Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma

Keiko Onda; Kazutoshi Iijima; Yohko U. Katagiri; Hajime Okita; Masahiro Saito; Toshiaki Shimizu; Nobutaka Kiyokawa

doi:10.1007/s12185-010-0567-z

Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma

Keiko Onda, Kazutoshi Iijima, Yohko U. Katagiri, Hajime Okita, Masahiro Saito, Toshiaki Shimizu, Nobutaka Kiyokawa

Research output: Contribution to journal › Article › peer-review

8 Citations (Scopus)

Abstract

B cell-activating factor belonging to the tumor necrosis factor superfamily (BAFF) is a crucial factor for B cell development and is involved in the survival of malignant B cells, but its effect on B cell precursors (BCPs) remains unclear. We investigated BCP acute lymphoblastic leukemia (-ALL) cells for BAFF receptor (-R) expression and compared the effect of BAFF on BCP-ALL cells and Burkitt lymphoma (BL) cells. Expression of BAFF-R was detected in some cell lines and some clinical specimens of both BL and BCP-ALL. BAFF acted on both BL and BCP-ALL cells and promoted proliferation by both. BAFF also inhibited apoptosis by BL cells induced by cross-linking of cell surface molecules and anticancer drugs, but failed to inhibit apoptosis by BCP-ALL cells. BAFF induced prompt and obvious activation of the NF-κB signaling pathway in BL cells, but only weak and delayed activation of the pathway in BCP-ALL cells. The results of this study indicate that some BCP-ALL cells and some BL cells express BAFF-R, but that the effects of BAFF on BCP-ALL cells are different from its effects on mature B cell malignancies.

Original language	English
Pages (from-to)	808-819
Number of pages	12
Journal	International journal of hematology
Volume	91
Issue number	5
DOIs	https://doi.org/10.1007/s12185-010-0567-z
Publication status	Published - 2010 Jun
Externally published	Yes

Keywords

Apoptosis
B cell precursor ALL
BAFF
Burkitt lymphoma

ASJC Scopus subject areas

Hematology

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Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma. / Onda, Keiko; Iijima, Kazutoshi; Katagiri, Yohko U.; Okita, Hajime; Saito, Masahiro; Shimizu, Toshiaki; Kiyokawa, Nobutaka.

In: International journal of hematology, Vol. 91, No. 5, 06.2010, p. 808-819.

Research output: Contribution to journal › Article › peer-review

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title = "Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma",

abstract = "B cell-activating factor belonging to the tumor necrosis factor superfamily (BAFF) is a crucial factor for B cell development and is involved in the survival of malignant B cells, but its effect on B cell precursors (BCPs) remains unclear. We investigated BCP acute lymphoblastic leukemia (-ALL) cells for BAFF receptor (-R) expression and compared the effect of BAFF on BCP-ALL cells and Burkitt lymphoma (BL) cells. Expression of BAFF-R was detected in some cell lines and some clinical specimens of both BL and BCP-ALL. BAFF acted on both BL and BCP-ALL cells and promoted proliferation by both. BAFF also inhibited apoptosis by BL cells induced by cross-linking of cell surface molecules and anticancer drugs, but failed to inhibit apoptosis by BCP-ALL cells. BAFF induced prompt and obvious activation of the NF-κB signaling pathway in BL cells, but only weak and delayed activation of the pathway in BCP-ALL cells. The results of this study indicate that some BCP-ALL cells and some BL cells express BAFF-R, but that the effects of BAFF on BCP-ALL cells are different from its effects on mature B cell malignancies.",

keywords = "Apoptosis, B cell precursor ALL, BAFF, Burkitt lymphoma",

author = "Keiko Onda and Kazutoshi Iijima and Katagiri, {Yohko U.} and Hajime Okita and Masahiro Saito and Toshiaki Shimizu and Nobutaka Kiyokawa",

note = "Funding Information: Acknowledgments We thank Dr. K. J. Mori and Dr. Y. Matsuo for the gift of murine BM stromal cell line MS-5 and BL/BCP-ALL cell lines, respectively. We also thank Ms. H. Kiyokawa for her assistance in preparing the manuscript. This work was supported by a grant from the Japan Health Sciences Foundation for Research on Publicly Essential Drugs and Medical Devices (KHA1004), Health and Labour Sciences Research Grants (the 3rd-term comprehensive 10-year-strategy for cancer control H19-010), and a Grant for Child Health and Development from the Ministry of Health, Labour and Welfare of Japan.",

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doi = "10.1007/s12185-010-0567-z",

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AU - Onda, Keiko

AU - Iijima, Kazutoshi

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AU - Okita, Hajime

AU - Saito, Masahiro

AU - Shimizu, Toshiaki

AU - Kiyokawa, Nobutaka

N1 - Funding Information: Acknowledgments We thank Dr. K. J. Mori and Dr. Y. Matsuo for the gift of murine BM stromal cell line MS-5 and BL/BCP-ALL cell lines, respectively. We also thank Ms. H. Kiyokawa for her assistance in preparing the manuscript. This work was supported by a grant from the Japan Health Sciences Foundation for Research on Publicly Essential Drugs and Medical Devices (KHA1004), Health and Labour Sciences Research Grants (the 3rd-term comprehensive 10-year-strategy for cancer control H19-010), and a Grant for Child Health and Development from the Ministry of Health, Labour and Welfare of Japan.

PY - 2010/6

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N2 - B cell-activating factor belonging to the tumor necrosis factor superfamily (BAFF) is a crucial factor for B cell development and is involved in the survival of malignant B cells, but its effect on B cell precursors (BCPs) remains unclear. We investigated BCP acute lymphoblastic leukemia (-ALL) cells for BAFF receptor (-R) expression and compared the effect of BAFF on BCP-ALL cells and Burkitt lymphoma (BL) cells. Expression of BAFF-R was detected in some cell lines and some clinical specimens of both BL and BCP-ALL. BAFF acted on both BL and BCP-ALL cells and promoted proliferation by both. BAFF also inhibited apoptosis by BL cells induced by cross-linking of cell surface molecules and anticancer drugs, but failed to inhibit apoptosis by BCP-ALL cells. BAFF induced prompt and obvious activation of the NF-κB signaling pathway in BL cells, but only weak and delayed activation of the pathway in BCP-ALL cells. The results of this study indicate that some BCP-ALL cells and some BL cells express BAFF-R, but that the effects of BAFF on BCP-ALL cells are different from its effects on mature B cell malignancies.

AB - B cell-activating factor belonging to the tumor necrosis factor superfamily (BAFF) is a crucial factor for B cell development and is involved in the survival of malignant B cells, but its effect on B cell precursors (BCPs) remains unclear. We investigated BCP acute lymphoblastic leukemia (-ALL) cells for BAFF receptor (-R) expression and compared the effect of BAFF on BCP-ALL cells and Burkitt lymphoma (BL) cells. Expression of BAFF-R was detected in some cell lines and some clinical specimens of both BL and BCP-ALL. BAFF acted on both BL and BCP-ALL cells and promoted proliferation by both. BAFF also inhibited apoptosis by BL cells induced by cross-linking of cell surface molecules and anticancer drugs, but failed to inhibit apoptosis by BCP-ALL cells. BAFF induced prompt and obvious activation of the NF-κB signaling pathway in BL cells, but only weak and delayed activation of the pathway in BCP-ALL cells. The results of this study indicate that some BCP-ALL cells and some BL cells express BAFF-R, but that the effects of BAFF on BCP-ALL cells are different from its effects on mature B cell malignancies.

KW - Apoptosis

KW - B cell precursor ALL

KW - BAFF

KW - Burkitt lymphoma

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ER -

Differential effects of BAFF on B cell precursor acute lymphoblastic leukemia and Burkitt lymphoma

Abstract

Keywords

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