Bench to bedside: recent advances in lung cancer pathological research with implications for diagnostic clinical practice

After decades of relative stagnation lung cancer is emerging as a disease type where rapid progress is being made in diagnosis and therapy, as well as in our understanding of disease biology. Much of this progress is of immediate impact to diagnosticians, and more is likely to affect diagnostic practice in the near future. In this review we seek to briefly summarize several key areas of active research of immediate or probable imminent value to trainee and consultant pulmonary pathologists alike. We cover some major changes in tumour classification, grading, and patient stratification, as well as considering the state of the art in machine-assisted interpretation of lung cancer histology, and the use of genetically modified lung cancer models.     

A Pre-Protocol/Post-Protocol Quality Improvement Initiative Specific to One Hospital for Security of Pathologic Specimen

ObjectiveThe objective of this study was to reduce errors in a pathologic specimen with the help of a protocol systematizing the pathology specimen management process in the operating room.Materials and methodThis quasi-experimental study was carried out in the operating room unit of a research and training hospital. A protocol systematizing the process of specimen management in secure surgical pathology and prepared in light of the current literature was used as an intervention, and the effectiveness of the protocol was tested.ResultsIt was determined that the rate of adverse events decreased from .3226% (68 of 21,078) to .032% (6 of 18,706) after the protocol systematizing the surgical pathology specimen management process prepared by the researchers, and the protocol was found to be effective by 90% (P = .03).ConclusionBased on the data obtained in this study, we recommend the use of a pathologic specimen management protocol in the operating room.     

Outcomes after neoadjuvant or adjuvant chemotherapy for cT2-4N0-1 non–small cell lung cancer: A propensity-matched analysis

Objective

Comparative survival between neoadjuvant chemotherapy and adjuvant chemotherapy for patients with cT2-4N0-1M0 non–small cell lung cancer has not been extensively studied.

Fas/FasL在各阶段婴幼儿血管瘤中的表达及意义

目的 检测Fas／FasL在各阶段婴幼儿血管瘤组织中的表达，探讨Fas／FasL在婴幼儿血管瘤细胞凋亡中的作用。方法 应用EnVision法免疫组化染色和RT-PCR检测Fas／FasL蛋白及mRNA在各阶段血管瘤组织中的表达。结果 ①增生早期和增生中期，部分血管瘤细胞表达Fas；增生晚期，阳性细胞明显增多，Fas mRNA表达最强；消退早期，仍有少量微血管内皮细胞表达Fas，之后Fas表达迅速减弱。②最早期细胞团中没有FasL（＋）细胞；增生中期，血管瘤组织中出现少量FasL（＋）细胞；增生晚期FasL（＋）细胞显著增多，FasL mRNA表达最强；消退早期之后，FasL（＋）细胞迅速减少以至消失。结论 Fas／FasL与婴幼儿血管瘤演变过程有密切联系，Fas／FasL介导的血管瘤细胞凋亡可能是婴幼儿血管瘤自行消退的重要原因。     

微波对白斑上皮异常增生12项病理特征出现率的影响

上皮异常增生是白斑癌变的必经阶段，深入研究其镜下形态的特征性改变，不仅对加深认识白斑癌变规律有利，而且可以籍以研究治疗手段的有效性，本文采用ｓｅｌｌｙ法白斑动物模型，以微波辐射为阻断手段，采集金地鼠颊囊标本，行光镜下肉眼观察，并按照ＷＨＯ提出的上皮异常增生１２项病理特征进行观察记录，结果发现：特征性改变的出现颊率不同，为１５．５－６０．６％，微波处理与否对病理的出现率存在影响，与细胞增殖有关的改变     

胃癌动态增强MRI表现与肿瘤血管形成关系的研究

目的　探讨胃癌动态增强MRI强化表现与肿瘤血管形成的关系。方法　对 30例胃癌组织切片进行CD34和血管内皮生长因子 (VEGF)免疫组织化学染色。分析癌组织微血管密度 (MVD)和癌细胞VEGF的表达情况及其与临床病理特征的关系。并将动态增强MRI强化表现和扫描所获参数 (最大强化率 ,CERmax)与MVD、VEGF进行相关性研究。结果　 30例胃癌组织的MVD平均值为(4 2 95± 14 79)个 /视野 ,范围为 13 0 0～ 6 8 2 5个 /视野。VEGF低表达 30 % (9/ 30 ) ,高表达 70 % (2 1/30 )。MVD和VEGF表达与有无淋巴结转移密切相关 (P <0 0 5 ) ,与组织分化程度、有无浆膜层受侵无关 (P >0 0 5 )。MVD与胃癌TNM各分期密切相关 (P <0 0 5 )。TNM分期中Ⅰ期与Ⅳ期间VEGF表达差异有显著意义 (P <0 0 5 )。VEGF高表达者MVD值 [(4 7 30± 14 16 )个 /视野 ]与VEGF低表达者MVD值 [(32 81± 11 2 5 )个 /视野 ]间差异有显著意义 (t=- 2 716 ,P =0 0 11)。CERmax与MVD呈正相关 (r=0 5 5 6 ,P =0 0 0 14 )。微血管的分布及形态与胃癌动态增强表现的不规则强化及分层强化类型存在一致性。CERmax与VEGF蛋白表达无明显相关性 (t=- 0 84 7,P =0 4 0 4 )。结论　胃癌动态增强MRI表现反映了胃癌微血管的分布和形态。动态增强MRI可     

三氧化二砷-碘油化疗栓塞对兔肝移植瘤转移及与血管形成关系的研究

目的观察三氧化二砷（ As2O3）-碘油经肝动脉化疗栓塞对兔VX2肝移植瘤生长及转移的影响及与血管形成的关系。方法 48只家兔肝内肿瘤种植后2周，完全随机法分为4组，经肝动脉插管分别给予不同处理，实验设生理盐水灌注组、单纯碘油栓塞组、阿霉素．碘油栓塞组及 As2O3-碘油栓塞组。治疗后1周，免疫组织化学测定肿瘤区的微血管密度（MVD），治疗后3周，测量计算肝移植瘤的体积、坏死面积，观察肝内、双肺及其他器官肿瘤转移的发生率。结果 治疗后1周，各组MVD分别为（21．8±5．3）、（23．4±3．9）、（22．4±4．50）、（14．3±3．4）条／400倍视野（F=11．246，P=0．000）， As2O3-碘油栓塞治疗组与其他组相比差异有统计学意义；肿瘤植入后5周，各处理组肿瘤体积分别为（35．5±7．1）、（21．2±8．3）、（20．7±9．1）、（11．8±3．7）cm^3（F=21．203，P=0．000）。单纯碘油栓塞组、阿霉素一碘油栓塞组及 As2O3-碘油栓塞组与生理盐水灌注组相比差异有统计学意义（q值分别为6．723、6．940、11．119，P〈0．05）， As2O3-碘油栓塞组与单纯碘油栓塞及阿霉素-碘油栓塞组相比差异有统计学意义（g值分别为4．398、4．178，P值均〈0．05）；各组肿瘤坏死面积间差异无统计学意义（F=1．284，P=0．292）； As2O3-碘油栓塞治疗组双肺转移结节数目少于其他组（H=14．983，P=0．002），结节直径小于其他组（F=4．580，P=0．007），差异有统计学意义。腹腔转移淋巴结记分显示 As2O3-碘油栓塞治疗组腹腔淋巴结转移少于其他组（H=9．148，P=0．027）。双肺转移结节的数目、直径及腹腔转移淋巴结与肿瘤的微血管密度呈正相关（P〈0．05）。结论 As2O3-碘油联合经肝动脉栓塞治疗，抑制兔肝移植瘤的生长，抑制肿瘤的肺及腹腔淋巴结转移，其抑制转移的机制可能与抑制肿瘤血管形成有关。     

Pathological variables determining the prognosis of non-Hodgkin''s lymphomas

The aim of the study was to assess the role of pathological grade, cell proliferation, ploidy, immunophenotype and site in determining the prognosis of non-Hodgkin's lymphomas. Of particular interest was the relative value of grades derived from the Kiel classification as opposed to the National Cancer Institute (NCI) working formulation. The study consisted of 181 cases, treated in a relatively uniform way over an 18-month period spanning 1986. Using life table analysis, both NCI working formulation grade and Kiel grade correlated strongly with survival. However, the differences between grades were entirely due to an excess of early deaths in the high-grade and intermediate-grade categories. In patients surviving greater than 0.1 years (37 days), phenotype, site, ploidy and cell proliferation had no effect on survival. There was no evidence that intermediate-grade tumours, when subdivided into Kiel low- and high-grade types, differed in survival from tumours graded as low- or high-grade by both methods. However, NCI working, formulation high-grade tumours, especially those with a high proliferation rate, formed a group with a very high likelihood of death within 0.1 years.     

胰腺分裂与慢性胰腺炎的病因学关系及发病机制

目的:探讨胰腺分裂(PD)在慢性胰腺炎病因学中的作用及其发病机制。方法:将32只犬随机分为4组(每组8只)。Ⅰ组:部分结扎背-腹胰管间的交通支。Ⅱa组:切断并结扎交通支。Ⅱb组:在背胰管注入小乳头前2mm处将其切断并结扎断端。Ⅲ组:假手术对照组,除不结扎交通支外,其余操作同上。于手术前检测各组犬血清磷脂酶(PLA2)和淀粉酶(Ams)活性及背、腹胰管基础压并在胰泌素激发后15、30、45、60和90分钟各测压一次。于术后180天再行胰胆管测压和造影并观察背、腹胰和十二指肠乳头的病理改变。结果:⑴Ⅰ、Ⅱa组和Ⅱb组术后5-80天血清PLA2和Ams活性显著升高。⑵处死时Ⅰ、Ⅱa组腹胰管和Ⅱb组背、腹胰管压力在激发后30-60分钟显著高于注药前(P<0.01);在60分钟后,前两组压力恢复到术前水平(P>0.05),而Ⅱb组仍较高(P<0.05),该组压力在90分钟后恢复正常。⑶光镜:Ⅱb组犬背、腹胰小叶间或/和胰管周围显著纤维组织增生,腺细胞结构破坏和炎细胞浸润。Ⅰ和Ⅱa组腹胰见轻度上述改变。⑷电镜:Ⅰ、Ⅱa组腹胰和Ⅱb组背、腹胰腺细胞粗面内质网脱颗粒、融合和扩张。酶原颗粒减少,线粒体肿张。Ⅰ和Ⅱa组背胰及Ⅲ组背、腹胰未见异常。结论:PD是慢性胰腺炎的病因学因素之一,其引发胰腺炎的机制是在胰液分泌的高峰期副乳头功能性梗阻。