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New human myelodysplastic cell line, TER‐3: G‐CSF specific downregulation of Ca 2+ /calmodulin‐dependent protein kinase IV
Author(s) -
Mishima Yuji,
Terui Yasuhito,
Mishima Yuko,
Katsuyama Misa,
Mori Masaki,
Tomizuka Hiroshi,
Takizawa Toshiyuki,
Miyazato Akira,
Ueda Masuzu,
Yamada Muneo,
Hayasawa Hirotoshi,
Mizunuma Nobuyuki,
Ishizaka Yukihito,
Ikeda Kazuma,
Kato Takashi,
Ozawa Keiya,
Hatake Kiyohiko
Publication year - 2002
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.10095
Subject(s) - cd15 , myeloid , cd19 , haematopoiesis , cell culture , microbiology and biotechnology , interleukin 3 , biology , cd34 , stem cell , cancer research , cd33 , antigen , chemistry , immunology , cd8 , interleukin 21 , genetics
We have established a new hematopoietic cell line from a patient with myelodysplastic syndrome (MDS), which was refractory anemia with excess blasts (RAEB). This cell line, designated TER‐3, depends on several cytokines for long‐term survival and growth, and requires interleukin‐3 (IL‐3) for continuous growth. Cytochemical analysis revealed that TER‐3 cells are weakly dianisidine positive and nonspecific esterase positive, but peroxidase negative. The surface marker profile shows that the TER‐3 cells are strongly positive for myeloid, lymphoid, and megakaryocytic antigens such as CD15, CD19, and CD61, and negative for some common multilineage antigens such as CD13, CD33, and CD34. Thus, this cell line has a multilineage phenotype, suggesting that the transformation event occurred in multipotent stem cells. Dianisidine‐ and nonspecific esterase‐positive TER‐3 cells increase with granulocyte‐colony stimulating factor (G‐CSF) rather than with IL‐3. These results suggest that the cell line is useful for understanding the mechanism underlying G‐CSF‐associated hematopoietic cell differentiation and activation in the patient with MDS. J. Cell. Physiol. 191: 183–190, 2002. © 2002 Wiley‐Liss, Inc.