Changes in ad79249: more fixes

				morinlab.bib
			
          @@ -1,3 +1,23 @@

          +@article{grabinerDiverseArrayCancerassociated2014,

          +  title = {A Diverse Array of Cancer-Associated {{MTOR}} Mutations Are Hyperactivating and Can Predict Rapamycin Sensitivity},

          +  author = {Grabiner, Brian C. and Nardi, Valentina and Birsoy, Kıvanc and Possemato, Richard and Shen, Kuang and Sinha, Sumi and Jordan, Alexander and Beck, Andrew H. and Sabatini, David M.},

          +  date = {2014-05},

          +  journaltitle = {Cancer Discovery},

          +  shortjournal = {Cancer Discov},

          +  volume = {4},

          +  number = {5},

          +  eprint = {24631838},

          +  eprinttype = {pmid},

          +  pages = {554--563},

          +  issn = {2159-8290},

          +  doi = {10.1158/2159-8290.CD-13-0929},

          +  abstract = {Genes encoding components of the PI3K-AKT-mTOR signaling axis are frequently mutated in cancer, but few mutations have been characterized in MTOR, the gene encoding the mTOR kinase. Using publicly available tumor genome sequencing data, we generated a comprehensive catalog of mTOR pathway mutations in cancer, identifying 33 MTOR mutations that confer pathway hyperactivation. The mutations cluster in six distinct regions in the C-terminal half of mTOR and occur in multiple cancer types, with one cluster particularly prominent in kidney cancer. The activating mutations do not affect mTOR complex assembly, but a subset reduces binding to the mTOR inhibitor DEPTOR. mTOR complex 1 (mTORC1) signaling in cells expressing various activating mutations remains sensitive to pharmacologic mTOR inhibition, but is partially resistant to nutrient deprivation. Finally, cancer cell lines with hyperactivating MTOR mutations display heightened sensitivity to rapamycin both in culture and in vivo xenografts, suggesting that such mutations confer mTOR pathway dependency.},

          +  langid = {english},

          +  pmcid = {PMC4012430},

          +  keywords = {Animals,Antibiotics Antineoplastic,Cell Line Tumor,Databases Factual,HEK293 Cells,HeLa Cells,Humans,MAP Kinase Signaling System,MCF-7 Cells,Mechanistic Target of Rapamycin Complex 1,Mechanistic Target of Rapamycin Complex 2,Mice,Mice Nude,Multiprotein Complexes,Mutation,Neoplasms,Neoplasms Experimental,Protein Kinase Inhibitors,Sirolimus,TOR Serine-Threonine Kinases,Xenograft Model Antitumor Assays},

          +  file = {/Users/rmorin/Zotero/storage/9XHKLA8X/Grabiner et al. - 2014 - A diverse array of cancer-associated MTOR mutation.pdf}

          +}

          +

           @article{trissalMIR142LossofFunctionMutations2018,

             title = {{{MIR142 Loss-of-Function Mutations Derepress ASH1L}} to {{Increase HOXA Gene Expression}} and {{Promote Leukemogenesis}}},

             author = {Trissal, Maria C. and Wong, Terrence N. and Yao, Juo-Chin and Ramaswamy, Rahul and Kuo, Iris and Baty, Jack and Sun, Yaping and Jih, Gloria and Parikh, Nishi and Berrien-Elliott, Melissa M. and Fehniger, Todd A. and Ley, Timothy J. and Maillard, Ivan and Reddy, Pavan R. and Link, Daniel C.},

...	...	@@ -1,3 +1,23 @@
	1	+@article{grabinerDiverseArrayCancerassociated2014,
	2	+ title = {A Diverse Array of Cancer-Associated {{MTOR}} Mutations Are Hyperactivating and Can Predict Rapamycin Sensitivity},
	3	+ author = {Grabiner, Brian C. and Nardi, Valentina and Birsoy, Kıvanc and Possemato, Richard and Shen, Kuang and Sinha, Sumi and Jordan, Alexander and Beck, Andrew H. and Sabatini, David M.},
	4	+ date = {2014-05},
	5	+ journaltitle = {Cancer Discovery},
	6	+ shortjournal = {Cancer Discov},
	7	+ volume = {4},
	8	+ number = {5},
	9	+ eprint = {24631838},
	10	+ eprinttype = {pmid},
	11	+ pages = {554--563},
	12	+ issn = {2159-8290},
	13	+ doi = {10.1158/2159-8290.CD-13-0929},
	14	+ abstract = {Genes encoding components of the PI3K-AKT-mTOR signaling axis are frequently mutated in cancer, but few mutations have been characterized in MTOR, the gene encoding the mTOR kinase. Using publicly available tumor genome sequencing data, we generated a comprehensive catalog of mTOR pathway mutations in cancer, identifying 33 MTOR mutations that confer pathway hyperactivation. The mutations cluster in six distinct regions in the C-terminal half of mTOR and occur in multiple cancer types, with one cluster particularly prominent in kidney cancer. The activating mutations do not affect mTOR complex assembly, but a subset reduces binding to the mTOR inhibitor DEPTOR. mTOR complex 1 (mTORC1) signaling in cells expressing various activating mutations remains sensitive to pharmacologic mTOR inhibition, but is partially resistant to nutrient deprivation. Finally, cancer cell lines with hyperactivating MTOR mutations display heightened sensitivity to rapamycin both in culture and in vivo xenografts, suggesting that such mutations confer mTOR pathway dependency.},
	15	+ langid = {english},
	16	+ pmcid = {PMC4012430},
	17	+ keywords = {Animals,Antibiotics Antineoplastic,Cell Line Tumor,Databases Factual,HEK293 Cells,HeLa Cells,Humans,MAP Kinase Signaling System,MCF-7 Cells,Mechanistic Target of Rapamycin Complex 1,Mechanistic Target of Rapamycin Complex 2,Mice,Mice Nude,Multiprotein Complexes,Mutation,Neoplasms,Neoplasms Experimental,Protein Kinase Inhibitors,Sirolimus,TOR Serine-Threonine Kinases,Xenograft Model Antitumor Assays},
	18	+ file = {/Users/rmorin/Zotero/storage/9XHKLA8X/Grabiner et al. - 2014 - A diverse array of cancer-associated MTOR mutation.pdf}
	19	+}
	20	+
1	21	@article{trissalMIR142LossofFunctionMutations2018,
2	22	title = {{{MIR142 Loss-of-Function Mutations Derepress ASH1L}} to {{Increase HOXA Gene Expression}} and {{Promote Leukemogenesis}}},
3	23	author = {Trissal, Maria C. and Wong, Terrence N. and Yao, Juo-Chin and Ramaswamy, Rahul and Kuo, Iris and Baty, Jack and Sun, Yaping and Jih, Gloria and Parikh, Nishi and Berrien-Elliott, Melissa M. and Fehniger, Todd A. and Ley, Timothy J. and Maillard, Ivan and Reddy, Pavan R. and Link, Daniel C.},