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[Epidemiological characteristics of cancer mortality in the elderly in Qidong, 1972-2021]. 1972-2021年启东市老年人癌症死亡率流行病学特征分析
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20240529-00224
Y S Chen, J Wang, X H Tang, J Zhu

Objective: To analysis the prevalence characteristics of cancer mortality among the elderly in Qidong City, Jiangsu Province, from 1972 to 2021, and to provide scientific basis for the development of precise prevention and control strategies for cancer in the elderly. Methods: Data of cancers were obtained from Qidong Cancer Registry, a descriptive study method was used to calculate the crude mortality rate (CMR) of cancer among the elderly (≥60 years old). The China age-standardized rate (ASR-C) was calculated using the age structure of the Chinese population in 2000, and world age-standardized rate (ASR-W) was calculated using Segi's world standard population. Joinpoint regression analysis was performed using Joinpoint 4.9.1.0 software to calculate the annual percentage change (APC) and average annual percentage change (AAPC) of mortality. Results: From 1972 to 2021, there were 74 723 cancer deaths in the elderly in Qidong, with CMR of 752.08/105, ASR-C of 666.03/105 (994.22/105 for males and 470.29/105 for females) and ASR-W of 681.11/105. The ASR-C showed little fluctuation before 2000, increased rapidly from 2001 to 2011, and then decreased from 2011 to 2021. From 2017 to 2021, the CMR was 791.01/105, the ASR-C was 689.80/105 (956.77/105 for males and 469.98/105 for females), and the ASR-W was 657.53 /105. The CMR for the 60-64, 65-69, 70-74, 75-79, and 80+ age groups from 2012 to 2021 were 385.42/105 505.51/105, 721.64/105, 1 213.28/105, and 1 705.32/105, respectively. The CMR of elderly under 75 years old were lower from 2012 to 2021 than in other periods, while those of elderly people aged more than 75 years were higher from 2012 to 2021 than in other periods. The AAPC for ASR-C of all cancers over the 50 years was 0.22%, with APC of -1.59% in 2008-2021 (both P<0.05). Over the 50 years, the top five cancers in terms of mortality were lung cancer, gastric cancer, liver cancer, colorectal cancer, and esophageal cancer. Their AAPCs of ASR-C were 1.61%, -2.36%, -0.10%, 1.44%, and -2.03%, respectively. The increasing trends of mortality rates for lung cancer and colorectal cancer and the decreasing trends for gastric cancer and esophageal cancer were statistically significant (P<0.05). Conclusions: The mortality of cancers among elderly is at a high level in Qidong. The overall mortality since 2008 have shown a decreasing trend, and the prevention and control of some cancers have been effective.

目的:分析江苏省启东市1972 - 2021年老年人癌症死亡率流行特征,为制定精准的老年人癌症防治策略提供科学依据。方法:癌症数据来自启东市癌症登记处,采用描述性研究方法计算老年人(≥60岁)癌症的粗死亡率(CMR)。采用2000年中国人口年龄结构计算中国年龄标准化率(ASR-C),采用Segi世界标准人口计算世界年龄标准化率(ASR-W)。采用Joinpoint 4.9.1.0软件进行Joinpoint回归分析,计算死亡率年变化百分数(APC)和平均年变化百分数(AAPC)。结果1972 - 2021年,启东市老年人癌症死亡74 723例,CMR为752.08/105,ASR-C为666.03/105(男性994.22/105,女性470.29/105),ASR-W为681.11/105。ASR-C在2000年之前波动不大,2001 - 2011年快速上升,2011 - 2021年下降。2017 - 2021年,CMR为791.01/105,ASR-C为689.80/105(男性为956.77/105,女性为469.98/105),ASR-W为657.53 /105。2012 - 2021年60 ~ 64岁、65 ~ 69岁、70 ~ 74岁、75 ~ 79岁和80岁以上年龄组的CMR分别为385.42/105、505.51/105、721.64/105、1 213.28/105和1 705.32/105。2012 - 2021年75岁以下老年人CMR低于其他时期,而2012 - 2021年75岁以上老年人CMR高于其他时期。50年间所有癌症ASR-C的AAPC为0.22%,2008-2021年APC为-1.59% (P均<0.05)。50年来,死亡率排名前五的癌症分别是肺癌、胃癌、肝癌、结直肠癌和食道癌。ASR-C的AAPCs分别为1.61%、-2.36%、-0.10%、1.44%和-2.03%。肺癌、结直肠癌死亡率上升趋势,胃癌、食管癌死亡率下降趋势均有统计学意义(P<0.05)。结论:启东市老年人癌症死亡率较高。2008年以来,中国总体死亡率呈下降趋势,部分癌症防控工作取得成效。
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引用次数: 0
[Cancer incidence, mortality and trends among elderly in Hebei province, 2011-2020]. 2011-2020年河北省老年人癌症发病率、死亡率及趋势分析
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20240110-00019
Y Y Liu, D J Li, S S Wu, S Zhang, Y F Fu, Y T He

Objective: With the aggravation of population aging, the burden of malignant tumors in the elderly population is becoming more and more heavy. This study aims to analyze the incidence and mortality of malignant tumors in the elderly population in Hebei Province in the past decade. Methods: The incidence and mortality data of malignant tumors in people aged ≥60 years old in 38 cancer registration areas in Hebei Province from 2011 to 2020 were collected, and the incidence and mortality were analyzed by gender, urban and rural areas, and age groups. The age standardized rates were calculated using the 2000 Chinese population census and Segi's world population. The trend of incidence and mortality was analyzed using the Joinpoint model and the average annual percent change (AAPC). Results: From 2011 to 2020, 216 200 new cases of malignant tumors were reported in the elderly population in the cancer registration areas of Hebei Province, and 170 700 deaths were reported. The peak ages of incident cases number for males and females were 65-69 years old and 60-64 years old, respectively. The crude incidence rate of malignant tumors in the elderly was 905.42/105, and the crude mortality rate was 714.96/105. In general, the incidence and mortality in rural areas were higher than those in urban areas, and the incidence and mortality in males were higher than those in females. The peak ages of incidence and mortality were 80-84 years old and 85+ years old, respectively. From 2011 to 2020, lung cancer, gastric cancer, esophageal cancer, female breast cancer, and colorectal cancer were the main malignant tumors of incidence rate in the elderly population in Hebei Province, and lung cancer, gastric cancer, liver cancer, esophageal cancer, and colorectal cancer were the main malignant tumors in the mortality rate. From 2011 to 2020, the incidence and mortality of malignant tumors in the elderly population in Hebei Province showed a decreasing trend, and AAPC for the age-standardized incidence and mortality were -4.69% and -5.53%, respectively. The rank of incidence and mortality rate of each cancer had changed, but the top two were still lung cancer and stomach cancer. Conclusions: The incidence and mortality of cancer in the elderly population in Hebei province have decreased, but the burden is still heavy. Lung cancer and stomach cancer are still the focus of prevention and treatment in the elderly population in Hebei province.

目的:随着人口老龄化的加剧,老年人群的恶性肿瘤负担越来越重。本研究旨在分析近十年来河北省老年人群恶性肿瘤的发病率和死亡率。研究方法收集2011-2020年河北省38个肿瘤登记地区≥60岁老年人群恶性肿瘤的发病率和死亡率数据,按性别、城乡、年龄组对发病率和死亡率进行分析。采用 2000 年中国人口普查和 Segi 世界人口计算年龄标准化率。采用 Joinpoint 模型和年均百分比变化(AAPC)分析了发病率和死亡率的趋势。结果显示从 2011 年到 2020 年,河北省肿瘤登记地区老年人口中新发恶性肿瘤病例 216 200 例,死亡 170 700 例。男性和女性发病高峰年龄分别为 65-69 岁和 60-64 岁。老年人恶性肿瘤的粗发病率为 905.42/105,粗死亡率为 714.96/105。总体而言,农村地区的发病率和死亡率高于城市地区,男性的发病率和死亡率高于女性。发病和死亡的高峰年龄分别为 80-84 岁和 85 岁以上。从 2011 年到 2020 年,河北省老年人群恶性肿瘤发病率以肺癌、胃癌、食管癌、女性乳腺癌和结直肠癌为主,死亡率以肺癌、胃癌、肝癌、食管癌和结直肠癌为主。2011-2020年,河北省老年人口恶性肿瘤发病率和死亡率呈下降趋势,年龄标准化发病率和死亡率的AAPC分别为-4.69%和-5.53%。各种癌症的发病率和死亡率的排名发生了变化,但排名前两位的仍然是肺癌和胃癌。结论河北省老年人群癌症发病率和死亡率有所下降,但负担仍然较重。肺癌和胃癌仍是河北省老年人群的防治重点。
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引用次数: 0
[Evolution of grading for solitary fibrous tumors of the central nervous system: a clinical pathological and prognostic analysis]. [中枢神经系统孤立性纤维性肿瘤分级的演变:临床病理和预后分析]。
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20240810-00336
X L Li, H Zhang, C C Hu, J F Zhou, M Y Zhuang, X X Fan, L W Hu, Y P Chen, Q Huang, S Zhang, X F Wang

Objective: The 5th edition of the WHO classification of central nervous system (CNS) tumors in 2021 made significant revisions to the nomenclature and grading system of solitary fibrous tumors (SFT). This study aimed to explore the changes in the grading of CNS SFT and its relationship with clinical pathological features and prognosis. Methods: This study retrospectively reviewed the clinical and pathological data of 82 patients with CNS SFT diagnosed at the First Affiliated Hospital of Fujian Medical University from March 2006 to June 2021, reassessed their grading according to the WHO 5th edition CNS tumor classification, and conducted a comprehensive analysis of their histological morphology, immunohistochemical characteristics, and clinical imaging data. Results: The age of the patients ranged from 21 to 83 years, with a median age of 48 years. Follow-up was completed for 82 patients, during which 10 patients died, 24 recurred, and 5 metastasized. MRI imaging showed that SFT exhibited isointense signals on T1-weighted imaging (T1WI) and complex signals on T2-weighted imaging (T2WI), with signal intensity decreasing as the content of collagen fibers increased. According to the 2021 grading criteria, there was a significant change in the grading of SFT, with the number of grade 1 SFT increasing from 10 cases under the 2016 standard to 39 cases, while the number of grade 2 and 3 SFT decreased accordingly. The 2016 grading system was significantly correlated with the overall survival (OS) of patients (P=0.009), while the 2021 grading system did not reach statistical significance. Both grading systems were correlated with histological phenotype, Ki-67 index, mitotic figures, and necrosis (P<0.05). All cases expressed STAT6, and showed varying degrees of expression of vimentin, CD99, BCL-2, and CD34. The staining intensity of type Ⅳ collagen fibers, as analyzed semi-quantitatively, was correlated with the OS of the patients (P=0.017). Conclusions: The new grading system for CNS SFT has undergone significant changes, and its association with OS requires further validation. In-depth study of the content and fine structure of collagen fibers in SFT may have important clinical significance for the prognosis assessment and the formulation of treatment plans for patients. Moreover, quantitative analysis of T2WI signal intensity may provide a new method for preoperative preliminary assessment of the collagen fiber content in SFT.

目的:2021年WHO第五版中枢神经系统(CNS)肿瘤分类对孤立性纤维性肿瘤(SFT)的命名和分级体系进行了重大修订。本研究旨在探讨中枢神经系统SFT分级的变化及其与临床病理特征和预后的关系。方法:回顾性分析2006年3月至2021年6月在福建医科大学第一附属医院诊断的82例中枢神经系统SFT患者的临床和病理资料,根据WHO第5版中枢神经系统肿瘤分类重新评估其分级,并对其组织形态、免疫组织化学特征和临床影像学资料进行综合分析。结果:患者年龄21 ~ 83岁,中位年龄48岁。随访82例,死亡10例,复发24例,转移5例。MRI成像显示SFT在t1加权成像(T1WI)上表现为等信号,在t2加权成像(T2WI)上表现为复杂信号,信号强度随着胶原纤维含量的增加而降低。根据2021年的分级标准,SFT的分级发生了明显变化,一级SFT的数量从2016年标准下的10例增加到39例,而二级和三级SFT的数量相应减少。2016年分级系统与患者总生存期(OS)显著相关(P=0.009),而2021年分级系统未达到统计学意义。两种分级系统均与组织学表型、Ki-67指数、有丝分裂数和坏死相关(P<0.05)。所有病例均表达STAT6, vimentin、CD99、BCL-2、CD34均有不同程度表达。半定量分析Ⅳ型胶原纤维的染色强度与患者的OS相关(P=0.017)。结论:新的中枢神经系统SFT评分体系发生了显著变化,其与OS的相关性有待进一步验证。深入研究SFT中胶原纤维的含量和精细结构,对患者的预后评估和制定治疗方案具有重要的临床意义。此外,定量分析T2WI信号强度可为术前初步评估SFT中胶原纤维含量提供一种新的方法。
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引用次数: 0
[The expert consensus on the diagnosis and treatment of skull base and head-neck sarcomas (2024 edition)]. [颅底头颈部肉瘤诊治专家共识(2024年版)]。
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20240603-00235

Skull base sarcomas of the head and neck originate from the mesenchymal tissues of the skull base and head and neck region, exhibiting a highly aggressive behavior and can occur at all ages. Skull base sarcomas are rare in adults, with an incidence of less than 1% of head and neck tumors. However, in the pediatric population, the incidence can be as high as 35%. These tumors can arise in various locations, involving soft tissues, bones, or nerves of the skull base, face, and neck. The pathological types of skull base sarcomas are diverse, primarily including liposarcoma, angiosarcoma, leiomyosarcoma, rhabdomyosarcoma, Ewing sarcoma, osteosarcoma, undifferentiated pleomorphic sarcoma. Treatment typically involves a multimodal approach, with surgery being the preferred method. However, the surgical challenges posed by skull base sarcomas and the inconsistent efficacy of radiotherapy and chemotherapy contribute to the overall difficulty in treatment. Currently, there are no established guidelines or consensus for the diagnosis and management of skull base sarcomas in China. In response, Chinese Anti-Cancer Association Cancer Neurology Committee, Chinese Medical Education Association Head and Neck Oncology Professional Committee and Chinese Medical Education Association Oncology Chemotherapy Youth Committee have organized multidisciplinary expert discussions. Based on evidence from clinical research, we have summarized clinical application recommendations in the areas of epidemiology, histopathology, molecular pathology, imaging, surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy, with the aim of providing clinical practice evidence to enhance the treatment of skull base sarcomas and improve patient prognosis and quality of life.

头颈部的颅底肉瘤起源于颅底和头颈部的间充质组织,表现出高度侵袭性,可发生于所有年龄。颅底肉瘤在成人中很少见,发病率不到头颈部肿瘤的1%。然而,在儿科人群中,发病率可高达35%。这些肿瘤可以出现在不同的部位,包括软组织、骨骼或颅底、面部和颈部的神经。颅底肉瘤病理类型多样,主要有脂肪肉瘤、血管肉瘤、平滑肌肉瘤、横纹肌肉瘤、尤文氏肉瘤、骨肉瘤、未分化多形性肉瘤等。治疗通常包括多模式方法,手术是首选方法。然而,颅底肉瘤手术难度大,放化疗效果不一致,导致治疗总体困难。目前,对于颅底肉瘤的诊断和治疗,中国尚无明确的指南或共识。对此,中国抗癌协会肿瘤神经学专业委员会、中华医学教育协会头颈肿瘤专业委员会、中华医学教育协会肿瘤化疗青年专业委员会组织了多学科专家讨论。根据临床研究证据,总结流行病学、组织病理学、分子病理学、影像学、手术、放疗、化疗、靶向治疗、免疫治疗等方面的临床应用建议,以期为加强颅底肉瘤的治疗,改善患者预后和生活质量提供临床实践依据。
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引用次数: 0
[Clinicopathological features of primary pulmonary epithelioid hemangioendothelioma: a study of 7 cases]. 原发性肺上皮样血管内皮瘤7例临床病理特征分析
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20240421-00163
W Li, J K Li, X Zheng, L L Chen, Y H Yang

Objective: The clinicopathological features of pulmonary epithelioid hemangioendothelioma (PEHE) were analyzed to provide guidance for clinical practice. Methods: The clinical manifestations, imaging examination, pathological morphology and molecular characteristics, treatment and prognosis of patients with pulmonary epithelioid hemangioendothelioma were retrospectively collected. All cases were admitted to Fujian Medical University Union Hospital from January 2012 to May 2023. Results: Of 7 PEHE cases, 2 underwent tumor biopsy and 5 underwent tumor resection. There were 4 males and 3 females, with a median age of 58 years old. Six cases showed multiple bilateral nodules, and only one case showed a single lesion in the lower left lung lobe. Five patients presented with respiratory symptoms, like cough, sputum, hemoptysis, shortness of breath. There were round-like solid lesions with clear border and homogeneous density on lung CT. Histologically, it showed nodular growth with a distinctive myxohyaline stroma. Necrosis was seen in the center of some cases. Epithelioid tumor cells were arranged in cords, solid pattern or single cells, with abundant eosinophilic cytoplasm and occasional intracytoplasmic vacuoles. The plasmacytoid nucleus were round to oval in shape with obvious nucleoli, minimal pleomorphism and few mitoses. The tumor cells were positive for vascular endothelial markers: CD31 (7/7), CD34 (5/7), ERG (6/6), and Fli-1 (5/6); CKpan was focally positive in 3 cases (3/7), and TFE3 in 2 cases. Ki-67 index ranged from 5% to 10%. Additionally, the tumor cells partially express PD-L1 in two cases. Moreover, lung carcinoma-related gene detection was negative in one case. The TFE3 break-apart probe in two cases did not display a split signal. In terms of treatment, 4 cases were treated with surgery, 1 case was treated with chemotherapy and surgery, and 2 cases were follow-up observation. After the median 34.4 months follow-up time, one was lost to follow-up, six were survived. Their CT scans showed slight enlargement of pulmonary nodules without other organ metastases. Conclusions: PEHE is a rare vascular-derived tumor, which is usually characterized by multiple solid bilateral nodules with slow growth. It tends to lack specific clinical symptoms, and is prone to be misdiagnosed as a metastatic carcinoma. Diagnosis primarily rely on pathology, with the use of an immunohistochemical package being crucial for definitive and differential diagnosis.

目的:分析肺上皮样血管内皮瘤(PEHE)的临床病理特点,为临床提供指导。方法:回顾性收集肺上皮样血管内皮瘤患者的临床表现、影像学检查、病理形态及分子特征、治疗及预后。所有病例均于2012年1月至2023年5月在福建医科大学协和医院住院。结果:7例PEHE患者中2例行肿瘤活检,5例行肿瘤切除术。男4例,女3例,中位年龄58岁。6例表现为双侧多发结节,仅1例表现为左下肺叶单发病灶。5例患者出现咳嗽、咳痰、咯血、呼吸短促等呼吸道症状。肺部CT见圆形实性病灶,边界清晰,密度均匀。组织学上表现为结节状生长,间质粘液透明。部分病例中心可见坏死。上皮样肿瘤细胞呈索状、实状或单细胞排列,胞浆内嗜酸性丰富,偶见胞浆内空泡。浆细胞样核圆形至卵圆形,核仁明显,多形性极少,有丝分裂少。肿瘤细胞血管内皮标志物:CD31(7/7)、CD34(5/7)、ERG(6/6)、fl -1(5/6)阳性;CKpan局灶阳性3例(3/7),TFE3局灶阳性2例。Ki-67指数为5% ~ 10%。此外,2例肿瘤细胞部分表达PD-L1。肺癌相关基因检测阴性1例。在两种情况下,TFE3分离探针没有显示分离信号。治疗方面,手术治疗4例,化疗加手术治疗1例,随访观察2例。中位随访34.4个月后,1例失访,6例存活。CT扫描显示肺结节轻微肿大,无其他器官转移。结论:PEHE是一种罕见的血管源性肿瘤,多表现为双侧多发实性结节,生长缓慢。它往往缺乏特定的临床症状,并容易被误诊为转移性癌。诊断主要依靠病理,使用免疫组织化学包是决定性和鉴别诊断的关键。
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引用次数: 0
[Comparison of clinical outcomes between Ivor-Lewis and Mckeown esophagectomy for middle or lower esophageal cancer]. [Ivor-Lewis食管切除术与Mckeown食管切除术治疗中下段食管癌的临床疗效比较]。
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20230713-00010
L G Yuan, Y S Mao

Objective: To compare the short-term and long-term clinical effects of Ivor-Lewis and Mckeown esophagectomy in the treatment of middle or lower thoracic esophageal cancer. Methods: The clinical data of 716 patients with middle and lower thoracic esophageal cancer who underwent radical resection of Ivor Lewis or McKeown esophageal cancer in the Department of Thoracic Surgery, Cancer Hospital, Chinese Academy of Medical Science from March 2015 to October 2018 were analyzed retrospectively, and the perioperative indicators, postoperative complications and survival of the two surgical methods were compared. Results: Among 716 patients, 135 patients underwent Ivor Lewis esophagectomy and 581 patients underwent McKeown esophagectomy. Mckeown group was significantly superior to Ivor Lewis group in terms of total number of lymph node dissection [median number was 27 (19~37) vs 25(18~33)], total number of lymph node dissection stations [median number was 5(4~7) vs 5(4~5)], and number of lymph nodes dissection along recurrent laryngeal nerve [median number was 3 (1~6) vs 0 (0~3), P<0.05]. However, the incidence of recurrent laryngeal nerve palsy in Mckeown group was significantly higher than that in Ivor Lewis group [10.7% (62/581) vs 1.5%(2/135), P<0.001]. There was no significant difference in the 1 -, 3 -, 5-year overall survival between the Ivor Lewis group(91.0%, 70.5%, 52.9%) and the Mckeown group (89.7%, 68.4%, 62.4%, P>0.05), and there was also no significant difference in the 1 -, 3 -, 5-year disease free survival between the Ivor Lewis group(77.0%, 54.1%, 44.0%) and the Mckeown group (78.3%, 59.0%, 52.8%, P>0.05). Conclusions: Ivor Lewis esophagectomy and Mckeown esophagectomy are feasible, safe, good short-term efficacy and similar survival rate for middle and lower thoracic esophageal cancer. Ivor Lewis surgery has lower incidence of recurrent laryngeal nerve palsy. Mckeown operation has more advantages in lymph node dissection, especially in lymph node dissection beside the recurrent laryngeal nerve.

目的:比较Ivor-Lewis食管切除术与Mckeown食管切除术治疗胸椎中下段食管癌的近期和远期临床疗效。方法:回顾性分析2015年3月至2018年10月在中国医学科学院肿瘤医院胸外科行Ivor Lewis或McKeown食管癌根治术的716例胸椎中下段食管癌患者的临床资料,比较两种手术方式的围手术期指标、术后并发症及生存率。结果:716例患者中,Ivor Lewis食管切除术135例,McKeown食管切除术581例。Mckeown组淋巴结清扫总数[中位数为27 (19~37)vs 25(18~33)]、淋巴结清扫总站数[中位数为5(4~7)vs 5(4~5)]、喉返神经淋巴结清扫数[中位数为3 (1~6)vs 0 (0~3), P<0.05]均显著优于Ivor Lewis组。但Mckeown组喉返神经麻痹发生率明显高于Ivor Lewis组[10.7% (62/581)vs 1.5%(2/135), P<0.001]。Ivor Lewis组1、3、5年总生存率(91.0%、70.5%、52.9%)与Mckeown组(89.7%、68.4%、62.4%,P>0.05)比较差异无统计学意义;Ivor Lewis组1、3、5年无病生存率(77.0%、54.1%、44.0%)与Mckeown组(78.3%、59.0%、52.8%,P>0.05)比较差异无统计学意义。结论:Ivor Lewis食管切除术和Mckeown食管切除术治疗中、下段胸段食管癌可行、安全、近期疗效好、生存率相近。Ivor Lewis手术有较低的喉返神经麻痹发生率。Mckeown手术在淋巴结清扫,尤其是喉返神经旁淋巴结清扫方面更有优势。
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引用次数: 0
[MiR-4508 regulates chrysotile asbestos induced inflammation in human bronchial epithelial cells through the PI3K/AKT pathway]. [MiR-4508通过PI3K/AKT通路调控温石棉诱导的人支气管上皮细胞炎症]。
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20231116-00315
Y J Wang, L Huang, J R He, X Zhang, T T Huo, F Q Dong, J Yang, J J Deng

Objective: To explore the molecular mechanism of miR-4508 regulating the inflammatory response of human bronchial epithelial cells induced by representative chrysotile asbestos. Methods: The chrysotile asbestos was ground into ultrafine dust using a horizontal planetary instrument, and human bronchial epithelium (16HBE) cells were taken as the object of infection. Cell survival rate was detected by cell counting kit-8 method, cytotoxicity was detected by lactate dehydrogenase (LDH) kit. The released of inflammatory factor IL-6 was detected by electrochemical luminescence. The released inflammatory factor IL-8 was detected by enzyme-linked immunosorbent assay. The expression level of miR-4508 was screened and verified by reverse transcription-quantitative real-time polymerase chain reaction. After 16HBE cells were treated with AKT inhibitor MK2206, the phosphorylation levels of AKT and PTEN were detected by western blot. The expression levels of AKT and PTEN and the contents of IL-6 and IL-8 were detected in miR-4508 overexpression and interference experiments. Results: With the increase of chrysotile asbestos exposure concentration, the cell survival rate decreased in a concentration-dependent manner, and the LDH content gradually increased. The secretion of IL-6 and IL-8 in chrysotile 25, 50 and 75 µg/ml groups were (325.92±8.61) pg/ml, (331.51±4.96) pg/ml, (378.74±13.77) pg/ml, and (94.95±3.11) pg/ml, (357.60±1.80) pg/ml, (537.19±3.11) pg/ml, respectively, while the group with 0 µg/ml chrysotile was (95.85±1.20) pg/ml and (7.81±0.00) pg/ml (P<0.05). In addition, chrysotile asbestos exposure to 16HBE could induce the high expression of miR-4508. After pretreatment with MK2206, the phosphorylation levels of AKT and PTEN were decreased, the contents of IL-6 and IL-8 were significantly decreased, and the expression level of miR-4508 was significantly reduced. Overexpression of miR-4508 significantly increased the expressions of AKT and PTEN, and the contents of IL-6 and IL-8 (P<0.01). After interfering with miR-4508, the expressions of AKT and PTEN were significantly decreased, and the contents of IL-6 and IL-8 were significantly decreased (P<0.01). Conclusions: Chrysotile asbestos can induce the inflammatory response of 16HBE cells and up-regulate the expression level of miR-4508. The up-regulation of miR-4508 promotes the 16HBE inflammatory response induced by chrysotile asbestos through the PI3K/AKT pathway.

目的:探讨miR-4508调控代表性温石棉诱导人支气管上皮细胞炎症反应的分子机制。方法:采用卧式行星仪器将温石棉磨成超细粉尘,取人支气管上皮(16HBE)细胞作为感染对象。采用细胞计数试剂盒-8法检测细胞存活率,乳酸脱氢酶(LDH)试剂盒检测细胞毒性。电化学发光法检测炎症因子IL-6的释放。采用酶联免疫吸附法检测炎症因子IL-8的释放。通过逆转录-实时定量聚合酶链反应筛选并验证miR-4508的表达水平。用AKT抑制剂MK2206处理16HBE细胞后,western blot检测AKT和PTEN的磷酸化水平。通过miR-4508过表达和干扰实验检测AKT、PTEN的表达水平以及IL-6、IL-8的含量。结果:随着温石棉暴露浓度的增加,细胞存活率呈浓度依赖性下降,LDH含量逐渐升高。温石棉25、50、75µg/ml组IL-6、IL-8分泌量分别为(325.92±8.61)pg/ml、(331.51±4.96)pg/ml、(378.74±13.77)pg/ml、(94.95±3.11)pg/ml、(357.60±1.80)pg/ml、(537.19±3.11)pg/ml,而0µg/ml温石棉组IL-6、IL-8分泌量分别为(95.85±1.20)pg/ml、(7.81±0.00)pg/ml (P<0.05)。此外,温石棉暴露于16HBE可诱导miR-4508高表达。MK2206预处理后,AKT、PTEN磷酸化水平降低,IL-6、IL-8含量显著降低,miR-4508表达水平显著降低。过表达miR-4508可显著提高AKT、PTEN的表达及IL-6、IL-8的含量(P<0.01)。干扰miR-4508后,AKT、PTEN表达显著降低,IL-6、IL-8含量显著降低(P<0.01)。结论:温石棉可诱导16HBE细胞的炎症反应,上调miR-4508的表达水平。miR-4508的上调通过PI3K/AKT通路促进温石棉诱导的16HBE炎症反应。
{"title":"[MiR-4508 regulates chrysotile asbestos induced inflammation in human bronchial epithelial cells through the PI3K/AKT pathway].","authors":"Y J Wang, L Huang, J R He, X Zhang, T T Huo, F Q Dong, J Yang, J J Deng","doi":"10.3760/cma.j.cn112152-20231116-00315","DOIUrl":"10.3760/cma.j.cn112152-20231116-00315","url":null,"abstract":"<p><p><b>Objective:</b> To explore the molecular mechanism of miR-4508 regulating the inflammatory response of human bronchial epithelial cells induced by representative chrysotile asbestos. <b>Methods:</b> The chrysotile asbestos was ground into ultrafine dust using a horizontal planetary instrument, and human bronchial epithelium (16HBE) cells were taken as the object of infection. Cell survival rate was detected by cell counting kit-8 method, cytotoxicity was detected by lactate dehydrogenase (LDH) kit. The released of inflammatory factor IL-6 was detected by electrochemical luminescence. The released inflammatory factor IL-8 was detected by enzyme-linked immunosorbent assay. The expression level of miR-4508 was screened and verified by reverse transcription-quantitative real-time polymerase chain reaction. After 16HBE cells were treated with AKT inhibitor MK2206, the phosphorylation levels of AKT and PTEN were detected by western blot. The expression levels of AKT and PTEN and the contents of IL-6 and IL-8 were detected in miR-4508 overexpression and interference experiments. <b>Results:</b> With the increase of chrysotile asbestos exposure concentration, the cell survival rate decreased in a concentration-dependent manner, and the LDH content gradually increased. The secretion of IL-6 and IL-8 in chrysotile 25, 50 and 75 µg/ml groups were (325.92±8.61) pg/ml, (331.51±4.96) pg/ml, (378.74±13.77) pg/ml, and (94.95±3.11) pg/ml, (357.60±1.80) pg/ml, (537.19±3.11) pg/ml, respectively, while the group with 0 µg/ml chrysotile was (95.85±1.20) pg/ml and (7.81±0.00) pg/ml (<i>P</i><0.05). In addition, chrysotile asbestos exposure to 16HBE could induce the high expression of miR-4508<i>.</i> After pretreatment with MK2206, the phosphorylation levels of AKT and PTEN were decreased, the contents of IL-6 and IL-8 were significantly decreased, and the expression level of miR-4508 was significantly reduced. Overexpression of miR-4508 significantly increased the expressions of AKT and PTEN, and the contents of IL-6 and IL-8 (<i>P</i><0.01). After interfering with miR-4508, the expressions of AKT and PTEN were significantly decreased, and the contents of IL-6 and IL-8 were significantly decreased (<i>P</i><0.01). <b>Conclusions:</b> Chrysotile asbestos can induce the inflammatory response of 16HBE cells and up-regulate the expression level of miR-4508. The up-regulation of miR-4508 promotes the 16HBE inflammatory response induced by chrysotile asbestos through the PI3K/AKT pathway.</p>","PeriodicalId":39868,"journal":{"name":"中华肿瘤杂志","volume":"47 3","pages":"244-253"},"PeriodicalIF":0.0,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671372","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 application of ANXA2 gene knockout mouse models in lung cancer metastasis]. [ANXA2基因敲除小鼠模型在肺癌转移中的应用]。
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20240705-00277
W J Song, F Zhang, Z S Wang, J F Tian, R F Niu

Objective: ANXA2 plays a crucial role in cancer metastasis, but its mechanism is not yet fully understood. Therefore, it is necessary to establish an ANXA2 gene knockout mouse model to provide an effective tool for subsequent studies on ANXA2-related mechanisms. Methods: A gene knockout mouse model was constructed using CRISPR/Cas9 technology. The model was validated through tissue DNA extraction followed by polymerase chain reaction (PCR), sequencing, and western blot to confirm ANXA2 genotype and protein expression. The successfully constructed models were divided into a model group and a wild-type (WT) group for the creation of a mouse tail vein injection Lewis lung carcinoma (LLC) metastasis model. Metastatic foci formation was monitored using in vivo imaging technology, and the survival rates of the two groups were compared. Results: An sgRNA sequence targeting the first exon of ANXA2 was designed, and 16 founder mice were obtained through microinjection. Through consanguineous hybridization, 30 homozygous offspring were ultimately acquired. After establishing the strains of the mouse model, mice were divided into the ANXA2 knockout group and the WT group, with 8 mice in each group. An LLC lung metastasis model was established in both groups. Compared with the WT group, the number of metastatic foci was significantly increased in the ANXA2 knockout group (7 vs. 1), and the fluorescence intensity was stronger in the WT group than in the knockout group (P=0.002). Using the GEPIA2 database to analyze ANXA2 gene expression in tumor tissues and normal tissues of lung cancer patients, it was found that ANXA2 expression levels were significantly higher in lung cancer tumor tissues compared to normal tissues (P<0.05). The database included data from 478 lung cancer patients, and patients were stratified into high-expression and low-expression groups based on ANXA2 levels. Compared to the low-expression group, patients in the high-expression group exhibited significantly shorter disease-free survival and overall survival (P<0.05, respectively). The survival time of mice in the ANXA2 knockout group (median survival time, 43 days) was significantly longer compared to the WT group (median survival time, 26 days; P=0.017). Additionally, ANXA2 expression is significantly associated with the prognosis of lung cancer patients (P=6.4e-14). Conclusions: ANXA2 is closely associated with cancer metastasis and holds potential as a new target for metastasis treatment. Further in-depth research will greatly facilitate the transition of ANXA2 from basic research to clinical application.

目的:ANXA2在肿瘤转移中起重要作用,但其机制尚不完全清楚。因此,有必要建立ANXA2基因敲除小鼠模型,为后续研究ANXA2相关机制提供有效工具。方法:采用CRISPR/Cas9技术构建基因敲除小鼠模型。通过组织DNA提取、聚合酶链反应(PCR)、测序和western blot验证模型,确认ANXA2基因型和蛋白表达。将成功构建的模型分为模型组和野生型(WT)组,建立小鼠尾静脉注射Lewis肺癌(LLC)转移模型。采用活体成像技术监测转移灶的形成,并比较两组患者的生存率。结果:设计了靶向ANXA2第一外显子的sgRNA序列,并通过显微注射获得了16只创始小鼠。通过近亲杂交,最终获得30个纯合后代。小鼠模型建立品系后,将小鼠分为ANXA2敲除组和WT组,每组8只。两组均建立LLC肺转移模型。与WT组比较,ANXA2基因敲除组的转移灶数量显著增加(7 vs. 1),且WT组的荧光强度强于敲除组(P=0.002)。利用GEPIA2数据库分析肺癌患者肿瘤组织和正常组织中ANXA2基因表达情况,发现肺癌肿瘤组织中ANXA2表达水平明显高于正常组织(P<0.05)。该数据库包括来自478名肺癌患者的数据,并根据ANXA2水平将患者分为高表达组和低表达组。与低表达组相比,高表达组患者的无病生存期和总生存期均显著缩短(P<0.05)。与WT组相比,ANXA2基因敲除组小鼠的生存时间(中位生存时间,43天)显著延长(中位生存时间,26天;P = 0.017)。此外,ANXA2的表达与肺癌患者的预后显著相关(P=6.4e-14)。结论:ANXA2与肿瘤转移密切相关,有望成为肿瘤转移治疗的新靶点。进一步的深入研究将极大地促进ANXA2从基础研究向临床应用的过渡。
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引用次数: 0
[Guidelines for diagnosis, treatment management pathways, and quality control of ovarian cancer in county-level regions (2025 edition)]. [县级地区卵巢癌诊断、治疗管理途径及质量控制指南(2025年版)]。
Q3 Medicine Pub Date : 2025-03-23 DOI: 10.3760/cma.j.cn112152-20241129-00543

To establish diagnosis, treatment management pathways, and quality control guidelines tailored to county-level hospitals, standardize ovarian cancer care, improve treatment quality, and promote the equitable distribution of high-quality medical resources, the Expert Committee on Ovarian Cancer under the National Cancer Quality Control Center formulated the "Guidelines for diagnosis, treatment management pathways, and quality control of ovarian cancer in county-level regions (2025 edition)". This guideline integrates existing national standards for ovarian cancer diagnosis and treatment with evidence-based medicine and clinical expertise. Structured as a pathway framework, this guideline addresses hierarchical diagnosis and treatment, diagnostic workflows, therapeutic approaches, and follow-up protocols for ovarian cancer in county-level settings, offering 13 specific recommendations. The guideline clarifies the roles of county-level hospitals in ovarian cancer management, including primary diagnosis and treatment, administration of antitumor therapies, maintenance therapy, adverse event management, recurrence monitoring, rehabilitation guidance, two-way referrals, and follow-up. For cases beyond local capacity, timely referral to higher-level hospitals or qualified county-level facilities is advised. County-level hospitals may perform surgery for early-stage ovarian cancer, but suspected advanced-stage cases should be promptly referred. The guideline emphasizes the importance of multidisciplinary collaboration in county-level hospitals and recommend that initial chemotherapy for newly diagnosed patients should be conducted at higher-level or adequately equipped county-level institutions. Follow-up evaluations may be performed locally, but suspected recurrence or metastasis requires referral to higher-level hospitals for assessment. Detailed pathways are provided for diagnosis, treatment (including surgery, chemotherapy, maintenance therapy, and recurrence management), and follow-up, with recommendations for incorporating online follow-up methods to enhance patient monitoring. By defining the roles of county-level hospitals, standardizing referral processes, and strengthening multidisciplinary coordination, the guideline aims to promote standardized ovarian cancer care. Its implementation is expected to improve county-level hospitals' diagnostic and therapeutic capabilities, foster collaboration with higher-level institutions, and ultimately enhance patient outcomes and quality of life. These efforts will optimize medical resource allocation, elevate national ovarian cancer care standards, and advance balanced regional healthcare development.

为建立适合县级医院的诊断、治疗管理路径和质量控制指南,规范卵巢癌护理,提高治疗质量,促进优质医疗资源公平分配,国家癌症质量控制中心卵巢癌专家委员会制定了《县级地区卵巢癌诊断、治疗管理路径和质量控制指南(2025年版)》。本指南将现有的国家卵巢癌诊断和治疗标准与循证医学和临床专业知识相结合。本指南结构为途径框架,涉及县级环境下卵巢癌的分级诊断和治疗、诊断工作流程、治疗方法和随访方案,并提出13项具体建议。该指南明确了县级医院在卵巢癌管理中的作用,包括初步诊断和治疗、抗肿瘤治疗、维持治疗、不良事件管理、复发监测、康复指导、双向转诊和随访。对于超出当地能力的病例,建议及时转诊到更高一级的医院或有资质的县级机构。县级医院可以对早期卵巢癌进行手术治疗,但疑似晚期病例应及时转诊。该指南强调了县级医院多学科合作的重要性,并建议新诊断患者的初始化疗应在更高级别或设备充足的县级机构进行。随访评估可在当地进行,但怀疑复发或转移需要转诊到更高级别的医院进行评估。提供了诊断、治疗(包括手术、化疗、维持治疗和复发管理)和随访的详细途径,并建议采用在线随访方法来加强患者监测。通过明确县级医院的作用,规范转诊流程,加强多学科协调,该指南旨在促进卵巢癌规范化治疗。它的实施有望提高县级医院的诊断和治疗能力,促进与更高一级机构的合作,并最终提高患者的治疗效果和生活质量。这些努力将优化医疗资源配置,提高国家卵巢癌护理水平,促进区域卫生保健均衡发展。
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引用次数: 0
[CMTM3 regulates proliferation and migration of glioblastoma U251 cells via the NF-κB signaling pathway]. [CMTM3通过NF-κB信号通路调控胶质母细胞瘤U251细胞的增殖和迁移]。
Q3 Medicine Pub Date : 2025-02-23 DOI: 10.3760/cma.j.cn112152-20240213-00072
L S Jiang, W Teng, W J Qiu, Y G Ling, X P Shi, N Y Long, L Z Chu, J Liu
<p><p><b>Objective:</b> To explore the effects and potential mechanisms of chemokine-like factor-like MARVEL transmembrane domain-containing Protein 3 (CMTM3) on the proliferation and migration of glioblastoma (GBM) cells. <b>Methods:</b> Using CMTM3 expression data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases, we analyzed the differential expression of CMTM3 in GBM tissues and its impact on the prognosis of GBM patients. Immunohistochemical staining and protein content determination of CMTM3 was performed on GBM and adjacent non-cancerous tissue samples from 11 GBM patients who underwent surgical treatment at the Affiliated Hospital of Guizhou Medical University between November 3, 2022 and March 15, 2023. Additionally, the expression of CMTM3 was validated in GBM cell lines U87, U251, LN229, and the human astrocyte (NHA) cell line using real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot analyses. Stable cell lines with silenced and overexpressed CMTM3 (sh-CMTM3 group and OE-CMTM3 group) were constructed using U251 cells. The effect of CMTM3 expression on cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8) assay. Flow cytometry was employed to examine the impact of CMTM3 expression on the cell cycle. Transwell assays were conducted to evaluate the influence of CMTM3 expression on cell migration. Bioinformatics analysis, Western blotting, NF-κB activation-nuclear translocation assays, and the NF-κB pathway inhibitor pyrrolidine dithiocarbamate ammonium (PDTC) were used to validate the effect of CMTM3 on the NF-κB pathway. Finally, a subcutaneous tumorigenesis assay in nude mice was performed to observe the impact of CMTM3 expression on the <i>in vivo</i> growth of U251 cells. <b>Results:</b> Bioinformatics analysis revealed that CMTM3 is highly expressed in GBM tissues. Patients with a high CMTM3 expression had lower overall survival (OS) and disease-free survival (DFS) rates compared with those with a low CMTM3 expression (with <i>P</i> values of 0.010 and 0.032, respectively). Among the 11 GBM pathological specimens, 10 samples exhibited higher CMTM3 protein expression levels in the cancerous tissue compared with the adjacent non-cancerous tissue. The average CMTM3 protein expression in these samples was 0.44±0.09, significantly higher than that in the adjacent non-cancerous tissues (0.12±0.02, <i>P</i><0.001). In one sample, the difference in CMTM3 protein expression between the cancerous and adjacent non-cancerous tissues was not statistically significant (<i>P</i>=0.750).The RT-qPCR results showed that the mRNA expression level of CMTM3 in NHA cells was 1.0±0.1, whereas in GBM cells U87, LN229, and U251, the levels were 2.1±0.3, 3.4±0.5, and 3.7±0.8, respectively, all significantly higher than that in NHA cells (all <i>P</i><0.01). Western blot results demonstrated that the protein expression levels of CMTM3 in GBM cells U87, LN229, and U251 were 1.5±0.2, 1.8±0
目的:探讨趋化因子样MARVEL跨膜结构域蛋白3 (CMTM3)对胶质母细胞瘤(GBM)细胞增殖和迁移的影响及其潜在机制。方法:利用肿瘤基因组图谱(TCGA)和基因型-组织表达(GTEx)数据库的CMTM3表达数据,分析CMTM3在GBM组织中的差异表达及其对患者预后的影响。对2022年11月3日至2023年3月15日在贵州医科大学附属医院接受手术治疗的11例GBM患者的GBM及邻近非癌组织样本进行CMTM3免疫组化染色及蛋白含量测定。此外,通过实时定量聚合酶链反应(RT-qPCR)和Western blot分析,验证了CMTM3在GBM细胞系U87、U251、LN229和人星形胶质细胞(NHA)细胞系中的表达。利用U251细胞构建CMTM3沉默和过表达的稳定细胞系(sh-CMTM3组和OE-CMTM3组)。采用细胞计数试剂盒-8 (CCK-8)法评估CMTM3表达对细胞增殖的影响。流式细胞术检测CMTM3表达对细胞周期的影响。Transwell实验评估CMTM3表达对细胞迁移的影响。通过生物信息学分析、Western blotting、NF-κB活化-核易位实验和NF-κB通路抑制剂吡罗烷二硫代氨基磺酸铵(PDTC)验证CMTM3对NF-κB通路的影响。最后,通过裸鼠皮下肿瘤发生实验,观察CMTM3表达对U251细胞体内生长的影响。结果:生物信息学分析显示CMTM3在GBM组织中高表达。与CMTM3低表达患者相比,CMTM3高表达患者的总生存率(OS)和无病生存率(DFS)较低(P值分别为0.010和0.032)。11例GBM病理标本中,有10例癌组织中CMTM3蛋白表达水平高于癌旁非癌组织。CMTM3蛋白平均表达量为0.44±0.09,显著高于癌旁非癌组织(0.12±0.02,P<0.001)。在一个样本中,癌组织与癌旁非癌组织CMTM3蛋白表达差异无统计学意义(P=0.750)。RT-qPCR结果显示,CMTM3 mRNA在NHA细胞中的表达量为1.0±0.1,而在GBM细胞U87、LN229和U251中的表达量分别为2.1±0.3、3.4±0.5和3.7±0.8,均显著高于NHA细胞(均P<0.01)。Western blot结果显示,CMTM3蛋白在GBM细胞U87、LN229和U251中的表达量分别为1.5±0.2、1.8±0.2和1.9±0.1,均高于NHA细胞(0.7±0.2,均P<0.01),其中以U251细胞表达量最高。CCK-8、流式细胞术、Transwell迁移实验结果显示,sh-CMTM3组细胞活力受到抑制,G0/G1期细胞比例增加(P<0.01), S期细胞比例减少(P<0.01),迁移细胞数为233.6±35.5个,低于sh-NC组(P<0.001)。相反,OE-CMTM3组细胞活力增强,G0/G1期细胞比例降低(P<0.01), S期细胞比例增加(P<0.01),迁移细胞数为1212.0±20.8个,高于OE-NC组(P<0.001)。而OE-CMTM3+PDTC组细胞活力、细胞周期分布(G1、S、G2期)、细胞迁移数量无显著变化(P < 0.05)。Western blot分析和NF-κB活化-核转运实验结果显示,sh-CMTM3组P -p65/p65比值为0.51±0.04,P -κB α/ i -κB α比值为0.39±0.03,均低于sh-NC组(P<0.01)。细胞质染色率为(49.29±1.98)%,高于sh-NC组(P<0.01)。OE-CMTM3组P -p65/p65比值为2.27±0.10,P - κ b α/ i - κ b α比值为2.14±0.15,均高于OE-NC组(P<0.01)。细胞质染色率为(18.96±1.44)%,低于OE-NC组(P<0.01)。OE-CMTM3+PDTC组P -p65/p65比值、P - κ b α/ i - κ b α比值、细胞质染色率与OE-NC组比较差异均无统计学意义(P < 0.05)。裸鼠皮下肿瘤发生实验显示,sh-CMTM3组肿瘤体积为(408.9±96.2)mm³,小于sh-NC组(P=0.003)。OE-CMTM3组肿瘤体积为(1 514.5±251.5)mm³,明显大于OE-NC组(P=0.005)。 结论:在GBM中,CMTM3高表达,且与患者OS和DFS呈负相关。CMTM3通过NF-κB信号通路调控U251细胞的增殖和迁移能力。
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中华肿瘤杂志
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