加拿大McMaster 大学 用糖尿病药物修复骨髓红细胞造血功能 杀死白血病细胞
Leukemia: Cancer cells killed off with diabetes drug
科学家们可能已经找到了一种创新的方法来杀死急性骨髓性白血病中的癌细胞，同时保存和再生健康的红细胞。
白血病细胞
研究人员可能已经找到了一种方法来抑制白血病细胞(如图所示)，同时保护健康的红细胞。
这项新研究是由加拿大安大略省麦克马斯特大学麦克马斯特干细胞和癌症研究所的研究人员进行的。
图示：研究人员可能已经找到了一种方法来抑制白血病细胞(如图所示)，同时保护健康的红细胞。
麦克马斯特大学生物化学和生物医学科学教授、麦克马斯特干细胞和癌症研究所所长米克·巴蒂亚领导了这项研究，研究结果发表在《自然细胞生物学》杂志上。
正如科学家们解释的那样，治疗白血病的传统方法主要是针对白血病细胞，而很少关注红细胞的保护。
但是在骨髓中产生健康的血细胞对于防止白血病患者贫血或致命感染至关重要。
首先研究作者埃里森·博伊德——博士后干细胞和癌症研究所-麦克马斯特说,“我们的方法代表了一种不同的方式看待整个骨髓白血病和考虑作为一个生态系统, 而不是传统的研究方法,试图直接杀死病变细胞本身。”
“这些传统的治疗方法没有为病人提供足够的新的治疗选择，”她继续说道。“这种疾病的标准护理标准几十年来都没有改变。”
美国癌症协会(ACS)估计，2017年将有21380人被诊断出患有急性髓系白血病(AML)。其中大部分是成年人，因为“急性髓系白血病”倾向于针对老年人。几乎一半的这些病人会死于这种疾病。
糖尿病药物如何杀死癌细胞
为了改变这种可怕的生存前景，Boyd和他的同事从34名“基因多样”的AML患者身上采集了骨髓样本。
研究人员检查了患者的血细胞形成过程，并将其与健康捐赠者的血细胞形成过程进行了比较。博伊德和他的团队随后检测了单个细胞的行为，无论是在体外，还是在细胞培养中，还是在体内，或是在将人类细胞移植入小鼠体内的情况下。
研究人员发现这种疾病“破坏了骨髓中的脂肪细胞生态龛”。更具体地说，他们发现白血病抑制了骨髓脂肪细胞，即储存脂肪的细胞。
这导致了干细胞和祖细胞的功能紊乱，而在健康的身体中，祖细胞随后会形成红细胞。因此，红细胞的成熟停止了。
为了解决这个问题，研究人员给老鼠注射了一种叫做PPAR-gamma激活剂的药物——一种通常用于治疗2型糖尿病的药物——他们发现它恢复了骨髓中的脂肪细胞。
脂肪细胞的“再生”“拯救了健康的造血成熟，同时抑制了白血病的生长。”
换句话说，促进骨髓中的脂肪细胞再生健康的血细胞，同时杀死癌变的白血病细胞。
这一发现可能会带来新的治疗方法
Bhatia教授评论了这项发现在传统抗白血病疗法背景下的重要性，他说，“化疗和现有的标准治疗方法的重点是杀死癌细胞，但我们采取了完全不同的方法，改变了癌细胞生存的环境。”
“这不仅抑制了‘坏的’癌细胞，”他解释说，“还增强了‘好的’健康细胞，让它们在新的药物诱导环境中再生。”
Bhatia教授继续说:“事实上，我们可以用现有的药物在一种组织中针对一种细胞类型，这让我们对在病人身上进行试验的可能性感到兴奋。”
“我们可以预见，这将成为一种潜在的新的治疗方法，既可以添加到现有的治疗方法中，也可以在不久的将来取代其他的治疗方法。”
事实上，这种药物激活血液再生，可以通过激活自身健康的细胞，为等待骨髓移植的病人提供益处。
Leukemia: Cancer cells killed off with diabetes drug
Published Monday 16 October 2017 By Ana Sandoiu Fact checked by Jasmin Collier
Scientists may have found an innovative way to kill off cancer cells in acute myeloid leukemia, all the while preserving and regenerating healthy red blood cells.
leukemic cell
Researchers may have found a way to suppress leukemic cells (shown here) while preserving healthy red blood cells.
The new study was carried out by researchers from the McMaster Stem Cell and Cancer Research Institute at McMaster University in Ontario, Canada.
Mick Bhatia — a professor of biochemistry and biomedical sciences at McMaster University and director of the McMaster Stem Cell and Cancer Research Institute — led the investigation, and the findings have been published in the journal Nature Cell Biology.
As the scientists explain, conventional methods for treating leukemia focus on targeting leukemic cells, paying little attention to preserving red blood cells.
But the production of healthy blood cells in the bone marrow is crucial for preventing leukemia patients from having anemia or fatal infections.
First study author Allison Boyd — a postdoctoral fellow at the McMaster Stem Cell and Cancer Research Institute — says, "Our approach represents a different way of looking at leukemia and considers the entire bone marrow as an ecosystem, rather than the traditional approach of studying and trying to directly kill the diseased cells themselves."
"These traditional approaches have not delivered enough new therapeutic options for patients," she continues. "The standard-of-care for this disease hasn't changed in several decades."
The American Cancer Society (ACS) estimate that 21,380 people will be diagnosed with acute myeloid leukemia (AML) in 2017. Most of these will be adults, as AML tends to target seniors.
Almost half of these patients will die from the disease.
How a diabetes drug kills off cancer cells
To change these dire survival prospects, Boyd and colleagues collected bone marrow samples from 34 "genetically diverse" patients with AML.
The researchers examined the patients' blood cell formation process and compared it with that of healthy donors. Boyd and team then examined the behavior of individual cells both in vitro, or in cell cultures, and in vivo, or in mice that had human cells transplanted into them.
The researchers found that the disease "disrupts the adipocytic niche" in the bone marrow. And more specifically, they found that leukemia suppresses the bone marrow adipocytes — or the cells that store fat.
This led to dysfunction in the stem cells and progenitor cells, which, in a healthy body, would later go on to form red blood cells. The maturation of red blood cells was therefore stopped.
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To combat this, the researchers administered a so-called PPAR-gamma agonist — a drug commonly used to treat type 2 diabetes — to the mice, and they found that it restored the fat cells in the bone marrow.
This "rebirth" of fat cells "rescued healthy hematopoietic maturation while repressing leukemic growth."
In other words, boosting the fat cells in the bone marrow regenerated the healthy blood cells while killing off the cancerous leukemic ones.
Findings may lead to new therapies
Prof. Bhatia comments on the significance of the findings in the context of traditional anti-leukemia therapies, saying, "The focus of chemotherapy and existing standard-of-care is on killing cancer cells but instead, we took a completely different approach which changes the environment the cancer cells live in."
"This not only suppressed the 'bad' cancer cells," he explains, "but also bolstered the 'good' healthy cells, allowing them to regenerate in the new drug-induced environment."
"The fact that we can target one cell type in one tissue using an existing drug makes us excited about the possibilities of testing this in patients," continues Prof. Bhatia.
"We can envision this becoming a potential new therapeutic approach that can either be added to existing treatments or even replace others in the near future."
The fact that this drug activates blood regeneration may provide benefits for those waiting for bone marrow transplants by activating their own healthy cells."
Prof. Mick Bhatia
Leukemia: Cancer cells killed off with diabetes drug https://www.medicalnewstoday.com/articles/319761.php?sr
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