morinlab.bib
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+@article{ramirez-komoSpontaneousLossLineage2017,
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+ title = {Spontaneous Loss of {{B}} Lineage Transcription Factors Leads to Pre-{{B}} Leukemia in {{Ebf1}}+/-{{Bcl-xLTg}} Mice},
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+ author = {Ramírez-Komo, J. A. and Delaney, M. A. and Straign, D. and Lukin, K. and Tsang, M. and Iritani, B. M. and Hagman, J.},
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+ date = {2017-07-10},
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+ journaltitle = {Oncogenesis},
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+ shortjournal = {Oncogenesis},
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+ volume = {6},
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+ number = {7},
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+ eprint = {28692033},
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+ eprinttype = {pmid},
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+ pages = {e355},
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+ issn = {2157-9024},
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+ doi = {10.1038/oncsis.2017.55},
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+ abstract = {Early B-cell factor 1 (EBF1) plays a central role in B-cell lineage specification and commitment. Loss of this critical transcription factor is strongly associated with high-risk, relapsed and therapy-resistant B-cell-acute lymphoblastic leukemia, especially in children. However, Ebf1 haploinsufficient mice exhibit a normal lifespan. To determine whether prolonged survival of B cells would enable tumorigenesis in Ebf1 haploinsufficient animals, we generated Ebf1+/-Bcl-xLTg mice, which express the anti-apoptotic factor Bcl-xL in B cells. Approximately half of Ebf1+/-Bcl-xLTg mice develop aggressive oligoclonal leukemia as they age, which engrafts in congenic wild-type recipients without prior conditioning. The neoplastic cells display a pre-B phenotype and express early developmental- and natural killer cell/myeloid-markers inappropriately. In addition, we found tumor cell-specific loss of several transcription factors critical for maintaining differentiation: EBF1, TCF3 and RUNX1. However, in the majority of tumors, loss of Ebf1 expression was not due to loss of heterozygosity. This is the first spontaneous mouse model of pre-B leukemia to demonstrate inappropriate expression of non-B-cell-specific genes associated with loss of Ebf1, Tcf3 and Runx1 expression.},
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+ langid = {english},
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+ pmcid = {PMC5541707},
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+}
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+
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@article{wangETV6MutationCohort2014,
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title = {{{ETV6}} Mutation in a Cohort of 970 Patients with Hematologic Malignancies},
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author = {Wang, Qinrong and Dong, Shasha and Yao, Hong and Wen, Lijun and Qiu, Huiying and Qin, Llili and Ma, Liang and Chen, Suning},