阳和汤加减联合西医止痛药治疗骨转移癌疼痛的临床观察

【目的】观察阳和汤加减配合西医止痛药治疗骨转移癌疼痛的临床疗效及对便秘和患者生活质量的改善情况。【方法】将200例癌性疼痛患者按入院顺序随机分为治疗组和对照组各100例。对照组给予盐酸羟考酮控释片口服治疗,治疗组在对照组的基础上加用阳和汤加减治疗,2组均以21 d为1个周期,共观察1个周期。治疗前后进行疼痛评价,同时观察患者便秘及生活质量的改善情况。【结果】（1）在止痛效果方面,治疗组总有效率为95．0%,对照组为81．0%;治疗组的止痛效果优于对照组(P<0．05)。（2）在便秘改善情况方面,治疗组有92例出现便秘,其中88例有不同程度缓解,便秘改善有效率为95．7%;对照组有91例患者出现便秘,均不能自行缓解;治疗组对便秘的改善作用优于对照组（P<0．05）。（3）在生活质量改善方面,治疗组总有效率为89．0%,对照组为71．0%,治疗组疗效优于对照组(P<0．05)。（4）在不良反应方面,2组各有2例患者出现药物引起的肝功能轻度损害,经对症处理后均消失。【结论】阳和汤加减联合西医止痛药治疗癌性疼痛具有很好的减毒增效作用。     

食管癌根治性放疗191例疗效分析

目的:分析191例食管癌根治性放疗患者的长期疗效及其预后影响因素。方法:2009年5月至2012年5月首程接受根治性放疗的191例食管癌患者,依据《非手术治疗食管癌的临床分期标准(草案)》分为各个亚组,观察其近期疗效、生存率、局控率、治疗失败原因、死亡原因,用Kaplan-Meier法计算生存率及局控率,Log-rank法进行单因素预后分析,Cox法进行多因素预后分析。结果:随访率为99.5%。随访时间满2 a者61例,满3 a者24例。全组1、2、3 a局部控制率分别为83.2%、62.3%、48.7%,生存率分别为64.9%、36.6%、30.2%,中位生存期16个月。单因素分析显示病变部位、病变长度、最大病变横径、临近组织是否受侵、T分期、N分期、TNM分期与预后密切相关(χ2=7.881、12.756、5.491、9.972、18.825、11.739和14.353,P<0.05),Cox模型多因素预后分析结果显示T、N分期为影响总生存的因素(χ2=5.080、6.018,P<0.05)。结论:分期早晚仍是食管癌根治性放疗的经典预后影响因素,非手术治疗分期对判断预后有参考价值,治疗失败的主要原因是局部复发和未控,其次是远处转移。     

甲状腺髓样癌的外科治疗进展

甲状腺髓样癌(medullary thyroid carcinoma,MTC)为相对少见的恶性肿瘤之一,约占所有甲状腺癌的3%~5%,其组织来源为甲状腺滤泡旁细胞。MTC细胞能够产生降钙素(calcitonin)和其他具有内分泌活性的物质,其临床表现可有腹泻、潮红等类癌综合征或内分泌失调的表现,治疗上主张甲状腺全切除术,故不同于其他类型甲状腺癌。本文就MTC的外科治疗进展作一综述。     

HIF-1α、M ACC1、FOXO4与胃癌病理和预后的关系

目的：探究低氧诱导因子-1（HIF-1α）、结肠癌转移相关基因1（MACC1）和转录因子FOXO4在胃癌中的表达及与胃癌的临床病理特征和预后的关系。方法收集2006年12月至2008年5月安徽医科大学第一附属医院外科手术切除的原发性胃癌石蜡包埋标本110份,和距癌灶边缘5 cm以上且经病理检查确定为正常胃黏膜的癌旁组织标本46份,进行 HIF-1α、M ACC1和FOXO4蛋白免疫组织化学检测。统计标本来源患者的信息进行 HIF-1α、M ACC1和FOXO4蛋白与胃癌及转移淋巴结相关性分析。用Kaplan-M eier法分析术后胃癌患者的5年生存率和用Cox法进行生存率多因素回归分析。结果免疫组织化学法检测发现HIF-1α（P＜0．001）和MACC1（P＜0．001）蛋白在癌灶细胞中的表达明显高于癌旁组织,而FOXO4蛋白在癌灶细胞中的表达明显低于癌旁组织（P＜0．001）。统计分析发现细胞分化程度越低、浸润程度越大、伴随着淋巴结转移和TNM分期越高,HIF-1α和MACC1的阳性表达也越高,而FOXO4因子的表达降低。胃癌组织中3种因子的表达存在显著相关性。 HIF-1α、MACC1和FOXO43种因子的表达明显影响患者术后5年的生存率,而且是决定胃癌患者预后的独立因素。结论 HIF-1α、M ACC1和FOXO4在胃癌组织中存在异常表达,与胃癌的临床病理特征和胃癌患者的预后密切相关。     

c-cbl 基因沉默对卵巢癌 SKOV3细胞增殖和侵袭的影响

目的：探讨 c-cbl 在卵巢癌的表达及其对卵巢癌细胞增殖、侵袭的影响。方法通过免疫组织化学法（S-P 法）检测c-cbl 蛋白在卵巢癌组织的表达;EdU 检测卵巢癌 SKOV3细胞沉默 c-cbl 基因后细胞增殖能力变化;Transwell 检测卵巢癌 SK-OV3细胞侵袭能力;Western blot 检测 P21蛋白和 P53蛋白的表达。结果 c-cbl 蛋白在卵巢癌中表达位于细胞质,在卵巢癌中, c-cbl 蛋白呈强阳性表达,在正常卵巢组织 c-cbl 蛋白呈弱阳性或者阴性表达。与正常卵巢组织比较,c-cbl 蛋白在卵巢癌表达明显增高（P＜0．05）;c-cbl 蛋白在卵巢癌的表达与 FIGO 分期相关（P＜0．05）;沉默卵巢癌 SKOV3细胞 c-cbl 基因后,卵巢癌细胞增殖能力和侵袭能力降低（P＜0．05）;沉默 c-cbl 基因后,P21和 P53蛋白表达上调（P＜0．05）。结论 c-cbl 蛋白在卵巢癌表达上调,沉默 c-cbl 基因可能与上调 P21和 P53蛋白有关。     

Review of spectral domain enhanced depth imaging optical coherence tomography of tumors of the choroid

Background:Spectral domain enhanced depth imaging optical coherence tomography (EDI-OCT) can provide anatomic localization of intraocular tumors.Aims:The aim was to identify topographical and intrinsic patterns of choroidal tumors on EDI-OCT.Results:Using EDI-OCT, choroidal nevus displayed a smooth, dome-shaped topography with overlying retinal pigment epithelium alterations, drusen, and occasional subretinal cleft demonstrating photoreceptor loss. Small choroidal melanoma showed smooth, moderately dome-shaped topography, commonly with overlying shallow subretinal fluid that often depicted “shaggy” photoreceptors. Choroidal metastasis showed a minimally “lumpy, bumpy” surface topography and with overlying subretinal fluid and shaggy photoreceptors. Choroidal hemangioma showed a smooth, dome-shaped topography, with expansion of the affected small, medium, and large choroidal vessels. Choroidal lymphoma showed varying topography with increasing tumor thickness as “flat, rippled, or undulating (seasick)” surface. Choroidal osteoma displayed a smooth undulating surface with visible intralesional horizontal lines suggestive of bone lamellae and occasional horizontal and vertical tubules with intralesional “spongy” flecks. Choroidal melanocytosis appeared as uniformly thickened choroid with increased stromal density surrounding the normal choroidal vascular structures.Conclusions:Enhanced depth imaging-OCT can depict characteristic patterns that are suggestive of various choroidal tumors.     

Pro-migratory actions of the prostacyclin receptor in human breast cancer cells that over-express cyclooxygenase-2

Metastasis is the major cause of death in cancer patients. Elevated expression of cyclooxygenase-2 (COX-2) is observed in many human cancers and over-production of downstream prostaglandins (PGs) has been shown to stimulate metastasis. A role for increased PGE₂ production has been proposed, but whether other PGs contribute is currently unclear. In this study the pro-migratory actions of individual PGs were evaluated in MDA-MB-468 breast cancer cells that stably over-expressed COX-2 (MDA-COX-2 cells); cell migration was quantified using 3D-matrigel droplet assays. Inhibition of the prostacyclin and PGE synthases, but not alternate prostanoid synthases, prevented the increase in MDA-COX-2 cell migration produced by arachidonic acid (AA); direct treatment of cells with the stable prostacyclin analogue cicaprost also promoted migration. Pharmacological antagonism and knockdown of the IP receptor decreased cell migration, while antagonists of the alternate DP, EP2, FP, and TP prostanoid receptors were inactive. In support of these findings, activation of the IP receptor also enhanced migration in the MDA-MB-468, MDA-MB-231 and A549 cell lines, and IP receptor knock-down in MDA-COX-2 cells decreased the expression of a number of pro-migratory genes. In further studies, the prostacyclin/IP receptor and PGE₂/EP4 receptor pathways were found to be functionally independent and the inhibition of phosphatidylinositol 3-kinase (PI3K) and p38 mitogen-activated protein kinase (MAPK) selectively impaired the IP-receptor-dependent migration in MDA-COX-2 cells. Taken together, the prostacyclin/IP/PI3K-p38 MAPK axis has emerged as a novel pro-migratory pathway in breast cancer cells that over-express COX-2. This information could be utilized in novel treatment strategies to minimize tumor metastasis.     

Blastic Plasmacytoid Dendritic Cell Neoplasm: Single Center Experience on a Rare Hematological Malignancy

PurposeBlastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and poor prognostic hematological malignancy. There is still no standard treatment established for BPDCN patients. We aim to summarize the main clinical, biological features and treatment of 9 BPDCN patients.MethodsNine patients with BPDCN who had been diagnosed between July 2008 and December 2018 in Ankara University School of Medicine, were retrospectively evaluated.ResultsAll patients (n = 9) were male, median age was 64 (21–80). Five patients (55.6%) had bone marrow infiltration, 5 patients (55.6%) cutaneous lesions, 6 patients (66.7%) lymph node involvement, 2 patients (22.2%) central nervous system involvement and 2 patients (22.2%) spleen involvement at time of diagnosis. Complex karyotype was observed in 2 patients. CHOP was given to 5 patients (55.6%), hyper-CVAD to 2 patients (22.2%), fludarabine, cyclophosphamide and mitoxantrone to 1 patient (11.1%) and cyclophosphamide, etoposide, methylprednisolone to 1 patient (11.1%) as first line chemotherapy. Four patients (44.4%) underwent allogeneic hematopoietic stem cell transplantation (AHSCT) in complete remission (CR) 1. Venetoclax was given to a transplant ineligible patient who had skin and lymph node involvement, with the off-label use. The median follow-up time was 15.9 months (3–48.6 months). Estimated median overall survival was 15.9 + 1.6 (95% CI 12.7–19.1) months.ConclusionIntensive induction therapies followed by AHSCT in CR seems to be best approaches for patients with BPDCN. Thus, more effective treatment strategies particularly targeted therapies should be warranted to improve the survival of patients with this rare disease.