Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human

Naoki Morito; Keigyou Yoh; Yuki Fujioka; Takako Nakano; Homare Shimohata; Yuko Hashimoto; Akiko Yamada; Atsuko Maeda; Fumihiko Matsuno; Hiroyuki Hata; Atsushi Suzuki; Shigehiko Imagawa; Hiroaki Mitsuya; Hiroyasu Esumi; Akio Koyama; Masayuki Yamamoto; Naoyoshi Mori; Satoru Takahashi

doi:10.1158/0008-5472.CAN-05-2154

Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human

Naoki Morito, Keigyou Yoh, Yuki Fujioka, Takako Nakano, Homare Shimohata, Yuko Hashimoto, Akiko Yamada, Atsuko Maeda, Fumihiko Matsuno, Hiroyuki Hata, Atsushi Suzuki, Shigehiko Imagawa, Hiroaki Mitsuya, Hiroyasu Esumi, Akio Koyama, Masayuki Yamamoto, Naoyoshi Mori, Satoru Takahashi

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

61 Citations (Scopus)

Abstract

c-Maf translocation or overexpression has been observed in human multiple myeloma. Although c-maf might function as an oncogene in multiple myeloma, a role for this gene in other cancers has not been shown. In this study, we have found that mice transgenic for c-Maf whose expression was direct to the T-cell compartment developed T-cell lymphoma. Moreover, we showed that cyclin D2, integrin β₇, and AKK5 were upregulated in c-Maf transgenic lymphoma cells. Furthermore, 60% of human T-cell lymphomas (11 of 18 cases), classified as angioimmunoblastic T-cell lymphoma, were found to express c-Maf. These results suggest that c-Maf might cause a type of T-cell lymphoma in both mice and humans and that ARK5, in addition to cyclin D2 and integrin β₇, might be downstream target genes of c-Maf leading to malignant transformation.

Original language	English
Pages (from-to)	812-819
Number of pages	8
Journal	Cancer Research
Volume	66
Issue number	2
DOIs	https://doi.org/10.1158/0008-5472.CAN-05-2154
Publication status	Published - 2006 Jan 15
Externally published	Yes

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1158/0008-5472.CAN-05-2154

Cite this

Morito, N., Yoh, K., Fujioka, Y., Nakano, T., Shimohata, H., Hashimoto, Y., Yamada, A., Maeda, A., Matsuno, F., Hata, H., Suzuki, A., Imagawa, S., Mitsuya, H., Esumi, H., Koyama, A., Yamamoto, M., Mori, N., & Takahashi, S. (2006). Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human. Cancer Research, 66(2), 812-819. https://doi.org/10.1158/0008-5472.CAN-05-2154

Morito, N, Yoh, K, Fujioka, Y, Nakano, T, Shimohata, H, Hashimoto, Y, Yamada, A, Maeda, A, Matsuno, F, Hata, H, Suzuki, A, Imagawa, S, Mitsuya, H, Esumi, H, Koyama, A, Yamamoto, M, Mori, N & Takahashi, S 2006, 'Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human', Cancer Research, vol. 66, no. 2, pp. 812-819. https://doi.org/10.1158/0008-5472.CAN-05-2154

@article{bc31e196752d4f9baaf35039488b7972,

title = "Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human",

abstract = "c-Maf translocation or overexpression has been observed in human multiple myeloma. Although c-maf might function as an oncogene in multiple myeloma, a role for this gene in other cancers has not been shown. In this study, we have found that mice transgenic for c-Maf whose expression was direct to the T-cell compartment developed T-cell lymphoma. Moreover, we showed that cyclin D2, integrin β7, and AKK5 were upregulated in c-Maf transgenic lymphoma cells. Furthermore, 60% of human T-cell lymphomas (11 of 18 cases), classified as angioimmunoblastic T-cell lymphoma, were found to express c-Maf. These results suggest that c-Maf might cause a type of T-cell lymphoma in both mice and humans and that ARK5, in addition to cyclin D2 and integrin β7, might be downstream target genes of c-Maf leading to malignant transformation.",

author = "Naoki Morito and Keigyou Yoh and Yuki Fujioka and Takako Nakano and Homare Shimohata and Yuko Hashimoto and Akiko Yamada and Atsuko Maeda and Fumihiko Matsuno and Hiroyuki Hata and Atsushi Suzuki and Shigehiko Imagawa and Hiroaki Mitsuya and Hiroyasu Esumi and Akio Koyama and Masayuki Yamamoto and Naoyoshi Mori and Satoru Takahashi",

year = "2006",

month = jan,

day = "15",

doi = "10.1158/0008-5472.CAN-05-2154",

language = "English",

volume = "66",

pages = "812--819",

journal = "Cancer Research",

issn = "0008-5472",

number = "2",

}

TY - JOUR

T1 - Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human

AU - Morito, Naoki

AU - Yoh, Keigyou

AU - Fujioka, Yuki

AU - Nakano, Takako

AU - Shimohata, Homare

AU - Hashimoto, Yuko

AU - Yamada, Akiko

AU - Maeda, Atsuko

AU - Matsuno, Fumihiko

AU - Hata, Hiroyuki

AU - Suzuki, Atsushi

AU - Imagawa, Shigehiko

AU - Mitsuya, Hiroaki

AU - Esumi, Hiroyasu

AU - Koyama, Akio

AU - Yamamoto, Masayuki

AU - Mori, Naoyoshi

AU - Takahashi, Satoru

PY - 2006/1/15

Y1 - 2006/1/15

N2 - c-Maf translocation or overexpression has been observed in human multiple myeloma. Although c-maf might function as an oncogene in multiple myeloma, a role for this gene in other cancers has not been shown. In this study, we have found that mice transgenic for c-Maf whose expression was direct to the T-cell compartment developed T-cell lymphoma. Moreover, we showed that cyclin D2, integrin β7, and AKK5 were upregulated in c-Maf transgenic lymphoma cells. Furthermore, 60% of human T-cell lymphomas (11 of 18 cases), classified as angioimmunoblastic T-cell lymphoma, were found to express c-Maf. These results suggest that c-Maf might cause a type of T-cell lymphoma in both mice and humans and that ARK5, in addition to cyclin D2 and integrin β7, might be downstream target genes of c-Maf leading to malignant transformation.

AB - c-Maf translocation or overexpression has been observed in human multiple myeloma. Although c-maf might function as an oncogene in multiple myeloma, a role for this gene in other cancers has not been shown. In this study, we have found that mice transgenic for c-Maf whose expression was direct to the T-cell compartment developed T-cell lymphoma. Moreover, we showed that cyclin D2, integrin β7, and AKK5 were upregulated in c-Maf transgenic lymphoma cells. Furthermore, 60% of human T-cell lymphomas (11 of 18 cases), classified as angioimmunoblastic T-cell lymphoma, were found to express c-Maf. These results suggest that c-Maf might cause a type of T-cell lymphoma in both mice and humans and that ARK5, in addition to cyclin D2 and integrin β7, might be downstream target genes of c-Maf leading to malignant transformation.

UR - http://www.scopus.com/inward/record.url?scp=31544476523&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=31544476523&partnerID=8YFLogxK

U2 - 10.1158/0008-5472.CAN-05-2154

DO - 10.1158/0008-5472.CAN-05-2154

M3 - Article

C2 - 16424013

AN - SCOPUS:31544476523

VL - 66

SP - 812

EP - 819

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 2

ER -

Overexpression of c-Maf contributes to T-cell lymphoma in both mice and human

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this