9ca3570cd2742075ec9bb8c324b763ac2889865e
morinlab.bib
| ... | ... | @@ -870,11 +870,23 @@ |
| 870 | 870 | keywords = {Animals,B-cell,BAF,Chromatin,DNA Helicases,epigenetics,germinal center,Haploinsufficiency,Humans,Hyperplasia,immunology,lymphoma,Lymphoma B-Cell,Mice,Nuclear Proteins,SMARCA4,SWI/SNF,transcription,Transcription Factors} |
| 871 | 871 | } |
| 872 | 872 | |
| 873 | -@article{challa-malladiCombinedGeneticInactivation, |
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| 874 | - title = {Combined {{Genetic Inactivation}} of \β2-{{Microglobulin}} and {{CD58 Reveals Frequent Escape}} from {{Immune Recognition}} in {{Diffuse Large B Cell Lymphoma}}}, |
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| 875 | - author = {Challa-Malladi, Madhavi and Lieu, Yen K and Califano, Olivia and Holmes, Antony B and Bhagat, Govind and Murty, Vundavalli V and Dominguez-Sola, David and Pasqualucci, Laura and Dalla-Favera, Riccardo}, |
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| 873 | +@article{challa-malladiCombinedGeneticInactivation2011, |
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| 874 | + title = {Combined Genetic Inactivation of Β2-{{Microglobulin}} and {{CD58}} Reveals Frequent Escape from Immune Recognition in Diffuse Large {{B}} Cell Lymphoma}, |
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| 875 | + author = {Challa-Malladi, Madhavi and Lieu, Yen K. and Califano, Olivia and Holmes, Antony B. and Bhagat, Govind and Murty, Vundavalli V. and Dominguez-Sola, David and Pasqualucci, Laura and Dalla-Favera, Riccardo}, |
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| 876 | + date = {2011-12-13}, |
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| 876 | 877 | journaltitle = {Cancer Cell}, |
| 877 | - pages = {1--13} |
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| 878 | + shortjournal = {Cancer Cell}, |
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| 879 | + volume = {20}, |
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| 880 | + number = {6}, |
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| 881 | + eprint = {22137796}, |
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| 882 | + eprinttype = {pmid}, |
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| 883 | + pages = {728--740}, |
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| 884 | + issn = {1878-3686}, |
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| 885 | + doi = {10.1016/j.ccr.2011.11.006}, |
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| 886 | + abstract = {We report that diffuse large B cell lymphoma (DLBCL) commonly fails to express cell-surface molecules necessary for the recognition of tumor cells by immune-effector cells. In 29\% of cases, mutations and deletions inactivate the β2-Microglobulin gene, thus preventing the cell-surface expression of the HLA class-I (HLA-I) complex that is necessary for recognition by CD8(+) cytotoxic T~cells. In 21\% of cases, analogous lesions~involve the CD58 gene, which encodes a molecule involved in T and natural killer cell-mediated responses. In addition to gene inactivation, alternative mechanisms lead to aberrant expression of HLA-I and CD58 in {$>$}60\% of DLBCL. These two events are significantly associated in this disease, suggesting that they are coselected during lymphomagenesis for their combined role in escape from immune-surveillance.}, |
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| 887 | + langid = {english}, |
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| 888 | + pmcid = {PMC3660995}, |
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| 889 | + keywords = {beta 2-Microglobulin,CD58 Antigens,Cell Line Tumor,Coculture Techniques,Cytotoxicity Immunologic,DNA Copy Number Variations,DNA Mutational Analysis,Genetic Association Studies,Genotype,Histocompatibility Antigens Class I,Humans,Killer Cells Natural,Lymphoma Large B-Cell Diffuse,Mutation,Polymorphism Single Nucleotide,Protein Stability,Transcription Genetic}, |
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| 878 | 890 | } |
| 879 | 891 | |
| 880 | 892 | @article{nieGenomewideCRISPRScreens2021b, |