Pathophysiological interaction with normal bone marrow cells during the development of chronic myeloid leukemia

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460492
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Kanazawa University
• Principal Investigator: BABA Tomohisa 金沢大学, がん進展制御研究所, 助教 (00452095)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 慢性骨髄性白血病 / 白血病幹細胞 / 造血幹細胞 / 炎症性ケモカイン

Outline of Final Research Achievements

In the initiation process of chronic myeloid leukemia (CML), a small number of transformed leukemia cells coexist with a large number of normal hematopoietic cells, gradually increasing thereafter and eventually predominating in the bone marrow space. In this study, we newly established a mouse CML model, in which we can precisely observe the expansion of leukemia cells under the normal hematopoietic system. By using this CML model, we herein demonstrated that leukemia cells produce high levels of an inflammatory chemokine, CCL3, in the BM to selectively inhibit the proliferation of normal hematopoietic stem/progenitor cells. CCL3 eventually facilitates the dominant proliferation of leukemia cells, thereby contributing to CML progression.

Free Research Field

腫瘍病理学