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[A real-world study of the clinical application of the Paris system for reporting urinary cytology in cancer hospital]. [癌症医院尿液细胞学报告巴黎系统临床应用的实际研究]。
Q3 Medicine Pub Date : 2024-07-23 DOI: 10.3760/cma.j.cn112152-20230731-00049
H Zhao, Z H Zhang, H Q Guo, N Wei, H Y Ma, L L Zhao, Y Sun, C Wang, X X Chang, X G Bi, N Z Xing

Objectives: To evaluate the clinical value of the Paris system for reporting urinary cytology (TPS) in the diagnosis of urothelial carcinoma (UC). Methods: A total of 1 744 cytological diagnostic records (from 751 cases) were collected retrospectively. All specimens were voided urines and histopathology as the gold standard. The sensitivity and specificity of urinary cytological diagnosis of UC and risk of high grade malignant (ROHM) in each diagnostic category were compared. Results: There were 360 cases with histopathology. The percentage of negative for high-grade urothelial carcinoma (NHGUC) was 30.1% (226/751), atypical urothelial cells (AUC) was 29.8% (224/751), suspicious for high-grade urothelial carcinoma (SHGUC) was 16.8% (126/751), high grade urothelial carcinoma (HGUC) was 21.2% (159/751), and non-urothelial malignancy (NUM) was 2.1% (16/751). The histpathologic ROHM corresponding to each cytological diagnosis category were 27.3% for NHGUC, 32.7% for AUC, 74.7% for SHGUC, 96.6% for HGUC and 100.0% for NUM, respectively. ROHM of SHGUC was significantly higher than that of AUC group, and the difference between the two groups was statistically significant (P<0.001). ROHM of HGUC group was significantly higher than that of SHGUC group, and the difference was statistically significant (P<0.001). With SHGUC as the cut-off value, the sensitivity and specificity of cytological diagnosis of HGUC were 76.7% (165/215) and 85.7% (18/21), and with HGUC as the cut-off value, the sensitivity and specificity of cytological diagnosis of HGUC were 53.0% (114/215) and 100.0% (21/21), respectively. Conclusions: Urine cytology has high sensitivity and specificity in the diagnosis of HGUC. The malignant risk of TPS varies with different diagnosis category. The high malignant risk population in cancer hospital leads to the relatively high malignant proportion and ROHM in each diagnosis category. Urinary cytology TPS reporting system is helpful to clinical management and has good clinical application value.

目的评估巴黎尿液细胞学报告系统(TPS)在诊断尿路上皮癌(UC)中的临床价值。方法回顾性收集了 1 744 份细胞学诊断记录(来自 751 个病例)。所有标本均为排出的尿液,以组织病理学作为金标准。比较了尿液细胞学诊断 UC 的敏感性和特异性以及各诊断类别中的高级别恶性风险(ROHM)。结果有 360 例病例进行了组织病理学检查。高级别尿路上皮癌(NHGUC)阴性比例为 30.1%(226/751),非典型尿路上皮细胞(AUC)阴性比例为 29.8%(224/751),疑似高级别尿路上皮癌(SHGUC)为 16.8%(126/751),高级别尿路上皮癌(HGUC)为 21.2%(159/751),非尿路上皮恶性肿瘤(NUM)为 2.1%(16/751)。每个细胞学诊断类别对应的组织病理学ROHM分别为:NHGUC 27.3%、AUC 32.7%、SHGUC 74.7%、HGUC 96.6%、NUM 100.0%。SHGUC组的ROHM明显高于AUC组,两组间差异有统计学意义(P<0.001)。HGUC 组的 ROHM 明显高于 SHGUC 组,两组差异有统计学意义(P<0.001)。以SHGUC为临界值,细胞学诊断HGUC的敏感性和特异性分别为76.7%(165/215)和85.7%(18/21);以HGUC为临界值,细胞学诊断HGUC的敏感性和特异性分别为53.0%(114/215)和100.0%(21/21)。结论尿液细胞学诊断 HGUC 具有较高的敏感性和特异性。TPS的恶性风险因诊断类别而异。肿瘤医院的高恶性风险人群导致各诊断类别的恶性比例和ROHM相对较高。尿液细胞学 TPS 报告系统有助于临床管理,具有良好的临床应用价值。
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引用次数: 0
[Circ_0000263 improves radiosensitivity of Hela cells by inhibiting the activity of telomerase protein through miR-338-3p/TERT]. [Circ_0000263通过miR-338-3p/TERT抑制端粒酶蛋白的活性,从而提高Hela细胞的放射敏感性】。]
Q3 Medicine Pub Date : 2024-07-23 DOI: 10.3760/cma.j.cn112152-20231024-00244
C Wang, Y K Huo, M Y Li, C Li, X H Shen, S J Wang, Y F Liu, Z X Jiang

Objective: To explore the effect and molecular mechanism of circ_0000263 on HeLa cell activity, apoptosis, telomerase activity, and radiosensitivity. Methods: The Hela cells were divided into si-NC, si-circ, vector, circ_0000263, anti-NC, anti-miR-338-3p, miR-NC, miR-338-3p, si-circ+anti-NC, si-circ+ anti-miR-338-3p, si-circ+vector, si-circ+TERT, sh-NC, sh-circ groups. Reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of circ_0000263 and miR-338-3p. Cell clone formation array was used to detect cell survival; cell counting kit-8 (CCK-8) to detect cell proliferation; flow cytometry to detect apoptosis; western blot method to detect the expressions of proliferating cell nuclear antigen (PCNA), Cleaved-casp3, telomerase reverse transcriptase (TERT) proteins; double luciferase assay to detect the targeting relationships of circ_0000263 and miR-338-3p, miR-338-3p and TERT; telomere repeat amplification enzyme linked immunosorbent assay (TRAR-ELISA) to detect telomerase activity. Results: Circ_0000263 was highly expressed in Hela cells, miR-338-3p was low expressed, and TERT was highly expressed; circ_0000263 was also highly expressed in Hela cells treated with radiation (P<0.05). Knockdown of circ_0000263 inhibited the clone formation and cell proliferation ability of HeLa cells, and enhanced the radiosensitivity and apoptosis of HeLa cells. In contrast, knockdown of circ_0000263 decreased PCNA protein expression level and enhanced Cleaved-casp3 protein expression level in HeLa cells (P<0.05). The apoptosis rate in the si-circ group was (13.19±1.12)%, which was higher than (6.80±0.62)% of si-NC group (P<0.05). The apoptosis rate in the si-circ+4 Gy group was (24.82±1.57)%, which was higher than (17.00±0.96)% of si-NC+4 Gy group (P<0.05). Circ_0000263 targeted regulated miR-338-3p, and miR-338-3p targeted regulated TERT. MiR-338-3p was lowly expressed in HeLa cells, and knockdown of circ_0000263 elevated miR-338-3p expression level in HeLa cells. Circ_0000263 regulated TERT expression and inhibited telomerase activity through miR-338-3p. MiR-338-3p/TERT can restore the effect of circ_0000263 on the radiosensitivity of Hela cells. The apoptosis rate in the si-circ+anti-NC group was (27.37±0.89)%, which was higher than (18.22±1.18)% of the si-circ+anti-miR-338-3p group (P<0.05). The apoptosis rate in the si-circ+vector group was (27.55±0.48)%, which was higher than (20.10±0.68)% of si-circ+TERT group (P<0.05). After 72 hours of radiation by 4 Gy, the cell survival fraction of si-circ+anti-NC group was 0.41±0.02, which was lower than 0.66±0.03 of the si-circ+anti-miR-338-3p group (P<0.05); the cell survival fraction of si-circ+vector group was 0.42±0.05, which was lower than 0.70±0.03 of si-circ+TERT group (P<0.05). Conclusion: Inhibiting the expression of circ_0000263 supresses the proliferation of He

研究目的探讨circ_0000263对HeLa细胞活性、凋亡、端粒酶活性和放射敏感性的影响及分子机制。方法将 Hela 细胞分为 si-NC 组、si-circ 组、载体组、circ_0000263 组、anti-NC 组、anti-miR-338-3p 组、miR-NC 组、miR-338-3p 组、si-circ+anti-NC 组、si-circ+anti-miR-338-3p 组、si-circ+载体组、si-circ+TRT 组、sh-NC 组、sh-circ 组。采用逆转录-实时定量聚合酶链反应(RT-qPCR)检测 circ_0000263 和 miR-338-3p 的表达。细胞克隆形成阵列检测细胞存活;细胞计数试剂盒-8(CCK-8)检测细胞增殖;流式细胞仪检测细胞凋亡;Western印迹法检测增殖细胞核抗原(PCNA)、裂解-casp3、端粒酶逆转录酶(TERT)蛋白的表达;双荧光素酶试验检测circ_0000263与miR-338-3p、miR-338-3p与TERT的靶向关系;端粒重复扩增酶联免疫吸附试验(TRAR-ELISA)检测端粒酶活性。结果Circ_0000263在Hela细胞中高表达,miR-338-3p低表达,TERT高表达;Circ_0000263在经辐射处理的Hela细胞中也高表达(P<0.05)。敲除 circ_0000263 可抑制 HeLa 细胞的克隆形成和细胞增殖能力,增强 HeLa 细胞的辐射敏感性和凋亡能力。相反,敲除 circ_0000263 会降低 HeLa 细胞 PCNA 蛋白表达水平,提高 Cleaved-casp3 蛋白表达水平(P<0.05)。si-circ 组的细胞凋亡率为(13.19±1.12)%,高于 si-NC 组的(6.80±0.62)%(P<0.05)。si-circ+4 Gy组的细胞凋亡率为(24.82±1.57)%,高于si-NC+4 Gy组的(17.00±0.96)%(P<0.05)。Circ_0000263靶向调控miR-338-3p,miR-338-3p靶向调控TERT。MiR-338-3p在HeLa细胞中低表达,而敲除circ_0000263可提高HeLa细胞中miR-338-3p的表达水平。Circ_0000263 通过 miR-338-3p 调节 TERT 的表达并抑制端粒酶的活性。MiR-338-3p/TERT 可以恢复 circ_0000263 对 Hela 细胞辐射敏感性的影响。si-circ+anti-NC 组的细胞凋亡率为(27.37±0.89)%,高于 si-circ+anti-miR-338-3p 组的(18.22±1.18)%(P<0.05)。si-circ+vector 组的细胞凋亡率为(27.55±0.48)%,高于 si-circ+TERT 组的(20.10±0.68)%(P<0.05)。4Gy照射72小时后,si-circ+抗NC组细胞存活率为(0.41±0.02)%,低于si-circ+抗miR-338-3p组的(0.66±0.03)%(P<0.05);si-circ+载体组细胞存活率为(0.42±0.05)%,低于si-circ+TERT组的(0.70±0.03)%(P<0.05)。结论抑制circ_0000263的表达可通过调控miR-338-3p/TERT抑制Hela细胞的增殖,促进细胞凋亡,抑制端粒酶活性,提高癌细胞的放射敏感性,为提高Hela细胞的放射敏感性提供理论依据。
{"title":"[Circ_0000263 improves radiosensitivity of Hela cells by inhibiting the activity of telomerase protein through miR-338-3p/TERT].","authors":"C Wang, Y K Huo, M Y Li, C Li, X H Shen, S J Wang, Y F Liu, Z X Jiang","doi":"10.3760/cma.j.cn112152-20231024-00244","DOIUrl":"10.3760/cma.j.cn112152-20231024-00244","url":null,"abstract":"<p><p><b>Objective:</b> To explore the effect and molecular mechanism of circ_0000263 on HeLa cell activity, apoptosis, telomerase activity, and radiosensitivity. <b>Methods:</b> The Hela cells were divided into si-NC, si-circ, vector, circ_0000263, anti-NC, anti-miR-338-3p, miR-NC, miR-338-3p, si-circ+anti-NC, si-circ+ anti-miR-338-3p, si-circ+vector, si-circ+TERT, sh-NC, sh-circ groups. Reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of circ_0000263 and miR-338-3p. Cell clone formation array was used to detect cell survival; cell counting kit-8 (CCK-8) to detect cell proliferation; flow cytometry to detect apoptosis; western blot method to detect the expressions of proliferating cell nuclear antigen (PCNA), Cleaved-casp3, telomerase reverse transcriptase (TERT) proteins; double luciferase assay to detect the targeting relationships of circ_0000263 and miR-338-3p, miR-338-3p and TERT; telomere repeat amplification enzyme linked immunosorbent assay (TRAR-ELISA) to detect telomerase activity. <b>Results:</b> Circ_0000263 was highly expressed in Hela cells, miR-338-3p was low expressed, and TERT was highly expressed; circ_0000263 was also highly expressed in Hela cells treated with radiation (<i>P</i><0.05). Knockdown of circ_0000263 inhibited the clone formation and cell proliferation ability of HeLa cells, and enhanced the radiosensitivity and apoptosis of HeLa cells. In contrast, knockdown of circ_0000263 decreased PCNA protein expression level and enhanced Cleaved-casp3 protein expression level in HeLa cells (<i>P</i><0.05). The apoptosis rate in the si-circ group was (13.19±1.12)%, which was higher than (6.80±0.62)% of si-NC group (<i>P</i><0.05). The apoptosis rate in the si-circ+4 Gy group was (24.82±1.57)%, which was higher than (17.00±0.96)% of si-NC+4 Gy group (<i>P</i><0.05). Circ_0000263 targeted regulated miR-338-3p, and miR-338-3p targeted regulated TERT. MiR-338-3p was lowly expressed in HeLa cells, and knockdown of circ_0000263 elevated miR-338-3p expression level in HeLa cells. Circ_0000263 regulated TERT expression and inhibited telomerase activity through miR-338-3p. MiR-338-3p/TERT can restore the effect of circ_0000263 on the radiosensitivity of Hela cells. The apoptosis rate in the si-circ+anti-NC group was (27.37±0.89)%, which was higher than (18.22±1.18)% of the si-circ+anti-miR-338-3p group (<i>P</i><0.05). The apoptosis rate in the si-circ+vector group was (27.55±0.48)%, which was higher than (20.10±0.68)% of si-circ+TERT group (<i>P</i><0.05). After 72 hours of radiation by 4 Gy, the cell survival fraction of si-circ+anti-NC group was 0.41±0.02, which was lower than 0.66±0.03 of the si-circ+anti-miR-338-3p group (<i>P</i><0.05); the cell survival fraction of si-circ+vector group was 0.42±0.05, which was lower than 0.70±0.03 of si-circ+TERT group (<i>P</i><0.05). <b>Conclusion:</b> Inhibiting the expression of circ_0000263 supresses the proliferation of He","PeriodicalId":39868,"journal":{"name":"中华肿瘤杂志","volume":"46 7","pages":"676-685"},"PeriodicalIF":0.0,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[China clinical practice guideline for stage Ⅳ primary lung cancer (2024 edition)]. [中国原发性肺癌Ⅳ期临床实践指南(2024 年版)》。]
Q3 Medicine Pub Date : 2024-07-23 DOI: 10.3760/cma.j.cn112152-20240311-00104

Primary lung cancer (abbreviated as lung cancer) stands as the most prevalent malignant disease and the leading cause of cancer-related death in China, with an estimated 106.06×104 incident cases and 73.33×104 deaths in 2022. Due to the absence of effective early screening methods, most patients with lung cancer in China are in stage Ⅳ when diagnosed. Multi-disciplinary treatment based on systemic therapy is the treatment principle for patients with stage Ⅳ lung cancer. Chemotherapy remains the cornerstone, but its effectiveness is still unsatisfactory. In recent years, with the rapid development of molecular targeted therapy and immunotherapy, the treatment concept for stage Ⅳ lung cancer has been continually evolving, leading to significant improvements in patient treatment outcomes. To ensure timely updates on the global progress in the treatment of stage Ⅳ lung cancer and further improve the level of standardized diagnosis and treatment of stage Ⅳ lung cancer in China, Medical Oncology Branch of China International Exchange and Promotive Association for Medical and Health Care and Chinese Association for Clinical Oncologists organized experts to compile "China clinical practice guideline for stage Ⅳ primary lung cancer (2024 edition)". This guideline systematically and comprehensively updates epidemiological data, TNM staging, new drugs, treatment regimens, and new indications approved by China National Medical Products Administration before June 30, 2024, etc. Based on the " Clinical practice guideline for stage Ⅳ primary lung cancer in China(2021 version)" and the " Clinical practice guideline for stage Ⅳ lung cancer in China (2023 edition)." This guideline incorporates recommendation levels for therapeutic drugs and treatment flowcharts for stage Ⅳ lung cancer. The guideline covers common clinical issues and corresponding guidance in the diagnosis and treatment process of stage Ⅳ lung cancer. The guideline aims to guide the clinical practice of stage Ⅳ lung cancer, comprehensively improve the standardized diagnosis and treatment level in China, prolong the survival time of patients with stage Ⅳ lung cancer, and improve patients' quality of life.

原发性肺癌(简称 "肺癌")是中国发病率最高的恶性肿瘤,也是导致癌症相关死亡的首要原因,预计 2022 年中国将有 106.06×104 例肺癌患者发病,73.33×104 例肺癌患者死亡。由于缺乏有效的早期筛查方法,中国大多数肺癌患者确诊时已处于Ⅳ期。以系统治疗为基础的多学科治疗是Ⅳ期肺癌患者的治疗原则。化疗仍是基石,但疗效仍不理想。近年来,随着分子靶向治疗和免疫治疗的快速发展,Ⅳ期肺癌的治疗理念也在不断演变,患者的治疗效果得到了显著改善。为及时了解全球Ⅳ期肺癌治疗进展,进一步提高我国Ⅳ期肺癌规范化诊治水平,中国医疗保健国际交流促进会肿瘤内科分会和中国临床肿瘤医师协会组织专家编写了《中国Ⅳ期原发性肺癌临床实践指南(2024年版)》。该指南系统、全面地更新了流行病学数据、TNM分期、2024年6月30日前国家医疗器械监督管理局批准的新药、新治疗方案、新适应症等内容。以《中国Ⅳ期原发性肺癌临床实践指南(2021年版)》和《中国Ⅳ期肺癌临床实践指南(2023年版)》为基础。该指南纳入了Ⅳ期肺癌治疗药物推荐等级和治疗流程图。该指南涵盖了Ⅳ期肺癌诊疗过程中常见的临床问题及相应的指导意见。该指南旨在指导Ⅳ期肺癌的临床实践,全面提高我国Ⅳ期肺癌的规范化诊治水平,延长Ⅳ期肺癌患者的生存时间,改善患者的生活质量。
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引用次数: 0
[circ_BACH2 affects the malignant biological behavior of papillary thyroid cancer by regulating miR-370-3p]. [circ_BACH2通过调控miR-370-3p影响甲状腺乳头状癌的恶性生物学行为]
Q3 Medicine Pub Date : 2024-07-23 DOI: 10.3760/cma.j.cn112152-20231024-00245
P Sun, Y Feng, L Z Zhou, F Pei, B Su, X C Qiao

Objective: To investigate the influence of circ_BACH2 on the malignant biological behavior of papillary thyroid cancer and its molecular mechanism. Methods: Cancer tissues and paracancer tissues of 51 patients with papillary thyroid carcinoma from the Fourth Central Hospital of Tianjin between 2017 and 2019 were collected. Reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of circ_BACH2, miR-370-3p and G protein coupled receptor kinase interacting factor 1 (GIT1) mRNA in tissues and cells; flow cytometry to detect cell apoptosis and cell cycle; plate clone formation experiment to detect the number of cell clones; cell counting kit 8 (CCK-8) to detect cell proliferation; Transwell array to detect cell migration and invasion; western blot to detect protein expressions; dual luciferase report experiment to detect the targeting relationship between circ_BACH2, miR-370-3p and GIT1; the nude mouse tumor formation experiment to detect the effect of circ_BACH2 on tumors in mice. Results: Compared with adjacent tissues, the expressions of circ_BACH2 and GIT1 in papillary thyroid cancer tissues was increased, while the expression of miR-370-3p was decreased. Compared with Nthy-ori3-1 cells, the expressions of circ_BACH2 in papillary thyroid cancer cells TPC-1 and SW579 were increased, the mRNA and protein levels of GIT1 were increased, miR-370-3p expression was decreased. The expression level of GIT1 mRNA was negatively correlated with that of miR-370-3p (r=-0.634), and the expression level of circ_BACH2 was positively correlated with that of GIT1 (r=0.635). The expression level of circ_BACH2 was negatively correlated with that of miR-370-3p (r=-0.394, P<0.05). Circ_BACH2 and miR-370-3p has a binding site at the 3' UTR of GIT1. After knocking down circ_BACH2, the proportion of G0/G1 cells in papillary thyroid cancer cells TPC-1 and SW579 was increased, the proportion of S-phase cells was decreased and the proportion of G2/M-phase cells did not change significantly. The cell absorbance value was lower than that in si-NC group. The number of cell clone formation was decreased (43±5 vs 100±6, 54±8 vs 100±9); the cell apoptosis rate was increased [(19.60±2.40)% vs (4.30±0.20)%, (18.10±2.10)% vs (5.10±0.23)%]; cell migration number was decreased (61±7 vs 134±15, 58±6 vs 112±11), the invasion number was also decreased (45±6 vs 113±11, 47±4 vs 92±9); the expressions of Snail and Twist1 were decreased, and the expression of E-cadherin was increased (P<0.000). Inhibition of miR-370-3p expression reversed the effect of circ_BACH2 knockdown on proliferation, migration, invasion and apoptosis of thyroid papillary cancer cells. Overexpression of GIT1 reversed the effects of overexpression of miR-370-3p on proliferation, migration, invasion and apoptosis of thyroid papillary cancer cells. Mice injected with TPC-1

目的:研究 circ_BACH2 对甲状腺乳头状癌恶性生物学行为的影响及其分子机制:研究 circ_BACH2 对甲状腺乳头状癌恶性生物学行为的影响及其分子机制。方法收集天津市第四中心医院2017年至2019年间51例甲状腺乳头状癌患者的癌组织和癌旁组织。采用逆转录-定量实时聚合酶链反应(RT-qPCR)检测组织和细胞中circ_BACH2、miR-370-3p和G蛋白偶联受体激酶相互作用因子1(GIT1)mRNA的表达;流式细胞术检测细胞凋亡和细胞周期;平板克隆形成实验检测细胞克隆数量;细胞计数试剂盒8(CCK-8)检测细胞增殖;Transwell阵列检测细胞迁移和侵袭;Western印迹检测蛋白表达;双荧光素酶报告实验检测circ_BACH2、miR-370-3p和GIT1之间的靶向关系;裸鼠肿瘤形成实验检测circ_BACH2对小鼠肿瘤的影响。结果与邻近组织相比,甲状腺乳头状癌组织中circ_BACH2和GIT1的表达量增加,而miR-370-3p的表达量减少。与Nthy-ori3-1细胞相比,甲状腺乳头状癌细胞TPC-1和SW579中circ_BACH2的表达量增加,GIT1的mRNA和蛋白水平增加,miR-370-3p的表达量减少。GIT1 mRNA的表达水平与miR-370-3p的表达水平呈负相关(r=-0.634),circ_BACH2的表达水平与GIT1的表达水平呈正相关(r=0.635)。circ_BACH2的表达水平与miR-370-3p呈负相关(r=-0.394,P<0.05)。circ_BACH2 和 miR-370-3p 在 GIT1 的 3' UTR 有结合位点。敲除circ_BACH2后,甲状腺乳头状癌细胞TPC-1和SW579的G0/G1期细胞比例上升,S期细胞比例下降,G2/M期细胞比例无明显变化。细胞吸光度值低于 si-NC 组。细胞克隆形成数减少(43±5 vs 100±6,54±8 vs 100±9);细胞凋亡率增加[(19.60±2.40)% vs (4.30±0.20)%,(18.10±2.10)% vs (5.10±0.23)%];细胞迁移数减少(61±7 vs 134±15,58±6 vs 112±11),侵袭数减少(45±6 vs 113±11,47±4 vs 92±9);Snail和Twist1表达减少,E-cadherin表达增加(P<0.000)。抑制 miR-370-3p 的表达可逆转 circ_BACH2 敲除对甲状腺乳头状癌细胞增殖、迁移、侵袭和凋亡的影响。过表达 GIT1 逆转了过表达 miR-370-3p 对甲状腺乳头状癌细胞增殖、迁移、侵袭和凋亡的影响。小鼠注射稳定转染 sh-circ_BACH2 的 TPC-1 细胞,培养 35 天后,肿瘤体积缩小 [(535±91) mm3 vs (857±114) mm3];肿瘤重量减少 [(0.62±0.13)mg vs(1.06±0.15)mg,P<0.05];裸鼠肿瘤组织中circ_BACH2和GIT1表达量减少,miR-370-3p表达量增加。结论沉默circ_BACH2可抑制甲状腺乳头状癌细胞的体外增殖、迁移和侵袭,促进细胞凋亡,并通过靶向调控miR-370-3p/GIT1抑制体内肿瘤的生长。
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引用次数: 0
[Expert consensus on safety management of bone-modifying agents (2024 edition)]. [骨修饰剂安全管理专家共识(2024 年版)]。
Q3 Medicine Pub Date : 2024-07-23 DOI: 10.3760/cma.j.cn112152-20240111-00022

Bone-modifying agents are a class of drugs that alleviate a series of bone-related events such as pain, pathologic fracture, spinal cord compression, and hypercalcemia caused by bone metastases, and currently include bisphosphonates and RANKL inhibitors. Due to the widespread use of bone-modifying agents, the adverse effects of them are gradually increasing and affecting patients' quality of life. The Breast Cancer Group, Chinese Medical Doctor Association, and the International Medical Society, Chinese Anti-Cancer Association have organized relevant experts to focus on the treatment of bone metastases of advanced malignant tumors based on evidence-based medicine, discuss the management of adverse reactions to bone-modifying agents and form the consensus. Based on the first Expert Consensus on Safety Management of Bone-modifying Agents in China, this consensus added the definition of osteonecrosis of the jaw related to bone-modifying agents, the occurrence of adverse reactions of bone-modifying drugs reported in the literature, and summarized the clinical experience of clinicians in the management of adverse reactions in practice in recent years, and ultimately, the expert group members discussed and proposed reasonable suggestions to guide clinicians in the safety management of bone-modifying agents.

骨修饰药物是一类缓解骨转移引起的疼痛、病理性骨折、脊髓压迫、高钙血症等一系列骨相关事件的药物,目前包括双膦酸盐类和RANKL抑制剂。由于骨修饰药物的广泛使用,其不良反应也逐渐增加,影响了患者的生活质量。中国医师协会乳腺癌学组、中国抗癌协会国际医学会组织相关专家,以循证医学为基础,聚焦晚期恶性肿瘤骨转移的治疗,探讨骨修饰药物不良反应的处理,并形成共识。本次共识在《中国首届骨改良药物安全管理专家共识》的基础上,增加了与骨改良药物相关的颌骨坏死定义、文献报道的骨改良药物不良反应发生情况,并总结了近年来临床医生在实践中处理不良反应的临床经验,最终经专家组成员讨论提出合理建议,指导临床医生进行骨改良药物的安全管理。
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引用次数: 0
[Tumor mechanomedicine]. 【机制蛋白肿瘤】。
Q3 Medicine Pub Date : 2024-06-23 DOI: 10.3760/cma.j.cn112152-20230904-00118
H Guo, Y S He, M J Liu, B Cheng, F Xu

Malignant tumors represent a significant health challenge, critically impacting human well-being. Malignant tumors have become one of the leading causes of death worldwide. According to statistics from the World Health Organization, nearly one-sixth of global deaths in 2020 were caused by malignant tumors. The burden of malignant tumors in our country is also increasing. In recent years, with population aging and changes in lifestyle, the incidence and mortality rates of malignant tumors in China have been steadily rising, malignant tumors have gradually become one of the main causes of death in China. Developing effective diagnostic and treatment methods is of great significance in reducing the burden of malignant tumors in our country. Historically, the focus has been on leveraging the biochemical cues of tumors for both diagnosis and treatment. While valuable, this strategy does not recapitulate the full complexity of tumor diagnosis and management. Recently, the integration of biomechanics and mechanobiology with oncology has highlighted the importance of mechanical cues, which have emerged as new hallmarks of tumors, regulating tumor initiation and development are expected to open potential novel routes for cancer diagnosis and therapeutic interventions. Despite the advances, a thorough literature review suggests a pronounced gap in our understanding of the mechanical properties of tumors. The clinical community has not yet completely recognized the diagnostic and therapeutic relevance of the mechanical cues of tumors. To bridge this knowledge gap, we propose and introduce the paradigm of "Tumor Mechanomedicine". We provide a comprehensive overview of the multi-scale mechanical characteristics of tumors, exploring their influence on tumor biology, from the aspects of tumor biomechanics, tumor mechanobiology, tumor mechanodiagnostics, and tumor mechanotherapeutics. By elucidating the diagnostic and therapeutic potential of these mechanical cues, we aim to furnish the oncology community with fresh insights, paving the way for innovative solutions to persistent clinical conundrums.

恶性肿瘤是一项重大的健康挑战,严重影响人类福祉。从历史上看,重点一直是利用肿瘤的生化线索进行诊断和治疗。尽管这一策略很有价值,但它并没有充分体现肿瘤诊断和管理的复杂性。最近,生物力学和机械生物学与肿瘤学的结合突出了机械提示的重要性,机械提示已成为肿瘤的新特征,为癌症诊断和治疗干预开辟了潜在的新途径。尽管取得了这些进展,但一项全面的文献综述表明,我们对肿瘤力学性质的理解存在明显差距。临床界尚未完全认识到肿瘤机械提示的诊断和治疗相关性。为了弥补这一知识差距,我们提出并引入了“肿瘤机制医学”的范式。我们从肿瘤生物力学、肿瘤机械生物学、肿瘤机械诊断学和肿瘤机械治疗学等方面全面综述了肿瘤的多尺度力学特征,探讨了它们对肿瘤生物学的影响。通过阐明这些机械提示的诊断和治疗潜力,我们旨在为肿瘤学界提供新的见解,为解决持续存在的临床难题的创新解决方案铺平道路。
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引用次数: 0
[Effect of SIRT7 on inhibiting the epithelial-mesenchymal transformation in pancreatic cancer cells and related mechanism]. [SIRT7对抑制胰腺癌细胞上皮-间质转化的作用及相关机制]
Q3 Medicine Pub Date : 2024-06-23 DOI: 10.3760/cma.j.cn112152-20231024-00241
M D Wang, T Y Gao, W Huang, Y K Yang, Y Wang
<p><p><b>Objective:</b> To investigate the effect and mechanism of SIRT7 in epithelial mesenchymal transformation (EMT) of pancreatic cancer cells. <b>Methods:</b> The pancreatic cancer cells were divided into siControl, siSIRT7, over-expression SIRT7, siSIRT7+siCOL4A1, and siSIRT7+siSLUG groups using siRNA or plasmid transfection. The proliferation, migration and invasion of pancreatic cancer cells were detected by EdU, wound healing assay and Transwell experiments, respectively. The expression of EMT and cancer stem cell (CSC) markers were detected by quantitative real-time reverse transcription polymerase chain reaction assay (qRT-PCR) and western blot. RNA sequencing (RNA-seq) in SIRT7 knockdown PANC-1 cells was performed to explore the signaling pathways and target genes regulated by SIRT7. Then the target genes directly regulated by SIRT7 were identified with quantitative chromatin immunoprecipitation experiment (q-ChIP) and chromatin immunoprecipitation polymerase chain reaction (ChIP-PCR). The expressions of SIRT7 and target genes were detected by immunohistochemical (IHC) in pancreatic cancer tissues, and the correlation between SIRT7 and target gene expression was analyzed using TCGA dataset. The correlation between expression of SIRT7 or target genes and survival was analyzed on KM-plotter website. Finally, GeneMANIA, STRING and ENCORI were used to predict SIRT7-related proteins and miRNAs. <b>Results:</b> EdU assay showed that the cell proliferation rates in SIRT7-overexpressed PANC-1 [(19.33±0.35)%] and BxPC-3 cells [(17.00±1.89)%] were lower than those in the control group [(31.60±1.37)% and (24.33±0.78)%, respectively, <i>P</i><0.05]. The proliferation rates of SIRT7-knockdown PANC-1 [(23.94±1.00)% and (27.08±0.97)%] and BxPC-3 cells [(22.00±1.86)% and (25.96±1.61)%] were higher than those of the siControl group [(11.80±1.86)% and (13.42±1.39)%, respectively, <i>P</i><0.05]. In PANC-1 cells, the wound healing assay showed that the relative migration rate of SIRT7-overexpression cells [(76.67±2.74)%] was lower than that of control cells [(100.00±2.13)%, <i>P</i><0.05]; the relative migration rate of cells with SIRT7 knockdown [(134.22±4.08)% and (199.82±9.20)%, respectively] was higher than that of siControl group [(102.24±3.13)%, <i>P</i><0.05]. Compared with the control group, SIRT7 overexpression decreased the number of migrated BxPC-3 cells (45.66±1.69 vs 28.33±2.62, <i>P</i><0.05); while SIRT7 knockdown increased these numbers (65.66±2.86 and 82.00±2.94 versus 33.00±0.81, <i>P</i><0.01). Transwell experiment revealed that the number of invaded cells in SIRT7 overexpression groups (16.33±2.05 and 34.66±1.69) was lower than that control groups (54.33±4.64 and 58.66±5.90, <i>P</i><0.05); with SIRT7 knockdown, the numbers of invaded PANC-1 (63.66±2.49 and 69.33±3.29) and BxPC-3 cells (134.33±3.09 and 181.66±4.02) were higher than those in control groups (35.33±2.49 and 42.00±0.81, <i>P</i>˂0.05). Also, SIRT7 knockdown decreased the
目的研究 SIRT7 在胰腺癌细胞上皮间质转化(EMT)中的作用及机制。方法用 siRNA 或质粒转染胰腺癌细胞,将其分为 siControl 组、siSIRT7 组、过表达 SIRT7 组、siSIRT7+siCOL4A1 组和 siSIRT7+siSLUG 组。分别用 EdU、伤口愈合实验和 Transwell 实验检测胰腺癌细胞的增殖、迁移和侵袭。通过实时逆转录聚合酶链反应定量分析(qRT-PCR)和蛋白印迹检测EMT和癌症干细胞(CSC)标记物的表达。对敲除SIRT7的PANC-1细胞进行RNA测序(RNA-seq),以探索SIRT7调控的信号通路和靶基因。然后通过染色质免疫共沉淀定量实验(q-ChIP)和染色质免疫共沉淀聚合酶链反应(ChIP-PCR)确定了 SIRT7 直接调控的靶基因。免疫组化(IHC)检测了胰腺癌组织中SIRT7和靶基因的表达,并利用TCGA数据集分析了SIRT7和靶基因表达的相关性。在 KM-plotter 网站上分析了 SIRT7 或靶基因表达与生存期的相关性。最后,利用GeneMANIA、STRING和ENCORI预测SIRT7相关蛋白和miRNA。结果EdU检测显示,SIRT7表达组PANC-1细胞[(19.33±0.35)%]和BxPC-3细胞[(17.00±1.89)%]的增殖率低于对照组[(31.60±1.37)%和(24.33±0.78)%,P<0.05]。SIRT7敲除组 PANC-1 细胞[(23.94±1.00)%和(27.08±0.97)%]和 BxPC-3 细胞[(22.00±1.86)%和(25.96±1.61)%]的增殖率分别高于 siControl 组[(11.80±1.86)%和(13.42±1.39)%,P<0.05]。在 PANC-1 细胞中,伤口愈合试验表明,SIRT7 表达组细胞的相对迁移率[(76.67±2.74)%]低于对照组细胞[(100.00±2.13)%,P<0.05];SIRT7敲除组细胞的相对迁移率[(134.22±4.08)%和(199.82±9.20)%]分别高于siControl组[(102.24±3.13)%,P<0.05]。与对照组相比,SIRT7过表达组BxPC-3细胞迁移数减少(45.66±1.69 vs 28.33±2.62,P<0.05);而SIRT7敲除组BxPC-3细胞迁移数增加(65.66±2.86和82.00±2.94 vs 33.00±0.81,P<0.01)。Transwell实验显示,SIRT7过表达组的侵袭细胞数(16.33±2.05 和 34.66±1.69)低于对照组(54.33±4.64 和 58.66±5.90,P<0.05);敲除 SIRT7 后,被侵染的 PANC-1 细胞(63.66±2.49 和 69.33±3.29)和 BxPC-3 细胞(134.33±3.09 和 181.66±4.02)的数量高于对照组(35.33±2.49 和 42.00±0.81,P˂0.05)。此外,SIRT7敲除还降低了上皮标志物的表达,增加了间质和 CSC 标志物的表达。RNA-seq分析表明,SIRT7参与调控多种癌症相关信号通路,包括胰腺癌通路和EMT通路。此外,SIRT7还能直接与COL4A1和SLUG等靶基因的启动子区域结合。SIRT7与胰腺癌细胞中COL4A1和SLUG的表达和功能呈负相关。通过 IHC 验证了 SIRT7、COL4A1、SLUG 和 SOX2 在胰腺癌组织中的表达。最后,根据 GeneMANIA、STRING 和 ENCORI 在线工具预测,SIRT7 与许多蛋白质和 miRNA 相关。结论SIRT7 可通过转录抑制 COL4A1 和 SLUG 等靶基因的表达来抑制胰腺癌细胞的 EMT。因此,SIRT7 可能是胰腺癌的潜在抑癌基因。
{"title":"[Effect of SIRT7 on inhibiting the epithelial-mesenchymal transformation in pancreatic cancer cells and related mechanism].","authors":"M D Wang, T Y Gao, W Huang, Y K Yang, Y Wang","doi":"10.3760/cma.j.cn112152-20231024-00241","DOIUrl":"10.3760/cma.j.cn112152-20231024-00241","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;b&gt;Objective:&lt;/b&gt; To investigate the effect and mechanism of SIRT7 in epithelial mesenchymal transformation (EMT) of pancreatic cancer cells. &lt;b&gt;Methods:&lt;/b&gt; The pancreatic cancer cells were divided into siControl, siSIRT7, over-expression SIRT7, siSIRT7+siCOL4A1, and siSIRT7+siSLUG groups using siRNA or plasmid transfection. The proliferation, migration and invasion of pancreatic cancer cells were detected by EdU, wound healing assay and Transwell experiments, respectively. The expression of EMT and cancer stem cell (CSC) markers were detected by quantitative real-time reverse transcription polymerase chain reaction assay (qRT-PCR) and western blot. RNA sequencing (RNA-seq) in SIRT7 knockdown PANC-1 cells was performed to explore the signaling pathways and target genes regulated by SIRT7. Then the target genes directly regulated by SIRT7 were identified with quantitative chromatin immunoprecipitation experiment (q-ChIP) and chromatin immunoprecipitation polymerase chain reaction (ChIP-PCR). The expressions of SIRT7 and target genes were detected by immunohistochemical (IHC) in pancreatic cancer tissues, and the correlation between SIRT7 and target gene expression was analyzed using TCGA dataset. The correlation between expression of SIRT7 or target genes and survival was analyzed on KM-plotter website. Finally, GeneMANIA, STRING and ENCORI were used to predict SIRT7-related proteins and miRNAs. &lt;b&gt;Results:&lt;/b&gt; EdU assay showed that the cell proliferation rates in SIRT7-overexpressed PANC-1 [(19.33±0.35)%] and BxPC-3 cells [(17.00±1.89)%] were lower than those in the control group [(31.60±1.37)% and (24.33±0.78)%, respectively, &lt;i&gt;P&lt;/i&gt;<0.05]. The proliferation rates of SIRT7-knockdown PANC-1 [(23.94±1.00)% and (27.08±0.97)%] and BxPC-3 cells [(22.00±1.86)% and (25.96±1.61)%] were higher than those of the siControl group [(11.80±1.86)% and (13.42±1.39)%, respectively, &lt;i&gt;P&lt;/i&gt;<0.05]. In PANC-1 cells, the wound healing assay showed that the relative migration rate of SIRT7-overexpression cells [(76.67±2.74)%] was lower than that of control cells [(100.00±2.13)%, &lt;i&gt;P&lt;/i&gt;<0.05]; the relative migration rate of cells with SIRT7 knockdown [(134.22±4.08)% and (199.82±9.20)%, respectively] was higher than that of siControl group [(102.24±3.13)%, &lt;i&gt;P&lt;/i&gt;<0.05]. Compared with the control group, SIRT7 overexpression decreased the number of migrated BxPC-3 cells (45.66±1.69 vs 28.33±2.62, &lt;i&gt;P&lt;/i&gt;<0.05); while SIRT7 knockdown increased these numbers (65.66±2.86 and 82.00±2.94 versus 33.00±0.81, &lt;i&gt;P&lt;/i&gt;<0.01). Transwell experiment revealed that the number of invaded cells in SIRT7 overexpression groups (16.33±2.05 and 34.66±1.69) was lower than that control groups (54.33±4.64 and 58.66±5.90, &lt;i&gt;P&lt;/i&gt;<0.05); with SIRT7 knockdown, the numbers of invaded PANC-1 (63.66±2.49 and 69.33±3.29) and BxPC-3 cells (134.33±3.09 and 181.66±4.02) were higher than those in control groups (35.33±2.49 and 42.00±0.81, &lt;i&gt;P&lt;/i&gt;˂0.05). Also, SIRT7 knockdown decreased the","PeriodicalId":39868,"journal":{"name":"中华肿瘤杂志","volume":"46 6","pages":"566-582"},"PeriodicalIF":0.0,"publicationDate":"2024-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141332042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[The influence of knocking down the expression of low-density lipoprotein receptor associated proteins on the vascular abnormalities in hepatocellular carcinoma and its mechanisms]. [敲除低密度脂蛋白受体相关蛋白的表达对肝细胞癌血管异常的影响及其机制]。
Q3 Medicine Pub Date : 2024-05-23 DOI: 10.3760/cma.j.cn112152-20230809-00071
Q Wu, L L Zhan, Y Wang, Y C He, L Chen, Z Z Chen, G T Li, D M Liu, X Bao, X M Liu, H Guo, T Q Song

Objectives: To investigate the effect of the expression of low-density lipoprotein receptor associated protein (LDLR) on the vascular abnormalities in hepatocellular carcinoma (HCC) and its mechanisms. Methods: Based on the information of Oncomine Cancer GeneChip database, we analyzed the correlation between the expression level of LDLR and the expression level of carcinoembryonic antigen (CEA) and CD31 in hepatocellular carcinoma tissues. Lentiviral transfection of short hairpin RNA target genes was used to construct LDLR-knockdown MHCC-97H and HLE hepatocellular carcinoma cells. The differential genes and their expression level changes in LDLR-knockdown hepatocellular carcinoma cells were detected by transcriptome sequencing, real-time fluorescence quantitative polymerase chain reaction, and protein immunoblotting. The gene-related signaling pathways that involve LDLR were clarified by enrichment analysis. The effect of LDLR on CEA was assessed by the detection of CEA content in conditioned medium of hepatocellular carcinoma cells. Angiogenesis assay was used to detect the effect of LDLR on the angiogenic capacity of human umbilical vein endothelial cells, as well as the role of CEA in the regulation of angiogenesis by LDLR. Immunohistochemical staining was used to detect the expression levels of LDLR in 176 hepatocellular carcinoma tissues, and CEA and CD31 in 146 hepatocellular carcinoma tissues, and analyze the correlations between the expression levels of LDLR, CEA, and CD31 in the tissues, serum CEA, and alanine transaminase (ALT). Results: Oncomine database analysis showed that the expressions of LDLR and CEA in the tissues of hepatocellular carcinoma patients with portal vein metastasis were negatively correlated (r=-0.64, P=0.001), whereas the expressions of CEA and CD31 in these tissues were positively correlated ( r=0.46, P=0.010). The transcriptome sequencing results showed that there were a total of 1 032 differentially expressed genes in the LDLR-knockdown group and the control group of MHCC-97H cells, of which 517 genes were up-regulated and 515 genes were down-regulated. The transcript expression level of CEACAM5 was significantly up-regulated in the cells of the LDLR-knockdown group. The Gene Ontology (GO) function enrichment analysis showed that the differential genes were most obviously enriched in the angiogenesis function. The Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway enrichment analysis showed that the relevant pathways involved mainly included the cellular adhesion patch, the extracellular matrix receptor interactions, and the interactions with the extracellular matrix receptors. The CEA content in the conditioned medium of the LDLR-knockdown group was 43.75±8.43, which was higher than that of the control group (1.15±0.14, P<0.001). The results of angiogenesis experiments showed that at 5 h, the number of main junctions, the number of main

研究目的研究低密度脂蛋白受体相关蛋白(LDLR)的表达对肝细胞癌(HCC)血管异常的影响及其机制。研究方法根据Oncomine癌症基因芯片数据库的信息,分析肝细胞癌组织中低密度脂蛋白受体相关蛋白的表达水平与癌胚抗原(CEA)和CD31表达水平的相关性。用慢病毒转染短发夹RNA靶基因构建LDLR敲除的MHCC-97H和HLE肝癌细胞。通过转录组测序、实时荧光定量聚合酶链反应和蛋白免疫印迹法检测了LDLR敲除肝癌细胞中的差异基因及其表达水平变化。通过富集分析,明确了涉及 LDLR 的基因相关信号通路。通过检测肝癌细胞条件培养基中的 CEA 含量,评估了 LDLR 对 CEA 的影响。血管生成试验用于检测 LDLR 对人脐静脉内皮细胞血管生成能力的影响,以及 CEA 在 LDLR 调节血管生成中的作用。免疫组化染色法检测了 176 例肝癌组织中 LDLR 的表达水平,以及 146 例肝癌组织中 CEA 和 CD31 的表达水平,并分析了组织中 LDLR、CEA 和 CD31 的表达水平与血清 CEA 和丙氨酸转氨酶(ALT)之间的相关性。结果Oncomine数据库分析显示,门静脉转移的肝细胞癌患者组织中LDLR和CEA的表达呈负相关(r=-0.64,P=0.001),而这些组织中CEA和CD31的表达呈正相关(r=0.46,P=0.010)。转录组测序结果显示,MHCC-97H细胞的LDLR敲除组和对照组共有1 032个差异表达基因,其中517个基因上调,515个基因下调。LDLR敲除组细胞中CEACAM5的转录表达水平明显上调。基因本体(GO)功能富集分析表明,差异基因在血管生成功能方面的富集最为明显。京都基因和基因组百科全书(KEGG)信号通路富集分析表明,涉及的相关通路主要包括细胞粘附补丁、细胞外基质受体相互作用以及与细胞外基质受体的相互作用。LDLR敲除组条件培养基中的CEA含量为(43.75±8.43),高于对照组(1.15±0.14,P<0.001)。血管生成实验结果显示,5 h时,LDLR-敲除组用MHCC-97H细胞条件培养液培养的HUVEC细胞形成的主连接数、主节段数和晶格总面积分别为295.3±26.4、552.5±63.8、2 239 781.0±13 8211.9平方像素,分别高于对照组(113.3±23.5、194.8±36.5、660 621.0±280 328.3平方像素,均P<0.LDLR敲除组的HUVEC细胞与HLE细胞在条件培养液中培养形成的血管主要连接点数、主要节段数和晶格总面积分别为245.3±42.4、257.5±20.4 和 2 535 754.5±249 094.2 平方像素,均高于对照组(分别为 113.3±23.5、114.3±12.2 和 1 565 456.5±219 259.7 平方像素,均 P<0.01)。在 MHCC-97H 细胞对照组的条件培养液中,培养的 HUVEC 细胞加入 CEA 后形成的主连接数、主区段数和晶格总面积分别为 178.9±12.0、286.9±12.3和1 966 990.0±126 249.5像素,分别高于对照组(119.7±22.1、202.7±33.7和1 421 191.0±189 837.8平方像素)。肝细胞癌组织中 LDLR 的表达与 CEA 的表达无关,但与 CD31 的表达(r=-0.167,P=0.044)、血清 CEA 水平(r=-0.061,P=0.032)和血清 ALT 水平(r=-0.147,P=0.05)呈负相关。肝细胞癌组织中 CEA 的表达与 CD31 的表达呈正相关(r=0.192,P=0.020)。血清 CEA 水平与血清 ALT 水平呈正相关(r=0.164,P=0.029)。结论敲除 LDLR 可通过释放 CEA 促进 HCC 血管异常。
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引用次数: 0
[Expert consensus on safety management of bone-modifying agents]. [关于骨修饰剂安全管理的专家共识]。
Q3 Medicine Pub Date : 2024-04-29 DOI: 10.3760/cma.j.cn112152-20240111-00022

Bone-modifying agents are a class of drugs that alleviate a series of bone-related events such as pain, pathologic fracture, spinal cord compression, and hypercalcemia caused by bone metastases, and currently include bisphosphonates and RANKL inhibitors. Due to the widespread use of bone-modifying agents, the adverse effects of them are gradually increasing and affecting patients' quality of life. The Breast Cancer Group, Chinese Medical Doctor Association, and the International Medical Society, Chinese Anti-cancer Association have organized relevant experts to focus on the treatment of bone metastases of advanced malignant tumors based on evidence-based medicine, discuss the management of adverse reactions to bone-modifying agents and form the consensus. Based on the first Expert Consensus on Safety Management of Bone-modifying Agents in China, this consensus added the definition of osteonecrosis of the jaw related to bone-modifying agents, the occurrence of adverse reactions of bone-modifying drugs reported in the literature, and summarized the clinical experience of clinicians in the management of adverse reactions in practice in recent years, and ultimately, the expert group members discussed and proposed reasonable suggestions to guide clinicians in the safety management of bone-modifying agents.

骨修饰药物是一类缓解骨转移引起的疼痛、病理性骨折、脊髓压迫、高钙血症等一系列骨相关事件的药物,目前包括双膦酸盐类和RANKL抑制剂。由于骨修饰药物的广泛使用,其不良反应也逐渐增加,影响了患者的生活质量。中国医师协会乳腺癌学组、中国抗癌协会国际医学会组织相关专家,以循证医学为基础,聚焦晚期恶性肿瘤骨转移的治疗,探讨骨修饰药物不良反应的处理,并形成共识。本次共识在《中国首届骨改良药物安全管理专家共识》的基础上,增加了与骨改良药物相关的颌骨坏死定义、文献报道的骨改良药物不良反应发生情况,并总结了近年来临床医生在实践中处理不良反应的临床经验,最终经专家组成员讨论提出合理建议,指导临床医生进行骨改良药物的安全管理。
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引用次数: 0
[Chinese expert consensus on the diagnosis and management of ocular adnexal extranodal marginal zone mucosa-associated lymphoid tissue lymphoma (2023 edition)]. [眼附件外边缘区粘膜相关淋巴组织淋巴瘤诊治中国专家共识(2023 年版)]。
Q3 Medicine Pub Date : 2024-04-23 DOI: 10.3760/cma.j.cn112152-20230727-00042

Ocular adnexal extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (OAML) is a common malignant tumor that affects the ocular adnexal region. The incidence of OAML is increasing due to the aging population. The tumor invades the ocular adnexal region, which can result in abnormal ocular appearance and function, thereby reducing the quality of life. Currently, there is no standardized diagnosis and management guideline for OAML. To enhance the standardization of diagnosis and management in OAML, a collaborative effort was undertaken by esteemed organizations in China. The Cellular Immune Therapy Committee of China Association for Promotion of Health Science and Technology, the Ocular Tumor Committee of Chinese Medical Doctor Association for Ophthalmologist Branch, the Imaging Medicine Branch of Chinese International Exchange and Promotion Association for Medical and Healthcare, the Tumor and Microecology Professional Committee of China Anti-cancer Association, and the Lymphoma Immunotherapy Committee of Beijing Cancer Prevention Society jointly convened a panel of experts to develop the inaugural "Chinese Expert Consensus on the Diagnosis and Management of ocular adnexal extranodal marginal zone mucosa-associated lymphoid tissue lymphoma (2023 edition)"..

眼附件粘膜相关淋巴组织结节外边缘区淋巴瘤(OAML)是一种常见的影响眼附件区域的恶性肿瘤。由于人口老龄化,OAML 的发病率正在上升。肿瘤侵犯眼部附件区,可导致眼部外观和功能异常,从而降低生活质量。目前,还没有针对 OAML 的标准化诊断和管理指南。为了加强 OAML 诊断和管理的标准化,中国的一些权威机构开展了一项合作。中国卫生科技促进会细胞免疫治疗专业委员会、中国医师协会眼科医师分会眼部肿瘤专业委员会、中国医疗保健国际交流促进会影像医学分会、中国肿瘤微生态专业委员会、中国抗癌协会肿瘤专业委员会、中国抗癌协会肿瘤微生态专业委员会、中国抗癌协会肿瘤微生态专业委员会、中国抗癌协会肿瘤微生态专业委员会、中国抗癌协会肿瘤微生态专业委员会、中国抗癌协会肿瘤与微生态专业委员会、北京抗癌协会淋巴瘤免疫治疗专业委员会共同召集专家,制定了首部《眼附件结节外边缘区粘膜相关淋巴组织淋巴瘤诊治中国专家共识(2023年版)》。.
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中华肿瘤杂志
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