Changes in b9a6238: Added King 2013

				morinlab.bib
			
          @@ -1,4 +1,23 @@

          +@article{kingUbiquitinLigaseFBXW72013,

          +	title = {The ubiquitin ligase {FBXW7} modulates leukemia-initiating cell activity by regulating {MYC} stability},

          +	volume = {153},

          +	issn = {1097-4172},

          +	doi = {10.1016/j.cell.2013.05.041},

          +	abstract = {Sequencing efforts led to the identification of somatic mutations that could affect the self-renewal and differentiation of cancer-initiating cells. One such recurrent mutation targets the binding pocket of the ubiquitin ligase Fbxw7. Missense FBXW7 mutations are prevalent in various tumors, including T cell acute lymphoblastic leukemia (T-ALL). To study the effects of such lesions, we generated animals carrying regulatable Fbxw7 mutant alleles. Here, we show that these mutations specifically bolster cancer-initiating cell activity in collaboration with Notch1 oncogenes but spare normal hematopoietic stem cell function. We were also able to show that FBXW7 mutations specifically affect the ubiquitylation and half-life of c-Myc protein, a key T-ALL oncogene. Using animals carrying c-Myc fusion alleles, we connected Fbxw7 function to c-Myc abundance and correlated c-Myc expression to leukemia-initiating activity. Finally, we demonstrated that small-molecule-mediated suppression of MYC activity leads to T-ALL remission, suggesting an effective therapeutic strategy.},

          +	language = {eng},

          +	number = {7},

          +	journal = {Cell},

          +	author = {King, Bryan and Trimarchi, Thomas and Reavie, Linsey and Xu, Luyao and Mullenders, Jasper and Ntziachristos, Panagiotis and Aranda-Orgilles, Beatriz and Perez-Garcia, Arianne and Shi, Junwei and Vakoc, Christopher and Sandy, Peter and Shen, Steven S. and Ferrando, Adolfo and Aifantis, Iannis},

          +	month = jun,

          +	year = {2013},

          +	pmid = {23791182},

          +	pmcid = {PMC4146439},

          +	keywords = {Animals, Cell Cycle Proteins, Disease Models, Animal, F-Box Proteins, F-Box-WD Repeat-Containing Protein 7, Hematopoietic Stem Cells, Humans, Mice, Mice, Knockout, Mutation, Missense, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Proto-Oncogene Proteins c-myc, Receptor, Notch1, Tumor Suppressor Protein p53, Ubiquitin-Protein Ligases, Ubiquitination},

          +	pages = {1552--1566},

          +	file = {Full Text:C\:\\Users\\gbanc\\Zotero\\storage\\669DC46T\\King et al. - 2013 - The ubiquitin ligase FBXW7 modulates leukemia-initiating cell activity by regulating MYC stability.pdf:application/pdf},

          +}

          +

           @article{rysFasMutationsNonHodgkins2019,

           	title = {Fas {Mutations} in {Non}-{Hodgkin}'s {Lymphoma} ({NHL}): {Implications} for {Disease} {Progression} and {Therapeutic} {Resistance}},

           	volume = {134},

...	...	@@ -1,4 +1,23 @@
1	1
	2	+@article{kingUbiquitinLigaseFBXW72013,
	3	+ title = {The ubiquitin ligase {FBXW7} modulates leukemia-initiating cell activity by regulating {MYC} stability},
	4	+ volume = {153},
	5	+ issn = {1097-4172},
	6	+ doi = {10.1016/j.cell.2013.05.041},
	7	+ abstract = {Sequencing efforts led to the identification of somatic mutations that could affect the self-renewal and differentiation of cancer-initiating cells. One such recurrent mutation targets the binding pocket of the ubiquitin ligase Fbxw7. Missense FBXW7 mutations are prevalent in various tumors, including T cell acute lymphoblastic leukemia (T-ALL). To study the effects of such lesions, we generated animals carrying regulatable Fbxw7 mutant alleles. Here, we show that these mutations specifically bolster cancer-initiating cell activity in collaboration with Notch1 oncogenes but spare normal hematopoietic stem cell function. We were also able to show that FBXW7 mutations specifically affect the ubiquitylation and half-life of c-Myc protein, a key T-ALL oncogene. Using animals carrying c-Myc fusion alleles, we connected Fbxw7 function to c-Myc abundance and correlated c-Myc expression to leukemia-initiating activity. Finally, we demonstrated that small-molecule-mediated suppression of MYC activity leads to T-ALL remission, suggesting an effective therapeutic strategy.},
	8	+ language = {eng},
	9	+ number = {7},
	10	+ journal = {Cell},
	11	+ author = {King, Bryan and Trimarchi, Thomas and Reavie, Linsey and Xu, Luyao and Mullenders, Jasper and Ntziachristos, Panagiotis and Aranda-Orgilles, Beatriz and Perez-Garcia, Arianne and Shi, Junwei and Vakoc, Christopher and Sandy, Peter and Shen, Steven S. and Ferrando, Adolfo and Aifantis, Iannis},
	12	+ month = jun,
	13	+ year = {2013},
	14	+ pmid = {23791182},
	15	+ pmcid = {PMC4146439},
	16	+ keywords = {Animals, Cell Cycle Proteins, Disease Models, Animal, F-Box Proteins, F-Box-WD Repeat-Containing Protein 7, Hematopoietic Stem Cells, Humans, Mice, Mice, Knockout, Mutation, Missense, Precursor T-Cell Lymphoblastic Leukemia-Lymphoma, Proto-Oncogene Proteins c-myc, Receptor, Notch1, Tumor Suppressor Protein p53, Ubiquitin-Protein Ligases, Ubiquitination},
	17	+ pages = {1552--1566},
	18	+ file = {Full Text:C\:\\Users\\gbanc\\Zotero\\storage\\669DC46T\\King et al. - 2013 - The ubiquitin ligase FBXW7 modulates leukemia-initiating cell activity by regulating MYC stability.pdf:application/pdf},
	19	+}
	20	+
2	21	@article{rysFasMutationsNonHodgkins2019,
3	22	title = {Fas {Mutations} in {Non}-{Hodgkin}'s {Lymphoma} ({NHL}): {Implications} for {Disease} {Progression} and {Therapeutic} {Resistance}},
4	23	volume = {134},