3.0T MR弥散加权成像定量分析表观弥散系数对乳腺良恶性病变的诊断

目的 探讨3.0T MR弥散加权成像(DWI)定量分析表观弥散系数(ADC)对乳腺良恶性病变的诊断价值.方法 对经病理证实的50例乳腺病变57个病灶行MR弥散加权成像及动态增强扫描(DCE-MRI),绘制病灶感兴趣区(ROI)时间-信号强度曲线(TIC),分析曲线类型、测量病灶ADC值.结果 在b取50 s/mm2和800 s/mm2情况下,本组良性病变ADC值为(1.483±0.358)×10-3mm2/s,明显大于恶性病变的(0.952±0.148)×10-3 mm2/s(P＜0.05).经受试者工作曲线(ROC)分析得出良恶性病变ADC诊断阈值为1.219×10-3mm2/s.该值对乳腺恶性病变诊断的敏感性及特异性分别为90.6%和84.0%.DCE-MRI对乳腺恶性病变诊断的敏感性和特异性分别为87.5%和80.8%.ADC值与DCE-MRI结合诊断的敏感性和特异性提高为93.8%和88.0%.ADC值与DCE-MRI对乳腺恶性病变诊断的敏感性和特异性差异无统计学意义(P＞0.05).结论 3.0TMRI DWI定量分析ADC值对于乳腺病变的诊断及鉴别诊断有重要价值.     

磁共振扩散加权成像对乳腺癌的诊断价值

目的 探讨磁共振扩散加权成像(DWI)的表观扩散系数(ADC)值对乳腺肿块鉴别诊断价值,提高乳腺癌的诊断特异性.方法 对93例105个乳腺肿块患者行常规MR平扫DWI成像,测量ADC值.结果 37例43个良性病灶的平均ADC值:(1.37±0.36)×10-3 mm2/s,最大、最小ADC差值(0.63±0.19)×10-3mm2/s;58例62个恶性病灶的平均ADC值:(0.90±0.53)×10-3mm2/s,最大、最小ADC差值(0.91±0.27)×10-3 mm2/s;两者平均ADC值,最大、最小ADC差值的差异均有统计学意义(均P＜0.01).绘制诊断良、恶性病变ADC值ROC曲线,以1.1×10-3mm2/s作为临界值作为判断良、恶性的标准,敏感性为67％,特异性为72％;以1.0×10-3mm2/s为临界值,特异性可提高到84％.而敏感度降为60％.以最大、最小ADC差值0.75×10-3mm2/s为临界值,敏感性为67％,特异性为68％,如以0.80×10-3mm2/s为临界值,敏感性为53％,特异性为82％.结论 DWI的ADC值对乳腺良恶性病变的鉴别诊断具有一定的意义.     

磁共振扩散加权成像在软组织肿瘤诊断中的应用

目的 探讨磁共振扩散加权成像( DWI)在软组织肿瘤诊断中的应用价值.方法 对经手术病理证实的48例软组织肿瘤患者行MRI扩散加权成像,其中软组织恶性肿瘤28例,良性肿瘤20例.选择感兴趣区进行表观扩散系数( ADC)值的测定,并进行统计学分析.结果 软组织恶性肿瘤感兴趣区的ADC值(0.95±0.31)×10-3mm2/s明显低于软组织良性肿瘤的ADC值(1.87±0.66)×10-3mm2/s和肌肉组织( 1.62±0.50)×10-3mm2/s的ADC值(t=2.975、2.067,P＜0.05),软组织良性肿瘤与肌肉组织的ADC值差异无统计学意义(P＞0.05).ADC值为s1.35×10-3mm2/s时,鉴别良恶性肿瘤的敏感性为75％,特异性为89％.结论 软组织肿瘤ADC值测定在良恶性鉴别诊断中有重要价值.     

DWI在鉴别急性胆囊炎和肝病所致胆囊壁增厚中的诊断价值

目的探讨弥散加权成像(DWI)在急性胆囊炎和肝病所致胆囊壁增厚中的鉴别诊断价值。方法胆囊壁增厚患者103例分为急性胆囊炎(A组,52例)和肝病(B组,51例)两组,比较常规T2加权成像(T2WI)和DWI图像,测量DWI图像的表观弥散系数(ADC)值,绘制ROC曲线分析T2WI和DWI视觉评估及ADC值的鉴别诊断效能。结果两组T2WI图上胆囊壁厚度相仿(P>0.05)。两组在T2WI及DWI图上视觉评估信号比较有统计学差异(P<0.01)。A组ADC值低于B组[(2.02±0.35)×10^-3 mm²/s vs.(2.92±0.28)×10^-3 mm²/s](P<0.01)。取ADC值2.43×10^-3 mm²/s作为最佳诊断阈值时,其诊断急性胆囊炎的准确率、灵敏度和特异度分别为92%、90%和94%。以胆囊壁在DWI图上呈高或稍高信号(与同层面脑脊液信号相比)作为诊断急性胆囊炎的标准,DWI诊断急性胆囊炎的准确率、灵敏度和特异度分别为9...     

磁共振弥散加权成像联合CRP对急性缺血性脑梗死时间窗的鉴别价值

目的磁共振弥散加权成像(DWI)联合血清C反应蛋白(CRP)对急性缺血性脑梗死时间窗的鉴别价值。方法回顾性分析2021年6月至2023年6月宝鸡市中心医院收治的195例急性缺血性脑梗死患者床资料, 其中男111例, 女84例, 年龄范围57～75岁。按发病至接受磁共振检查前时间分为超急性期组(病程≤6 h)67例、急性期组(病程6～72 h)79例、亚急性期组(≥72～168 h)49例;比较3组患者的DWI检查结果[表观弥散系数(ADC)]及CRP水平, 受试者操作特征曲线(ROC)分析DWI联合CRP对急性缺血性脑梗死时间窗的鉴别价值, 采用t检验、F检验进行统计分析。结果超急性期组患侧ADC为(0.33±0.08)×10-3 mm2/s, 低于急性期组的(0.40±0.09)×10-3 mm2/s、亚急性期组的(1.56±0.25)×10-3 mm2/s, 3组比较差异有统计学意义(F=34.455, P<0.05);且超急性期组、急性期组患者患侧ADC值低于健侧, 但亚急性期组患者ADC值高于健侧, 差异有统计学意义(均P<0.05)。超急性期组CRP为(9.39±...     

磁共振全身弥散加权成像技术在肿瘤诊断和鉴别诊断中的应用

目的评价磁共振全身弥散加权成像(WB-DWI)技术的临床应用价值。方法回顾性分析59例经手术病理和临床随访证实的肿瘤患者WB-DWI影像表现特征,均采用1.5T MR体部线圈进行扫描,利用三维最大密度投影(3D MIP)及黑白翻转技术重建出类PET图像,测量病灶的表观弥散系数(ADC值),并进行良恶性病变的ADC值对比。结果 59例肿瘤病灶在WB-DWI呈高信号,且均经常规MRI证实,恶性肿瘤平均ADC值(1.15±0.32)×10-3mm2/s,良性肿瘤平均ADC值(2.48±0.36)×10-3mm2/s,二者之间有统计学差异(P<0.05)。结论 WB-DWI对肿瘤病变的检出及良恶性肿瘤的鉴别诊断有重要的临床应用价值。     

常规MR和弥散加权成像对原发性中枢神经系统淋巴瘤和胶质母细胞瘤的鉴别诊断价值

目的 探讨常规MR和弥散加权成像(DWI)在原发性中枢神经系统淋巴瘤(PCNSL)和胶质母细胞瘤(GBM)鉴别诊断中的价值.方法 回顾性分析27例GBM和22例PCNSL病例的常规MR图像,分析其信号特点.测量肿瘤平均表观弥散系数(mean ADC,ADCM).同时测量对侧正常脑白质区的ADC值,计算肿瘤校正ADC值(corrected ADC,ADCc=ADC肿瘤实质、ADC对侧白质).两组间常规MR信号特点采用卡方检验比较,ADCM和ADCc值采用f检验比较.采用受试者工作特性曲线(ROC)分析ADCM和ADCc值对GBM和PCNSL的鉴别诊断价值.结果 GBM和PCNSL组在T1WI(P=O.06)和T2WI(P=0.86)上的信号特点比较差异无统计学意义,在强化均匀性方面比较差异有统计学意义(P<0.01).GBM组的ADCM和ADCc值均明显高于PCNSL组[ADCM:(0.97±0.17)×10-3 mm2/s比(0.69+0.11)×10-3 mm2/s,P＜0.01];[ADCc:(1.28±+0.21)比(0.92±0.13),P＜0.01].ROC曲线分析结果提示,以ADCM值≤0.85×10-3 mm2/s为阈值,可获得最优的诊断效能(AUC:0.911,敏感度:95.5％,特异度:81.5％).以ADCc值≤1.09为阈值,可获得最优的诊断效能(AUC:0.936,敏感度:95.5％,特异度:85.2％).结论 DWI和ADC值可辅助GBM和PCNSL的鉴别诊断,为常规MR提供补充信息.     

磁共振弥散加权成像在肝局灶性病变中的价值

目的:探讨磁共振弥散加权成像(diffusion weighted imaging,DWI)对肝脏局灶性病变的诊断价值。方法:对50例肝局灶性病变(其中肝细胞癌14例,肝转移瘤17例、肝囊肿5例、肝血管瘤11例、局灶性结节增生3例)行MRI平扫、DWI及动态增强扫描。分析各病变的弥散成像的信号特点,并测量正常肝脏和病变的表观弥散系数(apparent diffusion coefficient,ADC值)。结果:肝局灶性病变在DWI上为高信号,随b值的增加信号有不同程度下降;当b值为500s/mm2时,肝细胞癌、肝转移瘤、肝囊肿、肝血管瘤和局灶性结节增生(FNH)的ADC值分别为(0.81±0.12)×10-3mm2/s、(1.13±0.26)×10-3mm2/s、(3.07±0.37)×10-3mm2/s、(2.18±0.30)×10-3mm2/s、(1.67±0.17)×10-3mm2/s。肝内良性病变与恶性病变ADC值之间有统计学差异(P<0.05)。结论:依据对肝脏局灶性病变的DWI图像、ADC值及其特点分析,能比较准确地判断肝局灶性病变的良恶性,对肝局灶性病变的诊断及鉴别诊断有一定价值。     

表观扩散系数鉴别低及中高级别前列腺癌的应用价值

目的探讨表观扩散系数(ADC)鉴别低、中高级别前列腺癌的应用价值。方法收集2017年3月至2021年6月经连云港市第二人民医院病理证实的58例前列腺癌患者的磁共振成像(MRI)检查资料, 平均年龄65岁。根据术后病理结果分为低级别组(Gleason评分≤6分, 20例)和中高级别组(Gleason评分≥7分, 38例)。所有患者均行完善的MRI平扫及扩散加权成像(DWI)检查, 分别测量癌灶的最小ADC值(ADCmin)、平均ADC值(ADCmean)、标准化ADC值(ADCn), 采用独立样本t检验比较两组间ADCmin、ADCmean、ADCn差异;绘制3种不同ADC值鉴别前列腺癌病理分级的受试者工作特征曲线(ROC), 获取曲线下面积(AUC), 评估各指标鉴别诊断低级别和中高级别前列腺癌的效能。采用Z检验比较各AUC之间差异。结果低级别组ADCmin、ADCmean、ADCn值分别为(0.734±0.063)×10-3mm2/s、(0.816±0.091)×10-3mm2/s、(0.631±0.037)×10-3mm2/s, 均高于中高级别组(0.646±0.055)×10-3...     

磁共振弥散成像技术在星形细胞肿瘤诊断中的应用

目的评价近似弥散系数(ADC)值、张量D值(trace D)值及各向异性分数(FA)值在鉴别星形细胞肿瘤实质、瘤周水肿及正常组织中的作用以及评估星形细胞肿瘤良恶性的价值。方法采用GE 1.5T MR仪,对23例1~2级星形细胞肿瘤及22例3~4级星形细胞肿瘤进行了常规磁共振成像(MRI)、弥散加权成像(DWI)及弥散张量(DTI)成像,弥散敏感系数(b值,b=os/mm2及b=1000s/mm2)测量病变感兴趣区的数值。结果1~2级星形细胞肿瘤实质的最低ADC值(1.46±0.32)×10-3mm2/s和trace D值(0.64±0.19)×10-3mm2/s,明显高于3~4级ADC值(0.87±0.18)×10-3mm2/s和(0.48±0.15)×10-3mm2/s,(P<0.01)。低度恶性肿瘤肿瘤实质与瘤周水肿之间ADC值无显著性差异;高度恶性肿瘤肿瘤实质与瘤周水肿间有显著性差异。FA图像可清楚显示肿瘤与白质纤维的关系。结论结合常规MRI,ADC值及trace D值有助于鉴别星形细胞肿瘤良恶性。     

肾细胞癌56例的CT诊断分析

目的分析肾细胞癌的CT表现,探讨CT平扫及增强扫描对该类疾病的诊断价值。方法对手术和病理证实的56例肾细胞癌进行回顾性分析,所有病例均行平扫和增强扫描。结果肾透明细胞癌48例,肾乳头状癌6例,肾嫌色细胞癌1例,肾集合管癌1例。上述各型有其特征性的CT表现,肾透明细胞癌呈不均匀而富血供;乳头状癌不均匀而少血供;嫌色细胞癌呈少血供改变,内可见星茫状强化;集合管癌累及肾皮质和肾髓质,呈少血供改变,边界不清。结论常见RCC亚型有其特征性的CT表现,有助于鉴别诊断。     

Axitinib for renal cell carcinoma

Background: The approval of sunitinib, sorafenib and temsirolimus has dramatically altered the management of renal cell carcinoma (RCC). Bevacizumab plus IFN may also be added to the therapeutic armamentarium. Axitinib (AG-013736) is an oral and selective tyrosine kinase inhibitor. Objective: Data supporting the development of axitinib for RCC are reviewed. Methods: Preclinical and clinical data available for axitinib for RCC are presented. Results: Axitinib inhibits VEGFR-1, VEGFR-2 and VEGFR-3 with picomolar potencies, and PDGFR-α, PDGFR-β and c-kit with nanomolar potencies. Phase II clinical trials of axitinib in pretreated RCC following sorafenib or cytokine treatment have demonstrated promising activity accompanied by a favorable toxicity profile. Further development of axitinib for RCC is warranted.     

Targeted therapy of renal cell cancer

Rapid development of treatment strategies for renal cell cancer (RCC) has occurred in recent years. Elucidation of the crucial role of the Von Hippel-Lindau (VHL) tumor suppressor gene in upregulating growth factors associated with angiogenesis has provided new insight into RCC biology and has identified specific targets for novel therapeutic strategies. For almost two decades, cytokine-based immunotherapy has remained a treatment of choice in advanced RCC patients. However, it has provided only modest improvement in clinical outcome and has been associated with severe toxicity. With the advent of novel therapies directly targeting the VEGF molecule or VEGF receptor signal transduction pathway, the clinical outcome in high-risk, advanced RCC has significantly improved. In phase III clinical trials, novel targeted agents - temsirolimus, sorafenib, sunitinib and bevacizumab - significantly prolonged progression-free survival of patients with metastatic RCC and, crucially, temsirolimus also prolonged overall survival in patients with high-risk disease. Despite the obvious clinical efficacy of novel targeted therapies in the treatment of RCC, many unanswered questions still remain; in particular, the efficacy of targeted agents in patients with low-risk RCC, the optimal sequence and combination of therapies for first-, second-, or third-line treatment, and the efficacy of this strategy in adjuvant settings.     

Perifosine in renal cell carcinoma

Importance of the field: Tagatose is a naturally occurring simple sugar that is a more palatable bulk low-calorie (1.5 kcal/g) sweetener. It was approved as a food additive by the FDA in 2003. Tagatose has been studied as a potential antidiabetic and antiobesity medication. In preliminary studies in humans, tagatose has shown a low postprandial blood glucose and insulin response. Its proposed mechanism of action may involve interference in the absorption of carbohydrates by inhibiting intestinal disaccharidases and glucose transport. It may also act through hepatic inhibition of glycogenolysis.

Areas covered in this review: This article summarizes tagatose Phase I and II diabetes trials. It describes the pharmacodynamics and possible mechanism of action of this agent. Literature from 1974 to 2009 is reviewed.

What the reader will gain: Better understanding of the implications of postprandial hyperglycemia. An appreciation of the liver as a target of glucose control. Increased awareness of tagatose, a sweetener, as a potential new medication that operates through improvement of postprandial hyperglycemia.

Take home message: Tagatose is currently being studied as a postprandial antihyperglycemic agent that may be safer with regard to hypoglycemia. Ongoing Phase III clinical trials will provide more definitive answers.     

Effects of deferasirox on renal function and renal epithelial cell death

Iron-chelating therapy results in a significant improvement in the life expectancy of patients with transfusional iron overload. However, alterations of renal function have been observed in some patients undergoing chelation therapy. In the present study we evaluated the effect of treatment with deferasirox iron chelator on the renal function in normal Wistar rats and in mouse and human cultured tubular cell lines.Results indicate that deferasirox given daily via intraperitoneal route for 7 days induced: (1) an increased urinary protein, albumin and glucose excretion, (2) tubular necrosis/apoptosis, (3) and increased tubular damage markers, in spite of normal glomerular function. Moreover, in vitro studies revealed that: (1) mouse MCT cultures resulted more susceptible to the antiproliferative/cytotoxic effect of deferasirox, mainly at 24 h after treatment, than human HK-2 cultures, (2) MCT cell content of damage molecules increased after 24 h of iron chelator treatment with slight changes in their excretion into the culture medium and (3) MCT cultures showed a significant evidence of apoptotic cell death through an increased expression and activation of caspase-3 and marked DNA fragmentation. In conclusion, this renal side effect of deferasirox-chelating therapy seems to be based on direct toxic effects of deferasirox on renal tubular cells.     

Expression of NDRG2 in clear cell renal cell carcinoma

Clear cell renal cell carcinoma (CCRCC) is the most common pathological type of renal cell carcinoma and the main cause of renal carcinoma mortality. NDRG2, a new member of the N-Myc downstream-regulated gene (NDRG) family, is a focus for study at present. Up to now, its expression and function in carcinoma remain unclear. The aim of this study was to investigate its expression in CCRCC tissues and several renal carcinoma cell lines. The expression of NDRG2 was evaluated in renal cell carcinoma cell lines, tumor and adjacent non-tumor tissues from same clear cell renal cell carcinoma patients, by using immunohistochemistry, immunofluorescence, RT-PCR and Western blot. By immunohistochemistry and immunofluorescence we found that NDRG2 was predominantly located in the cytoplasm and membrane of renal carcinoma cancer cells, and the positive rate of NDRG2 in renal carcinoma specimens was 30.3% (40/132), which is significantly lower than 91.67% (121/132) in normal renal tissues (p<0.01). The average staining score in normal renal tissues was significantly higher than renal carcinoma (6.12+/-1.84 versus 2.65+/-1.23, p<0.01). Moreover, NDRG2 mRNA and protein were down-regulated in 6 fresh CCRCC tissues compared with their adjacent noncancerous tissues and normal tissues. Its expression was also lower in the human CCRCC-derived cell lines A-498 and 786-O than in the human proximal tubular cell lines HK-2 and HKC. These results indicated that NDRG2 might play an important role in the carcinogenesis and development of CCRCC and may function as a tumor suppressor in CCRCC.     

Pharmacotherapy for treating metastatic clear cell renal cell carcinoma

Introduction: Over the past decade metastatic renal cell carcinoma (RCC) treatment landscape has dramatically evolved from the era of cytokines-based immunotherapy (which benefited very few patients, at the expenses of high toxicities) to the present era of targeted agents and novel immunotherapeutics, greatly improving the prognosis of our patients.

Areas covered: Here we have reviewed the present status of the medical treatment of metastatic RCC. To do this, we interrogated the Medline database, as well as the proceedings of the main Oncological and Urological conferences for the relevant trials coducted so far.

Expert opinion: Despite all the advances made in these relatively few years, further improvements are needed, since none of the available agents proved able to cure even a sigle metastatic RCC patient. In particular, advances are awaited from the results of ongoing trial of combinations of different immune checkpoint inhibitors and of immune checkpoint inhibitors with anti-VEGF/VEGFRs agents. Furthermore, a better understanding of the molecular escape pathways used by the tumor to overcome VEGFR blockade or immune activation will hopefully bring soon to the clinic more active, tailored treatments, to be used in second line and beyond.     

转移性肾细胞癌药物治疗方法的研究

肾细胞癌在我国的发病率逐年升高,且对于放化疗不敏感,免疫治疗效果有限,尤其是转移性肾细胞癌的预后较差。该文就转移性肾细胞癌的药物治疗方案的作用机制、现状及展望进行综述。     

Targeted therapy in renal cell carcinoma

Hypoxia-regulated genes such as vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) are both important for tumour progression in renal cell carcinoma (RCC). Drugs that block these and other pathways have been examined in Phase I and II clinical trials in patients with advanced or metastatic RCC. Results from a randomised study of an anti-VEGF antibody demonstrate a delay in the time to disease progression, suggesting a biological effect and change in the natural history of the disease. Results using small-molecule inhibitors of VEGF, FLT3, KIT and platelet-derived growth factor receptor tyrosine kinases, such as sunitinib, show a 40% objective response rate. Results from a Phase III clinical trial with sorafenib, an inhibitor of multiple tyrosine kinases, show only a 2% response rate; however, a statistically significant improvement in progression-free survival was observed. Objective responses have also been noted using an inhibitor of the mammalian target of rapamycin. Conversely, EGF receptor inhibitors, proteosome inhibitors, microtubule stabilising agents, cell-cycle inhibitors and imatinib were also examined with few objective responses. Ultimately, identifying the predictive factors for responsiveness to these targeted therapies may improve the clinical benefit; for example, RCC with biallelic mutations in the von Hippel-Lindau gene would have higher levels of hypoxia-inducible factor-1alpha, and may be more responsive to inhibitors of angiogenesis. Phase III studies comparing the combinations of targeted therapy could lead to a new standard of care for RCC.