Giant cell reparative granuloma of posterior ethmoid: A case report

Giant cell reparative granuloma (GCRG) is an unusual, nonneoplastic fibrous lesion affecting maxillary and mandibular bones and only rarely, the cranial bones. Giant cell reparative granuloma of the posterior ethmoid is exceedingly rare. To the best of our knowledge none of such case has been previously reported. Being a soft fleshy lesion of bone, if tends to have a benign course, not aggressive, it often recurs following incomplete excision. We report the case of a woman with a GCRG of right posterior ethmoid. We discuss the clinical picture, differential diagnosis, histologic evaluation and appearance on computed tomography.     

ｍｉＲＮＡ：新一代肿瘤生物标志

微小ＲＮＡ（ｍｉＲＮＡ）是一类小分子非编码ＲＮＡ,能够在转录后水平调控蛋白合成,几乎参与了调控细胞活动的各个环节。到目前为止,ｍｉＲＮＡ给予人们一个新的视野理解肿瘤的发生发展,展示了作为肿瘤标志物以及肿瘤治疗靶点的巨大潜能。作者从肿瘤标志物的角度,归纳了ｍｉＲＮＡ用于肿瘤诊断、药物疗效预测以及预后判断所获得的成就,并对其临床应用前景作了展望。     

尼洛替尼:一种新的抗肿瘤靶向药物

分子靶向药物伊马替尼能够与Bcr-Abl激酶结合而成功治疗慢性粒细胞性白血病,然而该激酶的点突变常导致伊马替尼耐药,使治疗失败.尼洛替尼是一种比伊马替尼更有效的新型Bcr-abl激酶抑制剂.在Ⅰ期临床研究中,119例伊马替尼耐药的患者接受了不同剂量水平的尼洛替尼,最大耐受剂量为600mg,每日二次口服.推荐Ⅱ期研究的剂量为400mg,每日二次.最常见的不良反应是骨髓抑制、皮疹、脂肪酶和胆红素升高.在慢性期、加速期、急变期的慢性粒细胞性白血病患者中,分别有92%(53%)、72%(48%)、39%(27%)获得了血液学/细胞遗传学缓解.联合应用几种不同的Bcr-Abl激酶抑制剂有相加或协同作用,如伊马替尼、尼洛替尼和达沙替尼,并有可能延迟或预防耐药的出现.一些研究试图通过鉴定病人的突变类型而预测这些药物的效果.     

A case of oxaliplatin-related posterior reversible encephalopathy syndrome

We report the first case of oxaliplatin-related posterior reversible encephalopathy syndrome (PRES) in the medical literature. A 19-year-old woman with metastatic adenocarcinoma of the rectum received modified FOLFOX (5-fluorouracil/oxaliplatin) chemotherapy. Ten days after the fourth treatment, she presented to the hospital with seizures and altered mental status. Magnetic resonance imaging of the brain demonstrated hyperintensity in the white matter of the posterior hemispheres consistent with PRES. Herein, we briefly review the PRES syndrome and its management.     

抗癌治疗新靶标——去整合素金属蛋白酶10

去整合素金属蛋白酶(ADAM)10基因是ADAM家族成员,其相应的细胞膜蛋白含有解聚素域和金属蛋白酶域,在细胞黏附、细胞融合、细胞迁移、膜蛋白脱落和分解等生物学行为中起作用.ADAM10蛋白在多种肿瘤中有过表达现象,能与数种黏附分子和癌症信号分子相互作用,促进肿瘤的侵袭和转移.以调控ADAM10的表达为靶目标,抑制肿瘤细胞的转移和侵袭,有望成为肿瘤治疗的新策略.

Abstract：

Gene ADAM10 (a disintegrin and metalloproteinase 10) is a member of ADAMs gene family. The corresponding membrane protein contains a disintegrin domain and a metalloproteinase domain. It is involved in various biological events such as cell adhesion, cell fusion, cell migration, and membrane protein shedding and proteolysis. ADAM10 protein is overexpressed in many tumors, which interacts with adhesion molecules and critical signaling molecules associated with cancer development and tumor progression, and promotes tumor invasion and metastasis. Regulating the expression of ADAM 10 can inhibit tumor invasion and metastasis , which may become a new strategy for anticancer therapy.     

后路脊柱截骨术与牵引辅助后路广泛松解术治疗重度脊柱畸形的比较研究

目的：比较后路脊柱截骨术和牵引辅助后路广泛松解术治疗重度脊柱畸形的围手术期并发症和初步疗效。方法回顾性比较研究我科收治的29例重度脊柱畸形患者资料。2013年8月至2014年6月,行牵引辅助后路广泛松解术矫形患者（牵引组）12例;2012年6月至2013年8月,行后路脊柱截骨手术矫形患者（对照组）17例。牵引组术前主弯Cobb’s角平均为111.8°,对照组平均为115.2°;牵引组术前最大后凸角度平均为113.3°,对照组为118.5°。比较两组间术后90天内的并发症发生率以及临床疗效。结果两组术前平均年龄、性别比、体重指数、主弯角度、主弯柔韧度、最大后凸角差异无统计学意义。手术时间,牵引组和对照组分别为（322.1±102.5）min和（426.3±100.4）min（P＝0.012）;术中出血量,牵引组和对照组分别为（1241.7±999.5）ml和（2300.0±1449.1）ml（P＝0.040）;置钉密度,牵引组和对照组分别为（58.0±16.2）%和（77.4±13.1）%（P＝0.001）;而围手术期并发症,牵引组和对照组分别为16.7%和58.8%（P＝0.049）;两组比较,牵引组显著小于对照组,差异有统计学意义,但两组的畸形矫正率相当。结论重度脊柱畸形患者的后路脊柱截骨术和牵引辅助后路广泛松解术,疗效相当,但牵引辅助后路广泛松解术,可避免侵袭性大的操作、缩短手术时间、减少出血量,并显著减少了围手术期并发症的发生率。     

Survivin: A new target for anti-cancer therapy

Survivin is one of the most cancer-specific proteins identified to date, being upregulated in almost all human tumors. Biologically, survivin has been shown to inhibit apoptosis, enhance proliferation and promote angiogenesis. Because of its upregulation in malignancy and its key role in apoptosis, proliferation and angiogenesis, survivin is currently attracting considerable attention as a new target for anti-cancer therapies. In several animal model systems, downregulation of survivin or inactivation of its function has been shown to inhibit tumor growth. Strategies under investigation to target survivin include antisense oligonucleotides, siRNA, ribozymes, immunotherapy and small molecular weight molecules. The translation of these findings to the clinic is currently ongoing with a number of phase I/II clinical trials targeting survivin in progress. These include use of the antisense oligonucleotide LY2181308, the low molecular weight molecule inhibitor YM155 and survivin-directed autologous cytotoxic T lymphocytes. The optimum use of survivin antagonists in the treatment of cancer is likely to be in combination with conventional cancer therapies.     

Esophagus in-field: A new predictor for esophagitis

Purpose

To define optimization parameters for limiting esophageal toxicity with concurrent chemoradiation (CRT) for non-small cell lung cancer (NSCLC).

Materials and methods

A retrospective analysis of patients treated with concurrent chemoradiation at the Dana-Farber/Brigham and Women’s Hospital Cancer Center was done with IRB approval. All patients were treated with concurrent CRT. All patients underwent 3-D conformal radiotherapy planned with ECLIPSE (Varian, Palo Alto, CA) treatment planning system. Patients had their esophagus contoured in two ways: the entire esophagus (Esoph) and esophagus in-field (Esoph_in). Together with clinical variables, dose volume metrics including mean dose, V5-V60 of both structures (Esoph and Esoph_in) were analyzed for correlation with acute esophagitis (?grade 3) and late esophageal stricture. The analyses and graphics were completed using R (R Development Core Team, 2006). Logistic regression analysis was used to assess the relationships between dosimetric factors and swallowing complications while controlling for non-dosimetric variables.

Results

109 patients were studied between 2000 and 2006. 25% of patients had grade 3 or greater acute esophagitis. 5/109 (5.5%) had late esophageal stricture with a six-month actuarial risk of stricture of 6.5% (95% CI = 1-11%). Mean dose and V45-V60 for both Esoph and Esoph_in significantly correlated with development of acute esophagitis. V55 and V60 for both Esoph and Esoph_in significantly correlated with development of stricture. On Multivariate analysis V55 of the Esoph and Esoph_in was most predictive of toxicity. Limiting the V55 Esoph_in to 50% was the best cut-point for acute esophagitis.

Conclusions

In the setting of concurrent CRT, V55 of the Esoph or Esoph_in is the best predictor of acute esophagitis.     

A new era in prostate cancer therapy: new targets and novel therapeutics

The results of two phase III trials demonstrating a significant prolongation of survival with docetaxel-based chemotherapy has fueled interest in expanding therapeutic development in prostate cancer. This coupled with improved understanding of the mechanisms responsible for prostate cancer development and progression has lead to discovery of several biologic targets that can be exploited using novel therapeutics in what has been referred to as the era of “targeted therapy.” Several of these therapies have shown promise either as single agents or in combination with proven chemotherapeutic agents. This review focuses upon some of the more promising targeted therapies under investigation for the treatment of hormone refractory prostate cancer and highlights some of challenges faced in therapeutic development.     

Oxaliplatin: A new agent for colorectal cancer

For nearly 40 years, the medical treatment of colorectal cancer had been limited to the fluoropyrimidines until the recent development of irinotecan (CPT-11). In the past decade, a new agent has appeared, oxaliplatin. This third-generation platinum compound has synergistic activity with 5-fluorouracil and is non-cross-resistant with 5-fluorouracil, CPT-11, and other platinum agents. Numerous clinical trials in Europe have demonstrated the activity of oxaliplatin in patients with untreated and refractory metastatic colorectal cancer. Nevertheless, the US Food and Drug Administration recently denied approval for oxaliplatin as first-line treatment of colorectal cancer because of a lack of clear-cut survival advantage in clinical trials. Additional clinical trials in patients with colorectal cancer are ongoing in the United States and will test the activity of oxaliplatin in the metastatic and adjuvant setting. These studies will define the role for what appears to be a very useful and important agent.     

The addition of pravastatin to chemotherapy in advanced gastric carcinoma: A randomised phase II trial

PurposeStatins have for long been considered to play a potential role in anticancer treatment based upon their ability to inhibit the mevalonate synthesis pathway. This randomised phase II trial compared the efficacy and safety of pravastatin added to epirubicin, cisplatin and capecitabine (ECC versus ECC + P) in patients with advanced gastric carcinoma.MethodsPatients were randomised to receive up to six cycles of 3-weekly ECC with or without pravastatin (40 mg, once daily from day 1 of the first cycle until day 21 of the last cycle). Primary end-point was progression-free rate at 6 months (PFR_6months). Secondary end-points were response rate (RR), progression-free survival (PFS), overall survival (OS) and safety. For early termination in case of futility, a two-stage design was applied (P₀ = 50%; P₁ = 70%; α = 0.05; β = 0.10).ResultsThirty patients were enrolled. PFR_6months was 6/14 patients (42.8%) in the ECC + P arm, and 7/15 patients (46.7%) in the control arm, and therefore the study was terminated after the first stage. In the ECC and ECC + P arm, RR was 7/15 (46.7%) and 5/15 (33.3%), median PFS was 5 and 6 months and median OS was 6 and 8 months, respectively. Toxicity data showed no significant differences, although there was a trend towards more gastrointestinal side-effects such as diarrhoea and stomatitis in the ECC + P arm.ConclusionIn this randomised phase II trial the addition of pravastatin to ECC did not improve outcome in patients with advanced gastric cancer. Therefore, further testing of this combination in a randomised phase III trial cannot be recommended.