艾日布林治疗相关的皮肤毒性二例

甲磺酸艾日布林(eribulin mesylate,以下简称艾日布林)是一种软海绵素类微管动力学抑制剂,通过阻止细胞分裂的微管动力学发挥作用.艾日布林对肿瘤微环境具有独特的作用,增加肿瘤核心的血管灌注和通透性,降低乳腺癌细胞的迁移能力 [1].法国一项多中心观察研究显示,艾日布林与其他化疗比较可提高乳腺癌患者三线和四线...     

亚砷酸治疗复发性APL并发毛细血管渗漏综合征1例

1病例介绍 患者,男,48岁,工人.因低热、全身皮肤出血点、齿龈渗血于2002年8月10日入院,经临床、血、骨髓象、PML/RARα基因检测确诊为急性早幼粒细胞白血病(APL),以全反式维A酸(ATRA)口服治疗48 d达完全缓解(CR),缓解后定期进行强化化疗2次,此后不定期在门诊检查.随访至2004年5月12日,患者自感全身乏力,门诊血象检查早幼粒细胞0.52,Plt46×109/L,考虑APL复发,1个月后患者全身出血倾向加重,伴发热、血尿,于2004年6月20日入院治疗.     

注射用重组人白介素-11致毛细血管渗漏综合征1例

毛细血管渗漏综合征(capillary leak syndrome,CLS)是一种突发、可逆性的毛细血管高渗透性疾病,主要表现为全身皮肤、黏膜进行性水肿,浆膜腔积液,血压及中心静脉压降低,低氧血症,甚至呼吸、循环衰竭,严重时可出现多器官功能衰竭,病死率较高[1]。引起CLS的病因较多,其中生物制剂可引起肿瘤患者出现CLS。为提高对该并发症的认识,现     

生物制剂白介素11致严重毛细血管渗漏综合征死亡一例

患者,男性,64岁,小细胞肺癌合并肝转移,曾行卡铂、VP-16化疗6个周期,肝转移灶消失,因纵隔淋巴结增大,更改化疗方案:泰素、奈达铂化疗两周期,纵隔淋巴结继续增大。调整治疗方案:开普拓240mg单药化疗,同时行纵隔部位放疗,患者第二次化疗后三周,因血小板下降,应用白介素11(巨和粒)     

艾立布林治疗晚期乳腺癌疗效和安全性的多中心真实世界研究

目的探讨真实世界艾立布林治疗晚期乳腺癌的疗效及安全性。方法选取2019年12月至2020年12月就诊于北京市朝阳区三环肿瘤医院、山东省肿瘤医院、北京大学肿瘤医院、包头市肿瘤医院、中国医科大学附属盛京医院及中国医学科学院肿瘤医院的晚期乳腺癌患者。生存分析采用Kaplan-Meier法和Log rank检验, 多因素分析采用Cox回归模型。结果 77例患者中位无进展生存时间为5个月, 客观缓解率(ORR)为33.8%, 疾病控制率(DCR)为71.4%。三阴性乳腺癌患者ORR为23.1%, DCR为57.7%;Luminal型乳腺癌患者ORR为40.0%, DCR为77.8%;人表皮生长因子受体2过表达型乳腺癌患者ORR为33.3%, DCR为83.3%。艾立布林为一线至二线治疗患者的ORR为50.0%, DCR为66.7%;三线至四线治疗患者的ORR为29.4%, DCR为76.5%;五线至十一线治疗患者的ORR为28.6%, DCR为71.4%。艾立布林单药治疗组患者的ORR为40.0%, DCR为66.0%;联合化疗或靶向治疗组患者的ORR为22.2%, DCR为81.5%。在辅助治...     

股骨毛细血管扩张型骨肉瘤1例

毛细血管扩张型骨肉瘤很少见,我院收治1例,现报告如下:患者男,18岁.20天前因跑步后出现左大腿中下段隐痛,跛行,局部无红肿,休息一周后好转,3天前夜间睡眠时突感左大腿中下段剧痛,不能下地行走.入院体检:左大腿中下段轻度肿胀,皮肤不红,皮温较对侧略高,局部深压痛,左膝不能完全伸曲.白细胞计数为7.5×10~9/L.X片仅见左股骨中下段薄层骨膜反应.初诊为骨膜炎、骨髓炎.10天后患者下床时不慎摔倒,当即左大腿下段剧痛、畸形,不能站立.X线片示左股骨下段骨折、错位,骨膜反应较前片更加明显,并掀起、断裂,骨折断端及邻近骨质片未见明显吸收破坏征象.手术所见骨折周围肌肉淤血较多,软组织机化,色泽灰暗,肌肉质地较硬,水肿明显.断端罱有大量骨膜反应.断端骨髓腔骨小梁色泽灰黄,骨皮质变薄,疏松呈灰白,     

Poland综合征合并乳腺癌一例

Poland综合征是一种罕见的先天畸形症候群,包括胸大肌、胸小肌缺如或发育不良,同侧乳腺发育不良或缺如,同侧胸廓发育不良,同侧上肢发育不良或缺如。Poland综合征合并恶性肿瘤的病例文献曾有报道,但是合并乳腺癌的病例并不多见,笔者报告1例本院收治的Poland综合征合并乳腺癌患者。     

艾立布林用于多线治疗后晚期乳腺癌5例报告

近年来,转移性乳腺癌患者的生存率有所提高,以蒽环类、紫杉醇、吉西他滨、卡培他滨、长春瑞滨、铂类为基础的化疗方案延长了乳腺癌患者的总生存期(overall survival,OS)[1].但晚期转移性乳腺癌患者长期生存率仍然不佳,因此,需要更加有效的治疗手段来改善患者的生活质量并延长生存期[2].艾立布林是一种非紫杉烷类...     

Gemcitabine-induced systemic capillary leak syndrome

Systemic capillary leak syndrome (SCLS) is a rare disorder with ahigh mortality rate, characterized by rapidly developing edema, weightgain and hypotension, hemoconcentration and hypoproteinemia. Thissyndrome is caused by sudden, reversible capillary hyperpermeabilitywith a rapid extravasation of plasma from the intravascular to theinterstitial space. Even though SCLS has been suggested to be thepathogenic mechanism for the pulmonary toxicity of gemcitabine (GCB), anew deoxycytidine analogue with structural similarities to cytosinearabinoside, a direct correlation between GCB and SCLS has never beenreported. We describe a case of repeated SCLS after GCB administrationin a 51-year-old male with locally-advanced non-small-cell lung cancertreated with a combination of cisplatin and GCB. The detection ofGCB-induced SCLS supports the hypothesis that SCLS could be thepathogenic way of GCB pulmonary toxicity. This finding can help tobetter understand and treat the potentially deadly GCB-related acuterespiratory distress syndrome that is being recognized.     

Role of nitric oxide in IL-2 therapy-induced capillary leak syndrome

Nitric oxide (NO) is a potent short-lived and short range bioactive molecule, which plays a key role in physiological and pathological processes including inflammation and cancer. Detrimental effects of excessive NO production during septic shock have been well recognized. We tested the hypothesis that capillary leak syndrome following systemic interleukin-2 (IL-2) therapy resulted from a cascade of events leading to the induction of NO which, directly or indirectly, injured capillaries and caused fluid leakage. Our results provided the first direct evidence that the induction of active NO synthase (NOS) leading to the overproduction of NO is instrumental in IL-2-induced capillary leakage in mice and that successful blocking of this overproduction with chronic oral administration of NOS inhibitors can mitigate this leakage without interfering with the beneficial antitumor effects of IL-2 therapy. NO blocking agents can, in fact, improve IL-2-induced antitumor effector cell activation, as well as tumor regression. In our studies, NO blocking agents alone reduced the growth and metastasis of a murine mammary carcinoma, at least in part, by mitigating the invasion and angiogenesis-stimulating role of tumor-derived NO. Thus, NOS inhibitors may be useful in treating certain tumors and serve as valuable adjuncts to systemic IL-2 based immunotherapy of cancer and infectious diseases.     

Breast cancer in a patient with McCune-albright syndrome

We treated a patient with breast cancer associated with McCune-Albright syndrome. A 40-year-old woman with a history of precocious puberty visited our hospital complaining of a mass in the upper lateral quadrant of the right breast. Although bone scintigraphy revealed multiple high uptake of^99mTc, plain X-ray demonstrated ground-glass appearance, suggesting fibrous dysplasia rather than bone métastases. Serum levels of tumor markers and alkaline phosphatase were within the normal range. Breast cancer associated with McCune-Albright syndrome was diagnosed, and she subsequently underwent breast conserving surgery, excision of abdominal wall myxoma and bone biopsy of the left clavicula. The bone lesion was histologically confirmed as fibrous dysplasia. Although McCune-Albright syndrome is a rare clinical entity, it should be considered as a possible differential diagnosis of bone metastasis in patients with breast cancer. As recent molecular studies have suggested genetic mutations in McCune-Albright syndrome, this syndrome may possibly predispose patients to breast cancer.     

Early breast cancer following treatment of myelodysplastic syndrome: Report of a case

A 45-year-old woman was admitted to our hospital complaining of a mass in her left breast. She had previously been diagnosed with myelodysplastic syndrome (MDS), a type of refractory anemia, based on bone marrow findings and chromosome analysis. She received a preoperative transfusion of fresh packed platelets and a recombinant human granulocyte colony-stimulating factor (rhG-CSF) injection. Left partial mastectomy and axillary lymph nodes dissection were performed to treat early breast cancer. Postoperatively, prophylactic radiotherapy of the residual breast and administration of medroxyprogesterone acetate (MPA) were performed because the tumor tissue was positive for progesterone receptors. She has remained clinically stable, with no evidence of recurrence, for more than three years to date. We report a rare case of breast cancer with MDS, treated with breast-conserving therapy. The strategy of pre- or postoperative platelet transfusion, rhG-CSF injections, and hormonal therapy (AAPA) appears to be suitable treatment for progesterone receptor (PgR)-positive breast cancer patients with AADS.     

乳腺癌术后放疗引起放射性肺损伤的临床分析

目的 分析乳腺癌术后放疗引起放射性肺损伤的临床相关因素,为优化放疗计划提供参考。方法 对96例术后放疗的乳腺癌患者进行回顾性分析,观察手术方式,术后放疗的照射野、照射剂量,辅助化疗的种类、年龄、肺部原有基础疾病与放射性肺损伤发生率的关系。结果 96例乳腺癌患者中发生放射性肺损伤19例,放射性肺损伤的发生与照射野、照射剂量有关(P＜0.05)。结论 术后放疗照射野的设计和放疗剂量的增加是放射性肺损伤发生率增高的主要因素。     

Eribulin mesylate reduces tumor microenvironment abnormality by vascular remodeling in preclinical human breast cancer models

Eribulin mesylate is a synthetic macrocyclic ketone analog of the marine sponge natural product halichondrin B and an inhibitor of microtubule dynamics. Some tubulin‐binding drugs are known to have antivascular (antiangiogenesis or vascular‐disrupting) activities that can target abnormal tumor vessels. Using dynamic contrast‐enhanced MRI analyses, here we show that eribulin induces remodeling of tumor vasculature through a novel antivascular activity in MX‐1 and MDA‐MB‐231 human breast cancer xenograft models. Vascular remodeling associated with improved perfusion was shown by Hoechst 33342 staining and by increased microvessel density together with decreased mean vascular areas and fewer branched vessels in tumor tissues, as determined by immunohistochemical staining for endothelial marker CD31. Quantitative RT‐PCR analysis of normal host cells in the stroma of xenograft tumors showed that eribulin altered the expression of mouse (host) genes in angiogenesis signaling pathways controlling endothelial cell–pericyte interactions, and in the epithelial–mesenchymal transition pathway in the context of the tumor microenvironment. Eribulin also decreased hypoxia‐associated protein expression of mouse (host) vascular endothelial growth factor by ELISA and human CA9 by immunohistochemical analysis. Prior treatment with eribulin enhanced the anti‐tumor activity of capecitabine in the MDA‐MB‐231 xenograft model. These findings suggest that eribulin‐induced remodeling of abnormal tumor vasculature leads to a more functional microenvironment that may reduce the aggressiveness of tumors due to elimination of inner tumor hypoxia. Because abnormal tumor microenvironments enhance both drug resistance and metastasis, the apparent ability of eribulin to reverse these aggressive characteristics may contribute to its clinical benefits.