三氧化二砷抗肿瘤作用研究进展

三氧化二砷治疗急性早幼粒白血病疗效肯定，但对其他血液肿瘤及实体瘤的治疗作用及抗肿瘤作用机理仍未明确。综述国内，外有关研究，探索其治疗作用及抗肿瘤机制，为开辟三氧化二砷新的治疗作用提供参考。     

三氧化二砷抗肿瘤临床应用进展

三氧化二砷(As2O3)治疗急性早幼粒细胞白血病(APL)有特效，在其他恶性肿瘤治疗中也有应用。其抗肿瘤作用涉及诱导细胞分化与凋亡、细胞周期阻滞、抗肿瘤血管生成及调节多种基因表达。现综述As2O3抗肿瘤作用机制及临床应用。     

三氧化二砷抗肿瘤临床应用进展

三氧化二砷(As2O3)治疗急性早幼粒细胞白血病(APL)有特效,在其他恶性肿瘤治疗中也有应用.其抗肿瘤作用涉及诱导细胞分化与凋亡、细胞周期阻滞、抗肿瘤血管生成及调节多种基因表达.现综述As2O3抗肿瘤作用机制及临床应用.     

三氧化二砷应用于肝癌治疗的实验研究进展

三氧化二砷(arsenictrioxide, As2O3)是中药砒霜的主要成分,有剧毒,但 近年来人们研究发现其具有显著的抗肿瘤作 用。综述其在肝癌治疗方面的实验研究进 展,阐明As2O3的抗肿瘤机制主要为通过调 控多种基因选择性诱导肝癌细胞凋亡、选择 性细胞毒作用、抗肿瘤血管形成作用、改变肝 癌细胞核基质蛋白成分及抑制肝癌细胞增殖 细胞抗原(PCNA)的表达等;细胞周期分析 显示As2O3可以阻滞肝癌细胞于S+G2/M 期;与ADM、DDP等化疗药物联合应用可明 显提高对肝癌细胞的杀伤率,丁硫氨酸亚矾 氨(BSO)可增加肝癌细胞对As2O3敏感性。     

肝动脉化疗栓塞联合灌注三氧化二砷治疗原发性肝癌初步观察

探讨三氧化二砷肝动脉灌注治疗原发性肝癌的临床疗效。对62例和56例原发性肝癌患者分别采用常规药物联合三氧化二砷和单纯常规药物介入治疗,分析治疗效果。结果常规药物联合三氧化二砷组1年生存率优于单纯常规药物组,P=0·017,P<0·05,半年生存率及近期疗效差异无统计学意义,P>0·05。初步研究结果提示,原发性肝癌患者肝动脉常规药物联合三氧化二砷介入治疗能提高1年生存率。     

三氧化二砷抗肿瘤研究

用三氧化二砷(As2O3)治疗急性早幼粒细胞白血病(APL)疗效显著。研究表明As2O3还可以诱导多种实体瘤细胞生长阻滞和凋亡,但As2O3对实体瘤的治疗作用及抗肿瘤作用机制仍未明确。     

三氧化二砷抗肿瘤研究

用三氧化二砷（As2O3）治疗急性早幼粒细胞白血病（APL）疗效显著。研究表明As2O3还可以诱导多种实体瘤细胞生长阻滞和凋亡,但As2O3对实体瘤的治疗作用及抗肿瘤作用机制仍未明确。     

三氧化二砷抗肿瘤机制研究进展

三氧化二砷(As2O3)又称白砒或砒霜,在我国医药中称为信石。多年来研究表明As2O3既能治疗血液系统恶性疾病,又对其他多种实体肿瘤有抗肿瘤作用。As2O3抗肿瘤作用机制错综复杂,本文根据国内外相     

三氧化二砷用于实体肿瘤化疗的实验研究

三氧化二砷用于治疗白血病已有 2 0余年 ,并取得显著疗效。近年来 ,已开展了三氧化二砷用于实体肿瘤的实验研究 ,如食管癌、胃癌、结肠癌、肝癌、肺癌、膀胱癌等 ,取得了一定成果 ,为其用于实体肿瘤的临床化学治疗提供了实验基础。     

2-甲氧基雌二醇的抗肿瘤作用研究进展

目的:探讨2-甲氧基雌二醇(2-ME)在抗肿瘤作用中的研究进展。方法:应用Medline及CNKI期刊全文数据库检索系统,以2-ME、肿瘤治疗和细胞周期为关键词,检索2002-2007年2-ME抗肿瘤作用方面的研究相关文献24篇。结果:2-ME为雌二醇在体内的生理代谢产物,但对雌激素受体的亲和力较低,而对多种肿瘤细胞具有抑制作用,其主要机制为抑制细胞增殖、诱导肿瘤细胞和内皮细胞凋亡、抗血管新生、促进细胞周期停滞及增强肿瘤细胞对辐射的敏感性等。2-ME对正常细胞和组织无作用,不良反应较小。结论:2-ME具有广泛的抗肿瘤作用,有望成为一种新的抗肿瘤药物。     

三氧化二砷作用机制研究进展

砷化合物在我国作为药物应用已有2400多年的历史了。自从20世纪90年代,我国学者应用三氧化二砷（As2O3）治疗急性早幼粒细胞性白血病并获得成功以来,人们对砷化合物进行了深入的研究,发现As2O3不仅对各型白血病有效,对其他多种恶性肿瘤也有良好的治疗效果。As2O3主要是通过抑制肿瘤细胞生长和肿瘤新生血管形成、诱导肿瘤细胞部分分化和凋亡等发挥抗肿瘤作用的。本文不仅对上述问题进行总结,还展望了新发展起来的基因表达谱分析技术--基因芯片技术在研究As2O3作用机制方面的应用前景。     

三氧化二砷诱导恶性肿瘤细胞凋亡机制的研究进展

三氧化二砷已广泛应用于白血病和各种实体瘤化学治疗的基础研究和临床实践中。近年来国内外多项研究证实三氧化二砷诱导凋亡是其杀伤肿瘤的主要机制,其分子机制尚未得到系统阐明,本文就其抗凋亡作用机制的研究进展作一综述。     

砷剂联合全反式维甲酸治疗 M3型小儿急性早幼粒细胞白血病

目的：探讨全反式维甲酸联合使用亚砷酸治疗 M3型小儿急性早幼粒细胞白血病的临床疗效。方法：选取我院2010年1月至2013年7月收治的80例急性早幼粒细胞白血病患儿,随机分为观察组和对照组,每组40例。观察组给予全反式维甲酸（ATAR）联合亚砷酸治疗,对照组给予 ATAR 进行治疗。两组患者均接受2个疗程的治疗,治疗过程中达到完全缓解（CR）的患者改用维持治疗。测定患者经过2个疗程治疗后的血象和骨髓象,并评价两组患者的治疗效果。结果：与单纯使用 ATAR 治疗相比,采用 ATAR 联合亚砷酸治疗,可以使患者更快的恢复血红蛋白水平和血小板数量;同时可以显著抑制患儿骨髓内的细胞异常增生和分化。疗效结果也表明,联合治疗 APL 可以显著的增加疗效,且能显著降低复发人数和复发率。结论：ATAR联合亚砷酸治疗 APL 效果可靠,起效迅速,值得临床推广使用。     

In the War Against Solid Tumors Arsenic Trioxide Need Partners

In the past decade, the therapeutic potential of arsenic trioxide (ATO) in the treatment of acute promyelocytic leukemia (APL) was recognized. This encouraged other investigators to test the efficacy of ATO in the management of other hematological and solid tumor malignancies. Notably, as a single agent, arsenic trioxide did not benefit patients diagnosed with solid tumors. However, when it was combined with other agents, treatment benefit emerged. In this article, we have summarized the outcome of clinical trials that used arsenic trioxide as a single agent as well as in combination settings in patients diagnosed with solid tumors. We have also reviewed possible additional mechanisms by which ATO may be useful as a chemosensitizer in combination therapy. We hope that our review will encourage clinical investigators to rationally combine ATO with additional chemotherapeutic agents in treating patients diagnosed with solid tumors.     

白血病端粒酶活动度与三氧化二砷治疗观察

目的观察白血病端粒酶活性与三氧化二砷的治疗效果。方法端粒重复扩增法结合光密度测定和临床治疗观察。结果急性白血病均表现出较高的端粒酶活性，用三氧化二砷治疗后，获得临床血液学缓解及端粒酶活性降低，并在维持缓解间保持较低水平。结论观察端粒酶活动度有助于l临床判断病情转归及三氧化二砷的治疗反应。     

Arsenic trioxide in multiple myeloma: rationale and future directions

Multiple myeloma remains an incurable malignancy with a median survival that does not exceed 3 years. At least one third of patients with multiple myeloma fail to respond to induction chemotherapy, and those who initially achieve remission eventually relapse and require additional therapy. Recent reports demonstrating the efficacy of arsenic trioxide in acute promyelocytic leukemia have prompted a revival in the clinical use of this compound. The achievement of clinical responses marked by molecular conversion of the malignant phenotype and remissions in patients who had failed to respond to multiple courses of conventional chemotherapy provided the impetus to explore its use in multiple myeloma. Properties that favor the use of arsenic trioxide are its ability to target selectively malignant cells for apoptosis through enhancementof reactive oxygen species, to induce differentiation, and to inhibit angiogenesis. Multiple events involved in the pathogenesis of multiple myeloma coincide with pathways targeted by arsenic trioxide, and early results have suggested that clinical responses and safety in patients are promising with advanced disease.     

History of the development of arsenic derivatives in cancer therapy

Arsenic is a natural substance that has been used medicinally for over 2,400 years. In the 19th century, it was the mainstay of the materia medica. A solution of potassium arsenite (Fowler's solution) was used for a variety of systemic illnesses from the 18th until the 20th century. This multipurpose solution was also primary therapy for the treatment of chronic myelogenous leukemia until replaced by radiation and cytotoxic chemotherapy. The past 100 years have seen a precipitous decline in arsenic use and, by the mid-1990s, the only recognized indication was the treatment of trypanosomiasis. Much of this decline was due to concerns about the toxicity and potential carcinogenicity of chronic arsenic administration. The rebirth of arsenic therapy occurred in the 1970s when physicians in China began using arsenic trioxide as part of a treatment for acute promyelocytic leukemia (APL). Their accumulated experience showed that a stable solution of arsenic trioxide given by intravenous infusion was remarkably safe and effective both in patients with newly diagnosed APL leukemia and in those with refractory and relapsed APL. The mechanisms of action of arsenic derivatives in this disease and other malignancies are many and include induction of apoptosis, partial cytodifferentiation, inhibition of proliferation, and inhibition of angiogenesis. Molecular studies and ongoing clinical trials suggest that, as a chemotherapeutic agent, arsenic trioxide shows great promise in the treatment of malignant disease.     

Differentiating agents in pediatric malignancies: All-trans-retinoic acid and arsenic in acute promyelocytic leukemia

Acute promyelocytic leukemia (APL) is the most potentially curable type of acute myeloid leukemia. It is characterized by the chromosomal translocation t(15;17), which results in the fusion gene PML-RAR-α. The introduction of all-trans- retinoic acid (ATRA) was a major advance in treatment of this disease. This agent induces terminal differentiation of malignant myeloid cells to mature neutrophils, and its side effects are usually well tolerated in children. ATRA does not eradicate the malignant myeloid clone in APL and, eventually, resistance develops. Arsenic trioxide induces nonterminal differentiation of malignant promyelocytes and promotes apoptosis. APL patients treated with ATRA or arsenic trioxide have rapid resolution of their coagulopathy. Because both of these drugs are well tolerated in children and their synergy has been shown in animal models, the possibility of combining ATRA and arsenic trioxide in frontline therapy for children with APL is being considered.     

Clinical activity of arsenic trioxide for the treatment of multiple myeloma.

Arsenic has been used since ancient times as a therapeutic agent. However, until recently its use in modern medicine has been restricted to the treatment of a limited number of parasitic infections. In the early 1990s, reports from China described impressive results with arsenic trioxide in patients with de novo, relapsed, and refractory acute promyelocytic leukemia (APL). Other investigators subsequently confirmed these results leading to approval of its use for relapsed or refractory APL in the United States. Investigations of this agent have demonstrated that its efficacy in APL and preclinical tumor models is dependent upon a number of mechanisms, including induction of apoptosis, effects on cellular differentiation, cell cycling, and tumor angiogenesis. Subsequent preclinical studies showed significant activity of arsenic trioxide in multiple myeloma (MM). Based on this, in a phase II trial, we have evaluated the activity of arsenic trioxide in 14 patients with relapsed MM, refractory to conventional salvage therapy. With the dose and schedule used, treatment with arsenic trioxide produced responses in three patients and prolonged stable disease in a fourth patient, with the longest response lasting 6 weeks. Although treatment was reasonably well tolerated, in these patients with extensive prior therapy, 11 developed cytopenia, five associated with infectious complications and three developed deep vein thromboses. The results of this small trial support further investigation of this novel drug for the treatment of patients with relapsed or refractory MM.