in the model group decreased significantly （P<0.05）， and CD8⁺ increased significantly （P<0.05）. The plasma content of FITC-D in the model group was significantly increased （P<0.05）， and the expression of Cyclin D₁， CDK2， and CDK4 proteins in colon tissue was significantly increased （P<0.05， P<0.01）. In addition， the expression of Occludin and Claudin-1 was significantly decreased. Compared with the model group， the body weight of mice in the mesalazine group and the high- and low-dose Huangqintang groups increased. DAI score decreased， and the colon became longer. IL-6， TNF-α， and IL-1β expression decreased （P<0.05， P<0.01）， but there was no significant change in IL-4 and IL-10. The content of CA199 was significantly reduced （P<0.05）， and the colomatoid lesions and inflammatory infiltrates were reduced in the mesalazine group and the Huangqintang group. The crypt structure damage was lighter， and the positive expression of Ki67 was reduced. CD4⁺， CD4⁺/CD8⁺， and CD49b⁺ increased， and the difference was not statistically significant. FITC-D content decreased （P<0.05）. The expression of Cyclin D₁， CDK2， and CDK4 decreased （P<0.05， P<0.01）， and Claudin-1 and Occludin protein expression increased in the high-dose Huangqintang group （P<0.05）. ConclusionHuangqintang has a certain delay and inhibitory effect on AOM/DSS-induced inflammatory cancer transformation， and its mechanism of action may be related to regulating immune function and inflammatory response， inhibiting the release of pro-inflammatory factors， repairing damaged intestinal barriers， inhibiting abnormal proliferation of colon cells， and intervening in the formation and development of CAC colon tumors.

BACKGROUND: Low-density computed tomography (LDCT) improved early lung cancer diagnosis but introduces an excess of false-positive pulmonary nodules data. Hence, accurate diagnosis of early-stage lung cancer remains challenging. The purpose of the study was to assess the feasibility of using circulating tumour cells (CTCs) to differentiate malignant from benign pulmonary nodules. METHODS: 122 patients with suspected malignant pulmonary nodules detected on chest CT in preparation for surgery were prospectively recruited. Peripheral blood samples were collected before surgery, and CTCs were identified upon isolation by size of epithelial tumour cells and morphological analysis. Laser capture microdissection, MALBAC amplification, and whole-exome sequencing were performed on 8 samples. The diagnostic efficacy of CTCs counting, and the genomic variation profile of benign and malignant CTCs samples were analysed. RESULTS: Using 2.5 cells/5 mL as the cut-off value, the area under the receiver operating characteristic curve was of 0.651 (95% confidence interval: 0.538-0.764), with a sensitivity and specificity of 0.526 and 0.800, respectively, and positive and negative predictive values of 91.1% and 30.3%, respectively. Distinct sequence variations differences in DNA damage repair-related and driver genes were observed in benign and malignant samples. TP53 mutations were identified in CTCs of four malignant cases; in particular, g.7578115T>C, g.7578645C>T, and g.7579472G>C were exclusively detected in all four malignant samples. CONCLUSIONS CTCs play an ancillary role in the diagnosis of pulmonary nodules. TP53 mutations in CTCs might be used to identify benign and malignant pulmonary nodules.
Humans ; Lung Neoplasms ; Exome Sequencing ; Multiple Pulmonary Nodules ; Carcinoma ; DNA Repair

Objective:To compare the prognosis of fluoroucil combined with cisplatin and paclitaxel combined with cisplatin regimens with concurrent radiotherapy in treatment of esophageal squamous cell carcinoma.Methods:A total of 120 patients with esophageal squamous cell carcinoma who were admitted to Anyang Tumor Hospital of Henan Province from December 2012 to November 2018 were randomly divided into group A and group B by using a random number generator. Group A was given cisplatin combined with 5-fluorouracil, and group B was given cisplatin combined with paclitaxel. Both groups had the same radiotherapy regimen, and both used intensity-modulated radiation therapy (IMRT). Completions of 50 Gy radiotherapy and at least one cycle of chemotherapy were considered to be in line with the plan. Survival data was analyzed in the term of intention-to-treat (ITT) and per-protocol (PP) set.Results:Of the 120 patients, 114 patients were treated and the adverse reactions could be evaluated, including 55 cases in group A and 59 cases in group B. The incidence of grade Ⅲ-Ⅳ leukopenia in group B was higher than that in group A [49.2% (29/59) vs. 25.5% (14/55)], and the difference was statistically significant ( χ2 = 6.805, P = 0.012), and there were no statistical differences in the other adverse reactions between the two groups (All P > 0.05). A total of 113 cases can be analyzed for survival. According to ITT analysis, the median progression-free survival (PFS) time in group A and group B was 28.0 months (95% CI 15.5-34.5 months) and 27.0 months (95% CI 17.0-41.0 months), the median overall survival (OS) time was 28.0 months (95% CI 15.8-34.2 months) and not reached, the differences were not statistically significant (both P > 0.05). According to PP analysis, the median PFS time in group A and group B was 28.0 months (95% CI 15.8-34.2 months) and 29.0 months (95% CI 14.9-45.1 months), the median OS time in group A and group B was 28.0 months (95% CI 3.7-52.3 months) and not reached, the differences were not statistically significant (both P > 0.05). Conclusions:The fluorouracil combined with cisplatin regimen and paclitaxel combined with cisplatin regimen with concurrent radiotherapy have similar PFS and OS time in treatment of esophageal squamous cell carcinoma, the adverse reactions are different, but they are all tolerable. In individualized clinical practice, the toxicities and costs of the two regimens can be comprehensively considered.