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Novel non-TCR chromosome translocations t(3;11)(q25;p13) and t(X;11)(q25;p13) activating LMO2In T-cell acute lymphoblastic leukemia (T-ALL) cytogenetic alterations juxtapose the LIM-domain-only-2 gene (LMO2) with T-cell receptor loci.


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Analysis of tandem E-box motifs within human Complement receptor 2 (CR2/CD21) promoter reveals cell specific roles for RP58...Complement receptor 2 (CR2/CD21) plays an important role in the generation of normal B cell immune responses.
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Drug-gene modeling in pediatric T-cell acute lymphoblastic leukemia highlights importance of 6-mercaptopurine for outcomeThis study advances our understanding of drug resistance in T-ALL and provides new markers for patient stratification.
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The evolution of clinical trials for infant acute lymphoblastic leukemiaDespite initial improvements in survival of infants with ALL since establishment of the first pediatric cooperative group ALL trials, the poor outcome has...
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Returning raw genomic data to research participants in a pediatric cancer precision medicine trialIn pediatric cancer precision medicine clinical trials settings, parents proactively seeking treatment and answers to causation may request return of their child's raw data and/or biospecimen. To satisfy such requests, the ZERO Childhood Cancer Program required a guidance document.
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Murine bone-derived mesenchymal stem cells undergo molecular changes after a single passage in cultureThe rarity of the mesenchymal stem cell (MSC) population poses a significant challenge for MSC research. Therefore, these cells are often expanded in vitro, prior to use. However, long-term culture has been shown to alter primary MSC properties.
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Precision-guided treatment in high-risk pediatric cancersRecent research showed that precision medicine can identify new treatment strategies for patients with childhood cancers. However, it is unclear which patients will benefit most from precision-guided treatment.
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Characterization of mesenchymal stem cells in pre-B acute lymphoblastic leukemiaComponents of the bone marrow microenvironment (BMM) have been shown to mediate the way in which leukemia develops, progresses and responds to treatment. Increasing evidence shows that leukemic cells hijack the BMM, altering its functioning and establishing leukemia-supportive interactions with stromal and immune cells.