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1.
Aim: To evaluate whether or not transforming growth factor‐beta1 is related to inflammation markers and to intercellular and vascular cell adhesion molecules in patients with stable renal transplantation. Methods: Serum concentrations of transforming growth factor‐beta1, tumour necrosis factor‐alpha, C‐reactive protein and adhesion molecules were analysed in 33 renal transplanted patients, 33 patients with chronic renal insufficiency (matched to the transplanted group for level of renal function), and 33 hypertensives with normal renal function. anova , Student's t‐test and simple regression analysis were used to analyse the data. Results: Transplanted patients showed higher values than hypertensives of transforming growth factor‐beta1, tumour necrosis factor‐alpha, C‐reactive protein and adhesion molecules (P < 0.0001 for all). Renal insufficiency group exhibited higher concentrations of transforming growth factor‐beta1, tumour necrosis factor‐alpha, C‐reactive protein and adhesion molecules than hypertensives (P < 0.0001 for all). Transplanted and renal insufficiency patients had similar blood pressure and renal function levels, and transforming growth factor‐beta1, tumour necrosis factor‐alpha, C‐reactive protein and adhesion molecules were not significantly different. In transplanted and in renal insufficiency groups transforming growth factor‐beta1, adhesion molecules and tumour necrosis factor‐alpha correlated significantly each other and with glomerular filtration rate (P < 0.001 for all). Conclusion: In long‐term renal transplantation inflammation and endothelial activation biomarkers, the pro‐fibrotic cytokine transforming growth factor‐beta1 and kidney function are interrelated. Because of the relevant role that inflammation, organ fibrosis and graft dysfunction may play against renal and cardiovascular survival of graft recipients, a better comprehension of the interactions between these variables is needed.  相似文献   

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Objective: This study was to investigate the invasiveness of pregnancy-induced hypertension (PIH) trophoblast cells and evaluate the effects of IGF-Ⅱand TGF-β1 on cytotrophoblast invasion.Methods: Cytotrophoblast cells from normal and PIH placenta were separated and purified. Cytotrophoblast invasiveness of normal and PIH placenta was measured by in vitro invasion assay. Effects of IGF-Ⅱand TGF-β1 on cytotrophoblast invasion were also studied.Results: In PIH group, cytotrophoblast invasiveness was dramatically decreased. In normal group, trophoblast invasiveness was significantly enhanced by IGF-Ⅱ but inhibited by TGF-β1. Neither IGF-Ⅱ nor TGF-β1 had statistically significant effects on PIH trophoblast invasion.Conclusions: PIH cytotrophoblast invasiveness dramatically decreases as compared to the normal level. IGF-Ⅱand TGF-β1 may play an important role in shallow trophoblast invasion on PIH.  相似文献   

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目的:观察邻苯二甲酸二乙基己酯(DEHP)及代谢产物邻苯二酸-单-2-乙基己酯(MEHP)对幼鼠睾丸组织转化生长因子-β1(TGF-β1)表达和端粒酶活性的影响,探讨DEHP和MEHP损害生精功能可能的机制。方法:生后2周龄的Wistar雄性幼鼠96只,随机分8组,每组12只。随机选择1组行生理盐水[0.9%NS0.2 ml/(kg.d),喂养3周]灌胃,作为正常对照组(NC组);再选1组行环磷酰胺[CTX 100 mg/(kg.d),喂养1周]灌胃,作为阳性对照组(PC组);余各组分别用DEHP、MEHP按低剂量[100 mg/(kg.d),喂养3周]、中剂量[200 mg/(kg.d),喂养2周]、高剂量[300 mg/(kg.d),喂养1周]灌胃制作动物模型。观察不同时期、不同剂量下睾丸组织精子形态变化,光镜下计数精子头部及畸形率;应用免疫组化SABC法及RT-PCR法检查睾丸组织TGF-β1的表达,并测定面密度;ELISA法检查睾丸组织中端粒酶活性。结果:①睾丸组织内精子形态变化:用药组精子数量减少,出现精子断头、无钩、双尾等畸形精子;在光镜下精子计数,与NC组比较,用药各组精子头部显著减少(P<0.05),畸形率增加(P<0.05),但高剂量短时间用药组与低剂量长时间用药组比较,差异无统计学意义(P>0.05)。②睾丸组织TGF-β1的表达变化:NC组低表达,DEHP及代谢产物MEHP染毒各组生精细胞内表达增多,PC组大量表达,阳性细胞呈黄褐色,主要分布于胞膜及胞质。NC组面密度为0.156 0±0.003 5、TGF-β1mRNA为1.51±0.20,PC组面密度为0.534 0±0.003 1、TGF-β1 mRNA为8.43±1.75;用药的DEHP组面密度均值为0.289 0±0.003 6、TGF-β1 mRNA为3.83±1.57,MEHP组面密度均值为0.284 0±0.003 1、TGF-β1 mRNA为3.51±1.41,用药各组与NC组、PC组比较差异有统计学意义(P<0.01),但高剂量短时间用药组与低剂量长时间用药组比较,差异无统计学意义(P>0.05);③睾丸组织中端粒酶活性:与NC组比较,用药各组睾丸组织中端粒酶活性下降(P<0.05),高剂量短时间用药组与低剂量长时间用药组比较,差异无统计学意义(P>0.05)。结论:DEHP及代谢产物MEHP对幼鼠生精功能有明显损害,其损害机制可能与DEHP及代谢产物MEHP诱导睾丸组织TGF-β1的表达水平升高、端粒酶活性降低有关。  相似文献   

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目的:探讨水动力辅助吸脂对自体脂肪移植隆乳患者手术效果、脂肪移植成活率及并发症的影响。方法:选取2015年8月-2018年8月在笔者医院行自体脂肪移植隆乳术的202例患者为研究对象,其中98例接受常规隆乳患者为对照组,104例接受水动力辅助吸脂进行隆乳患者为研究组,记录患者治疗有效率和并发症发生情况。结果:研究组总有效率为100.00%高于对照组的79.59%,差异有统计学意义(χ^2=22.423,P=0.000)。研究组吸脂时间少于对照组,乳房体积增大量、移植脂肪成活率高于对照组,差异有统计学意义(P<0.05)。研究组术后并发症总发生率为1.92%低于对照组的10.20%,差异有统计学意义(χ^2=26.751,P=0.000)。结论:水动力辅助吸脂可降低自体脂肪移植隆乳患者并发症发生率,提高脂肪移植成活率和治疗效果,可在临床推广应用。  相似文献   

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BACKGROUND: This study evaluates the expression of transforming growth factors TGFbeta1, TGFbeta2 and TGFbeta3 in cases of gastric carcinoma and their possible correlation with classic prognostic markers and patient survival. MATERIALS AND METHODS: The study included 110 gastrectomy specimens obtained from equal number of patients with gastric cancer. According to the TNM classification, 7 tumors were identified as being stage I, 33 stage II, 52 stage III, and 18 stage IV, whereas 92 tumors were low-grade and 18 high-grade malignancies. On paraffin sections, the streptavidin-biotin technique using antibodies against TGFbeta1, TGFbeta2, and TGFbeta3 was applied. Morphological and immunohistochemical results were correlated with clinicopathologic parameters. RESULTS: TGFbeta1 was expressed in 78 out of 110 (71%) carcinomas, whereas TGFbeta2 and TGFbeta3 were detected in all tumors examined. Normal gastric mucosal epithelial cells expressed TGFbeta2 and TGFbeta3, but not TGFbeta1. Statistical analysis revealed higher expression of TGFbeta1 in low grade carcinomas (P = 0.009). TGFbeta2 presence was higher in advanced stage tumors (P = 0.008) and was correlated with worse prognosis (P < 0.05). TGFbeta1 expression was related to increased disease-free survival (P < 0.05) while Cox analysis revealed that TGFbeta1 expression constituted an independent prognostic factor. CONCLUSIONS: Gastric carcinoma is related to differential expression of TGFbeta1, TGFbeta2, and TGFbeta3. TGFbeta1 may be implicated in the pathogenesis of the tumors, since it is expressed only in neoplastic tissue. TGFbeta1 is related with an increased disease-free and overall survival constituting an independent prognostic factor. In advanced stages, TGFbeta2 seems to be involved in tumor progression related to worse prognosis.  相似文献   

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BACKGROUND: Dysregulated renal expression of matrix metalloproteinases (MMPs), tissue inhibitors of MMPs (TIMP) and TGF-beta1 contribute to the development of tubulo-interstitial fibrosis characteristic of progressive forms of primary glomerulonephritis (GN). There is little information on the circulating levels of these proteins in human GNs. Here, we assessed whether different histopathological GN types could be associated with distinct plasma patterns of MMPs and regulatory proteins. METHODS: Protein levels of MMP-2, MMP-9, TGF-beta1 and TIMP-1 were measured by ELISA in plasma from venous blood of 108 untreated patients with various types of primary GN defined by kidney biopsy, namely IgAN (n=63), membranous GN (MN, n=26), minimal change nephrotic syndrome (MCNS, n=12) and focal and segmental glomerular sclerosis (FSGS, n=7), and were compared with levels in 50 healthy subjects. Plasma samples were assayed for gelatinolytic activity (zymography). RESULTS: Zymography detected the proforms of MMP-2 and MMP-9. Compared with controls, IgAN patients exhibited a significant, parallel decrease in plasma levels of MMP-2, MMP-9 and TGF-beta1. In MN patients, decreased MMP-9 level contrasted with a high MMP-2 level and a normal TGF-beta1 level. In the MCNS/FSGS group, increased MMP-2 level contrasted with unchanged MMP-9 and decreased TGF-beta1 levels. Plasma concentration of TIMP-1 was elevated in all GN groups. There was no correlation between baseline MMP-2/MMP-9/TIMP-1/TGF-beta1 levels and the degree of renal dysfunction or with progression toward ESRD. CONCLUSIONS: Plasma concentrations of MMP-2, MMP-9 and TGF-beta1 significantly differed between the various histopathological types of primary GNs, thus suggesting the involvement of different underlying mechanisms in the regulation of glomerular and tubulointerstitial fibrosis in these renal diseases.  相似文献   

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目的探索Apert综合征患者中两个常见突变Ser252Trp和Pro253Arg对临床表型影响的差异。方法分别以"Apert and FGFR2"、"Apert综合征和FGFR2突变"为关键词,在PubMed和中国知网中进行检索,从227篇文献中筛选出29篇同时包含FGFR2基因突变和临床表型的文章。本研究的样本量为230例Apert综合征患者,涉及37种临床表型。其中男女比率为1∶1,平均年龄为(8.9±9.6)岁。利用t检验、卡方检验或Fisher精确检验,比较两个突变(Ser252Trp和Pro253Arg)之间临床表型的差异。结果 87%的患者能检测到FGFR2基因上的Ser252Trp和Pro253Arg两个常见突变,低于之前报道的98%。其中伴发腭裂的频率,Ser252Trp突变约为Pro253Arg突变的2.3倍(55%vs 24%,P<0.001);Pro253Arg突变中Ⅲ型并指发生频率显著高于Ser252Trp突变(69%vs 29%,P<0.001);其他临床表型在两个突变中的差异不具有统计学意义。结论本研究通过整合1995年至2017年间的相关文献,发现Apert综合征中两个常见突变的发生频率可能存在一定程度的高估;两个突变之间的表型影响具有细微差异,两者相较,Ser252Trp突变者较常出现腭裂畸形,而Pro253Arg突变则会出现较为严重的并指畸形。  相似文献   

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Aim Colorectal cancer is associated with inflammatory bowel disease. The mechanisms of how different genetic make‐ups of cytokines might influence the individual susceptibility to develop particular types of tumours are still unknown. The authors analysed the association between genetic polymorphisms in cytokine/cytokine receptor genes and the risk of colorectal cancer in a Korean population. Method The authors assessed polymorphisms of the interleukin: IL‐1, IL‐1R, IL‐2, IL‐4, IL‐4R, IL‐10, transforming growth factor (TGF)‐β1, IFN‐γ genes in Korean patients with colorectal cancer (n = 170) and in a normal healthy control group (n = 130) to investigate the association between theses cytokine gene polymorphisms and the risk of colorectal cancer. Results The IL‐4R 1902*T allele was found to be associated with an increased risk of colon cancer (P < 0.01, OR = 2.0) and rectal cancer (P < 0.05, OR = 1.8). The IL‐4R 1902*C allele was associated with a decreased risk of both colon cancer (P < 0.01, OR = 0.51) and rectal cancer (P < 0.05, OR = 0.5). The TFG‐β1 10*T allele was found to be associated with an increased risk of colon cancer (P < 0.00, OR = 2.3) and the TFG‐β1 10*C allele with a decreased risk of colon cancer (P < 0.00, OR = 0.43). Conclusion These results suggest that the genetic polymorphisms of IL‐4R and TGF‐β1 are associated with the risk of colorectal cancer in a Korean population.  相似文献   

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目的 探究血清基质金属蛋白酶11(MMP-11)、转化生长因子-β(TGF-β1)水平在胸主动脉瘤患者中的检测意义。方法 选取我院2020年7月~2020年12月收治的30例胸主动脉瘤患者为研究对象,将其纳入研究组;再以30例健康体检志愿者为对照,将其纳入对照组。对比两组受试者初检时血清MMP-11、TGF-β1表达水平差异,经Pearson相关系数分析胸主动脉瘤患者血清MMP-11与血清TGF-β1水平的相关性;根据病理类型,将研究组患者分为真性动脉瘤组和主动脉夹层动脉瘤组两个亚组,比较其血清MMP-11、TGF-β1水平的差异。结果 研究组血清MMP-11、TGF-β1水平明显高于对照组(P<0.05);胸主动脉瘤患者血清MMP-11与血清TGF-β1水平呈正相关性(P<0.05);真性动脉瘤组患者血清MMP-11、TGF-β1水平明显高于主动脉夹层动脉瘤组(P<0.05)。结论 胸主动脉瘤患者中血清MMP-11表达与TGF-β1调控关系密切,了解MMP-11、TGF-β1表达水平有利于临床防治胸主动脉瘤。  相似文献   

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目的 了解2型糖尿病合并骨质疏松患者其类胰岛素生长因子-1(IGF-1)的变化与骨转换之关系。方法 分别测定2型糖尿病合并骨质疏松组(A组)、2型糖尿病未合并骨质疏松组(B组)、绝经后骨质疏松组(C组)和对照组(D组)的血清IGF-1、总碱性磷酯酶(总AKP)、骨特异碱性磷酸酶(骨AKP)、骨钙素(BGP)、尿吡啶啉(PYD)、尿脱氧吡啶啉(DPD),全段甲状旁腺素(IPTH),并进行组间比较和聚类相关分析。结果 A、C组病例其尿PYD和DPD值明显高于B、D组;而IGF-1水平则A、C组明显低于B和D组。聚类相关性分析表明在2型糖尿病合并骨质疏松组骨密度值与IGF-1关系最为密切,而在绝经后骨质疏松组则主要为绝经时间和骨吸收指标(PYD和DPD)。结论 骨形成减少是2型糖尿病合并骨质疏松的原因之一,而IGF-1的减少可能与2型糖尿病的骨形成减少有关。  相似文献   

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目的探讨黄体生成素(LH)对多囊卵巢综合征(PCOS)患者卵巢黄素化颗粒细胞胰岛素受体底物(IRS)-1和IRS-2 mRNAs及蛋白质表达的影响,其及在卵巢局部胰岛素抵抗中的作用。方法收集行体外受精-胚胎移植(IVF-ET)治疗的11例PCOS患者(PCOS组)和15例排卵正常的输卵管性不育患者(对照组)促排卵后黄素化颗粒细胞行体外培养,分别用不同浓度LH(0、20、200、2,000 mIU/ml)处理细胞48 h,采用逆转录聚合酶链反应(RT-PCR)和免疫印迹法(Western-blot)检测黄素化颗粒细胞IRS-1和IRS-2 mRNAs及蛋白质的表达。结果(1)与对照组比较,PCOS组黄素化颗粒细胞IRS-1 mRNA及蛋白质表达显著增加(P<0.05),IRS-2 mRNA及蛋白质表达显著降低(P<0.05);(2)不同浓度LH作用后,PCOS组黄素化颗粒细胞IRS-1 mRNA及蛋白质的表达显著增加,IRS-2 mRNA及蛋白质的表达变化不明显;对照组则均无显著变化。结论PCOS异常增高的LH可能通过增加黄素化颗粒细胞IRS-1 mRNA及蛋白质的表达参与了患者卵巢局部选择性胰岛素抵抗的发生。  相似文献   

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Objective To compare the effect of insulin-like growth factor-1 receptor (IGF-1R) inhibitor and insulin on renal interstitial macrophage infiltration in mice with type 2 diabetic kidney disease (DKD) mice. Methods Twenty-four male C57BL/6 mice were selected. After 1 week of adaptive feeding, 6 rats were randomly selected as the control group. The other mice were intraperitoneally injected with streptozotocin (30 mg/kg) after 8 weeks of high-fat and high-sugar feeding. After 72 h, the type 2 diabetes mellitus (DM) models were successfully established if random blood glucose was greater than 16.7 mmol/L. After 8 weeks, if the proteinuria of DM mice increased, the DKD models were successful. DKD mice were divided into 3 groups by random number remainder method: DKD group (n=6), DKD+insulin group (insulin group, n=6, subcutaneous injection of 1-2 U/d insulin) and DKD+IGF-1R inhibitor (IGF-1R inhibitor group, n=6, administered with 30 mg?kg-1?d-1 IGF-1R inhibitor). They were continuously treated for 8 weeks. Random blood glucose was tested by glucometer. Blood and urine were collected, and biochemical indicators, such as serum creatinine, urea nitrogen and urine protein were measured by biochemical analyzer. Renal pathological changes were detected by hematoxylin-eosin staining (HE) and periodic acid-schiff staining (PAS). Suppressor of cytokine signaling 2 (SOCS2) mRNA and insulin-like growth factor-1 (IGF-1) mRNA were detected by in situ hybridization. The protein expressions of SOCS2, F4/80, Toll-like receptor 4 (TLR4) and CD68 were detected by immunohistochemistry. Results Compared with the control group, blood glucose, serum creatinine, serum urea nitrogen and urinary protein excretion rate were significantly higher in DKD mice (all P<0.05), and CD68+ cells number, F4/80+ cells number and the expression of TLR4 in the tubulointerstitial of DKD mice were significantly higher (all P<0.05). After intervention with insulin or IGF-1R inhibitor, serum creatinine, serum urea nitrogen and urinary protein excretion rate of DKD mice were significantly reduced (all P<0.05). Insulin intervention could significantly reduce blood glucose in mice (P<0.05), but had no significant effect on macrophages. Although IGF-1R inhibitor did not significantly reduce blood glucose, it could significantly reduce the number of CD68, F4/80 positive cells and the expression of TLR4 protein in renal interstitium of DKD mice (all P<0.05). Compared with the DKD group, insulin intervention significantly reduced the expression of IGF-1 protein and mRNA (both P<0.01), and increased the expression of SOCS2 mRNA and protein (both P<0.01). And the expression of SOCS2 protein was correlated with the number of F4/80+ cells in insulin group (R2=0.8461, P=0.005). However, IGF-1R inhibitors had no significant effect on SOCS2 expression, but had better inhibition of macrophage infiltration. Conclusion IGF-1R inhibitor has a better inhibitory effect on DKD renal interstitial macrophage infiltration than insulin. The mechanism may be related to the fact that IGF-1R inhibitor does not up-regulate SOCS2 expression, whereas insulin up-regulates SOCS2 expression to activate some potential pathways.  相似文献   

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Aim Colorectal cancer is common, accounting for nearly 10% of all cancers. Transforming growth factor‐β1 (TGF‐β1) is a pleiotropic cytokine that has been implicated in the pathogenesis of colorectal neoplasia. The most studied −509C>T polymorphism of TGF‐β1 gene has been associated with various kinds of cancer. This study investigated the association between this genetic variant and the risk and/or progression of colorectal cancer. Method A case–control study was carried out of 150 colorectal cancer cases and 503 healthy controls. DNA was extracted from blood cell nuclear materials, and −509C>T polymorphism in the TGF‐β1 gene promoter was genotyped by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP). Colorectal cancer tissues (n = 70) were obtained from the studied cases for measurement of TGF‐β1 mRNA expression levels. We also assessed the plasma TGF‐β1 levels of cases (n = 88) and healthy subjects (n = 120). Results The TGF‐β1 producer genotype, −509TT, was not associated with an increased risk of colorectal cancer compared with other genotypes. Colorectal cancer patients especially those with a more aggressive disease behaviour were more frequently associated with C allele. Conclusion The results suggest that TGF‐β1 −509C>T polymorphism is not associated with either an increased risk or progression of colorectal cancer.  相似文献   

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BACKGROUND: There is growing evidence describing an association of hK2 and IGFs with cancer. The aim of this study is to investigate the differences in serum levels of hK2 and IGFs in a large group of patients with benign prostatic hyperplasia (BPH) or prostatic carcinoma (CaP) and to examine the value of these variables, as well as their various combinations with PSA, for discriminating between these two clinical entities. METHODS: Human glandular kallikrein 2 (hK2), insulin-like growth factor-1 (IGF-1), free and total PSA concentrations were measured with non-competitive immunological procedures. Receiver operating characteristic (ROC) analysis as well as univariate and multivariate logistic regression analysis were performed to investigate the potential utility of the various markers and their combinations for discriminating between BPH and CaP. RESULTS: hK2 and IGF-1 concentrations were increased in CaP patients, in comparison to BPH patients. hK2/free PSA and free/total PSA ratios (area under the curve, AUC = 0.70) were stronger predictors of prostate cancer than the IGF-1/total PSA ratio (AUC = 0.56) in the group of patients with total PSA <4 microg/L. The hK2/free PSA ratio (AUC = 0.74) was found to have significant discriminatory value in patients with total PSA within the "gray zone" (4-10 microg/L). Multivariate logistic regression models confirmed the observed relationships and identified IGF-1/free PSA and hK2/free PSA as independent predictors of CaP. CONCLUSIONS: hK2/free PSA and IGF-1/free PSA ratios may be useful adjuncts in improving patient selection for prostate biopsy.  相似文献   

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PurposeTo analyze the relationships between background parenchymal enhancement (BPE) of the contralateral healthy breast and tumor response after neoadjuvant chemotherapy (NAC) in women with breast cancer.Materials and methodsA total of 228 women (mean age, 47.6 years ± 10 [SD]; range: 24–74 years) with invasive breast cancer who underwent NAC were included. All patients underwent breast magnetic resonance imaging (MRI) before and after NAC and 127 patients underwent MRI before, during (after the 4th cycle of NAC) and after NAC. Quantitative semi-automated analysis of BPE of the contralateral healthy breast was performed. Enhancement level on baseline MRI (baseline BPE) and MRI after chemotherapy (final BPE), change in enhancement rate between baseline MRI and final MRI (total BPE change) and between baseline MRI and midline MRI (early BPE change) were recorded. Associations between BPE and tumor response, menopausal status, tumor phenotype, NAC type and tumor stage at diagnosis were searched for. Pathologic complete response (pCR) was defined as the absence of residual invasive cancer cells in the breast and ipsilateral lymph nodes.ResultsNo differences were found in baseline BPE, final BPE, early and total BPE changes between pCR and non-pCR groups. Early BPE change was higher in non-pCR group in patients with stages 3 and 4 breast cancers (P = 0.019) and in human epidermal growth factor receptor 2 (HER2)-negative patients (P = 0.020).ConclusionEarly reduction of BPE in the contralateral breast during NAC may be an early predictor of loss of tumor response, showing potential as an imaging biomarker of treatment response, especially in women with stages 3 or 4 breast cancers and in HER2 – negative breast cancers.  相似文献   

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