穿刺活检术在早期乳腺癌诊断上的价值

对乳腺病变常规行 X线检查 ,定位后穿刺活检取得病理学诊断 ,对提高乳腺癌的诊断、确定治疗方案确有帮助。我院 1996年 1月— 1999年 6月间采用此技术对 16 6例患者进行了乳腺穿刺活检 ,获得了满意的结果 ,现报告如下。1　材料与方法1.1　临床资料　我们对 1996年 1月—1999年 6月间因乳腺疾病就诊的患者中 ,摄患乳 X线片 ,从中选出 16 6例患者。均为女性 ,年龄 2 1岁～ 73岁 ,其中 30岁以内 2 6例 (15 .7%) ,31岁～ 5 0岁 12 2例(73.5 %) ,5 1岁以上 18例 (10 .8%)。1.2　操作方法　选用 PRO- MA2 .2型自动活检枪和乳腺活检针。患者取坐…     

乳腺癌腋窝淋巴结穿刺活检的临床应用

<正>乳腺癌发病率逐年递增,2014年其发病率已居全球女性肿瘤发病率的第1位[1]。对乳腺癌腋窝临床分期,前哨淋巴结活检(sentinel lymph node biopsy,SLNB)已逐步取代腋窝淋巴结清扫术,成为临床腋窝淋巴结阴性早期乳腺癌腋窝淋巴结分期的金标准。虽然SLNB有很高的可靠性,但SLNB为有创检查,同时会引起伤口感染、血肿、感觉异常、淋巴水肿等并发症,而那些在腋窝位置较深、与血管紧密相邻的淋巴结,活检存在一定的困难和风险[2-4]。因此,寻找创伤更小的评估乳腺癌腋窝临床分期方法显得尤为必要。     

乳腺癌骨转移患者生存分析

目的 提高对乳腺癌骨转移患者预后影-向因素的进一步认识，指导临床个体化治疗。方法 回顾分析有完整病例资料的乳腺癌骨转移患者68例。结果 68例患者的中位生存期20个月，乳腺癌骨转移合并肝脏和/或肺转移同时存在时，患者的中位生存期13．5个月；乳腺癌骨转移不合并肝脏和/或肺转移患者的中位生存期为26个月；仅有骨转移而不合并其他脏器转移的患者的平均生存时间为44.2个月。结论 乳腺癌转移患者中肝脏和/或肺转移是预后不良指标。骨转移而不合并其他转移的患者生存期较长，其次是骨转移合并肺转移者、合并淋巴结转移、骨转移合并多个脏器转移者及合并肝脏转移者。     

非开放式活检在乳腺癌普查中的应用

近年来,在政府倡导下,两癌(宫颈癌和乳腺癌)普查已广泛展开,查出大量可疑病例最终必经病理检查确定诊断。本文就乳腺癌普查可疑病例的病理活检相关问题作一简介。     

骨代谢指标在乳腺癌骨转移的临床应用

乳腺癌骨转移在复发转移乳腺癌中的发生率为65%～75%。骨痛、骨损伤、骨相关事件(skeletal related event,SRE)的发生及生活质量的降低是乳腺癌骨转移的常见并发症,其将进一步降低癌症患者的生活质量并缩短生存期。随着疗效的增加,生存期的延长,骨转移在临床上出现的频率亦在增加,因此,乳腺癌骨转移的诊治日益成为乳腺癌治疗的     

乳腺癌骨转移机制研究进展

乳腺癌是一种容易发生骨转移的女性常见恶性肿瘤。乳腺癌细胞的特异性、骨微环境及两者间相互作用是形成骨转移的共同因素。乳腺癌细胞表达的趋化因子受体、整合素、溶骨因子和成骨因子等使肿瘤细胞易于扩散到骨,而骨微环境可以为肿瘤细胞的生长提供丰富的生长因子和细胞因子。一旦乳腺癌细胞侵入骨质,肿瘤细胞分泌的因子就会作用于骨的外在结构和内在结构（如造血干细胞、T细胞、血小板、内皮细胞等）,使骨质破坏且分泌相关因子反作用于癌细胞,从而引起转移的级联反应和恶性循环形成。     

改良EDTA脱钙法和酸脱钙法在乳腺癌骨转移免疫组织化学中的比较研究

背景与目的：晚期乳腺癌骨转移发生率大于70%,对骨组织进行脱钙处理是一大技术难点。探索乳腺癌骨转移的临床特点及更适合对骨组织进行脱钙的方法。方法：收集2012年1月—2018年1月期间病理学诊断为乳腺癌骨转移患者的临床资料,分析临床特征;分析改良乙二胺四乙酸二钠（ethylenediaminetetraacetic acid,EDTA）脱钙法及酸脱钙法对骨转移组织进行处理后,骨组织形态、结构的差异;比较两组原发灶与转移灶免疫组织化学检查结果中雌激素受体（estrogenreceptor,ER）、孕激素受体（progesterone receptor,PR）的一致性;分析两组骨转移组织ER、PR、Ki-67的阳性率;分析乳腺癌骨转移患者ER、PR阳性和阴性的生存差异。结果：116例乳腺癌骨转移患者中91.4%为溶骨性骨转移,80.1%骨转移的数量为4~20,81.9%发生骨相关事件（skeletal-related event,SRE）。41例为改良EDTA脱钙,75例为酸脱钙,两组骨组织的形态结构无明显差异。改良EDTA脱钙组ER一致性为95.1%,明显高于酸脱钙组（69.3%）（P<0.05）;改良EDTA脱钙组骨组织ER的阳性率为90.2%,明显高于酸脱钙组（73.3%）（P<0.05）;改良EDTA组PR的阳性率（58.5%）明显高于酸脱钙组（36.0%）（P<0.05）,Ki-67增殖指数明显高于酸脱钙组（P<0.05）;骨转移组织ER + 患者的平均生存时间为（41.09±4.26）个月,明显优于ER - 患者［（25.81±5.71）个月］（P<0.05）。结论：乳腺癌骨转移多为多发溶骨性,且SRE发生率高。改良EDTA脱钙法优于酸脱钙法,更适于对骨组织进行脱钙和免疫组织化学制片。     

ICTP在诊断乳腺癌骨转移中的临床价值

目的:探讨ICTP在诊断乳腺癌骨转移中的临床价值.方法:用EIA法测定60例乳腺癌患者和23例健康体检者的ICTP血清水平.结果:乳腺癌骨转移患者ICTP血清水平较非骨转移和正常对照组显著升高,其诊断敏感性为77.8%,特异性为91.3%.多处骨转移患者血清ICTP阳性率和血清水平较单处骨转移患者显著升高且随着乳腺癌分期的升高,血清ICTP阳性率和血清水平也升高.结论:ICTP对乳腺癌骨转移患者的早期诊断,病情监测和临床分期判断具有重要意义.     

前哨淋巴结活检在乳腺癌病人中的应用

目的 探讨前哨淋巴结（sentined lymph node,SLN）定位和活检（SLNB）及其对预测乳腺癌腋窝淋巴结（axillary lymph node,ALN）转移的准确性。方法 对本院自2004年6月至2006年6月收治的56例乳腺癌病人进行回顾,56例病人临床分期均为TmNoMo,术中在肿瘤周围或活检腔的正常乳腺组织皮下注射美蓝,进行SLN定位和活检。结果 SLNB的检出成功率为91．07％（51／56）,准确性为92．16％（47／51）,灵敏度为94．12％（32／34）,假阴性率为5．88％（2／34）,特异性为89．47％（17／19）。结论 用美蓝作SLN定位进行SLNB能准确预测乳腺癌腋窝淋巴结（ALN）转移状态。     

乳腺癌骨转移靶向性机制研究进展

骨骼是乳腺癌优先且最常见的转移部位之一。患者常先出现骨骼微转移（转移前龛影）,进而发展为明显的转移灶,这一过程有赖于骨微环境提供的生长支持和癌细胞对这一环境的适应能力。骨微环境可产生多种因子促进肿瘤细胞的生长和骨转移的进展,而癌细胞也经常模拟骨和骨髓环境的细胞行为和基因表达。对乳腺癌骨转移的特异性分子与机制的研究对乳腺癌晚期骨转移的治疗有重要意义。     

Osteolytic bone metastasis in breast cancer

Summary Metastasis of breast cancer cells to bone consists of multiple sequential steps. To accomplish the process of metastasis to bone, breast cancer cells are required to intrinsically possess or acquire the capacities that are necessary for them to proliferate, invade, migrate, survive, and ultimately arrest in bone. These capacities are essential for any cancer cells to develop distant metastases in organs such as lungs and liver as well as bone. Once breast cancer cells arrest in bone, bone is a storehouse of a variety of cytokines and growth factors and thus provides an extremely fertile environment for the cells to grow. However, breast cancer cells are unable to progress in bone unless they destroy bone with the assistance of bone-resorbing osteoclasts. Thus, the capacity of breast cancer cells to collaborate with osteoclasts is likely to be specific and is likely critical for them to cause osteolytic bone metastases. Evidence to support the concept that there is an intimate relationship between breast cancer cells and osteoclasts is described using anin vivo bone metastasis model in which human breast cancer cells are inoculated into the left ventricle of nude mice. The roles of cell adhesion molecules including cadherins and laminin and matrix metalloproteinases in the development of osteolytic bone metastases by breast cancer are also discussed.     

Biology of breast cancer bone metastasis

Breast carcinoma ranks among the most prevalent malignancies in women. Breast carcinoma frequently metastasizes to bone and approximately 70% of patients with breast cancer have bone metastases, which generally are osteolytic lesions. They cause major morbidity and mortality in patients; and the available treatment options are limited. Bone-specific homing and colonization of cancer cells are important and interesting features of metastasis. There are complex and multiple steps in the process of bone metastasis; and the elaborate interaction between breast carcinoma and bone involves various cytokines, growth factors and cellular signals, which results in a vicious cycle and promotes tumor cell accumulation and osteolysis. Recent advances in molecular biology have resulted in major breakthroughs in our understanding of the pathogenesis of bone metastasis in breast cancer, which is critical in preventing metastasis, designing novel and targeted treatments and prolonging survival in this devastating condition.     

Mechanisms of breast cancer bone metastasis

Bone, as well as liver and lung, is one of the most preferential metastatic target sites for cancers including breast, prostate, and lung cancers and the consequences are always devastating. Like other metastasis, breast cancer bone metastasis consists of several steps from the escape of primary site to the colonization in target site. This review focuses on several key steps including: 1. Invasion and escape from primary tumor site. 2. Target migration toward bone. 3. Specific adhesion and arrest in bone. 4. Establishment of metastasis in bone. The factors involved in this process will provide good targets for therapy.     

乳腺癌骨转移研究进展

骨是乳腺癌最常见的转移部位之一,乳腺癌骨转移以溶骨性病变为主,也有少部分为成骨性病变,目前的研究表明趋化因子、整合素、血管生成以及骨微环境与癌细胞的相互作用等在乳腺癌骨转移的过程中起了重要作用.     

Evaluation of bone metabolic markers in breast cancer with bone metastasis

PURPOSE: In the present study, four bone metabolic markers were examined to clarify them meaning and clinical value in the detection of bone metastasis (BM) from breast cancer. METHODS: we examined serum carboxyterminal telopeptide of type I collagen (ICTP), tartrate resistant acid phosphatase (TRACP), total alkaline phosphatase (ALP) and urinary type I collagen cross-linked N-telopeptides (NTx) as potential markers. These bone markers were evaluated simultaneously in 156 breast cancer patients; 114 patients without metastasis (group A), 23 patients with BM (group B) and 19 patients with metastasis at sites other than bone (group C). RESULTS: The mean values of ICTP and TRACP in group B were significantly greater than those in group A. Group B consisted of the patients with varying degrees of BM and variation in their treatments. The patients in group B were divided into BM (+) and BM (++) according to hot spots in bone scan. ICTP and TRACP were elevated in BM (++) patients compared to BM (+) patients (p<0.05). The values of ICTP and TRACP of the twelve patients without treatment in group B were significantly higher than those in group A. In the treated patients of group B, the mean values of ICTP and TRACP were lower in responders and cases of stable disease than those with progression. NTx and ALP were inferior to ICTP and TRACP for clinical evaluation of BM. CONCLUSIONS: We confirmed that ICTP and TRACP might be useful markers for screening and monitoring BM in breast cancer.     

Efficacy of etoposide in bone metastasis of breast cancer

We have used ADM, MMC, CDDP and other drugs for a case of bone metastasis of breast cancer, but the bone destruction was advanced and she could not walk. We have also used etoposide, a new chemotherapeutic drug, for the same case. Two months later bone sclerosis was seen by X-ray film and pain disappeared. Bone sclerosis then advanced after 6 months, she has begun to stand, and after 8 months she has been able to walk with a cane. There was no severe side effect. Etoposide was very effective for bone metastasis of the breast cancer.     

Bone metabolic markers in bone metastasis of breast cancer

Background. The efficacy and cost-performance benefit of radionuclide bone scintigraphy in monitoring metastatic bone activity remain controversial. Bone metabolic markers are now expected to play a role in the diagnosis and follow-up of bone metastasis. Methods. We investigated several bone metabolic markers in patients with breast cancer. We measured three metabolic markers of bone resorption: pyridinoline cross-linked carboxy terminal telopeptide (ICTP), C-telopeptides of type I collagen (CTx), and the free form of deoxypyridinoline (fDPD), and four metabolic markers of bone formation: procollagen I carboxy terminal peptide (PICP), total alkaline phosphatase (Al-p), bone-specific alkaline phosphatase (BAl-p), and osteocalcin (BGP) in 210 patients without and 268 patients with bone metastasis. Patients without bone metastasis were analyzed in terms of menstruation status. Patients with bone metastasis were analyzed in terms of bone metastatic burden and tumor lesion "condition" (ie, determination by X-ray and/or computed tomography and bone scan findings of new lesion, progression of disease, no change, improvement, and complete remission, according to the criteria of the International Unite Against Cancer). Results. In patients without bone metastasis, ICTP did not change with menopause. All markers other than ICTP were significantly elevated with menopause. In patients with bone metastasis, all markers, except for BGP, were significantly elevated according to metastatic bone tumor burden. Among the seven markers, ICTP showed the best receiver operating characteristic curves. ICTP also showed the best correlation to bone metastatic burden among the markers by Spearman's rank correlation coefficient. In patients stratified by "condition", ICTP, CTx, fDPD, Al-p, and BAl-p showed significant elevation in patients with progression, new lesion, and no change, while PICP and BGP showed only minimal elevation in those patients. Conclusion. Bone metabolic markers, particularly ICTP, appear to be valuable for the diagnosis of bone metastasis from breast cancer. Received: April 22, 1999 / Accepted: July 15, 1999     

高强度聚焦超声治疗乳腺癌骨转移的疗效

目的:研究高强度聚焦超声（high intensity focused ultrasound,HIFU）治疗乳腺癌骨转移的疗效。方法:选取乳腺癌骨转移患者50例,随机将患者分为观察组与对照组,每组各25名。观察组采用HIFU治疗,对照组采用放疗。观察2组患者治疗前后的疼痛缓解率及骨显像浓集影区别。结果:观察组与对照组疼痛缓解显效分别为15例（60%）、5例（20%）（P＜0.01）,观察组与对照组治疗前后骨显像CR分别为19例（76%）、1例（4%）（P＜0.01）。结论:HIFU是一种从体外无创治疗骨转移瘤的有效手段。与传统治疗方法相比,治疗时间短,一般需2~3小时,治疗即可完成。局部复发后可再次应用HIFU治疗。HIFU治疗将成为骨转移的又一有效治疗手段。     

Cortactin potentiates bone metastasis of breast cancer cells

Gene amplification of the chromosome 11q13 in breast cancer and squamous carcinomas in the head and neck results in frequent overexpression of cortactin, a prominent substrate of Src-related tyrosine kinases in the cell cortical areas. To investigate the role of cortactin in tumor progression, we analyzed MDA-MB-231 breast cancer cells overexpressing green fluorescent protein-tagged murine cortactin (GFP-cortactin) and a cortactin mutant deficient in tyrosine phosphorylation under the control of a retroviral vector. Injection of MDA-MB-231 cells overexpressing GFP-cortactin into nude mice through cardiac ventricles caused bone osteolysis at a frequency approximately 85% higher than that of cells expressing the vector alone, whereas injection of cells overexpressing the mutant deficient in tyrosine phosphorylation induced 74% fewer osteolytic metastases as compared with the control group. Interestingly, the cells expressing either GFP-cortactin or the mutant did not show significant differences in growth in vitro or when injected m.f.p. in vivo. On the other hand, the cells overexpressing GFP-cortactin but not the mutant acquired a >60% enhanced capability for transendothelial invasion and endothelial cell adhesion. These data suggest that cortactin contributes to tumor metastasis by enhancing the interaction of tumor cells with endothelial cells and the invasion of tumor cells into bone tissues.