数字化乳腺X线引导下切除活检及导丝定位钙化患者的影像学病理及相关表现

目的:分析数字化乳腺X线引导下切除活检及导丝定位钙化患者的X线征象。方法:回顾性分析2015年12月至2017年12月间收治102例数字化乳腺X线引导下切除活检及导丝定位钙化患者进行实验研究,观察X影像中分布征象及微钙化形态,比较X征象与乳腺癌A、B、C不同数据系统(BI-RADS)分型之间的差异。结果:102例乳腺癌患者中,良性病变患者80例(78.43%),恶性病变患者22例(21.56%)。不同类型病变的钙化类型与BI-RADS分型差异明显(P <0.05);恶性病变在BI-RADS4C中占比最大(9/12,75.00%),良性病变在BI-RADS4A中占比最大(24/27,88.88%),良性病变在BI-RADS类患者构成比差异明显(P<0.05)。结论:乳腺疾病可通过数字化乳腺X线引导下活检术诊断乳腺癌,乳腺病灶是否钙化的主要影响因素是BI-RADS和钙化类型,具有一定的临床价值,值得推广应用。     

芪胶升白胶囊对曲妥珠单抗和多西紫杉醇治疗转移性乳腺癌的影响

目的 探讨芪胶升白胶囊对曲妥珠单抗和多西紫杉醇治疗转移性乳腺癌的影响。方法 选择我院肿瘤内科转移性乳腺癌患者100 例,分为对照组与观察组,各50 例。对照组给予曲妥珠单抗和多西紫杉醇治疗;观察组给予芪胶升白胶囊联合曲妥珠单抗和多西紫杉醇治疗：疗程均25 周,疗程结束时观察两组临床疗效、生活质量和不良反应,并观察1 年内生存情况。结果 两组临床效果比较,差异无显著性（Z=-1.50,P＞0.05）;两组1 年内生存情况比较,差异无显著性（χ2=1.00,P＞0.05）;两组生活质量比较,观察组高于对照组（t=2.37,P＜0.05）;两组治疗后骨髓抑制比较差异有显著性（χ2=4.76,P＜0.05）,而肝肾功能损害比较差异具有显著性（χ2=7.90,P＜0.01）。结论芪胶升白胶囊可提高曲妥珠单抗和多西紫杉醇治疗转移性乳腺癌患者的生活质量,显著减轻化疗所引起的肝肾损伤和骨髓抑制。     

BI-RADS分类联合超微血管成像技术在乳腺实性结节鉴别诊断中的价值

目的 探讨数据系统分类标准（BI-RADS）联合超微血管成像（SMI）技术在乳腺实性结节鉴别诊断中的应用效果。方法 回顾性分析2018 年7 月～2019 年8 月收治的94 例乳腺结节患者临床资料。所有患者均行常规超声和SMI 检查,根据二维超声结果予以BI-RADS 分类,并经手术或穿刺病理活检。评估BI-RADS 分类、SMI 技术单独及联合诊断乳腺实性结节的诊断结果,计算诊断效能（准确度、敏感度、特异度、阳性及阴性预测值）,绘制ROC曲线比较不同诊断方法效能。结果 ①SMI 诊断乳腺结节良恶性灵敏度、阴性预测值高于BI-RADS 分类,特异度、准确率、阳性预测值低于BI-RADS 分类,联合检测灵敏度、特异度、准确率、阳性预测值、阴性预测值均高于BI-RADS 分类及SMI 单独诊断;②联合检查诊断曲线下面积（AUC）高于BI-RADS 分类和SMI,SMI 诊断AUC 高于BI-RADS 分类（P＜0.05）。结论BI-RADS 分类联合SMI 技术在乳腺实性结节鉴别诊断中效能较高,临床应用前景可观。     

国产乳腺彩色三维多普勒超声市场问卷调查分析

目的对比分析国产与进口乳腺彩色三维多普勒超声(简称乳腺三维彩超)在市场供给服务方面的优劣,发现国产设备在市场供给服务上问题,总结原因并提出改进建议,推动国产化高品质乳腺三维彩超的发展,振兴民族品牌,提升国产医疗器械品牌的市场竞争力和市场影响力。方法选取辽宁省内八个市县区区域内所辖的所有三级医疗机构、二级医疗机构、社区卫生服务中心、乡镇卫生院、部分民营医疗机构及妇幼保健机构的全部可用于乳腺疾病筛查的彩超的市场供给服务信息进行调查,采用对设备使用人员发放问卷,现场填写的方式进行数据采集,确保对每台乳腺三维彩超在配置、使用、故障、售后、维修、培训等市场供给服务方面做出准确、客观、真实的评价,并对采集的数据建立数据库及进行数据分析。结果国产乳腺三维彩超配置比例明显低于进口乳腺三维彩超,市场占有率不足进口设备的一半。进口设备主要配置在三级、二级医疗机构,国产设备主要配置在乡镇卫生院,社区服务中心等基层医疗机构。国产与进口乳腺三维彩超在市场供给服务情况方面相比较,在设备满足临床需求度、设备发生故障频率与使用可及性、设备售后服务及维修满意度、设备技术培训满意度方面上总体无明显差异。在设备改进提升需求方面中的设备技术功能的改进与创新、售后服务提升、质量提升、设备安全防护方面总体无明显差异。对进口设备在改善设备操作便利程度的需求高于国产设备。结论国产乳腺三维彩超在满足市场需求和临床诊疗需求上总体与进口乳腺三维彩超无明显差异,但在品牌定位及地域分布上均不平衡,国产设备仍以中低端产品为主,主要配置在基层医疗机构,故应加大对优秀国产设备的扶持,引导民族品牌的创建和宣传,提高国产品牌的市场占有率,扭转高端医疗器械长期以来依赖进口的局面,对我国医疗设备产业及医疗卫生事业的发展都有着十分重要的意义。     

“互联网+”健康教育模式在乳腺外科的构建及应用

目的 探索“互联网+”健康教育模式在乳腺外科的构建及应用效果。方法 选择2019年3月至2020年3月在河北大学附属医院乳腺外科手术治疗的160例乳腺癌(breast cancer,BC)患者作为研究对象,按照入院先后顺序分为对照组和观察组,每组80例。对照组采取传统健康宣教模式,观察组在对照组的传统健康教育模式基础上,重点运用“317护”微信平台开展健康宣教。比较干预后两组患者健康教育内容掌握情况、依从性以及患者满意度指标。结果 干预后,观察组乳腺癌患者健康教育内容掌握情况、依从性、满意度评分均明显高于对照组,差异均有统计学意义(P<0.05)。结论 “互联网+”健康教育模式在乳腺外科的应用效果较传统健康教育方式有显著优势, 值得临床推广应用。     

两用型乳头保护加奶器对乳头凹陷产妇母乳喂养成功率的影响

目的：探讨两用型乳头保护加奶器对乳头凹陷产妇母乳喂养成功率的影响。方法：将2017年10月至2018年10月间温州医科大学附属第二医院育英儿童医院分娩的II型乳头凹陷产妇80例随机分为对照组及观察组,每组40例,对照组采用常规护理方法进行纠正,观察组采用自制两用乳头保护加奶器进行纠正,比较2组产妇在产后3 d的母乳喂养率、产后3 d的状态焦虑（S-AI）及特质焦虑（T-AI）分值。结果：观察组产妇在产后3 d的母乳喂养率显著高于对照组,差异有统计学意义（P＜0.05）;观察组产妇在产后3 d的S-AI及T-AI水平均明显低于对照组,差异有统计学意义（P＜0.05）。结论：对乳头凹陷产妇采用两用乳头保护加奶器进行纠正,可降低S-AI、T-AI评分,提高母乳喂养率,促进母婴健康。     

他莫昔芬对ER- GPER+乳腺癌细胞上皮间质转化的影响及机制

目的：探讨他莫昔芬（TAM）对雌激素受体（ER）阴性、G蛋白偶联雌激素受体（GPER）阳性乳腺癌细胞上皮间质转化（EMT）的影响。方法：以ER阴性（ER-）、GPER阳性（GPER+）乳腺癌MDA-MB-468细胞为研究对象,用TAM处理细胞,GPER特异性抑制剂G15抑制胞内GPER活性,siRNA干扰GPER蛋白表达,侵袭小室实验检测细胞侵袭能力,Western blot检测ERα、GPER、Vimentin、E-cadherin及N-cadherin蛋白表达变化。结果：TAM（5 μmol/L）可明显增强MDA-MB-468细胞的侵袭能力（P＜0.01）;G15（10 μmol/L）预处理能显著抑制TAM诱导的细胞侵袭活动（P＜0.01）;GPER-siRNA可明显干扰MDA-MB-468细胞GPER蛋白表达（P＜0.01）;干扰GPER蛋白表达能有效抑制TAM诱导的细胞侵袭活动（P＜0.01）。TAM处理明显诱导Vimentin和N-cadherin蛋白表达上调（P＜0.01）,E-cadherin蛋白表达下调（P＜0.01）;G15预处理或干扰GPER蛋白表达均能抑制TAM的上述诱导作用（均P＜0.05）。结论：TAM能诱导ER- GPER+乳腺癌MDA-MB-468细胞EMT,其作用与其激活GPER有关。     

Exome sequencing identifies FANCM as a susceptibility gene for triple-negative breast cancer

Inherited predisposition to breast cancer is known to be caused by loss-of-function mutations in BRCA1, BRCA2, PALB2, CHEK2, and other genes involved in DNA repair. However, most families severely affected by breast cancer do not harbor mutations in any of these genes. In Finland, founder mutations have been observed in each of these genes, suggesting that the Finnish population may be an excellent resource for the identification of other such genes. To this end, we carried out exome sequencing of constitutional genomic DNA from 24 breast cancer patients from 11 Finnish breast cancer families. From all rare damaging variants, 22 variants in 21 DNA repair genes were genotyped in 3,166 breast cancer patients, 569 ovarian cancer patients, and 2,090 controls, all from the Helsinki or Tampere regions of Finland. In Fanconi anemia complementation gene M (FANCM), nonsense mutation c.5101C>T (p.Q1701X) was significantly more frequent among breast cancer patients than among controls [odds ratio (OR) = 1.86, 95% CI = 1.26–2.75; P = 0.0018], with particular enrichment among patients with triple-negative breast cancer (TNBC; OR = 3.56, 95% CI = 1.81–6.98, P = 0.0002). In the Helsinki and Tampere regions, respectively, carrier frequencies of FANCM p.Q1701X were 2.9% and 4.0% of breast cancer patients, 5.6% and 6.6% of TNBC patients, 2.2% of ovarian cancer patients (from Helsinki), and 1.4% and 2.5% of controls. These findings identify FANCM as a breast cancer susceptibility gene, mutations in which confer a particularly strong predisposition for TNBC.Breast cancer is the most common cancer affecting women worldwide. It is also the principal cause of death from cancer among women globally, accounting for 14% of all cancer deaths (1). The etiology of breast cancer is multifactorial, and the risk depends on various factors like age, family history, and reproductive, hormonal, or dietary factors. The majority of breast cancers are sporadic, but approximately 15% of cases show familial aggregation (2, 3). Since the identification of the first breast and ovarian cancer susceptibility genes breast cancer 1 and 2 (BRCA1 and BRCA2, respectively) by linkage analysis and positional cloning, several breast cancer susceptibility genes and alleles with different levels of risk and prevalence in the population have been recognized. BRCA1 and BRCA2 mutation carriers have more than 10-fold increased risk of breast cancer compared with women in the general population, and mutations in TP53, PTEN, STK11, and CDH1 have also been associated with a high lifetime risk of breast cancer in the context of rare inherited cancer syndromes (4). In addition, rare variants in genes such as checkpoint kinase 2 (CHEK2), ataxia telangiectasia mutated (ATM), and BRCA1 interacting helicase BRIP1, that confer a two- to fourfold increased risk, and in partner and localizer of BRCA2 (PALB2), with even higher risk estimates, have been found with candidate gene approaches (5, 6), and an increasing number of common low-risk loci with modest odds ratios (ORs; as much as 1.26-fold increased risk for heterozygous carriers) have been identified by genome-wide association studies (7).However, the major portion of hereditary breast cancer still remains unexplained, and many susceptibility loci are yet to be found. Exome sequencing combined with genotyping of the identified variants in case-control analysis is an effective method to recognize novel risk alleles, based on the assumption that disease-causing variants are rare and often accumulate in the protein-coding areas of the genome (8–10).Since the discovery that proteins encoded by the BRCA1 and BRCA2 breast/ovarian cancer susceptibility genes are directly involved in homologous recombination repair of DNA double-strand breaks, it has been evident that other genes involved in DNA repair are attractive breast cancer susceptibility candidates (4). Biallelic mutations in ATM gene cause rare ataxia telangiectasia disease and are associated with an increased risk for breast cancer as a result of improper DNA damage response (11). Fanconi anemia (FA) is a rare genetic disorder caused by biallelic mutations in FA genes that also participate in DNA repair. At least 15 FA genes have been identified (12). Patients with heterozygous mutations in certain FA genes have an elevated risk for various cancers, and monoallelic mutations in at least four of these genes [BRCA2, BRIP1, PALB2, and RAD51 paralog C (RAD51C)] are associated with an increased risk of breast or ovarian cancer (12, 13). Recurrent founder mutations in several cancer susceptibility genes, including the BRCA2, PALB2, and RAD51C FA genes, have been identified in the Finnish population (14–16). The PALB2 and RAD51C founder mutations have been detected at 2% frequency in Finnish breast or ovarian cancer families (15–17), whereas, in other populations, mutations in these genes are rare and often unique for each family. Founder effects in the isolated populations such as Finland or Iceland may enrich certain mutations and thus explain a significant proportion of all mutations in certain genes (18, 19). This provides an advantage in the search for novel susceptibility genes and alleles.In this study, we used exome sequencing to uncover previously unidentified recurrent breast or ovarian cancer predisposing variants in the Finnish population with a focus on DNA repair genes. Selected variants were further genotyped in a large case-control sample set. Our investigation revealed an association of a nonsense mutation (rs147021911) in an FA complementation gene, FANCM, with breast cancer, especially with triple-negative (TN) breast cancer (TNBC).     

A multicentre study of primary breast diffuse large B‐cell lymphoma in the rituximab era

Primary breast diffuse large B‐cell lymphoma (DLBCL) is a rare subtype of non‐Hodgkin lymphoma (NHL) with limited data on pathology and outcome. A multicentre retrospective study was undertaken to determine prognostic factors and the incidence of central nervous system (CNS) relapses. Data was retrospectively collected on patients from 8 US academic centres. Only patients with stage I/II disease (involvement of breast and localized lymph nodes) were included. Histologies apart from primary DLBCL were excluded. Between 1992 and 2012, 76 patients met the eligibility criteria. Most patients (86%) received chemotherapy, and 69% received immunochemotherapy with rituximab; 65% received radiation therapy and 9% received prophylactic CNS chemotherapy. After a median follow‐up of 4·5 years (range 0·6–20·6 years), the Kaplan–Meier estimated median progression‐free survival was 10·4 years (95% confidence interval [CI] 5·8–14·9 years), and the median overall survival was 14·6 years (95% CI 10·2–19 years). Twelve patients (16%) had CNS relapse. A low stage‐modified International Prognostic Index (IPI) was associated with longer overall survival. Rituximab use was not associated with a survival advantage. Primary breast DLBCL has a high rate of CNS relapse. The stage‐modified IPI score is associated with survival.