Personal comorbidities and their subsequent risks for liver,gallbladder and bile duct cancers

Many environmental risk factors for hepatobiliary cancers are known but whether they are associated with specific cancer types is unclear. We present here a novel approach of assessing standardized incidence ratios (SIRs) of previously diagnosed comorbidities for hepatocellular carcinoma (HCC), gallbladder cancer (GBC), cholangiocarcinoma (CCA) and ampullary cancer. The 13 comorbidities included alcohol and nonalcohol related liver disease, chronic obstructive pulmonary disease, gallstone disease, viral and other kinds of hepatitis, infection of bile ducts, hepatic and other autoimmune diseases, obesity and diabetes. Patients were identified from the Swedish Inpatient Register from 1987 to 2018, and their cancers were followed from 1997 onwards. SIRs for HCC were 80 to 100 in men and women diagnosed with hepatitis C virus and they were also >10 in patients diagnosed with hepatitis B virus, other kind of hepatitis, hepatic autoimmune disease and nonalcohol related liver disease. Many of these risks, as well as alcohol related liver disease, were either specific to HCC or were shared with intrahepatic CCA. For GBC, CCA and ampullary cancer infection of bile ducts was the main risk factor. Gallstone disease, nonhepatic autoimmune diseases and diabetes were associated with all hepatobiliary cancers. The limitations of the study include inability to cover some rare risk factors and limited follow-up time. Many of the considered comorbidities are characterized by chronic inflammation and/or overt immune disturbance in autoimmune diseases. The results suggest that local chronic inflammation and a related immune disturbance is the carcinogenic trigger for all these cancers.     

早产儿消化道穿孔的病因及影响预后的危险因素分析

目的:探讨早产儿消化道穿孔的病因，分析影响早产儿消化道穿孔短期预后不良的危险因素。方法:回顾性分析山西省 儿童医院新生儿外科2015年1月—2021 年5月诊治的89 例早产儿消化道穿孔的临床资料。根据术后3 个月时结局分为生存 组和预后不良组。比较两组术前、术中及术后与早产儿消化道穿孔预后不良相关的因素，采用Logistic 回归分析筛选早产儿消 化道穿孔预后不良的危险因素。结果:早产儿消化道穿孔的病死率为25.84%，坏死性小肠结肠炎（NEC）和胃壁肌层缺损是早产 儿消化道穿孔常见的病因。单因素分析显示生存组患儿从发现气腹至手术时间在8 h 之内的比例显著高于预后不良组 （χ2=15.22，P＜0.01）。预后不良组合并脓毒性休克的比例显著高于生存组（χ2=33.19，P＜0.01）。预后不良组术后合并需非计划二次 手术的并发症比例显著高于生存组（χ2=7.24，P＜0.01）。Logistic 回归分析显示脓毒性休克（OR=0.06，95%CI:0.02~0.21，P＜0.01）和 气腹至手术时间大于8 h（OR=0.23，95%CI:0.07~0.81，P＜0.05）是早产儿消化道穿孔短期预后不良的危险因素。结论:NEC 和胃 壁肌层缺损是早产儿消化道穿孔的主要病因，脓毒性休克和从气腹发生至手术时间大于8 h 是早产儿消化道穿孔短期预后 不良的危险因素。     

Non-canonical role of Hippo tumor suppressor serine/threonine kinase 3 STK3 in prostate cancer

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Synthesis and automated fluorine-18 radiolabeling of new PSMA-617 derivatives with a CuAAC radiosynthetic approach

In the last decade, the development of new radiopharmaceuticals for the imaging and therapy of prostate cancer has been a highly active and important area of research, especially focusing on the prostate-specific membrane antigen (PSMA), an antigen which is upregulated in prostate, as well as in other tumor cells. A large variety of PSMA ligands have been radiolabeled, to date. Among the various derivatives, PSMA-617 resulted to be one of the most interesting in terms of interaction with the antigen and clinical properties, and its lutetium-177 labeled version has recently been approved by regulatory agencies for therapeutic purposes. For this reasons, the radiolabeling with fluorine-18 of a PSMA-617 derivative might be of interest. Beside other methodologies to radiolabel macromolecules with fluorine-18, the “click-chemistry” approach resulted to be very useful, and the copper-catalyzed azide-alkyne cycloaddition (CuAAC) is considered one of most efficient and reliable. This paper proposes the synthesis of a suitable precursor for the radiolabeling with fluorine-18 of a new PSMA-617 derivative. The whole radiosynthetic procedure has been fully automated, and the final product, which proved to be stable in plasma, has been obtained with radiochemical yield and purity suitable for subsequent preclinical studies.     

同型半胱氨酸、维生素D、C、E、B12及叶酸与胃癌关系的研究进展北大核心

胃癌作为临床最常见的肿瘤之一,常因确诊疾病较晚而影响治疗效果,胃镜活检后的病理虽然作为确诊的金标准,但是由于此方式过程痛苦,操作复杂,费用较高,且具有侵入性,可能会导致患者拒绝操作而难普及于临床,因此积极找寻胃癌有效的监测指标十分必要。近年来,很多学者研究维生素与胃癌的相关关系,并试图通过摄取某些维生素降低胃癌发生率,延缓病情及改善预后,也有通过检测血清中维生素的水平给早期胃癌的诊断提供帮助。本文就同型半胱氨酸、维生素D、维生素C、维生素E、维生素B12及叶酸在胃癌中的作用机制,及其在血清中水平与胃癌关系的相关研究进展进行简要综述,为临床胃癌诊疗提供新思路。     

Lymph node micrometastasis of poorly differentiated node-negative gastric cancer risks a worse-than-expected survival outcome under standard management algorithm

BackgroundInvestigation of lymph node micrometastasis (mN) of gastric cancer has been focused on either T1 disease or T1-4N0 disease. Yet, it is unclear whether standard management algorithm toward poorly differentiated gastric cancer (PDGC) is more vulnerable to existence of mN, given its inherently biological aggressiveness, as compared with other histological types.Patients and methodsA surgical series (n = 3456) of gastric cancer categorized by histological differentiation was enrolled to analyze survival stratification. Of them, a cohort of T1-T4 N0 PDGC (n = 100) were subjected to cytokeratin immunohistochemistry, a surrogate of mN.ResultsCancer-specific survival by AJCC8 staging system could be nicely differentiated in both well-/moderately differentiated and signet ring cell types, while those between stage IA versus IB (p = 0.105), and stage IB versus IIA (p = 0.141) in PDGC could not. Thirteen (13%) out of 100 node-negative PDGC cases exhibited mN, with 5, 2, 5 and 1 cases occurring in T1, T2, T3, and T4 stage, respectively, without identifiable contributing factors. Prognostic performance of AJCC8 working upon PDGC became more discriminative by incorporating mN, as hazard ratio of stage IIIC referenced to stage IA increased from 43 to 78.ConclusionDefective discriminative survival of PDGC by standard staging algorithm prompted us to survey mN occurring in T1-T4N0 PDGC. The prognostic performance of AJCC8 working upon PDGC was enhanced by incorporating mN. As so, we recommend documentation of mN exclusively on node-negative PDGC that helps unveil stage migration phenomenon and switch to appropriate adjuvant therapy in need.     

Multiomic analysis reveals conservation of cancer-associated fibroblast phenotypes across species and tissue of origin

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