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Clin Cancer Res:维生素E或降低多发性错构瘤综合征患者的癌症风险

  1. Clin Cancer Res
  2. 多发性错构瘤综合征
  3. 癌症风险
  4. 维生素E

来源:生物谷 2012-11-18 23:39

2012年9月18日 讯 /生物谷BIOON/ --近日,来自美国克利夫兰诊所的研究者通过研究发现,维他命E可以预防遗传性疾病患者癌症的发生。“目前我们发现在多发性错构瘤综合征中(Cowden Syndrome)存在一系列的遗传突变,多发性错构瘤综合征可以使得患者引发许多癌症,包括乳腺癌和甲状腺癌等。

2012年9月18日 讯 /生物谷BIOON/ --近日,来自美国克利夫兰诊所的研究者通过研究发现,维他命E可以预防遗传性疾病患者癌症的发生。“目前我们发现在多发性错构瘤综合征中(Cowden Syndrome)存在一系列的遗传突变,多发性错构瘤综合征可以使得患者引发许多癌症,包括乳腺癌和甲状腺癌等。琥珀酸脱氢酶(SDH)基因突变或许可以引发癌症,”研究者Charis Eng这样说到,目前相关的研究成果已经刊登在了9月17日的杂志Clinical Cancer Research上。

SDH基因主要负责产生能量,其突变会导致机体活性氧的积累,这些改变将损伤细胞并且使得细胞对细胞凋亡出现耐受性,而细胞凋亡是机体清除癌性细胞的一种机体过程。

然而研究者发现,当在突变细胞中添加维生素E时,活性氧的积累水平就会降低,从而减少细胞损伤。

这项研究发现揭示了维生素E或许可以作为一种抗癌制剂或者预防因子来进行应用,尤其是对于携带有SDH突变的多发性错构瘤综合征患者。

多发性错构瘤综合征可以产生多种类型的癌症,患乳腺癌的风险为85%,上皮甲状腺癌风险为35%,而且其它风险也会随之升高,粗略估计有200,000个个体受到多发性错构瘤综合征的影响。(生物谷Bioon.com)

编译自:Vitamin E May Decrease Cancer Risk in Cowden Syndrome Patients

Vitamin E Protects against Lipid Peroxidation and Rescues Tumorigenic Phenotypes in Cowden/Cowden-like Patient-Derived Lymphoblast Cells with Germline SDHx Variants

Ying Ni1,4 and Charis Eng1

Purpose: Cowden syndrome (CS), a Mendelian autosomal-dominant disorder, predisposes to breast, thyroid, and other cancers. Germline variations in succinate dehydrogenase genes (SDHx) occur in approximately 10% PTEN mutation-negative CS and CS-like (CSL) individuals (SDHvar+). We previously showed that SDHx variants result in elevated reactive oxygen species (ROS), disruption of nicotinamide adenine dinucleotide (NAD) equilibrium, and destabilization of p53 hence apoptosis resistance in CS/CSL patient-derived lymphoblastoid cells. In the present study, we sought to address the tumorigenic impacts of increased ROS and the potential of protecting SDHvar+ cells with antioxidants. Experimental Design: We measured the lipid peroxidation levels in patient-derived SDHvar+ lymphoblastoid cells and sequenced 74 controls or SDHvar+ germline DNA samples for mitochondrial hypervariable region II (HVRII) polymorphisms. SDHvar+ lymphoblastoid cells were treated with various antioxidants to check p53 expression and sub-G1 cell population with cell-cycle analysis. Results: We showed that elevated ROS results in higher lipid peroxidation in SDHvar+ cells. Accumulation of polymorphisms in mitochondrial HVRII was observed in SDHvar+ samples. Interestingly, α-tocopherol (vitamin E) treatment, but not other antioxidants, rescued SDHvar+ cells from apoptosis resistance and protected SDHvar+ cells from oxidative damage such as decreased lipid peroxidation as well as partially recovered p53 expression and NAD/NADH levels. Conclusions: We conclude that disruption of complex II because of SDHx variants leads to increased ROS generation, specifically accompanied by lipid peroxidation. The lipid soluble antioxidant α-tocopherol can selectively protect SDHvar+ cells from oxidative damage, apoptosis resistance, and rebalance redox metabolites NAD/NADH. Clin Cancer Res; 18(18); 4954–61. ©2012 AACR.

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