@article{oai:repo.qst.go.jp:00044867,
 author = {Kakinuma, Shizuko and Kodama, Youtarou and Amasaki, Yoshiko and Shang, Yi and Tokairin, Yutaka and Arai, Masami and Nishimura, Mayumi and Monobe, Manami and Kojima, Shuji and Shimada, Yoshiya and 柿沼 志津子 and 小玉 陽太郎 and 甘崎 佳子 and 尚 奕 and 東海林 裕 and 新井 正美 and 西村 まゆみ and 物部 真奈美 and 島田 義也},
 issue = {20},
 journal = {Oncogene},
 month = {Nov},
 note = {Deficiencies in DNA mismatch repair (MMR) result in replication errors within key tumor suppressor genes or oncogenes, and cause hereditary nonpolyposis colorectal cancer (HNPCC). Hematological malignancy with microsatellite instability is also associated with defective MMR, but little is known about the target genes for MMR. Here we identified Ikaros, a master transcription factor of lymphoid lineage commitment and differentiation, as a mutational target in spontaneous and radiation-induced T-cell lymphomas in Mlh1-deficient mice. Three quaters of lymphomas lacked Ikaros protein expression, which resulted from a frameshift mutation that created a stop codon. Mononucleotide repeat sequences at 1029-1034(C)6 and 1567-1572(G)6 in Ikaros were mutational hot spots with a one-base deletion occurring with a frequency of 45% and 50%, respectively. Point mutations and splicing alterations were also observed.  In total, 85% of the lymphomas showed aberrations in Ikaros. The characteristics of Mlh1-deficient lymphomas is harboring of multiple mutations simultaneously in the same tumor, displaying a combination of two frameshift mutations at different repeats, frameshift and point mutations, and/or deletion mutations. This is the first report of Ikaros mutations coupled with Mlh1 deficiency in lymphomagenesis.},
 pages = {2945--2949},
 title = {Ikaros is a mutational target for lymphomagenesis in Mlh1-deficient mice},
 volume = {26},
 year = {2006}
}