新药物或可增强伊马替尼抗白血病效果
Potential New Way To Make A Good Anti-leukemia Drug Even Better
http://www.sciencedaily.com/releases/2008/10/081020093402.htm
ScienceDaily (Oct. 21, 2008) — A recently identified cancer-causing protein makes the anti-leukemia drug imatinib, less effective. By blocking the protein, an international team of researchers was able to slow the spread of leukemia cells in culture.
The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.
Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.
CML is associated with the abnormal fusion of a portion of chromosome 21 with a cell growth-promoting enzyme called ABL, which makes the enzyme perpetually active. Imatinib slows down the spread of cancer by blocking the enzyme's activity. But the drug doesn't work in everyone and resistance often develops, most likely because the drug only targets mature cells, leaving self-renewing cancer stem cells behind.
Now, Xiaoyan Jiang and a team of researchers from the British Columbia Cancer Agency in Vancouver and other institutions may have discovered what protects the stem cells from imatinib.
The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells. When Zhou and colleagues blocked AHI-1 in cancer cells from imatinib-resistant CML patients, they restored the ability of the drug to kill the cells. The next step, says Jiang is finding a drug that blocks AHI-1, which could potentially be given in combination with imatinib in the future.
http://www.sciencedaily.com/releases/2008/10/081020093402.htm
ScienceDaily (Oct. 21, 2008) — A recently identified cancer-causing protein makes the anti-leukemia drug imatinib, less effective. By blocking the protein, an international team of researchers was able to slow the spread of leukemia cells in culture.
The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.
Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.
CML is associated with the abnormal fusion of a portion of chromosome 21 with a cell growth-promoting enzyme called ABL, which makes the enzyme perpetually active. Imatinib slows down the spread of cancer by blocking the enzyme's activity. But the drug doesn't work in everyone and resistance often develops, most likely because the drug only targets mature cells, leaving self-renewing cancer stem cells behind.
Now, Xiaoyan Jiang and a team of researchers from the British Columbia Cancer Agency in Vancouver and other institutions may have discovered what protects the stem cells from imatinib.
The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells. When Zhou and colleagues blocked AHI-1 in cancer cells from imatinib-resistant CML patients, they restored the ability of the drug to kill the cells. The next step, says Jiang is finding a drug that blocks AHI-1, which could potentially be given in combination with imatinib in the future.
Potential New Way To Make A Good Anti-leukemia Drug Even Better
可能使一种好的抗白血病药物（伊马替尼）疗效更好的潜在方法。
ScienceDaily (Oct. 21, 2008) — A recently identified cancer-causing protein makes the anti-leukemia drug imatinib, less effective. By blocking the protein, an international team of researchers was able to slow the spread of leukemia cells in culture.
每日科学（2008年10月21日）－最近发现的一种由肿瘤引起的蛋白使抗白血病药物伊马替尼的疗效减低。一组国际研究者通过阻滞该蛋白，使得培养基中的白血病细胞蔓延速度减慢。
The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.
该研究将在线发表在10月20日实验医学杂志上，它认为对白血病的最有效治疗应该基于联合应用靶向药物，而不是依赖于单一的特效药。
Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). 伊马替尼是目前治疗慢性髓细胞白血病的最普遍药物。CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. 慢性髓细胞白血病是一种发生于中年人的常见血液肿瘤，占西方成人所有白血病发病数的15－20%.Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.肿瘤细胞在患者血液中的聚集，导致感染、贫血和其他潜在生命风险的并发症。
CML is associated with the abnormal fusion of a portion of chromosome 21 with a cell growth-promoting enzyme called ABL, which makes the enzyme perpetually active. CML与21好染色体的部分异常融合相关，导致控制细胞增长的酶ABL永久激活。Imatinib slows down the spread of cancer by blocking the enzyme's activity. 伊马替尼通过阻滞该酶的活性来阻止肿瘤的进展。But the drug doesn't work in everyone and resistance often develops, most likely because the drug only targets mature cells, leaving self-renewing cancer stem cells behind.但是该药物并不适用于所有人，并经常产生耐药，很可能是因为该药物只针对成熟细胞，而漏掉了可自行更新的肿瘤干细胞。
Now, Xiaoyan Jiang and a team of researchers from the British Columbia Cancer Agency in Vancouver and other institutions may have discovered what protects the stem cells from imatinib. 现在来自温哥华英国哥伦比亚肿瘤研究所的江小燕和他的研究者联合其他研究机构可能已经发现了保护干细胞免于伊马替尼杀伤的途径。
The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells. 该研究组发现曾经发现于白血病细胞中的AHI-1蛋白在CML干细胞中高表达。When Zhou and colleagues blocked AHI-1 in cancer cells from imatinib-resistant CML patients, they restored the ability of the drug to kill the cells. 当周和他的同事阻滞了对伊马替尼耐药的白血病患者肿瘤细胞的AHI-1蛋白，他们恢复了该药对干细胞的杀伤作用。The next step, says Jiang is finding a drug that blocks AHI-1, which could potentially be given in combination with imatinib in the future.江表示，下一步是找一种阻滞AHI-1的药物，这种药物可能在将来与伊马替尼联用于治疗。
可能使一种好的抗白血病药物（伊马替尼）疗效更好的潜在方法。
ScienceDaily (Oct. 21, 2008) — A recently identified cancer-causing protein makes the anti-leukemia drug imatinib, less effective. By blocking the protein, an international team of researchers was able to slow the spread of leukemia cells in culture.
每日科学（2008年10月21日）－最近发现的一种由肿瘤引起的蛋白使抗白血病药物伊马替尼的疗效减低。一组国际研究者通过阻滞该蛋白，使得培养基中的白血病细胞蔓延速度减慢。
The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.
该研究将在线发表在10月20日实验医学杂志上，它认为对白血病的最有效治疗应该基于联合应用靶向药物，而不是依赖于单一的特效药。
Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). 伊马替尼是目前治疗慢性髓细胞白血病的最普遍药物。CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. 慢性髓细胞白血病是一种发生于中年人的常见血液肿瘤，占西方成人所有白血病发病数的15－20%.Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.肿瘤细胞在患者血液中的聚集，导致感染、贫血和其他潜在生命风险的并发症。
CML is associated with the abnormal fusion of a portion of chromosome 21 with a cell growth-promoting enzyme called ABL, which makes the enzyme perpetually active. CML与21好染色体的部分异常融合相关，导致控制细胞增长的酶ABL永久激活。Imatinib slows down the spread of cancer by blocking the enzyme's activity. 伊马替尼通过阻滞该酶的活性来阻止肿瘤的进展。But the drug doesn't work in everyone and resistance often develops, most likely because the drug only targets mature cells, leaving self-renewing cancer stem cells behind.但是该药物并不适用于所有人，并经常产生耐药，很可能是因为该药物只针对成熟细胞，而漏掉了可自行更新的肿瘤干细胞。
Now, Xiaoyan Jiang and a team of researchers from the British Columbia Cancer Agency in Vancouver and other institutions may have discovered what protects the stem cells from imatinib. 现在来自温哥华英国哥伦比亚肿瘤研究所的江小燕和他的研究者联合其他研究机构可能已经发现了保护干细胞免于伊马替尼杀伤的途径。
The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells. 该研究组发现曾经发现于白血病细胞中的AHI-1蛋白在CML干细胞中高表达。When Zhou and colleagues blocked AHI-1 in cancer cells from imatinib-resistant CML patients, they restored the ability of the drug to kill the cells. 当周和他的同事阻滞了对伊马替尼耐药的白血病患者肿瘤细胞的AHI-1蛋白，他们恢复了该药对干细胞的杀伤作用。The next step, says Jiang is finding a drug that blocks AHI-1, which could potentially be given in combination with imatinib in the future.江表示，下一步是找一种阻滞AHI-1的药物，这种药物可能在将来与伊马替尼联用于治疗。
