自动乳腺全容积成像结合超声乳腺影像报告和数据系统分类诊断常规超声征象不典型的乳腺癌

目的探讨自动乳腺全容积成像(ABVS)联合乳腺影像报告和数据系统(BI-RADS)分类对常规超声恶性征象不典型(BI-RADS分类3类及4A类)乳腺癌的诊断价值。方法对常规超声BI-RADS分类3类及4A类的832例患者共876个乳腺肿块行ABVS。结合ABVS冠状位图像特点对乳腺肿块重新进行BI-RADS分类。与术后病理结果对照,比较常规超声BI-RADS分类与ABVS结合BI-RADS分类为3类、4A类肿块中恶性率的差异;并以BI-RADS分类≥4B类为恶性肿块诊断标准,评价ABVS结合BI-RADS分类诊断乳腺恶性肿块的效能。结果常规超声BI-RADS分类为3类肿块558个,恶性率4.30%(24/558),4A类肿块318个,恶性率11.01%(35/318)。结合ABVS冠状位图像特点重新分类后,3类肿块455个,恶性率0.66%(3/455);4A类肿块176个,恶性率4.55%(8/176);4B类肿块218个,恶性率14.22%(31/218);4C类肿块27个,恶性率62.96%(17/27)。ABVS结合BI-RADS分类为3类、4A类肿块的恶性率明显低于常规超声分类为3类、4A类肿块(χ~2=11.447、5.951,P=0.001、0.015)。ABVS结合BI-RADS分类对恶性肿块的诊断敏感度、特异度及准确率分别为81.36%(48/59)、75.89%(620/817)及76.26%(668/876)。结论 ABVS结合BI-RADS分类对常规超声恶性征象不典型的乳腺癌具有重要诊断价值。     

超声乳腺影像学报告及数据系统鉴别诊断乳腺小肿块

目的探讨超声乳腺影像学报告及数据系统(BI-RADS)标准化描述术语鉴别诊断乳腺小肿块(最大直径均≤1.5cm)的价值。方法利用BI-RADS超声术语对159例患者共186个乳腺小肿块进行描述,并对这些超声征象进行二分类Logistic回归分析。结果良性肿块123个(123/186,66.13%),恶性肿块63个(63/186,33.87%)。超声对恶性肿块诊断的敏感度、特异度、准确率分别为71.43%(45/63)、87.80%(108/123)、82.26%(153/186)。单因素分析显示乳腺良恶性小肿块的形态、边缘、生长方向、后方回声、内部微钙化差异有统计学意义(P0.05);多因素分析显示边缘毛刺和内部微钙化进入回归模型(P0.05)。结论边缘毛刺及肿块内部微钙化对鉴别乳腺良恶性小肿块最具价值。     

超声ABVS对乳腺肿物的诊断价值研究

目的研究超声ABVS(自动乳腺全容积成像)检查对乳腺肿块的诊断价值及鉴别良恶性的作用。方法本研究选取2017年5月至2019年5月本院收治的乳腺肿块患者共200例,所有患者均行超声ABVS检查和X线钼靶检查。结果所有患者乳腺肿块中呈恶性者81例,良性者119例。81例乳房恶性肿块中,64例为浸润性乳腺癌,14例为导管原位癌,3例为黏液癌;119例乳房良性肿块中,58例为纤维腺瘤,32例为纤维囊性乳腺病,19例为导管内乳头状瘤,2例为硬化性腺病,6例为浆细胞性乳腺炎,1例为叶状肿瘤,1例为脂肪坏死结节。乳房肿块ABVS检出率大于X线钼靶检查(χ~2=70439,P0.05),超声ABVS检查中,良恶性肿块汇聚征出现率具有统计学意义(χ~2=25.8631,P0.05)。超声ABVS检查的敏感度为86.42%,特异性为80.67%,准确率为83.0%,阳性预测值为75.26%,阴性预测值为82.05%;X线钼靶检查敏感度为64.20%,特异性为71.43%,准确率为68.50%,阳性预测值为60.47%,阴性预测值为74.56%,超声ABVS检查各项指标均优于X线钼靶,差异具有统计学意义(P0.05)。结论超声ABVS检查在乳腺肿块检出率及良恶性鉴别诊断方面,优势较X线钼靶更为明显,而两种检查联合应用可以有效提高准确率及敏感度,适合临床治疗人员选择应用。     

超声BI-RADS分级联合弹性评分鉴别乳腺肿块良恶性的诊断价值

目的探讨超声BI-RADS分级联合弹性评分鉴别乳腺肿块良恶性的诊断价值。方法回顾性分析2020-01—2020-08间于郑州大学第二附属医院行手术治疗并经术后病理检查确诊的268例乳腺肿块(318个肿块)患者的临床资料。以术后病理结果为"金标准",分析术前超声BI-RADS分级联合弹性评分鉴别乳腺肿块良恶性的诊断价值。结果本研究318个肿块的病理结果为:恶性结节127个,其中浸润性导管癌87个、浸润性小叶癌16个、腺癌9个、乳头状癌10个、导管内癌5个。良性结节191个,其中乳腺增生89个、纤维腺瘤66个、乳管内乳头状瘤25个、脂肪瘤11个。以病理结果为"金标准",术前依据超声BI-RADS分级联合弹性评分诊断恶性结节123个,良性结节187个,与病理学结果不符合8个。超声BI-RADS分级联合弹性评分鉴别乳腺肿块良恶性的灵敏度为92.13%,特异性为97.91%,准确率为96.86%。阳性预测值为96.80%,阴性预测值为96.89%。结论超声BI-RADS分级联合弹性评分鉴别乳腺肿块的良恶性,具有较高的灵敏度、特异性、准确率,以及阳性预测值和阴性预测值。可作为临床早期诊断和制订治疗方案的依据。     

动态增强MRI、超声及X射线对乳腺良恶性病灶诊断的对比研究

目的探讨动态增强MRI、超声及X射线在乳腺良、恶性病变鉴别诊断中的价值。方法回顾性分析四川大学华西医院2008年6月至2009年6月期间对50个乳腺病灶进行动态增强MRI、超声及X射线检查的影像资料,基于乳腺影像报告和数据系统(BI-RADS)分别判定病变的良、恶性,以病理诊断为标准,采用Z检验比较三者的受试者操作特征(ROC)曲线下面积,对比分析三者对乳腺良、恶性肿瘤的诊断效能。结果 44例患者50个乳腺病灶,26个恶性病灶,24个良性病灶。基于BI-RADS,X射线对26个乳腺恶性病灶判定结果为5类5个,4类7个,3类6个,2类3个,1类1个,0类4个;24个良性病灶判定结果为4类1个,3类3个,2类4个,1类13个,0类3个。超声对26个乳腺恶性病灶的诊断结果为5类17个,4类4个,3类1个,2类1个,1类3个;24个良性病灶的诊断结果为5类1个,4类2个,3类4个,2类14个,1类2个,0类1个。MRI对26个乳腺恶性病灶的诊断结果为5类6个,4类18个,3类1个,1类1个;24个良性病灶的诊断结果为1类20个,2类3个,3类1个。MRI、超声、X射线对乳腺肿瘤诊断的ROC曲线下面积分别为0.977、0.835、0.764,MRI与超声、X射线比较,差异有统计学意义(分别P=0.021、P=0.025),超声与X射线比较,差异无统计学意义(P=0.230)。结论动态增强MRI是鉴别乳腺病变良、恶性的一种准确检查方法,对乳腺良、恶性病变的鉴别诊断效能优于超声和X射线。     

自动全容积成像在乳腺疾病诊断中的应用：附173例报告

目的:研究自动乳腺全容积成像技术(ABVS)在乳腺疾病中的诊断价值。方法:选择2013年1月—2015年9月间的173例乳腺病变患者作为研究对象,分别采用弹性成像和ABVS方法进行诊断,并与病理结果对比,比较恶性病变和良性病变的ABVS征象及诊断准确率。结果:在病理检出的199个病灶中,良性病灶为77个(38.69%),恶性病灶为122个(61.31%);ABVS检查结果冠状面"太阳征"以及细小钙化征象在恶性病变中的检出率显著的高于良性病变,两者差异有统计学意义(P0.05);ABVS诊断的准确率以及对恶性肿瘤诊断的敏感度明显的高于弹性成像诊断,两者亦有统计学差异(P0.05)。结论:ABVS诊断提高了乳腺癌诊断的准确率以及敏感度,为乳腺良、恶性肿瘤的鉴别提供了新的角度。     

BI-RADS 3类及4A类乳腺结节超声分类新临床决策

目的:探究BI-RADS 3及4A类乳腺结节的超声图像特征与乳腺癌的关系,并提出一项指导BI-RADS 3类及4A类乳腺结节分类的新临床决策。方法:收集608例乳腺结节患者的病历资料(652个BI-RADS 3类及4A类乳腺结节),回顾性分析其超声图像特征与乳腺癌的相关性。结果:通过多因素Logistic回归分析显示,患者年龄≥45岁、结节呈圆形、边缘模糊、边缘毛刺状及内部血流信号与乳腺恶性肿瘤的发生显著相关(均P<0.05)。结论:提出一项新的临床决策,即当观察到以下特征中的至少两项时,患者应接受诊断性活检(BI-RADS 4A类)而非短期随访(BI-RADS 3类):患者年龄≥45岁、结节呈圆形、边缘不清晰(模糊或毛刺状)及内部血流信号。     

超声评分对乳腺良、恶性结节的诊断价值

目的探讨超声评分对乳腺结节的诊断价值。方法对乳腺良、恶性结节进行超声评分,并与术后病理结果对比分析。结果良性乳腺结节的二维评分及总评分与恶性乳腺结节相比差异有统计学意义（P〈0.01）,恶性结节超声评分高于良性结节（P〈0.01）;根据ROC曲线和Youden指数,可将超声评分≥11分作为二维超声诊断恶性占位的临界点,超声评分≥12分作为总评分诊断恶性占位的临界点。结论通过对乳腺占位的超声评分有助于提高乳腺良、恶性结节超声诊断的准确率。     

超声征象Logistic回归分析诊断甲状腺恶性结节

目的探讨Logistic回归分析在常规超声及CEUS诊断甲状腺良恶性结节中的价值。方法选取经超声引导下穿刺活检或术后病理证实的甲状腺结节患者218例,其中恶性结节74例,良性结节144例,观察结节边界、形态、纵横比、微钙化、回声类型、血流分级以及CEUS增强模式等超声特征,并对其行单因素分析,以有统计学意义的指标为因变量,行多因素Logistic回归分析,建立ROC曲线。结果单因素分析显示低回声、形态不规则、边界不清、纵横比≥1、微钙化、血流分级(Ⅰ、Ⅱ级)、不均匀增强及低增强是诊断甲状腺恶性结节的重要指标(P均0.01)。多因素分析显示形态不规则、微钙化、不均匀增强及低增强是甲状腺恶性结节的独立预测指标(P均0.05)。以Logistic回归模型预测甲状腺恶性结节的准确率为82.57%,ROC曲线下面积为0.906。结论根据甲状腺结节边界、形态、纵横比、微钙化、回声类型、血流分级以及CEUS增强特征建立的Logistic回归模型有助于诊断甲状腺恶性结节。     

乳腺空芯针活检为不典型导管上皮增生的病理低估研究

目的:计算乳腺空芯针穿刺活检(core needle biopsy,CNB)诊断为不典型导管上皮增生(atypical ductal hyperplasia,ADH)病人的病理低估率。分析病人临床及影像学信息,探讨低估的预测因素。方法:回顾性分析2010年1月至2013年2月期间,本中心60例CNB诊断为ADH病人。定义病理低估为CNB是ADH但切除活检诊断是恶性的。以卡方检验、Fisher精确检验和二分类Logistic回归分析病理低估的预测因素。结果:本研究60例CNB诊断为ADH病人的病理低估率为65.0%(39/60)。乳腺X线检查发现恶性征象的微钙化(OR=7.988,95%CI:4.997~12.810,P=0.001)、乳腺X线检查影像报告数据系统(BI-RADS)≥4级(OR=10.875,95%CI:2.747~43.051,P     

A clinicopathological analysis of breast cancer in patients with a family history

A study was conducted to investigate the clinical and pathological characteristics of breast cancer in patients with a family history (FH). Among 4,481 primary breast cancer patients, 394 (8.8%) had families which included two or more breast cancer patients within three generations (FH(+) group). This group was compared with the remaining 3,969 patients (FH(–) group) with the following results: (1) The tumor diameter in the FH(+) group was slightly less than that in the FH(–) group [not significant (NS)], with fewer lymph node metastases (P<0.05); (2) the positive rates for the estrogen receptor were 52% (138/266) and 49% (1,216/2,481), respectively (NS); (3) expression of the c-erbB-2 protein was observed in 14 out of 40 (35%) and 32 out of 100 cases (32%), respectively (NS); (4) the relative risk of bilateral occurrence in the FH(+) group was 1.4, with a 95% confidence interval of 0.9–2.4; (5) the 15-year survival rate was 72% and 60%, respectively, suggesting a better prognosis for the FH(+) group (P<0.01); and (6) multivariate analysis showed that the contribution of FH to postoperative survival was marginal (P=0.07). Factors related to the hormonal environment such as age at menarche (P=0.08) and age at menopause (P=0.08) made a greater but non-significant contribution to the prognosis of the FH(+) group than to that of the FH(–) group. However, further genetic and molecular biological analyses of familial breast cancer are needed in order to clarify the mechanisms of cancer accumulation within families.     

Glutathione S-transferase polymorphisms associated with risk of breast cancer in southern Taiwan

In this study, the genetic polymorphisms associated with breast cancer in southern Taiwan were investigated. Two categories of genes were analyzed: (1) BRCA1, BRCA2, and Rad51, the DNA repair factors involved in homologous recombinational repair; and (2) CYP1A1, COMT, GST, and NAT2, the xenobiotic-metabolizing enzymes (XME) involved in estrogen metabolism. We found that the number of deletions and/or mutations in the GST genes was highly correlated with the occurrence of breast cancer. These data suggest that the GST enzymes, which detoxify the catechol estrogen quinones, are important target molecules for screening in populations at high risk of breast cancer.     

Decreased expression of the DCC gene in human breast carcinoma

Inactivation of the deleted in colon cancer (DCC) gene on chromosome 18 is known to be associated with the tumorigenesis and metastasis of colorectal cancer. In the present study, we investigated the expression of DCC and the c-erbB-2 product in surgical specimens from 45 patients with breast cancer by immunohistochemical staining, and found the expression of DCC to be decreased in 23 (51%) tumors. In 8 years of follow-up, 11 of 22 (50%) patients with DCC-positive staining tumors, and 17 of 23 (74%) patients with DCC-negative tumors developed recurrence. The stratified analysis, according to the status of axillary lymph node metastasis, showed the same tendency. Overexpression of erbB-2 was detected in 13 (29%) of the 45 breast cancer specimens, but there were no differences in the relapse rate between patients with erbB-2 positive and those with erbB-2 negative tumors. Although the individual alteration of DCC or erbB-2 did not possess independent prognostic significance for the prediction of recurrence, patients with tumors having the double alteration of DCC-negative and erbB-2-positive showed adverse relapse-free survival (0.025<P<0.05). These findings suggest that a decrease in DCC expression and erbB-2 overexpression may influence the progression of breast carcinoma.     

NOEY2 mutations in primary breast cancers and breast hyperplasia

PurposeThe NOEY2 gene mutations and protein expression in human breast cancers, adjacent breast tissues and breast benign lesions were analysed to explore the potential correlation between the mutation spectrum and breast cancer development and progression.Experimental designThe promoter, exon and intron regions of NOEY2 gene were amplified by polymerase chain reaction (PCR) with DNA extracted from 50 human breast cancer and corresponding adjacent breast tissues as well as 50 breast benign lesions, respectively. The PCR products were then sequenced and analysed. The effect of mutations on the expression of NOEY2 protein by immunohistochemistry were proven as well.ResultsTwenty-one of 50 (42%) breast cancer mutations were identified in promoter (11 cases) and exon 2 (seven cases on untranslation region and three on coding region) and 17 of 50 (34%) adjacent breast tissues (all were atypical hyperplasia lesions) occurred mutations, including six promoter mutations and 11 exon 2 changes (10 cases on untranslation region and one on coding region). Interestingly, the mutations were identified in both breast cancers and the corresponding adjacent breast tissues collected from the same patient in seven of them. No mutation was identified in all benign breast tissues. Immunohistochemical analysis showed that two of 17 mutational adjacent breast tissue samples were NOEY2 immunoreaction negative, and in all 21 mutations of breast cancers five cases were of loss of NOEY2 expression. All mutations with immunoreaction negative factor were located at promoter and/or exon 2 coding region. NOEY2 gene mutations were not correlated with patient ages, histological types, tumour sizes, histological grades, clinical stages, axillary lymph node metastases or with the condition of hormone receptor (ER, PR) expression and HER2 amplification.ConclusionsThe mutations of human NOEY2 were identified in human breast cancers and the corresponding adjacent breast tissues. The hot mutation spots were its promoter and exon 2 regions, and those occurring at the exon2 coding region and part of the promoter may alter the expression of NOEY2. The presence of NOEY2 mutations in human breast cancer and early-stage lesions indicates that NOEY2 mutations may be partly associated with breast tumourigenesis.     

The contribution of inherited factors to the clinicopathological features and behavior of breast cancer

This review is focused on genetic factors that may influence the development and/or appearance of breast cancer metastases. Over the last decade there have been significant advances in the understanding of genetic predisposition to breast cancer. The first breast cancer predisposing gene to be identified was TP53, and this was followed over the next 5 years by two more genes, BRCA1 and BRCA2, which from a population perspective are much more important than TP53. Other rarer genes have subsequently been identified, but the role of more common, less penetrant genes in breast cancer susceptibility remains unknown. Recent work has shown that breast cancers occurring in women carrying germ-line BRCA1 mutations tend to have clinicopathological features that are usually associated with a poor prognosis, such as high grade, estrogen receptor negative status and somatic TP53 mutations. On the other hand, they are usually ERBB2 negative. Whether or not such tumors are more or less likely to metastasize, and hence be associated with a poor outcome, is currently uncertain and has been the subject of much debate. Here, we outline some of the clinicopathological features of hereditary breast cancer, discuss the prognostic studies that have been performed, and introduce some possible new research directions.     

Genetic analysis of breast cancer progression

At the histological level, breast tumors display a variety of morphologic lesions which suggest the existence of an increasingly aberrant pathway of intermediate steps leading to the invasive primary tumor and its metastatic dissemination. In order to obtain direct evidence for this presumed progression, underlying genetic changes must be identified. Analyses of primary breast tumors have revealed a large number of dominant and recessive gene alterations encompassing several cellular attributes and activities. It is quite likely that some of these alterations are of a causal nature and thus enable the tumor to attain distinctive malignant phenotypes, such as, dysregulated proliferation, invasion, angiogenesis, and ability to metastasize. Considerable heterogeneity has been observed in the sequence of acquisition of these genetic changes, which is substantiated by recent comparative analyses between carefully microdissected preinvasive and invasive tumor. The data are evaluated here in the context of existing models of breast cancer progression. Implications and prospects for translational application to the clinic are also discussed.     

Loss of c-met protooncogene in primary and metastatic sites of breast cancer

Background: It has been proposed that clones of tumor cells acquire higher metastatic potential as a result of specific genetic alterations. This study was designed to determine the role of the c-met protooncogene in systemic spread by comparing the loss of the c-met protooncogene between primary and metastatic breast carcinomas. Methods: Only patients who had not received chemotherapy or radiotherapy in the preceding 6 months were included in this study. Histologically proven malignant tissue was obtained from the primary tumor, involved nodes, and distant metastatic and recurrent tumors of patients with breast carcinomas. Allelic loss of the c-met protooncogene in tumor tissue was determined by Southern blotting using a polymerase chain reaction-generated 347-bp human met-H probe. Restriction digestion was performed usingTaq I andMsp I, with the patient's lymphocyte DNA as controls. Results: Of 52 patients, lymphocyte DNA from 36 patients was heterozygous for the c-met protooncogene (69% informative). Forty-six tumors from these 36 patients were analyzed. Four of 30 primary tumors (13%) showed allelic loss of c-met. Of the nine nodal metastases examined, three (33%) showed allelic loss of the c-met protooncogene. Of seven distant metastatic breast tumors or recurrent disease, two (29%) showed allelic loss (both in patients with skin metastasis in the chest wall). Conclusions: Allelic loss of the c-met protooncogene was detected in both primary (13%) and metastatic sites (31%) of breast cancer. Although a higher proportion of allelic loss of c-met was noted in nodal and distant/recurrent disease, the difference when compared with the primary tumor was not statistically significant. These findings indicate a limited role of the c-met protooncogene in breast cancer metastases.     

Immunohistochemical overexpression of C-erbB-2 in the prognosis of breast cancer

Immunohistochemical c-erbB-2 protein overexpression was detected in 34 of 124 (27.4%) paraffin-embedded breast cancer specimens. Although no difference was seen between the c-erbB-2 positive and negative groups in 5-year disease-free survival, 5-year overall survival was significantly less favorable in the c-erbB-2 positive group. Furthermore, patients graded as having positive c-erbB-2 staining and aneuploid DNA showed significantly poorer survival than those in other categories. The significant prognostic factors, determined by a multivariate analysis, were nodal status and c-erbB-2 overexpression. Our findings therefore suggest that c-erbB-2 expression is a prognostic factor in breast cancer and that it could be useful in the determination of postoperative adjuvant therapy.     

Overexpression ofbax enhances the radiation sensitivity in human breast cancer cells

Bax-a, a splice variant ofbax which promotes apoptosis, is expressed in many kinds of untransformed cell lines and breast tissue, whereas only weak or no expression could be detected in breast cancer cell lines and malignant breast tissue. Human breast cancer MCF-7 cells, which have a weakbax gene expression, were stably transfected with pCX2neobax encoding humanbax and neomycin-resistant genes, and two unique clones (MCF-7/bax-1 and MCF-7/bax-2) were thus generated which expressed different levels ofbax-. Sensitivity to ionizing radiation (IR) was examined and each was more sensitive to IR than the parental MCF-7 cells. The degree of enhancement in radiosensitivity was dependent on the expression level ofbax, and IR was found to induce intranucleosomal DNA fragmentation in stable transfectant but not in parent cells, thus suggesting that this sensitization is due to apoptosis. We suggest that exogenousbax- expression might therefore be one of the factors determining cellular radiosensitivity in MCF-7 breast cancer cells and may potentially have a therapeutic application by enhancing radiation sensitivity in breast cancer cells.     

Carcinoma arising in fibroadenoma of the breast —A case report and review of the literature—

A 47 year old woman with two isolated lumps in her right breast underwent an excisional biopsy and the histological findings of both lesions revealed fibroadenoma with anin situ lobular carcinoma. Patey’s modified radical mastectomy was performed after which careful follow-up was continued. To date, a total 161 cases of carcinoma arising in a fibroadenoma have been reported in the world literature and a review of these literature is given following the case report.