Changes in b3d6f12: more fixes

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

          +@article{jungnickelClonalDeleteriousMutations2000,

          +  title = {Clonal Deleterious Mutations in the {{IkappaBalpha}} Gene in the Malignant Cells in {{Hodgkin}}'s Lymphoma},

          +  author = {Jungnickel, B. and Staratschek-Jox, A. and Bräuninger, A. and Spieker, T. and Wolf, J. and Diehl, V. and Hansmann, M. L. and Rajewsky, K. and Küppers, R.},

          +  date = {2000-01-17},

          +  journaltitle = {The Journal of Experimental Medicine},

          +  shortjournal = {J Exp Med},

          +  volume = {191},

          +  number = {2},

          +  eprint = {10637284},

          +  eprinttype = {pmid},

          +  pages = {395--402},

          +  issn = {0022-1007},

          +  doi = {10.1084/jem.191.2.395},

          +  abstract = {Members of the nuclear factor (NF)-kappaB family of transcription factors play a crucial role in cellular activation, immune responses, and oncogenesis. In most cells, they are kept inactive in the cytosol by complex formation with members of the inhibitor of NF-kappaB (IkappaB) family, whose degradation activates NF-kappaB in response to diverse stimuli. In Hodgkin's lymphoma (HL), high constitutive nuclear activity of NF-kappaB is characteristic of the malignant Hodgkin and Reed-Sternberg (H/RS) cells, which occur at low number in a background of nonneoplastic inflammatory cells. In single H/RS cells micromanipulated from histological sections of HL, we detect clonal deleterious somatic mutations in the IkappaBalpha gene in two of three Epstein-Barr virus (EBV)-negative cases but not in two EBV-positive cases (in which a viral oncogene may account for NF-kappaB activation). There was no evidence for IkappaBalpha mutations in two non-HL entities or in normal germinal center B cells. This study establishes deleterious IkappaBalpha mutations as the first recurrent genetic defect found in H/RS cells, indicating a role of IkappaBalpha defects in the pathogenesis of HL and implying that IkappaBalpha is a tumor suppressor gene.},

          +  langid = {english},

          +  pmcid = {PMC2195754},

          +  keywords = {Adult,Child,DNA-Binding Proteins,Female,Gene Deletion,Hodgkin Disease,Humans,I-kappa B Proteins,Male,NF-KappaB Inhibitor alpha,Tumor Cells Cultured},

          +  file = {/Users/rmorin/Zotero/storage/CABELY4P/Jungnickel et al. - 2000 - Clonal deleterious mutations in the IkappaBalpha g.pdf}

          +}

          +

           @article{kuoRolePIM1Ibrutinibresistant2016,

             title = {The Role of {{PIM1}} in the Ibrutinib-Resistant {{ABC}} Subtype of Diffuse Large {{B-cell}} Lymphoma},

             author = {Kuo, Hsu-Ping and Ezell, Scott A. and Hsieh, Sidney and Schweighofer, Karl J. and Cheung, Leo Wk and Wu, Shiquan and Apatira, Mutiah and Sirisawad, Mint and Eckert, Karl and Liang, Yu and Hsu, Jeff and Chen, Chun-Te and Beaupre, Darrin and Chang, Betty Y.},

...	...	@@ -1,3 +1,23 @@
	1	+@article{jungnickelClonalDeleteriousMutations2000,
	2	+ title = {Clonal Deleterious Mutations in the {{IkappaBalpha}} Gene in the Malignant Cells in {{Hodgkin}}'s Lymphoma},
	3	+ author = {Jungnickel, B. and Staratschek-Jox, A. and Bräuninger, A. and Spieker, T. and Wolf, J. and Diehl, V. and Hansmann, M. L. and Rajewsky, K. and Küppers, R.},
	4	+ date = {2000-01-17},
	5	+ journaltitle = {The Journal of Experimental Medicine},
	6	+ shortjournal = {J Exp Med},
	7	+ volume = {191},
	8	+ number = {2},
	9	+ eprint = {10637284},
	10	+ eprinttype = {pmid},
	11	+ pages = {395--402},
	12	+ issn = {0022-1007},
	13	+ doi = {10.1084/jem.191.2.395},
	14	+ abstract = {Members of the nuclear factor (NF)-kappaB family of transcription factors play a crucial role in cellular activation, immune responses, and oncogenesis. In most cells, they are kept inactive in the cytosol by complex formation with members of the inhibitor of NF-kappaB (IkappaB) family, whose degradation activates NF-kappaB in response to diverse stimuli. In Hodgkin's lymphoma (HL), high constitutive nuclear activity of NF-kappaB is characteristic of the malignant Hodgkin and Reed-Sternberg (H/RS) cells, which occur at low number in a background of nonneoplastic inflammatory cells. In single H/RS cells micromanipulated from histological sections of HL, we detect clonal deleterious somatic mutations in the IkappaBalpha gene in two of three Epstein-Barr virus (EBV)-negative cases but not in two EBV-positive cases (in which a viral oncogene may account for NF-kappaB activation). There was no evidence for IkappaBalpha mutations in two non-HL entities or in normal germinal center B cells. This study establishes deleterious IkappaBalpha mutations as the first recurrent genetic defect found in H/RS cells, indicating a role of IkappaBalpha defects in the pathogenesis of HL and implying that IkappaBalpha is a tumor suppressor gene.},
	15	+ langid = {english},
	16	+ pmcid = {PMC2195754},
	17	+ keywords = {Adult,Child,DNA-Binding Proteins,Female,Gene Deletion,Hodgkin Disease,Humans,I-kappa B Proteins,Male,NF-KappaB Inhibitor alpha,Tumor Cells Cultured},
	18	+ file = {/Users/rmorin/Zotero/storage/CABELY4P/Jungnickel et al. - 2000 - Clonal deleterious mutations in the IkappaBalpha g.pdf}
	19	+}
	20	+
1	21	@article{kuoRolePIM1Ibrutinibresistant2016,
2	22	title = {The Role of {{PIM1}} in the Ibrutinib-Resistant {{ABC}} Subtype of Diffuse Large {{B-cell}} Lymphoma},
3	23	author = {Kuo, Hsu-Ping and Ezell, Scott A. and Hsieh, Sidney and Schweighofer, Karl J. and Cheung, Leo Wk and Wu, Shiquan and Apatira, Mutiah and Sirisawad, Mint and Eckert, Karl and Liang, Yu and Hsu, Jeff and Chen, Chun-Te and Beaupre, Darrin and Chang, Betty Y.},