The HMG-I oncogene causes highly penetrant, aggressive lymphoid malignancy in transgenic mice and is overexpressed in human leukemia

HMG-I/Y is overexpressed in human cancer, although a direct role for this gene in transformation has not been established. We generated transgenic mice with HMG-I targeted to lymphoid cells. All seven informative founder HMG-I mice developed aggressive lymphoma by a mean age of 4.8 months. Tumors ex...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2004-05, Vol.64 (10), p.3371-3375
Main Authors: YI XU, SUMTER, Takita Felder, BHATTACHARYA, Raka, TESFAYE, Abeba, FUCHS, Ephraim J, WOOD, Lisa J, HUSO, David L, RESAR, Linda M. S
Format: Article
Language:English
Subjects:
Animals
Antineoplastic agents
Biological and medical sciences
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Female
HMGB1 Protein - biosynthesis
HMGB1 Protein - genetics
Humans
Lymphoma - genetics
Lymphoma - metabolism
Lymphoma - pathology
Male
Medical sciences
Mice
Mice, Transgenic
Neoplasm Transplantation
Pharmacology. Drug treatments
Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics
Precursor Cell Lymphoblastic Leukemia-Lymphoma - metabolism
RNA, Messenger - biosynthesis
RNA, Messenger - genetics
Transgenes
Tumors
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Summary:HMG-I/Y is overexpressed in human cancer, although a direct role for this gene in transformation has not been established. We generated transgenic mice with HMG-I targeted to lymphoid cells. All seven informative founder HMG-I mice developed aggressive lymphoma by a mean age of 4.8 months. Tumors express T-cell markers and are transplantable. We also demonstrate that HMG-I mRNA and protein are increased in human acute lymphocytic leukemia samples. Our results show that HMG-I functions as an oncogene and suggest that it contributes to the pathogenesis of leukemia and other cancers with increased HMG-I expression.
ISSN:0008-5472
1538-7445
DOI:10.1158/0008-5472.CAN-04-0044