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Target genes of the LMO1-regulated microRNAs and their relevant pathways may be a potential therapeutic targe
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IKZF1 rs10235796 C allele, IKZF1 rs6964969A>G, CDKN2A rs3731246 G>C, and CDKN2A rs3731246 C allele were signi fi cantly associated with Acute Lymphoblastic Leukemia in Yemenis of Arab-Asian descent. Borderline association found in IKZF1 rs4132601 T>G variant. No associations found with LMO1 rs442264; rs3794012; rs4237770
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These results suggested that LMO1 gene rs110419 A > G polymorphism may contribute to protection against neuroblastoma
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A C-to-T single nucleotide transition occurs as a somatic mutation in noncoding sequences 4 kb upstream of the transcriptional start site of the LMO1 oncogene in primary samples from patients with T-cell acute lymphoblastic leukaemia. This conforms to an APOBEC-like cytidine deaminase mutational signature and a new MYB binding site driving high levels of LMO1 expression.
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LMO1 is an important oncogene that promotes neuroblastoma initiation, progression, and widespread metastatic dissemination.
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LMO1 appears to be a coactivator of AR involved in the progression of prostate cancer
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data suggest that genetic variants in LMO1 are associated with increased NB risk in Chinese children.
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a polymorphism within a super-enhancer element in the first intron of LMO1 influences neuroblastoma susceptibility through differential GATA transcription factor binding and direct modulation of LMO1 expression in cis
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LMO1 is a commonly activated tumor promoter that activates AKT signaling in non-small cell lung cancer.
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LMO1 is a commonly activated tumor promoter that activates AKT signaling in colorectal cancer and a new predictive marker for targeted therapy.
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results show that LMO1 is poised for expression in normal progenitors, where activation of SCL/TAL1 together with a breakdown of epigenetic repression of LMO1 regulatory elements
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genetic variants within LMO1 are associated with acute lymphoblastic leukemia and identify this gene as a strong candidate for precursor B-cell leukemogenesis.
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data show that common polymorphisms at the LMO1 locus are strongly associated with susceptibility to developing neuroblastoma, but also may influence the likelihood of further somatic alterations at this locus, leading to malignant progression
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60% of transgenic mice that overexpressed both OLIG2 and LMO1 developed pre-T lymphoblastic lymphoma/leukemia with large thymic tumor masses.
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The present data suggest that TGF-beta, LMO1, possibly RUNX3, and GSDM form a regulatory pathway for directing the pit cells to apoptosis.
