Changes in 97df984: more fixes

				morinlab.bib
			
          @@ -1,3 +1,22 @@

          +@article{pinyolInactivationRB1Mantlecell2007,

          +  title = {Inactivation of {{RB1}} in Mantle-Cell Lymphoma Detected by Nonsense-Mediated {{mRNA}} Decay Pathway Inhibition and Microarray Analysis},

          +  author = {Pinyol, Magda and Bea, Silvia and Plà, Laura and Ribrag, Vincent and Bosq, Jacques and Rosenwald, Andreas and Campo, Elias and Jares, Pedro},

          +  date = {2007-06-15},

          +  journaltitle = {Blood},

          +  shortjournal = {Blood},

          +  volume = {109},

          +  number = {12},

          +  eprint = {17332242},

          +  eprinttype = {pmid},

          +  pages = {5422--5429},

          +  issn = {0006-4971},

          +  doi = {10.1182/blood-2006-11-057208},

          +  abstract = {Mantle-cell lymphoma (MCL) is genetically characterized by the translocation t(11;14)(q13;q32) and a high number of secondary chromosomal abnormalities. To identify genes inactivated in this lymphoma, we examined 5 MCL cell lines following a strategy previously described in tumors with microsatellite instability that is based on the combined inhibition of the nonsense-mediated mRNA decay pathway and gene-expression profiling. This approach, together with the design of a conservative algorithm for analysis of the results, allowed the identification of 3 genes carrying premature stop codons. These genes were p53 with a mutation previously described in JEKO-1, the leukocyte-derived arginine aminopeptidase (LRAP) gene in REC-1 that showed a new splicing isoform generating a premature stop codon, and RB1 in UPN-1 that contained an intragenic homozygous deletion resulting in a truncated transcript and total loss of protein expression. The new LRAP isoform was detected also in 2 primary MCLs, whereas inactivating intragenic deletions of RB1 were found in the primary tumor from which UPN-1 was derived and 1 additional blastoid MCL. These tumors carried a concomitant inactivation of p53, whereas p16INK4a was wild type. These results indicate for the first time that RB1 may be inactivated in aggressive MCL by intragenic deletions.},

          +  langid = {english},

          +  keywords = {Algorithms,Cell Line Tumor,Codon Nonsense,Dental Enamel Proteins,Gene Expression Profiling,Gene Silencing,Humans,Lymphoma Mantle-Cell,Microarray Analysis,Protein Isoforms,Retinoblastoma Protein,RNA Messenger,Tumor Suppressor Protein p53},

          +  file = {/Users/rmorin/Zotero/storage/AVNQXD5P/Pinyol et al. - 2007 - Inactivation of RB1 in mantle-cell lymphoma detect.pdf}

          +}

          +

           @article{freieGermlinePointMutation2024,

             title = {A Germline Point Mutation in the {{MYC-FBW7}} Phosphodegron Initiates Hematopoietic Malignancies},

             author = {Freie, Brian and Carroll, Patrick A. and Varnum-Finney, Barbara J. and Ramsey, Erin L. and Ramani, Vijay and Bernstein, Irwin and Eisenman, Robert N.},

...	...	@@ -1,3 +1,22 @@
	1	+@article{pinyolInactivationRB1Mantlecell2007,
	2	+ title = {Inactivation of {{RB1}} in Mantle-Cell Lymphoma Detected by Nonsense-Mediated {{mRNA}} Decay Pathway Inhibition and Microarray Analysis},
	3	+ author = {Pinyol, Magda and Bea, Silvia and Plà, Laura and Ribrag, Vincent and Bosq, Jacques and Rosenwald, Andreas and Campo, Elias and Jares, Pedro},
	4	+ date = {2007-06-15},
	5	+ journaltitle = {Blood},
	6	+ shortjournal = {Blood},
	7	+ volume = {109},
	8	+ number = {12},
	9	+ eprint = {17332242},
	10	+ eprinttype = {pmid},
	11	+ pages = {5422--5429},
	12	+ issn = {0006-4971},
	13	+ doi = {10.1182/blood-2006-11-057208},
	14	+ abstract = {Mantle-cell lymphoma (MCL) is genetically characterized by the translocation t(11;14)(q13;q32) and a high number of secondary chromosomal abnormalities. To identify genes inactivated in this lymphoma, we examined 5 MCL cell lines following a strategy previously described in tumors with microsatellite instability that is based on the combined inhibition of the nonsense-mediated mRNA decay pathway and gene-expression profiling. This approach, together with the design of a conservative algorithm for analysis of the results, allowed the identification of 3 genes carrying premature stop codons. These genes were p53 with a mutation previously described in JEKO-1, the leukocyte-derived arginine aminopeptidase (LRAP) gene in REC-1 that showed a new splicing isoform generating a premature stop codon, and RB1 in UPN-1 that contained an intragenic homozygous deletion resulting in a truncated transcript and total loss of protein expression. The new LRAP isoform was detected also in 2 primary MCLs, whereas inactivating intragenic deletions of RB1 were found in the primary tumor from which UPN-1 was derived and 1 additional blastoid MCL. These tumors carried a concomitant inactivation of p53, whereas p16INK4a was wild type. These results indicate for the first time that RB1 may be inactivated in aggressive MCL by intragenic deletions.},
	15	+ langid = {english},
	16	+ keywords = {Algorithms,Cell Line Tumor,Codon Nonsense,Dental Enamel Proteins,Gene Expression Profiling,Gene Silencing,Humans,Lymphoma Mantle-Cell,Microarray Analysis,Protein Isoforms,Retinoblastoma Protein,RNA Messenger,Tumor Suppressor Protein p53},
	17	+ file = {/Users/rmorin/Zotero/storage/AVNQXD5P/Pinyol et al. - 2007 - Inactivation of RB1 in mantle-cell lymphoma detect.pdf}
	18	+}
	19	+
1	20	@article{freieGermlinePointMutation2024,
2	21	title = {A Germline Point Mutation in the {{MYC-FBW7}} Phosphodegron Initiates Hematopoietic Malignancies},
3	22	author = {Freie, Brian and Carroll, Patrick A. and Varnum-Finney, Barbara J. and Ramsey, Erin L. and Ramani, Vijay and Bernstein, Irwin and Eisenman, Robert N.},