姐妹同患乳腺癌三例报告

1 病历摘要 例1：姐姐，51岁。2002年发现左乳腺肿块，2004年2月行左乳腺改良根治术，术后病理：小叶性浸润癌。肿块大小：4．0cm×3．5cm×2．5cm，腋淋巴结转移2／11，术后分期T2N1M0ⅡB期，受体实验：ER（-），PR（±），Her-Ⅱ（＋），术后CAF方案（环磷酰胺＋吡柔比星＋5-氟尿嘧啶）化疗1个疗程，由于经济原因停止治疗。妹妹，44岁。2004年7月行右乳腺癌改良根治术，术后病理：左乳浸润性导管癌。     

炎性乳癌误诊 1例

患者，女，３１岁。左侧乳腺肿块伴腋窝淋巴结肿大半年余。查左乳腺外上象限放射状切口疤痕２．５cm，其下方一肿块８cm×８cm，境界不清，质硬，与皮肤粘连，皮肤红肿。皮温高，有触痛，活动度差。同侧腋窝扪及一枚鸽蛋大小淋巴结，有压痛。门诊医师予肿块穿刺，细胞学检查发现癌细胞。追溯病史，患者半年前曾因左乳腺蚕豆大小肿块在门诊行肿块切除。病理报告为乳腺小叶增生症。术后原手术部位红肿硬结，半个月后左腋窝可扪及一枚蚕豆大小淋巴结，有压痛。嗣后半年时间，左乳腺肿块逐渐增大，局部皮肤呈暗红色，左腋窝淋巴结疼痛，在门诊就…     

小细胞肺癌乳腺转移1例

患者,女,37岁.2009年11月行胸部CT示:左肺门肿块,考虑中心型肺癌伴纵隔淋巴结转移.支气管镜病理:小细胞未分化癌.遂行依托泊甙+顺铂方案化疗4周期,并行局部放疗1疗程.2010年5月患者第4周期化疗后无意中发现左乳外上象限肿物,彩超检查示:右侧乳腺平乳头外侧可见0.8 cm×0.4 cm低回声;左侧乳腺外上象限可见1.9 cm×1.6 cm不均质团块,边界不清,呈蟹足状,内可见穿支血流;双侧腋下可见多个低回声,左侧最大1.3 cm ×0.9 cm,右侧腋下最大2.8 cm×1.4 cm.5月27日行左乳肿物切除活检,病理为小细胞未分化癌,结合病史考虑肺癌转移.后患者逐渐出现左乳红肿胀痛,行左侧乳腺放疗及全身化疗后疼痛症状改善不明显.     

谷胱甘肽(阿拓莫兰)致过敏反应1例

患者,女,5 4岁。因发现左乳肿块2月于2 0 0 3年4月2 3日收入我院外科,既往无药物过敏史。体检:左乳腺外上限可触及3cm×3cm大小质硬肿块,边界欠清楚,表面结节状,无压痛,与皮肤及胸肌无明显黏连,左乳皮肤无桔皮样改变,左乳头无溢血溢液,左腋下可及一约2cm×2cm质硬尚可活动淋巴结。入院后左乳肿块穿刺证实为“左乳腺腺癌”;X线及胸部CT提示“左乳癌伴腋窝淋巴结转移,左肺下叶基底段肿块:原发性肺癌,肺转移癌?右肝前叶动脉期异常强化灶,转移可能性大”;B超及腹部CT提示“右侧肾上腺转移癌首先考虑”;ECT检查示“左髂骨代谢活跃”。因不能…     

乳腺腺肌上皮瘤1例

患者,女,66岁,于7个月前发现左乳肿块。自述肿块约黄豆大小,无痛感,无明显增大。查体:双乳对称,皮肤无红肿、溃烂、橘皮样改变及酒窝征,双乳头朝向一致,左乳5点乳晕外2cm触及一肿块,大小1cm×1cm,质中,无压痛,形态较规则,边界不清晰,挤压双乳头无溢液,右乳未触及明显异常,双侧腋窝及锁骨上未触及肿大淋巴结。行乳腺钼靶检查示:左乳片状     

父子乳腺癌

父亲,李××,75岁、因右乳腺发现肿块1年余,近1月生长较快,无疼痛不适。过去未患慢性肝炎及慢性前列腺炎史,也无结核史。体检:右乳腺明显突起,局部可触及4×5cm凸凹不平之质硬肿块。且和乳晕皮肤粘连,边缘清楚,局部皮肤无破溃,水肿。腋淋巴结未触及。左乳腺未见异常,患者因年迈拒作根治术,仅作右乳腺单纯性局部扩大切除术,切除肿块7×10×12cm,病理报告右乳单纯癌。术后患者拒放疗、化疗及去势治疗,于术后10个月死于全身衰竭。儿,李××,54岁,左乳腺下发现肿块3月,无特     

儿童双侧乳腺原发性恶性淋巴瘤1例报告

患者男,13岁。左右乳腺同时长肿物3月,近1个月来左乳增大迅速。体检:左右乳房不对称,左乳明显增大,肿块大小7×6×4cm,尚能活动,表面皮肤紧张,血管扩张呈污红色,略有胀痛。右乳肿块4×3×2cm,活动,局部皮肤正常,左右乳头正常大小,无溢液,体表淋巴结、胸透纵隔淋巴结不肿大,血常规、腹部B超等皆无特殊。以往亦无淋巴瘤病史。于1988年7月在外院作左乳腺肿块活检,诊断为     

乳腺神经内分泌癌2例报告

乳腺神经内分泌癌十分罕见。现对我科于1998-2005年治疗的2例神经内分泌癌进行分析,报道如下。1临床资料例1.女性,40岁,因发现右乳腺肿块2月就诊。查体：右乳腺外上象限可触及一肿块,约1.5cm×1cm×0.5cm大小,质硬,无压痛,活动度欠佳,与皮肤无粘连,挤压乳头无分泌物,腋窝未触及肿大淋巴结。彩超示右乳腺实性占位病变。     

副乳腺癌二例报告

副乳腺在乳腺发育畸形中较常见,但发生于副乳腺的癌很少见,现报告二例.病例1 女性,40岁,已婚.发现右腋下肿块一年,轻度触痛,直径约4cm,肿块与乳腺尾叶无关,右乳房亦未查及肿块.抗炎治疗无效后行手术切除.病理检查见肿块4cm×4cm×3cm,周围附有软组织,肿块切面为灰白、灰黄色,与周围境界不清.镜检见以浸润性导管癌为主,小部分仍为导管内癌,癌边缘可见乳腺小叶结构,且少数导管上皮呈实性增生及不典型增生.术后一周又行乳癌根治术,经详查未见癌     

鲍温病伴乳腺导管浸润癌一例

患者女，38岁。主因“发现左乳、大、乳晕区皮肤改变10年”到我科就诊。10年前患行无意间发现左乳头、乳晕区皮肤改变，无渗液，伴有瘙痒，偶有乳房疼痛，在我院皮肤科病理检查诊断为鲍温病。住乳腺科准备手术治疗，拍乳腺钼靶片“左乳外上方泥沙样钙化”。专科检查：左乳头扁平，左乳头、乳晕区可见皮损，面积约4cm×4cm，表面无渗出，未触及肿块。手术病理检查乳腺组织为：乳腺导管癌早期浸润。遂行左乳癌改良根治术，术后淋巴结未见癌细胞转移，给予辅助化疗。     

Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming

Aim： Prenatal nicotine exposure （PNE） alters the hypothalamic-pituitary-adrenocortical （HPA） axis-associated neuroendocrine metabolic programming in intrauterine growth retardation offspring rats. In this study we aimed to clarify the susceptibility to metabolic diseases of PNE offspring rats fed a high-fat diet. Methods： Maternal Wistar rats were injected with nicotine （1.0 mg/kg, sc） twice per day from gestational day 11 until full-term delivery, and all pups were fed a high-fat diet after weaning and exposed to unpredictable chronic stress （UCS） during postnatal weeks 18-20. Blood samples were collected before and after chronic stress, and serum ACTH, corticosterone, glucose, insulin, total cholesterol, triglyceride and free fatty acids levels were measured. The hypothalamus, pituitary gland and liver were dissected for histological studies. Results： UCS significantly increased the serum ACTH, corticosterone and insulin levels as well as the insulin resistant index without changing the serum glucose, total cholesterol, triglyceride and free fatty acids levels in adult offspring rats without PNE. The body weight of PNE offspring rats presented a typical ＂catch-up＂ growth pattern. PNE not only aggravated the UCS-induced changes in the HPA axis programmed alteration （caused further increases in the serum ACTH and corticosterone levels）, but also significantly changed the glucose and lipid metabolism after UCS （caused further increases in the serum glucose level and insulin resistant index, and decrease in the serum free fatty acids）. The effects of PNE on the above indexes after UCS showed gender differences. Pathological studies revealed that PNE led to plenty of lipid droplets in multiple organs. Conclusion： PNE enhances not only the HPA axis, but also the susceptibility to metabolic diseases in adult offspring rats fed a high-fat diet after UCS in a gender-specific manner and enhances the susceptibility to metabolic diseases in adult offspring rats fed a high-fat diet.     

Hsp90 inhibitor BILBO21 enhances triptolide-induced apoptosis of human T-cell acute lymphoblastic leukemia cells in vitro mainly by disrupting p53- MDM2 balance

Aim： To investigate the effects of BILBO21, an inhibitor of heat shock protein 90 （Hsp90） alone or in combination with triptolide （TPL） on T-cell acute lymphoblastic leukemia （T-ALL） and the mechanisms of action. Methods： Human T-ALL cells line Molt-4 was examined. The cell viability was measured using M]-I- assay. Apoptotic cells were studied with Hoechst 33258 staining. Cell apoptosis and cell cycle were analyzed using flow cytometry with Annexin V/PI staining and PI staining, respectively. The levels of multiple proteins, including Akt, p65, CDK4/6, p18, Bcl-2 family proteins, MDM2, and p53, were examined with Western blotting. The level of MDM2 mRNA was determined using RT-PCR. Results： Treatment of Molt-4 cells with BILBO21 （50-800 nmol/L） inhibited the cell growth in a dose-dependent manner （the IC~ovalue was 384.6 and 301.8 nmol/L, respectively, at 48 and 72 h）. BILBO21 dose-dependently induced Go/G1 phase arrest, followed by apoptosis of Molt-4 cells. Furthermore, BILBO21 increased the expression of p18, decreased the expression of CDK4/6, and activated the caspase pathway in Molt-4 cells. Moreover, BILBO21 （50-400 nmol/L） dose-dependently decreased the phospho-MDM2 and total MDM2 protein levels, but slightly increased the phospho-p53 and total p53 protein levels, whereas TPL （5-40 nmol/L） dose- dependently enhanced p53 activation without affecting MDM2 levels. Co-treatment with BILBO21 and TPL showed synergic inhibition on Molt-4 cell growth. The co-treatment disrupted p53-MDM2 balance, thus markedly enhanced p53 activation. In addition, the co-treatment increased the expression of Bak and Bim, followed by increased activation of caspase-9. Conclusion： The combination of BILBO21 and TPL may provide a novel strategy for treating T-ALL by overcoming multiple mechanisms of apoptosis resistance.     

Stereoselective binding of doxazosin enantiomers to plasma proteins from rats,dogs and humans in vitro

Aim： （＋）Doxazosin is a long-lasting inhibitor of a1-adrenoceptors that is widely used to treat benign prostatic hyperplasia and lower urinary tract symptoms. In this study we investigated the stereoselective binding of doxazosin enantiomers to the plasma proteins of rats, dogs and humans in vitro. Methods： Human, dog and rat plasma were prepared. Equilibrium dialysis was used to determine the plasma protein binding of each enantiomer in vitro. Chiral HPLC with fluorescence detection was used to measure the drug concentrations on each side of the dialysis membrane bag. Results： Both the enantiomers were highly bound to the plasma proteins of rats, dogs and humans [（-）doxazosin： 89.4%-94.3%; （＋）doxazosin： 90.9%-95.4%]. （＋）Doxazosin exhibited significantly higher protein binding capacities than （-）doxazosin in all the three species, and the difference in the bound concentration （Cb） between the two enantiomers was enhanced as their concentrations were increased. Although the percentage of the plasma protein binding in the dog plasma was significantly lower than that in the human plasma at 400 and 800 ng/mL, the corrected percentage of plasma protein binding was dog〉human〉rat. Conclusion： （-）Doxazosin and （＋）doxazosin show stereoselective plasma protein binding with a significant species difference among rats, dogs and humans.     

三阴性乳腺癌的生物学特征和治疗策略

三阴性乳腺癌（triple negative breast cancer,T N B C）是指雌激素受体（E R）、孕激素受体（P R）和人表皮生长因子受体2（Her-2）均为阴性的乳腺癌。这类乳腺癌占乳腺癌病理类型的10%-23.8%^[1-5],     

美国与欧洲上市后药品安全风险管理进展概述

近10年来,美国食品药品管理局（FDA）、欧洲药品管理局（EMA）及其他相关单位,对上市后药品安全性监测日益重视,在这一领域取得了显著进展,并且制定了一系列新规定。     

芳香化酶抑制剂的耐药机制

内分泌治疗耐药其实是一个很古老的话题,从最经典的EBCTCT试验发现,应用他莫西酚（tamoxifen,TAM）5年,乳腺癌的复发率为15%,随访15年中,有33.2%的患者出现复发^[2,3]。     

外阴部异位乳腺纤维腺瘤病例报道与分析

乳腺纤维腺瘤为青年女性的常见病,多发病,是乳腺良性肿瘤中最为多见的一种,好发于乳腺外上象限｜1,引,发生于其他部位的异位乳腺纤维腺瘤十分少见。最近,我院收治了一例外阴部异位乳腺纤维腺瘤患者,现将其临床资料进行报道,并予以总结分析如下。     

Sodium hydrosulfide alleviates lung inflammation and cell apoptosis following resuscitated hemorrhagic shock in rats

Aim： To investigate the protective effects of hydrogen sulfide （H2S） against inflammation, oxidative stress and apoptosis in a rat model of resuscitated hemorrhagic shock. Methods： Hemorrhagic shock was induced in adult male SD rats by drawing blood from the femoral artery for 10 min. The mean arterial pressure was maintained at 35-40 mmHg for 1.5 h. After resuscitation the animals were observed for 200 min, and then killed. The lungs were harvested and bronchoalveolar lavage fluid was prepared. The levels of relevant proteins were examined using Western blotting and immunohistochemical analyses. NariS （28 pmol/kg, ip） was injected before the resuscitation. Results： Resuscitated hemorrhagic shock induced lung inflammatory responses and significantly increased the levels of inflammatory cytokines IL-6, TNF-a, and HMGB1 in bronchoalveolar lavage fluid. Furthermore, resuscitated hemorrhagic shock caused marked oxidative stress in lung tissue as shown by significant increases in the production of reactive oxygen species H202 and OH, the translocation of Nrf2, an important regulator of antioxidant expression, into nucleus, and the decrease of thioredoxin I expression. Moreover, resuscitated hemorrhagic shock markedly increased the expression of death receptor Fas and Fas-ligand and the number apoptotic cells in lung tissue, as well as the expression of pro-apoptotic proteins FADD, active-caspase 3, active-caspase 8, Bax, and decreased the expression of Bcl-2. Injection with NariS significantly attenuated these pathophysiological abnormalities induced by the resuscitated hemorrhagic shock. Conclusion： NariS administration protects rat lungs against inflammatory responses induced by resuscitated hemorrhagic shock via suppressing oxidative stress and the Fas/FasL apoptotic signaling pathway.