胰腺癌和其它胰腺肿瘤淋巴管密度的比较及意义

目的：探讨胰腺癌和其它胰腺肿瘤组织中淋巴管密度的差异及意义。方法：应用免疫组化方法,采用单克隆抗体D2-40检测经手术切除的33例胰腺癌（PC）、7例胰腺神经内分泌肿瘤（NETP）、7例胰腺实性假乳头状瘤（SPTP）和3例胰腺囊腺瘤（CP）组织的淋巴管密度（LVD）,比较胰腺癌组织与其它三种胰腺肿瘤组织淋巴管密度的差异。结果：NETP的LVD显著高于PC、SPTP、CP（P〈0.05）,PC的LVD显著高于SPTP、CP（P〈0.05）,SPTP和CP的LVD没有差异（P〉0.05）。结论：胰腺癌和胰腺神经内分泌肿瘤均具有较高的淋巴管密度,对于前者可能意味着为淋巴结转移作准备。     

胃肠胰腺神经内分泌肿瘤中血管表皮生长因子的表达与淋巴结转移的关系及意义

目的通过检测胃肠胰腺神经内分泌肿瘤中血管表皮生长因子(VEGF)、淋巴管密度(LVD)水平的变化,分析其与淋巴结转移的关系。方法选取胃肠胰神经内分泌肿瘤(GEP-NEN)患者,采用免疫组织化学法检测组织中VEGF、LVD的表达,分析其与淋巴结转移的关系。结果淋巴结转移组VEGF阳性率为55.26%(21/38),淋巴结未转移组VEGF阳性率为13.64%(3/22),差异有统计学意义(P<0.05)。淋巴结转移组的LVD均值达(0.83±0.14),较淋巴结未转移组患者明显升高(P<0.05);VEGF阳性表达的患者,其LVD较VEGF阴性表达者升高(P<0.05);VEGF与LVD呈正相关(P<0.05)。结论出现淋巴结转移的胃肠胰腺神经内分泌肿瘤患者,其VEGF表达阳性率升高,LVD值明显升高,VEGF的表达与LVD呈正相关。     

食管鳞癌淋巴管分布及密度与淋巴结转移的关系

目的:探讨食管鳞状细胞癌组织中淋巴管的分布及密度并分析其与淋巴结转移的关系.方法:应用单克隆抗体D2-40检测食管癌巢周围和癌巢中心区以及正常食管组织中淋巴管密度(LVD),分析其与临床病理因素的关系.结果:癌巢周围区LVD明显高于中心区和正常组织(P＜0.01).癌巢周围区LVD与淋巴结转移及分化程度相关(P＜0.05),与浸润深度无关(P＞0.05),癌巢中心区LVD与食管鳞癌分化程度、浸润深度和淋巴结转移均无相关性(P＞0.05).结论:D2-40是淋巴管特异和敏感的标记物,食管癌功能性淋巴管主要存在于食管癌巢周围,检测癌巢周围淋巴管可能是预测淋巴结转移的可靠指标.     

乳腺癌组织VEGF-D表达及淋巴管生成的临床意义探讨

目的:探讨乳腺癌组织中血管内皮生长因子-D(VEGF-D)、淋巴管密度(LVD)的表达及其与临床病理参数的关系.方法:应用Envision免疫组化技术对100例乳腺癌组织和20例乳腺纤维腺瘤组织中淋巴管内皮细胞透明质酸受体-1(LYVE-1)和VEGF-D的表达进行检测;计数LVD;并分析VEGF-D表达与LVD、乳腺癌临床病理参数的相关性.结果:乳腺癌癌旁组织中淋巴管密度显著高于乳腺纤维腺瘤组织(9.52±3.47 vs 1.31±1.02,P＜0.01);乳腺癌癌旁组织LVD与病理分期和淋巴结转移显著相关,P均＜0.01;乳腺癌组织VEGF-D蛋白表达的阳性率(76%)显著高于乳腺纤维腺瘤组织(10%),P＜0.0001;乳腺癌VEGF-D表达与淋巴结转移(P＜0.01)显著相关;乳腺癌VEGF-D蛋白表达阳性者的癌旁LVD(11.39±2.72 vs 3.81±1.71,P＜0.01)显著高于VEGF-D蛋白表达阴性者的癌旁LVD;乳腺癌VEGF-D表达与癌旁组织LVD存在明显的相关性.结论:乳腺癌组织VEGF-D与LVD的表达呈正相关,VEGF-D的表达与淋巴转移相关,VEGF-D的过表达可促进淋巴管生成,导致LMD的升高,进而促进乳腺癌淋巴转移,LVD与VEGF-D可作为乳腺癌淋巴转移的预测因子.     

MTDH在胰腺癌中的表达及其与E-cadherin、MVD的关系

[目的]研究MTDH在胰腺癌中的表达及其与钙黏蛋白(E-cadherin)、肿瘤微血管密度的关系及其临床意义.[方法]应用免疫组织化学SP法检测MTDH、E-cadherin、CD31在60例胰腺癌及其癌旁正常胰腺组织中的表达;并用抗CD31抗体标记微血管,计数微血管密度.应用即时荧光定量PCR检测10例胰腺癌及其癌旁正常胰腺组织中MTDH mRNA的表达水平.[结果]MTDH在胰腺癌组织中的表达率显著高于癌旁胰腺组织中的表达(P＜0.05);胰腺癌组织MTDH的表达与患者临床分期(P=0.014)、淋巴结转移(P=0.002)和远处转移(P=0.006)相关;E-cadherin的表达与患者临床分期(P=0.002)、淋巴结转移(P=-0.023)和组织学分级(P=-0.027)相关.MTDH在胰腺癌组织中的表达与E-cadherin表达负相关(P＜0.05),与MVD表达呈正相关(P＜0.05).[结论]MTDH在胰腺癌中高表达,其表达水平与肿瘤的进展和转移相关.MTDH蛋白的高表达可能通过影响肿瘤E-cadherin的表达和肿瘤微血管生成来促进胰腺癌的转移.     

肾细胞癌组织VEGF-C表达与淋巴管生成和淋巴转移的相关性

目的:应用特异的淋巴管内皮标志podoplanin检测肾细胞癌(RCC)组织中淋巴管,用淋巴管密度(LVD)表示淋巴管生成情况, 探讨RCC 内VEGF-C表达与淋巴管生成和淋巴转移的关系.方法:收集45例RCC和10例肾外伤致肾切除的正常肾组织标本,应用免疫组化检测VEGF-C、podoplanin 的表达,计算VEGF-C阳性表达率及淋巴管密度值,分析两者的关系.结果:RCC 组织内VEGF-C 阳性表达率(71.1%) 显著高于正常肾组织(10.0%),P<0.01,高中分化(70.6%) 和低分化(72.7%) 之间差异无统计学意义,P>0.05,淋巴结阳性组中VEGF-C阳性率(81.3 %)显著高于淋巴结阴性组(65.5%),P<0.05.RCC组织内LVD(6.8±1.3) 显著高于正常肾组织(1.2±0.3),P<0.01;VEGF-C阳性组LVD(7.6±1.5)显著高于VEGF-C 阴性组(4.7±0.9),P<0.05, 淋巴结阳性组LVD (8.3±1.4) 显著高于淋巴结阴性组(5.1±1.1),P<0.05.结论:淋巴管生成可能是RCC淋巴结转移的重要因素,VEGF-C参与RCC淋巴管生成,从而促进淋巴结转移.     

桩蛋白在胰腺癌中的表达及临床病理学意义

目的:探讨人类胰腺癌组织中桩蛋白的表达情况及临床病理学意义。方法:应用免疫组化法分别检测47例胰腺癌组织及47例正常胰腺组织中桩蛋白的表达情况,观察其与患者临床病理参数的关系,采用χ²及Fisher's exact检验统计学方法分析实验结果。结果:免疫组化检测结果显示,胰腺癌组织中桩蛋白的表达阳性率为76.60％(36／47),明显高于正常胰腺组织29.79％(14／47),两者差异有统计学意义（P＜0.05）。桩蛋白的表达与患者年龄、性别、肿瘤大小、分化程度、肿瘤位置无明显相关性（P＞0.05）,而与肿瘤TNM分期（P＜0.05）、肿瘤浸润范围（P＜0.05）、区域淋巴结转移（P＜0.05）相关,差异具有统计学意义。结论:桩蛋白与胰腺癌关系密切,进一步从基因水平的研究有助于寻找胰腺癌更佳的诊断和治疗方法。     

胃癌组织COX-2、VEGF-C表达与淋巴结转移及预后关系的研究

目的:探讨环氧化酶-2(cyclooxygenase-2,COX-2)、血管内皮生长因子C(VEGF-C)在胃癌组织中的表达及其与淋巴管生成、淋巴结转移及预后的关系.方法:采用免疫组织化学SABC法检测 51例胃癌及相应的癌旁组织COX-2、VEGF-C及受体VEGFR-3表达,计数肿瘤内淋巴管密度(LVD),并结合临床病理特征和随访资料进行分析.结果:胃癌组织COX-2、VEGF-C表达阳性率分别为62.8%(32/51),60.7%(31/51).COX-2表达与VEGF-C(r=O.74,P＜0.05)、临床分期(r=0.34,P＜0.05)、淋巴管密度(r=0.69,P＜0.01)和淋巴结转移(r=0.57,P＜0.01)呈正相关,与病理分化呈负相关(r=-0.58,P＜0.01).VEGF-C表达与淋巴管密度(r=0.45,P＜0.01)、淋巴结转移呈正相关(r=0.46,P＜0.05).随访5年,胃癌组织COX-2表达与生存率呈负相关,COX-2表达阴性组5年生存率(36.8%)显著高于COX-2表达阳性组(15.6%)(P＜0.05).结论:在胃癌组织中,COX-2、VEGF-C高表达,COX-2与VEGF-C、淋巴管密度、淋巴结转移呈正相关.推测COX-2通过诱导VEGF-C表达参与淋巴结转移.胃癌组织COX-2检测可能对推测预后具有重要意义.     

淋巴管密度与鼻咽癌淋巴结转移的关系

目的探讨鼻咽癌(NPC)组织中淋巴管密度(LVD)与其淋巴结转移的关系。方法应用单克隆抗体D2-40免疫组化法,检测66例NPC组织中的淋巴管密度,另选取30例轻度鼻咽黏膜炎的鼻咽组织作为对照,分析LVD与肿瘤淋巴结转移的关系。结果鼻咽癌组织LVD高于对照组(P<0.05);鼻咽癌组织瘤周LVD明显高于瘤内LVD(P<0.01);淋巴结转移患者NPC瘤周LVD高于无淋巴结转移者(P<0.05);瘤周LVD与鼻咽癌N分期的升高呈一致性(P<0.05);此外,瘤周LVD与鼻咽癌患者年龄、性别、远处转移、临床分期及T分期无相关性(P>0.05),年龄<49岁的NPC患者瘤内LVD高于年龄≥49岁的患者(P<0.05);瘤内LVD与患者性别、肿瘤T分期、N分期、M分期及临床分期无相关性(P>0.05)。结论鼻咽癌瘤周LVD与淋巴结转移密切相关,推测瘤周LVD对该肿瘤发生颈部淋巴结转移具有重要意义。     

VEGF-D在非小细胞肺癌组织中的表达及与淋巴管生长和淋巴转移的关系

目的:对非小细胞肺癌及正常肺组织中血管内皮生长因子-D(VEGF-D)的表达进行检测,旨在探讨VEGF-D在非小细胞肺癌(NSCLC)组织中的表达特点及与NSCLC相关临床病理因素之间的关系,并探讨VEGF-D在NSCLC淋巴管生成及淋巴结转移中的作用和可能机制.方法:采集NSCLC标本62例及正常肺组织10例,应用免疫组化SP法检测VEGF-D在组织中的表达,应用D2-40标记淋巴管内皮细胞以计数淋巴管密度(LVD).结果:NSCLC组VEGF-D表达阳性率显著高于正常肺组织组(P=0.000).VEGF-D表达阳性率在不同性别、年龄、病理类型、肿瘤大小之间差异无统计学意义.在有无淋巴结转移及不同临床分期之间差异有统计学意义(P=0.005,P=0.000).NSCLC组LVD高于正常肺组织组(P=0.000);有淋巴结转移组LVD高于无淋巴结转移组(P=0.006);相关分析证实LVD同淋巴结转移范围呈正相关(r=0.379,P=0.002).随VEGF-D表达强度的差异,各组LVD存在差异,各阳性组均高于阴性组,相关分析证实VEGF-D蛋白表达强度与LVD呈正相关(r=0.437,P=0.000).结论:淋巴管密度是NSCLC淋巴转移的重要影响因素,VEGF-D参与了NSCLC的淋巴管生成,从而促进NSCLC的淋巴管侵袭和局部淋巴结转移,是评估预后和制定治疗措施的重要指标.     

Recurrent pancreatic adenocarcinoma after pancreatic resection

The patient is a 57-year old Caucasian female who presented with right upper quadrant pain and obstructive jaundice and was diagnosed with resectable pancreatic cancer. She underwent pancreaticoduodenectomy (PD) after preoperative biliary stenting. She subsequently presented to the clinic, where it was noticed that she had an elevated CA 19-9. CT C/A/P revealed multiple new liver lesions.     

微生物群与胰腺癌

在高通量测序技术的推动下,近年来研究发现特定微生物群比例的变化与胰腺癌的发生发展有关,包括口腔中的微生物、胃肠道内菌群及胰腺内菌群等,其中口腔内牙龈卟啉单胞菌与胰腺癌风险呈正相关,这可能为胰腺癌的诊断提供新的生物学标志物。微生物群与胰腺癌的多种治疗方式密切相关,肠道菌群失调可影响化疗效果,胰腺癌内的细菌可诱导免疫耐受,合并细菌感染时可导致术后并发症发生率增多。     

Diabetes and pancreatic cancer

Type 2 diabetes mellitus is likely the third modifiable risk factor for pancreatic cancer after cigarette smoking and obesity. Epidemiological investigations have found that long-term type 2 diabetes mellitus is associated with a 1.5-fold to 2.0-fold increase in the risk of pancreatic cancer. A causal relationship between diabetes and pancreatic cancer is also supported by findings from prediagnostic evaluations of glucose and insulin levels in prospective studies. Insulin resistance and associated hyperglycemia, hyperinsulinemia, and inflammation have been suggested to be the underlying mechanisms contributing to development of diabetes-associated pancreatic cancer. Signaling pathways that regulate the metabolic process also play important roles in cell proliferation and tumor growth. Use of the antidiabetic drug metformin has been associated with reduced risk of pancreatic cancer in diabetics and recognized as an antitumor agent with the potential to prevent and treat this cancer. On the other hand, new-onset diabetes may indicate subclinical pancreatic cancer, and patients with new-onset diabetes may constitute a population in whom pancreatic cancer can be detected early. Biomarkers that help define high-risk individuals for clinical screening for pancreatic cancer are urgently needed. Why pancreatic cancer causes diabetes and how diabetes affects the clinical outcome of pancreatic cancer have yet to be fully determined. Improved understanding of the pathological mechanisms shared by diabetes and pancreatic cancer would be the key to the development of novel preventive and therapeutic strategies for this cancer.     

微RNA与胰腺癌

微RNA(miRNA)是一类非编码单链小分子RNA,在转录后水平调节靶基因的表达.miRNA的异常表达是胰腺癌发生发展的重要机制之一,对胰腺癌的临床诊断和防治具有潜在应用价值.     

Obesity and pancreatic cancer

BackgroundPancreatic cancer is an invariably fatal malignancy. Cigarette smoking and diabetes are established risk factors, but over the last two decades studies have shown that excess adiposity is an additional independent risk factor with 30–50% of cases thought to be attributed to nutritional factors. The aim of this narrative review is to analyze all the epidemiological evidence on the topic and possible pathophysiology.MethodsWe searched PubMed, Embase, Cochrane Library and Medline, and all available evidence was included. We firstly analyze meta- and pooled analysis. Then we discuss individual studies to identify sources of discrepancies between studies and attempt to delineate pathophysiology.ResultsIt is estimated that obese individuals have a relative risk (RR) ranging between 1.19 and 1.47, when compared with those of normal weight, regardless of diabetes or smoking status. No significant differences were found between gender.ConclusionThere is a measurable increased risk of developing pancreatic cancer in obese individuals, and excess adiposity is related to the condition with a “dose–response” curve.Hyperinsulinemia and possibly hyperestrogenism secondary to a metabolic syndrome, and independently from diabetes status, appear to be the key elements of the pathogenesis in pancreatic cancer secondary to excess body fat. Increased efforts should therefore be made in tackling the epidemic levels of obesity in the Western world countries.     

Depression and pancreatic cancer

Although pancreatic carcinoma and depression have been linked for years, the prevalence and relationship of these often coexisting diseases are still poorly understood. A clinical gestalt asserts that many patients present with depression before pancreatic carcinoma is diagnosed. Published studies reviewing this issue have found that many patients with pancreatic cancer are depressed. If the definition of depression is broadened to include mild depression in addition to major depression, these numbers increase. This article reviews the literature linking pancreatic carcinoma and depression.