研究提示骨髓增生异常综合征的治疗新策略

MD安德森新闻稿05 \/ 11 \/ 2015

一项研究揭示了染色体的“尾巴”被称为端粒可能给科学家们提供看开发治疗甚至预防组血细胞紊乱称为骨髓增生异常综合征的一种新的方式新的见解（MDS）。

在德克萨斯大学MD安德森癌症中心的研究人员发现了端粒的变性和MDS之间的直接联系。在尾部发现端粒，染色体的两端，有时被描述为类似塑料鞋带提示因为他们防止染色体末端的磨损，造成基因的破坏。

西蒙娜阿胶，博士

降解端粒有时会导致MDS，也被认为与年龄、性别（男性多见）、吸烟、辐射或化疗前癌家族史。MDS是中老年人更常见的血液疾病之一，60岁以上的人的影响百分之90例。

“MDS risk correlates with advancing age, therapy-induced DNA damage, and/or shorter telomeres, but whether telomere erosion directly causes MDS is unknown,” said 西蒙娜阿胶，博士, assistant professor of Leukemia。 “Our study provided genetic evidence that DNA damage caused by telomere loss is linked to this disorder。”

结果阿胶，同第一作者德里克Ong博士，奥德赛同基因组医学，和相应的作者Ron DePinho，医学博士，肿瘤生物学和 MD安德森总裁教授，发表在2015年5月11日发行的癌细胞。

Ron DePinho, M。D。

The team’s mouse and human cell study found that DNA damage caused by dysfunctional telomeres resulted in repressed expression of a gene called SRSF2。 SRSF2 is a RNA splicing gene that plays a role in cellular processes。 This change impacted blood cells named CMPs (common myeloid progenitors), affecting their ability to differentiate or fully mature。

“This study established an intimate link across telomere biology, aberrant RNA splicing and CMP differentiation,” said DiPinho。 “This may suggest that strategies to mitigate this DNA damage may be useful for preventing and/or treating MDS。”

Colla added that their findings “were consistent with long-standing observations that poor prognosis in MDS correlates strongly with short telomeres and elevated DNA damage in CMP cells。”

“This improved understanding should provide highly specific risk biomarkers for preventing and treating this incurable disease,” said Colla。

The study was funded by the National Cancer Institute (RO1 CA084628, CA 143883), the Laura and John Arnold Foundation and the National Institutes of Health (P30 CA16672)。

MD Anderson team members included Yamini Ogoti, Matteo Marchesini, Ph。D。, Irene Ganan Gomez, Ph。D。, Marcos Estecio, Ph。D。, Yu Wei, Ph。D。, Hui Yang, Ph。D。, Marianna D’Anca, Hagop Kantarjian, M。D。, and Guillermo Garcia-Manero, M。D。, all of Leukemia; Paola Storti, Ph。D。, Andrea Viale, M。D。, Ph。D。, David Weksberg, M。D。, Ph。D。, Yan Wing Ho, Baoli Hu, Ph。D。, Giannicola Genovese, Ph。D。,  Piergiorgio Pettazzoni, Ph。D。, Shan Jiang, Sujun Hua, Ph。D。, Alessandro Carugo, Luigi Nezi, Ph。D。, Alan Wang,Ph。D。, and Lynda Chin, M。D。, Genomic Medicine; Nipun Mistry, Li Zhang, Ph。D。, and Han Liang, Ph。D。, Bioinformatics and Computational Biology; Karen Clise-Dwyer, Ph。D。, and Kathryn Ruisaard, Stem Cell Transplantation and Cellular Therapy; Sonny Ang, Ph。D。, and Laurence Cooper, M。D。, Pediatrics; Christopher Bristow, Ph。D。, James Horner, Philip Jones, Ph。D。, and Timothy Heffernan, Ph。D。, Institute for Applied Cancer Science; Sarah Gaddis and Tim Gong, Ph。D。, Molecular Carcinogenesis; Asha Multani, Ph。D。, Genetics; and Carlos Bueso-Ramos, Ph。D。 Hematopathology。

Other participating institutions included the University of Parma, Parma, Italy, and In Silico Solutions, Falls Church, Va。

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