基于磁共振图像的乳腺癌分子分型研究进展

在基因表达水平上,乳腺癌分子亚型的分析对评价乳腺癌的恶性程度及制定个体化治疗方案具有重要的临床应用价值.除免疫组织化学染色和基因芯片技术外,影像组学的兴起也为乳腺癌分子分型提供新的预测方式.综述基于磁共振成像的乳腺癌分子分型的研究现状.在概述乳腺磁共振成像原理和特点的基础上,分别从统计学分析及机器学习方法的角度,阐述乳...     

Mast cells and the nodal sinus reaction in breast cancer

Mast cell counts in the sinuses of axillary nodes from breast cancer patients are shown to vary with the type of sinus reaction present. Few scattered mast cells were found in association with sinus histiocytosis. A mixed reaction, in which fewer histiocytes were present and more round cells, was accompanied by a significant increase in mast cell count, which in sinus catarrh showed a decrease. The possible role of sinus mast cells in relation to tumour spread is discussed.     

围术期静脉注射氟比洛芬酯在乳腺切除术后慢性疼痛中的作用

目的: 探讨围术期静脉注射氟比洛芬酯能否降低乳腺癌术后慢性疼痛的发生率和疼痛程度。方法: 采用随机、双盲、对照的研究方法, 入选60位在全麻下行乳房切除及腋窝淋巴结清扫的患者。术前1 d通过医院焦虑抑郁量表(HAD)评估所有患者的抑郁和焦虑。患者被随机均分为F组和对照组, 切皮前15 min和6 h后分别给予F组氟比洛芬酯50 mg静脉注射, 对照组脂肪乳剂5 mL静脉注射。术后2组患者均接受芬太尼静脉自控镇痛。术前、术后4 h和24 h分别抽取外周静脉血检测血浆中PGE₂和TNF-α的水平。观察并记录术后2, 6, 12, 24和48 h疼痛的数字等级评分(NRS)、芬太尼的剂量和不良反应。电话随访术后2至12个月期间疼痛的持续时间和强度。结果: 术后2, 4, 6, 12个月时疼痛的发生率分别为33%, 20%, 15%, 10%, 平均疼痛强度分别为0.77, 0.57, 0.28, 0.18。F组术后2, 4, 6和12个月时疼痛的强度均明显低于对照组(F=7.758, P=0.007), F组术后2, 4和6个月时疼痛的发生率也明显低于对照组(P<0.05), 12个月时慢性疼痛的发生率与对照组比较无明显差异(P>0.05)。术前、术后4 h和24 h两组患者血浆TNF-α的浓度无差异(F=0.530, P=0.470), 但F组血浆PGE₂的浓度明显低于对照组(F=5.646, P=0.021)。术后无1例患者发生异常出血、消化性溃疡、肝肾功能减退和呼吸抑制等不良反应。结论: 围术期100 mg氟比洛芬酯静脉注射能降低乳腺癌术后慢性疼痛的发生率和强度。     

BcL-2、Bax、CD44V6在乳腺癌表达及预后的研究

目的探讨影响乳腺癌患者预后的因素,协助临床制定手术方式及术后治疗方案。方法选择80例各型乳腺癌患者的标本,应用免疫组化SP方法,检测乳腺癌组织中癌基因BcL-2、Bax及黏附因子CD44V6的表达情况。结果乳腺癌中BcL-2、Bax及CD44V6的表达情况与肿瘤组织学分级、瘤体直径。有无转移及患者术后存活时间均有显著性相关(P<0.05或0.01)。结论BcL-2高表达、Bax低表达、CD44V6低表达的患者组织学分级好,肿瘤体积小,淋巴结转移少,术后存活时间长,这部分患者可做肿物扩大切除而保留乳房或即使已做乳房切除,术后也可减少放疗及化疗剂量。     

中西医结合治疗乳腺癌术后化疗药物性肝损害30例

目的观察中西医结合疗法治疗乳腺癌术后化疗药物性肝损害的临床疗效。方法对30例化疗药物性肝损害的乳腺癌术后患者给予疏肝健脾、清热解毒、利湿化瘀中药联合西药甘草酸二铵胶囊治疗,疗程为14天;观察临床症状及肝功能变化情况,并判定临床疗效。结果 30例患者经过治疗,临床总有效率达93.3%,AST、ALT水平明显下降（P〈0.05）。结论疏肝健脾、清热解毒、利湿化瘀中药联合西药甘草酸二铵胶囊治疗乳腺癌术后化疗药物性肝损害疗效确切。     

基质金属蛋白酶抑制剂抗肝癌细胞系侵袭作用的实验研究

目的探讨基质金属蛋白酶抑制剂-3（TIMP-3）对人肝癌细胞系（HXPG2）恶性表型的影响。方法利用基因重组技术构建含全长人TIMP-3cDNA的真核表达载体,利用脂质体法转染入HEPG2细胞。检测转染后鳓细胞的金属蛋白酶（MMPs）的活性、体外侵袭能力、制成裸鼠肝癌动物模型后体内成瘤性及自发转移能力等多项生物学行为的变化。结果HEPG2细胞在转染了TIMP-3cDNA后表达TIMP-3蛋白,与朱转染细胞及空载体对照组相比,体外侵袭能力、软琼脂集落形成能力均降低,裸鼠的肝癌肿瘤体积及重量也相应降低,且肿瘤组织中微血管密度降低,细胞外基质基本保持完整。结论特异性上调TIMP-3基因的表达可在一定程度上逆转HEPG2细胞的恶性表型。     

Comparative expressed sequence hybridization reveals differential gene expression in morphological breast cancer subtypes

In this study, comparative expressed sequence hybridization (CESH) has been used to compare gene expression patterns in three morphologically different breast cancer subtypes: classic-type invasive lobular carcinoma (ILC), poorly differentiated ERBB2-negative invasive ductal carcinoma-not otherwise specified (IDC-NOS), and poorly differentiated ERBB2-positive IDC-NOS. CESH allows global detection of chromosomal regions with differential gene expression in a way similar to that of comparative genomic hybridization (CGH). Eight cases of each breast cancer subtype were included in the study. For each subtype, two pools of four cases each were constructed. CESH was used to compare both pools within the same morphological subtype, followed by a comparison of pools belonging to different subtypes. This revealed three chromosomal regions that were differentially expressed in ductal and lobular carcinomas, including relative overexpression at 8q13-q23 and 16q22, and relative underexpression at 8p21-p22. In addition, an expression signature characterized by relative overexpression at 3q24-q26.3, 14q23-31, 17q12, and 20q12-13 was identified for ERBB2-positive IDC-NOS. In summary, CESH analysis highlights chromosomal regions of differential gene expression that are associated with morphologically defined breast cancer subtypes and suggests that regions on chromosome 8 are of interest in the discrimination between ductal and lobular carcinomas. In addition, using CESH, it was possible to identify an ERBB2 expression signature, comprising four chromosomal regions with potential significance in the aggressive behaviour of ERBB2-positive IDC-NOS.