71例肿瘤化疗致3~4级骨髓抑制的分析

目的：了解肿瘤科化疗致3~4级骨髓抑制不良反应的特点及相关因素，为临床合理用药提供参考。方法：选取某院2016年因化疗致3~4级骨髓抑制的住院肿瘤患者71例，分别从性别与年龄、药物种类、疾病类型、骨髓抑制类型及时间特点、化疗周期对抑制率的影响等多个因素进行回顾性分析。结果：3~4级骨髓抑制患者中男性多于女性，以41~60岁的中年人为主；药物以多西他赛、顺铂、吉西他滨为主，骨髓抑制的外周血象主要表现为白细胞及血小板下降；头颈部肿瘤所占比例最高，为67.7%；三系细胞开始下降时间和低值持续时间各不相同；白细胞及血小板最低值的发生率在化疗第4周期达到最大。结论：3~4级骨髓抑制的发生与多种因素有关，临床药师应该做好不良反应的报告和监测工作，减少反应的发生。     

Glioma grading using apparent diffusion coefficient map: application of histogram analysis based on automatic segmentation

The accurate diagnosis of glioma subtypes is critical for appropriate treatment, but conventional histopathologic diagnosis often exhibits significant intra‐observer variability and sampling error. The aim of this study was to investigate whether histogram analysis using an automatically segmented region of interest (ROI), excluding cystic or necrotic portions, could improve the differentiation between low‐grade and high‐grade gliomas. Thirty‐two patients (nine low‐grade and 23 high‐grade gliomas) were included in this retrospective investigation. The outer boundaries of the entire tumors were manually drawn in each section of the contrast‐enhanced T₁‐weighted MR images. We excluded cystic or necrotic portions from the entire tumor volume. The histogram analyses were performed within the ROI on normalized apparent diffusion coefficient (ADC) maps. To evaluate the contribution of the proposed method to glioma grading, we compared the area under the receiver operating characteristic (ROC) curves. We found that an ROI excluding cystic or necrotic portions was more useful for glioma grading than was an entire tumor ROI. In the case of the fifth percentile values of the normalized ADC histogram, the area under the ROC curve for the tumor ROIs excluding cystic or necrotic portions was significantly higher than that for the entire tumor ROIs (p < 0.005). The automatic segmentation of a cystic or necrotic area probably improves the ability to differentiate between high‐ and low‐grade gliomas on an ADC map. Copyright © 2014 John Wiley & Sons, Ltd.     

High‐grade serous carcinoma of tubo‐ovarian origin: recent developments

Extra‐uterine high‐grade serous carcinoma (HGSC) accounts for most of the morbidity and mortality associated with ovarian carcinoma, and is one of the leading causes of cancer death in women. Until recently our understanding of HGSC was very limited compared to other common cancers, and it has only been during the last 15 years that we have learned how to diagnose this ovarian carcinoma histotype accurately. Since then, however, there has been rapid progress, with identification of a precursor lesion in the fallopian tube, development of prevention strategies for both those with inherited susceptibility (hereditary breast and ovarian cancer syndrome) and without the syndrome, and elucidation of the molecular events important in oncogenesis. This molecular understanding has led to new treatment strategies for HGSC, with the promise of more to come in the near future. In this review we focus on these recent changes, including diagnostic criteria/differential diagnosis, primary site assignment, precursor lesions and the molecular pathology of HGSC.     

Low-Grade and High-Grade Invasive Ductal Carcinomas of the Breast Follow Divergent routes of Progression

Low-grade invasive ductal carcinoma is almost diploid,and has frequent losses of chromosome 16q,which is shared by other precancerous lesions of the mammary gland such as flat epithelial atypia(FEA),atypical ductal hyperplasia(ADH),and lownuclear grade ductal carcinoma in situ(DCIS).The genetic alterations accumulate in a stepwise fashion as the precancerous lesions progress to invasve ductal carcinoma.This supports the linear progression model of breast cancer from FEA,through ADH,to lownuclear grade DCIS as non-obligate early events in low-grade IDC evolution.In contrast,high-grade carcinoma tends to aneuploidy with complex genetic alterations-most importantly,frequent gains at chromosome 16q.Frequent losses at chromosome 16q in lowgrade IDC and gains in the same arm of the same chromosome in high-grade IDC imply that these lesions are two end outcomes of different disease processes and that they do not lie in the same continuum of a process.Therefore,low-grade and high-grade IDC are two distinct diseases with a divergent route of progression.     

Angiographically evident thrombus following fibrinolytic therapy is associated with impaired myocardial perfusion in STEMI: a CLARITY-TIMI 28 substudy.

AIMS: The presence of residual thrombus following fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) may predispose to greater embolization and microvascular dysfunction. METHODS AND RESULTS: We hypothesized that even in the presence of a patent epicardial artery, residual thrombus would be associated with worsened TIMI myocardial perfusion grades (TMPG), independent of epicardial flow. Data were analysed from the angiograms of 2684 patients enrolled in the CLARITY-TIMI 28 trial, with angiographically patent arteries (TIMI 2/3 flow) at a median of 88 h following fibrinolytic therapy. Thrombus in a patent epicardial artery was observed more frequently among patients with shorter times from randomization to angiography, among patients with non-left anterior descending infarctions, and among patients treated with placebo (vs. clopidogrel). Thrombus was associated with more frequent TIMI 2 flow (35.1 vs. 22.1%, P < 0.001), higher corrected TIMI frame counts (CTFC) (42 vs. 33 frames, P < 0.001), and a lower incidence of normal TMPG 3 (48.7 vs. 63.9%, P < 0.001), irrespective of treatment with clopidogrel or placebo. In multivariable analyses, thrombus remained associated with higher CTFC (P < 0.001) and worse TMPG (OR 1.6 for TMPG 0/1/2, P < 0.001) after adjustment for baseline covariates as well as known correlates of TMPG. The association between thrombus and impaired TMPG remained even after further adjustment for CTFC or TIMI flow grade. CONCLUSION: Residual angiographic thrombus following fibrinolytic therapy in STEMI patients is associated with impaired myocardial perfusion, independent of epicardial flow. This finding emphasizes the roles of platelet aggregation and distal embolization in the pathogenesis of microvascular dysfunction in STEMI.     

Survivin在子宫内膜样腺癌中的表达

目的研究Survivin在正常子宫内膜、子宫内膜不典型增生和子宫内膜样腺癌(EA)三种组织中表达的差异。方法选取华北石油管理局总医院2010年1月~2012年6月手术切除子宫并经病理证实的EA存档标本40例(EA组),经诊刮或宫腔镜检查病理结果示子宫内膜不典型增生20例(AHE组),同时选取同期因子宫脱垂或子宫肌瘤行子宫切除的正常子宫内膜20例作为对照(CON组)。通过免疫组织化学法检测三组中Survivin表达情况的差异。应用SPSS 16.0统计软件进行数据分析。结果 EA组的Survivin表达阳性率为90%,显著高于CON组(75%),差异有统计学意义(P<0.05)。在EA组中,组织分级为G1、G2、G3级的患者Survivin阳性率分别为85.0%、90.9%、100.0%,差异有统计学意义(P<0.05);手术-病理分期为Ⅰ期、Ⅱ期、Ⅲ期的患者Survivin阳性率分别为62.1%、85.7%、100.0%,差异有统计学意义(P<0.05);肌层浸润深度<1/2及≥1/2的患者Survivin阳性率分别为88.5%、92.9%,差异无统计学意义(P>0.05);存在淋巴结转移及无淋巴结转移的患者Survivin阳性率为100.0%、80.6%,差异无统计学意义(P>0.05);存在脉管浸润及无脉管浸润的患者Survivin阳性率分别为100.0%、84.2%,差异无统计学意义(P>0.05)。结论相较于正常子宫内膜,EA组织中Survivin表达显著增多。Survivin的阳性表达率与EA组织学分级和手术-病理分期相关,与肌层浸润、淋巴结转移及有无脉管浸润无关。     

A-kinase interacting protein 1 is sufficiently expressed and positively associates with WHO grade,meanwhile predicts unfavorable overall survival independently in glioma patients

The present study aimed to investigate the association of A-kinase interacting protein 1 (AKIP1) with clinical characteristics, and further explore the prognostic value of AKIP1 in glioma patients.Totally 168 glioma patients who underwent tumor resection were analyzed, and their tumor tissue specimens were acquired for the detection of AKIP1 expression by immunohistochemistry (IHC), which was scored by a semi-quantitative method considering staining intensity and staining density.According to AKIP1 expression in tumor tissues of glioma patients, there were 65 (38.7%) patients with AKIP1 low expression (IHC score 0–3), 48 (28.6%) patients with AKIP1 high + expression (IHC score 4–6), 42 (25.0%) patients with AKIP1 high++ expression (IHC score 7–9) and 13 (7.7%) patients with AKIP1 high+++ expression (IHC score 10–12), respectively. AKIP1 expression was positively associated with World Health Organization grade. Overall survival (OS) was the lowest in the patients with AKIP1 high+++ expression, followed by those with AKIP1 high++ expression and those with AKIP1 high+ expression, and highest in those with AKIP1 low expression. Further subgroup analysis exhibited that AKIP1 expression was negatively associated with OS especially in high-grade glioma patients. In addition, AKIP1 expression was negatively associated with OS in all subgroups of patients with/without adjuvant radiotherapy, with/without adjuvant chemotherapy. Further multivariate Cox''s regression exhibited that AKIP1 high expression was an independent predictive factor for worse OS.AKIP1 presents with the potential to be a novel biomarker for tumor management and prognosis surveillance in glioma patients.