Objective:To explore the clinical value of 18F-fluoromisonidazole (FMISO) PET/CT hypoxia imaging in early response to heavy ion radiotherapy in patients with non-small cell lung cancer(NSCLC). Methods:From April 2018 to January 2021, the 18F-FMISO PET/CT images of 23 NSCLC patients (19 males, 4 females; age (64.9±10.3) years) who received heavy ion radiotherapy in Shanghai Proton and Heavy Ion Center were retrospectively analyzed. The evaluation parameters included tumor volume (TV), tumor to background ratio (TBR) before and after radiotherapy. Patients were divided into hypoxia group and non-hypoxia group with the baseline TBR value≥1.4 as hypoxia threshold. Wilcoxon signed rank test was used to compare the differences of TV and TBR before and after radiotherapy in 2 groups. Results:Of 23 NSCLC patients, 17 were hypoxia and 6 were non-hypoxia. Compared with the baseline, TV after the radiotherapy (59.44(22.86, 99.43) and 33.78(8.68, 54.44) cm 3; z=-3.05, P=0.002) and TBR after the radiotherapy (2.25(2.09, 2.82) and 1.42(1.24, 1.67); z=-3.39, P=0.001) of the hypoxia group were significantly lower, while TV (16.19(6.74, 36.52) and 8.59(4.38, 25.47) cm 3; z=-1.57, P=0.120) and TBR (1.19(1.05, 1.27) and 1.10 (0.97, 1.14); z=-1.89, P=0.060) of the non-hypoxia group decreased with no significant differences. Conclusions:Hypoxic NSCLC tumors are sensitive to heavy ion radiation. Compared with non-hypoxic tumors, hypoxic tumors respond more quickly, and a significant reduction in TV can be observed early after radiotherapy. Heavy ion radiation can significantly improve tumor hypoxia.

Objective:To investigate the ultrasonic characteristics of eccrine spiradenoma (ES) and to analyze the diagnostic value.Methods:Nineteen ES patients with 24 lesions confirmed by pathology in 3 grade-A tertiary hospitals from October 2011 to October 2021 were enrolled as study group, and in the same time, 46 patients with 46 masses in the skin and muscular tissues with clinical features of automatic pain and/or tenderness were selected as control group. The ultrasonographic characteristics of the two groups were analyzed retrospectively, including anatomical location, shape, boundary, internal echogenicity, echogenic distribution, calcification, posterior acoustic effect, and vascularity. The ultrasonographic characteristics of the two groups were compared, and the risk sonographic characteristics of ES were obtained by multivariate logistic regression analysis. The sensitivity and specificity of ultrasound characteristics for the diagnosis of ES were calculated.Results:The ultrasonic characteristics of the two groups had significant differences in lobulated shape, boundary, internal echogenicity and posterior acoustic effect (χ 2=32.65, 15.65, 5.77, 13.63; all P<0.01). Multivariate logistic regression analysis showed that lobulated shape and posterior acoustic enhancement were the risk ultrasonic characteristics of ES. The sensitivity and specificity of lobulated shape and posterior acoustic enhancement characteristics in the diagnosis of ES were 79.17%, 89.13%, 95.83% and 47.83%, respectively; and the sensitivity and specificity of the combination of lobulated shape and posterior acoustic enhancement characteristics in the diagnosis of ES were 79.17% and 97.83%, respectively. Conclusions:The lobulated shape and posterior acoustic enhancement characteristics are important for the identification of ES, which have higher diagnostic efficacy for ES.

Objective: To analyze the spatial distribution of brain metastases in EGFR-mutant lung cancer and the risk of hippocampal metastasis. Methods: Patients with lung cancer brain metastases diagnosed and treated in the Shanghai Cancer Center Fudan University from 2006 to 2016 were enrolled. The brain metastasis with positive mutation of EGFR gene was screened. The magnetic resonance images of the patients were reviewed and the distribution characteristics of brain metastasis were analyzed. Results: A total of 920 lung cancer patients with brain metastases were screened, 266 of whom had EGFR gene mutation detection, and 131(49%) were identified as EGFR gene mutations. Excluding 17 patients who did not have a head magnetic resonance examination in our hospital, a total of 114 patients and 738 lesions were enrolled in this study. The proportion of brain metastases distributed in each brain region was 22.8%, 19.5%, 22.0%, 13.4%, 3.3%, 16.7%, and 2.2% for frontal, temporal, parietal, occipital lobe, insula, cerebellum, and brainstem, respectively. The number of metastases and cases located in the hippocampus, <5 mm from the hippocampus, <10 mm from the hippocampus, and<15 mm from the hippocampus were 6(0.8%), 10(1.3%), 11(1.4%), and 14(1.8%), 5 cases (4.4%), 8 cases (7.0%), 9 cases (7.9%), and 11 cases (9.6%), respectively. Conclusion EGFR-mutant lung cancer brain metastasis is low risk in the hippocampus and its surrounding 15 mm.

Regulatory T cells ( Treg) play important role in immune homeostasis in physics and hamper the anti-tumor immunity. Depletion of intra-tumor Treg is a critical step to boost the anti-tumor effect in immune therapy. Radiotherapy can induce secretion of TGF-βand IL33 from tumor cells and then increase Treg proliferation and recruitment into tumor through Langerhans cell. Depletion of Treg could increase the local control and abscopal effect of radiotherapy.

AIM:Toinvestigatewhetherautophagyisup-regulatedwhenresveratrol(Res)inducesapoptosis in chondrosarcoma , and to study the effects of autophagy inhibitor combined with Res on chondrosarcoma .METHODS:SW1353 cells were divided into 4 groups: control group, Res group, 3-methyladenine (3MA) group, and Res +3MA group.Electron microscopy was used to observe the autophagyosomes in control group and Res group .At the same time, the viability of the cells in the 4 groups was detected by CCK-8 assay.TUNEL staining and Western blotting (for determi-ning the levels of cleaved caspase-3, Bax and Bcl-2) were used to reflect levels of apoptosis in all groups .The expression of autophagy-related proteins Beclin 1, LC3-Ⅱ and p62 was detected by Western blotting .RESULTS: Exposure of the cells to Res resulted in a decrease in cell viability and an increase in the level of apoptosis ( P<0.05 ) .Compared with control group, the level of apoptosis was increased but the autophagy was decreased (P <0.05).Compared with Res group, the cell viability and the level of autophagy were decreased and the level of apoptosis was increased ( P<0.05 ) . CONCLUSION:Resveratrol induces apoptosis and autophagy , and inhibition of autophgay enhances resveratrol-induced apoptosis in chondrosarcoma .

OBJECTIVETo investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro.

METHODSCultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80 µmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1% DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment.

RESULTSEmodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time- and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05).

CONCLUSIONEmodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Carcinoma, Squamous Cell ; pathology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; drug effects ; Cyclin E ; metabolism ; Cyclin-Dependent Kinase 2 ; metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Emodin ; pharmacology ; Humans ; Mouth Neoplasms ; pathology ; Oncogene Proteins ; metabolism ; Signal Transduction

Objective To investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro. Methods Cultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80μmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1%DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment. Results Emodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time-and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05). Conclusion Emodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Objective To investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro. Methods Cultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80μmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1%DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment. Results Emodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time-and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05). Conclusion Emodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Background and purpose:Radiotherapy is one of the main treatment methods for brain tumor patients, but neurotoxicity was observed frequently. Because of the confounding factors in clinical data, it’s hard to summarize the characteristic of neurological changes after brain irradiation. This study used the brain irradiation injury model of rats to test whether brain irradiation change the mood and memory.Methods:Whole brain of SD rats (6-8 weeks old) was exposed to 22 Gy radiation. Open ifeld and elevated plus maze was used to assess the anxiety of rats, passive avoidance was used to assess the mood memory, and novel place recognition was used to assess the spatial memory at 1 month or 10 months after brain irradiation.Results:At 1 month post irradiation, rats moved with less distance and entrance to the central zone of open ifeld with less time, explored the open and closed arms with less time and the exploration of open arms also decreased, entered the darkroom more rapidly during the test phase of passive avoidance, and lose the interest to explore the novel place during novel place recognition. At 10 months post irradiation, rats exhibited similarly with control group during open ifeld and elevated plus maze test, but still entered the darkroom more rapidly during the test phase of passive avoidance, and lose the interest to explore the novel place during novel place recognition.Conclusion:Brain irradiation could decrease the locomotor activity, increase the anxiety mood, reduce the mood and spatial memory; mood dysfunction induced by brain irradiation could restore, but memory impairments would be long-standing.

Animals ; Disease Models, Animal ; Female ; Human papillomavirus 16 ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Uterine Cervical Neoplasms ; Xenograft Model Antitumor Assays