医学
造血
髓系白血病
骨髓
免疫学
干细胞
癌症研究
发病机制
免疫系统
白血病
酪氨酸激酶
慢性粒细胞白血病
髓样
内科学
生物
细胞生物学
受体
标识
DOI:10.1056/nejm199904293401706
摘要
In the past decade clinical and laboratory studies have led to important new insights into the biology of chronic myeloid leukemia (CML). Basic science has defined the molecular pathogenesis of CML as unregulated signal transduction by a tyrosine kinase. Clinical science has demonstrated that it is curable through immune-mediated elimination of leukemia cells by allogeneic T lymphocytes.Clinical FeaturesCML is a malignant clonal disorder of hematopoietic stem cells that results in increases in not only myeloid cells but also erythroid cells and platelets in peripheral blood and marked myeloid hyperplasia in the bone marrow (Figure 1A, Figure 1B, andFigure 1C). . . .
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