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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
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초록· 키워드
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It is known that acute myeloid leukemia (AML) is a heterogeneous blood cancer, which is enormously propagated by self-renewing leukemia stem cells (LSCs). The persistence of LSCs after chemotherapy can contribute to minimal residual disease and relapse by LSCs can be evoked promptly. Elucidating special molecules and cellular activity of LSCs is an extremely important to eliminate AML. Despite an increasing understanding of the origin of LSCs by incessant study, AML still remains a notorious disease with high mortality. An exact identification of the LSCs that sustain the proliferation of neoplastic clone is a fundamental issue in AML treatment. CD34+CD38- conventional phenotype is overall regarded as LSCs, but it has a limitation that is still hard to demarcate exactly due to similarity with normal hematopoietic stem cells (HSCs). Not all primary blasts and progenitors have equal function, thus a bona fide marker for identifying LSCs from HSCs is needed in hematologic malignancy, especially in AML. These findings have direct important implications in both in mechanistic study of LSCs as well as in the strategies of more effective therapies. In this review, I briefly summarized current advances in LSCs biology, focusing on membrane markers and a functional behavior of LSCs in AML treatment with monoclonal antibodies. Ultimately, it may be helpful in overviewing the status of LSC research, while expecting the clinic benefits of target therapy by specific inhibition.
목차
INTRODUCTION
Typical phenotypes of LSCs in AML I - from the beginning of LSC seeking
Phenotypes of LSCs in AML II - differential expression between LSC and HSC
Potential drugs, monoclonal antibodies that correspond to each target
CONCLUSION
REFERENCES
참고문헌 (35)
참고문헌 신청
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Bhatia M, Wang JC, Kapp U, Bonnet D, Dick JE. Purification of primitive human hematopoietic cells capable of repopulating immune-deficient mice. Proceedings of the National Academy of Sciences of the United States of America. 1997. 94: 5320 -5325.
Blair A, Hogge DE, Ailles LE, Lansdorp PM, Sutherland HJ. Lack of expression of thy-1 (CD90) on acute myeloid leukemia cells with long-term proliferative ability in vitro and in vivo. Blood. 1997. 89: 3104-3112.
Blair A, Sutherland HJ. Primitive acute myeloid leukemia cells with long-term proliferative ability in vitro and in vivo lack surface expression of c-kit (CD117). Experimental Hematology. 2000. 28: 660-671.
Bonnet D, Dick JE. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nature Medicine. 1997. 3: 730-737.
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UCI(KEPA) : I410-ECN-0101-2017-510-002402142