| the data in this study revealed a novel crosstalk between LMO2 and the Wnt signaling pathway during tumorigenesis and suggested that LMO2 might be a tumor suppressor in certain solid tumors. | None |
| Negative regulatory elements are present in the human LMO2 oncogene and may contribute to its expression in leukemia. | leukemia, |
| Negative regulatory elements are present in the human LMO2 oncogene and may contribute to its expression in leukemia. | leukemia, |
| The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia. | leukemia,pediatric, |
| identification of a new recurrent and cryptic deletion on chromosome 11 (del(11)(p12p13)) in about 4% (6/138) of pediatric T-ALL patients that activates the LMO2 oncogene in 4 of 6 del(11)(p12p13)-positive T-ALL patients | pediatric, |
| The oncoprotein LMO2 is expressed in normal germinal-center B cells and in human B-cell lymphomas. | lymphoma, |
| A novel post-transcriptional splicing form of the acute T cell leukemia proto-oncogene Lmo2. | leukemia, |
| Expression of the leukemia oncogene Lmo2 is controlled by an array of tissue-specific elements dispersed over 100 kb and bound by Tal1/Lmo2, Ets, and Gata factors. | leukemia, |
| The Lmo2 oncogene initiates leukemia in mice by inducing thymocyte self-renewal. | leukemia, |
| Structure of the leukemia oncogene LMO2: implications for the assembly of a hematopoietic transcription factor complex. | leukemia, |
| Data show that thymic expression of the Tal1 and Lmo2 oncogenes results in rapid development of T-ALL, and similar to T-ALL patients, more than half the leukemic mice develop spontaneous mutations in Notch1. | leukemia, |
| Lyl1 is critical for all oncogenic functions of Lmo2, including upregulation of a stem cell-like gene signature, aberrant self-renewal of thymocytes, and subsequent generation of T-cell leukemia. | leukemia, |
| recurrent activating intronic mutations of LMO2, a prominent oncogene in T-cell acute lymphoblastic leukemia (T-ALL). Heterozygous mutations were identified in PF-382 and DU.528 T-ALL cell lines in addition to 3.7% of pediatric (6 of 160) and 5.5% of adult (9 of 163) T-ALL patient samples. | leukemia,pediatric, |
| T-cell oncogene rhombotin-2 interacts with retinoblastoma-binding protein 2. | retinoblastoma, |
| The oncogenic LIM-only transcription factor Lmo2 regulates angiogenesis but not vasculogenesis in mice. | None |
| The LIM domain protein Lmo2 binds to AF6, a translocation partner of the MLL oncogene. | None |
| The LMO2 T-cell oncogene is activated via chromosomal translocations or retroviral insertion during gene therapy but has no mandatory role in normal T-cell development. | None |
| Activation of the T-cell oncogene LMO2 after gene therapy for X-linked severe combined immunodeficiency. | None |
| Assembly of the oncogenic DNA-binding complex LMO2-Ldb1-TAL1-E12. | None |
| biallelic activation of LMO2 in immature T-ALL cases may reflect their early T-cell development stage rather than it represents a true oncogenic mechanism. | None |