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【bio-news】science 突变可能触发了最难治的白血病
By Steve Mitchell
ScienceNOW Daily News
14 April 2008
Just like the fabled Ikaros who met his demise when he flew too close to the sun, a gene of the same name may spell trouble for cancer patients. A new study indicates that mutations in the Ikaros gene play a role in triggering acute lymphoblastic leukemia (ALL), an aggressive, treatment-resistant form of cancer. Researchers hope the find will lead to new ways to tackle the disease.
A chromosomal rearrangement called the Philadelphia chromosome causes chronic myelogenous leukemia (CML), a cancer of blood cells that patients can live with for years and generally recover from with treatment. But the same defect is also found in a small percentage of patients with ALL, which can be fatal in months and is difficult to treat. Researchers have long wondered what differentiates the two diseases. One possible culprit is Ikaros. Children with mutations in the gene, but who don't have the Philadelphia chromosome, develop ALL.
To find out if Ikaros also plays a role in Philadelphia chromosome-associated ALL, a team led by James Downing, a hematopathologist at St. Jude Children's Research Hospital in Memphis, Tennessee, looked at ALL patients who also had the Philadelphia chromosome, including 21 children and 22 adults. The majority of the patients had a flawed copy of the gene, with mutations occurring in 76.2% of the children and 90.9% of the adults, the researchers report this week in Nature. The Ikaros mutations were not found in 23 adults with CML, confirming the role of this gene in triggering ALL in those with the Philadelphia chromosome. Ikaros codes for a transcription factor protein that is essential for normal development of white blood cells called lymphocytes, but it is not yet clear how the mutations lead to cancer. One possibility is that the faulty protein produced by the mutations leads to abnormal lymphocytes that turn cancerous, Downing says.
Mitchell Smith, an oncologist at Fox Chase Cancer Center in Philadelphia, Pennsylvania, says the finding is "a big advance" that could pave the way for treatments. "There's nothing available today that will fix this, but once you know what you're after, it becomes easier to target," he adds. William Phelps, a molecular biologist at the American Cancer Society in Atlanta, Georgia, says the Ikaros protein itself probably won't make a good target for drugs because it's a transcription factor, and such proteins don't have binding sites to which compounds that block their action can adhere. But other genes or proteins that Ikaros regulates may make good targets for drugs, he adds. 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Mutation May Explain Deadly Form of Leukemia
突变可能触发了最难治的白血病
Just like the fabled Ikaros who met his demise when he flew too close to the sun, a gene of the same name may spell trouble for cancer patients. A new study indicates that mutations in the Ikaros gene play a role in triggering acute lymphoblastic leukemia (ALL), an aggressive, treatment-resistant form of cancer. Researchers hope the find will lead to new ways to tackle the disease.
好象寓言中的Ikaros在飞向太阳而走向毁灭，一个同名的基因也给癌症患者带来了麻烦。一项新的研究表明，Ikaros基因突变触发了急性淋巴细胞白血病（ALL）—— 一种进展性的，难治性白血病。研究人员希望这一发现能够为治疗这种疾病提供新的途径。
A chromosomal rearrangement called the Philadelphia chromosome causes chronic myelogenous leukemia (CML), a cancer of blood cells that patients can live with for years and generally recover from with treatment. But the same defect is also found in a small percentage of patients with ALL, which can be fatal in months and is difficult to treat. Researchers have long wondered what differentiates the two diseases. One possible culprit is Ikaros. Children with mutations in the gene, but who don't have the Philadelphia chromosome, develop ALL.
一种费城（Ph）染色体的重排导致了慢性粒细胞白血病（CML），这是一种血细胞肿瘤，病人能够生存数年，并随着治疗而逐渐康复。在一小部分ALL患者中也会发现类似的（Ph）染色体的重排，而ALL在数个月的时间内就可以致命，并且很难治。长期以来，研究人员一直在研究这两种疾病之间的差别。现在发现一个可能的原因便是Ikaros基因，那些有Ikaros基因突变而没有费城染色体的儿童，会患上ALL。
To find out if Ikaros also plays a role in Philadelphia chromosome-associated ALL, a team led by James Downing, a hematopathologist at St. Jude Children's Research Hospital in Memphis, Tennessee, looked at ALL patients who also had the Philadelphia chromosome, including 21 children and 22 adults.
为了阐明Ikaros基因是否也在费城染色体相关的ALL的关系中起作用，由美国田纳西州Memphis，裘德儿童研究医院的血液病理学家James Downing领导的一个研究小组，对同时具有费城染色体的ALL患者——包括21名儿童和22名成人——进行了研究。
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作者:admin@医学,生命科学 2010-12-29 05:14
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