Effects of FGF2 on the leukemia microenvironment in the bone marrow

我们研究了FGF 2对白血病细胞与其微环境之间相互作用的影响。与对照相比，从与用FGF 2处理的鼠基质单层的共培养物中回收的AML细胞显著更少。FGF 2还促进共培养中CML细胞对伊马替尼的敏感性。因此，在细胞周期静止期的AML细胞在FGF 2处理的单层中比对照少。我们接下来用Ara-C与w/wo FGF 2的组合处理人AML小鼠模型。与对照组相比，FGF 2处理小鼠的BM切片显示骨小梁增厚和白血病细胞数量增加。FGF 2不能帮助白血病细胞从脾脏中的Ara-C中存活。这些观察结果表明，由成骨细胞组成的骨内膜区域对于白血病细胞从化疗中存活至关重要，并且FGF 2通过促进成骨细胞功能而有利于BM中的白血病细胞。

We examined effects of FGF2 on interaction between leukemia cells and its microenvironment. Significantly fewer AML cells were recovered from cocultures with murine stromal monolayers treated with FGF2 than from control. FGF2 also facilitate the sensitivity of CML cells toward imatinib in the coculture. Accordingly, AML cells in cell cycle quiescent are less in FGF2-treated monolayers than control. We next treated human AML mouse model with Ara-C in combination w/wo FGF2. BM sections from FGF2-treated mice displayed thickened bone trabeculae and an increased number of leukemia cells compared to control. FGF2 did not help leukemia cells survive from Ara-C in the spleen. These observations suggest that the endosteal region consisting of osteoblasts is important for leukemia cells to survive from chemotherapy, and that FGF2 favors leukemia cell in the BM via promoting osteoblast functions.