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Myeloproliferative neoplasms and thrombosis. Blood 122, 2176–2184 (2013).",{"doi":304},"10.1182\u002Fblood-2013-03-460154",{"id":23,"text":306,"url":23,"identifiers":307},"Marchioli, R. et al. Cardiovascular events and intensity of treatment in polycythemia vera. N. Engl. J. Med. 368, 22–33 (2013).",{"doi":308},"10.1056\u002FNEJMoa1208500",{"id":23,"text":310,"url":23,"identifiers":311},"Landolfi, R. et al. Efficacy and safety of low-dose aspirin in polycythemia vera. N. Engl. J. Med. 350, 114–124 (2004).",{"doi":312},"10.1056\u002FNEJMoa035572",{"id":23,"text":314,"url":23,"identifiers":315},"Barbui, T. et al. Philadelphia chromosome-negative classical myeloproliferative neoplasms: revised management recommendations from European LeukemiaNet. Leukemia 32, 1057–1069 (2018).",{"doi":316},"10.1038\u002Fs41375-018-0077-1",{"id":23,"text":318,"url":23,"identifiers":319},"Tefferi, A., Vannucchi, A. M. & Barbui, T. Polycythemia vera treatment algorithm 2018. 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Risk factors for arterial versus venous thrombosis inpolycythemia vera: a single center experience in 587 patients. Blood Cancer J. 7, 662 (2017).",{"doi":339},"10.1038\u002Fs41408-017-0035-6",{"id":23,"text":341,"url":23,"identifiers":342},"Austin, P. C. An introduction to propensity score methods for reducing the effects of confounding in observational studies. Multivar. Behav. Res. 46, 399–424 (2011).",{"doi":343},"10.1080\u002F00273171.2011.568786",{"id":23,"text":345,"url":23,"identifiers":346},"Maugeri, N. et al. Inhibition of tissue factor expression by hydroxyurea in polymorphonuclear leukocytes from patients with myeloproliferative disorders: a new effect for an old drug? J. Thromb. Haemost. 4, 2593–2598 (2006).",{"doi":347},"10.1111\u002Fj.1538-7836.2006.02194.x",{"id":23,"text":349,"url":23,"identifiers":350},"Wendelboe, A. M. & Raskob, G. E. Global burden of thrombosis: epidemiologic aspects. Circ. 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Long-term treatment with antiplatelet drugs or vitamin K-antagonists (VKA) was given to 1391 (92.7%) patients; 975 (65%) patients received hydroxyurea (HU). We recorded 348 recurrences (venous in 142 cases) over 6075 patient-years, with an incidence rate of 5.7 per 100 pt-years (95% CI 5.1–6.4). The site of the first thrombosis predicted the site of recurrence. Independent factors influencing the rate of novel arterial thrombosis were HU (HR 0.67, 95% CI 0.46–0.98), antiplatelet treatment (HR 0.54, 95% CI 0.35–0.82), and VKA (HR 0.58, 95% CI 0.35–0.96). On the contrary, the recurrence of venous thromboses was significantly diminished only by VKA (HR 0.60, 95% CI 0.37–0.95), while HU prevented late but not early recurrences after venous thrombosis at common sites. Of note, we failed to demonstrate a positive effect of HU in the prevention of recurrent splanchnic vein thrombosis. In conclusion, in MPN patients, HU plays a role in the prevention of arterial thrombosis, together with aspirin and VKA, whereas its action in the prevention of recurrent venous thrombosis is uncertain. Such findings call for future studies to optimize and personalize secondary prophylaxis after MPN-related thrombosis.\u003C\u002Fjats:p>",{"EN":369},"Hydroxyurea prevents arterial and late venous thrombotic recurrences in patients with myeloproliferative neoplasms but fails in the splanchnic venous district. 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Risk for arterial and venous thrombosis in patients with myeloproliferative neoplasms: a population-based cohort study. Ann. Intern. Med. 168, 317–325 (2018).",{"doi":559},"10.7326\u002FM17-0028",{"id":23,"text":561,"url":23,"identifiers":562},"Patrono, C., Rocca, B. & De Stefano, V. Platelet activation and inhibition in polycythemia vera and essential thrombocythemia. Blood 121, 1701–1711 (2013).",{"doi":563},"10.1182\u002Fblood-2012-10-429134",{"id":23,"text":565,"url":23,"identifiers":566},"Barbui, T., Finazzi, G. & Falanga, A. Myeloproliferative neoplasms, and thrombosis. Blood 122, 2176–2184 (2013).",{"doi":304},{"id":23,"text":568,"url":23,"identifiers":569},"De Stefano, V. et al. Benefit-risk profile of cytoreductive drugs along with antiplatelet and antithrombotic therapy after transient ischemic attack or ischemic stroke in myeloproliferative neoplasms. 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Splanchnic vein thrombosis in myeloproliferative neoplasms: risk factors for recurrences in a cohort of 181 patients. Blood Cancer J. 6, e493 (2016).",{"doi":586},"10.1038\u002Fbcj.2016.103",{"id":23,"text":588,"url":23,"identifiers":589},"Cortelazzo, S. et al. Hydroxyurea for patients with essential thrombocythemia and a high risk of thrombosis. N. Engl. J. Med. 332, 1132–1136 (1995).",{"doi":590},"10.1056\u002FNEJM199504273321704",{"id":23,"text":592,"url":23,"identifiers":593},"Harrison, C. N. et al. Hydroxyurea compared with anagrelide in high-risk essential thrombocythemia. N. Engl. J. Med. 353, 33–45 (2005).",{"doi":594},"10.1056\u002FNEJMoa043800",{"id":23,"text":596,"url":23,"identifiers":597},"Gisslinger, H. et al. Anagrelide compared with hydroxyurea in WHO-classified essential thrombocythemia: the ANAHYDRET Study, a randomized controlled trial. Blood 121, 1720–1728 (2013).",{"doi":598},"10.1182\u002Fblood-2012-07-443770",{"id":23,"text":333,"url":23,"identifiers":600},{"doi":335},{"id":23,"text":602,"url":23,"identifiers":603},"Barbui, T., et al. Different effect of hydroxyurea and phlebotomy on prevention of arterial and venous thrombosis in polycythemia vera. Blood Cancer J., in press.",{},{"id":23,"text":314,"url":23,"identifiers":605},{"doi":316},{"id":23,"text":607,"url":23,"identifiers":608},"Franchini, M. & Mannucci, P. M. Association between venous and arterial thrombosis: clinical implications. Eur. J. Intern. Med. 23, 333–337 (2012).",{"doi":609},"10.1016\u002Fj.ejim.2012.02.008",{"id":23,"text":611,"url":23,"identifiers":612},"Spronk, H.M.H. et al. Atherothrombosis and thromboembolism: position paper from the Second MaastrichtConsensus Conference on thrombosis. Thromb. Haemost 118, 229–250 (2018).",{"doi":613},"10.1160\u002FTH17-07-0492",{"id":23,"text":345,"url":23,"identifiers":615},{"doi":347},{"id":23,"text":617,"url":23,"identifiers":618},"Swystun, L. L. & Liaw, P. C. The role of leukocytes in thrombosis. Blood 128, 753–762 (2016).",{"doi":619},"10.1182\u002Fblood-2016-05-718114",{"id":23,"text":621,"url":23,"identifiers":622},"Nahrendorf, M. Myeloid cell contributions to cardiovascular health and disease. Nat. Med. 24, 711–720 (2018).",{"doi":623},"10.1038\u002Fs41591-018-0064-0",{"id":23,"text":625,"url":23,"identifiers":626},"Landolfi, R. et al. Leukocytosis as a major thrombotic risk factor in patients with polycythemia vera. Blood 109, 2446–2452 (2007).",{"doi":627},"10.1182\u002Fblood-2006-08-042515",{"id":23,"text":629,"url":23,"identifiers":630},"Carobbio, A. et al. Leukocytosis and risk stratification assessment in essential thrombocythemia. J. Clin. 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The presence of JAK2 V617F mutation in the liver endothelial cells of patients with Budd-Chiari syndrome. Blood 113, 5246–5249 (2009).",{"doi":647},"10.1182\u002Fblood-2008-11-191544",{"id":23,"text":649,"url":23,"identifiers":650},"Rosti, V. et al. Spleen endothelial cells from patients with myelofibrosis harbor the JAK2V617F mutation. Blood 121, 360–368 (2013).",{"doi":651},"10.1182\u002Fblood-2012-01-404889",{"id":23,"text":653,"url":23,"identifiers":654},"Robertson, L., Yeoh, S. E. & Ramli, A. Secondary prevention of recurrent venous thromboembolism after initial oral anticoagulation therapy in patients with unprovoked venous thromboembolism. Cochrane Database Syst. Rev. 12, CD011088 (2017).",{},{"id":656,"createTime":657,"updateTime":657,"relativeEntities":658,"slug":659,"properties":660,"entityType":132,"verifyStatus":133,"verifyTime":657,"verifyNote":135,"syncStatus":22,"languages":676,"translateLanguages":23,"viewCount":24,"primaryUrl":677,"fullTextUrl":23,"authors":678,"publicationType":264,"publisherRelationship":1081,"citationCount":1114,"citationInfo":1115,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":1117,"isForceReanalyzing":352},"105a08d5-d551-4d94-ac14-acc9ace48425","2024-12-05T19:19:31.592+00:00",[],"EZH2-alterations-in-follicular-lymphoma-biological-and-clinical-correlations",{"mag":661,"keywords":663,"pmc":664,"openalex":666,"abstract":668,"title":670,"pm":672,"doi":674},{"VOID":662},"2607299002",{},{"VOID":665},"5436075",{"VOID":667},"W2607299002",{"EN":669},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The histone methyltransferase EZH2 has an essential role in the development of follicular lymphoma (FL). Recurrent gain-of-function mutations in\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>have been described in 25% of FL patients and induce aberrant methylation of histone H3 lysine 27 (H3K27). We evaluated the role of\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>genomic gains in FL biology. Using RNA sequencing, Sanger sequencing and SNP-arrays, the mutation status, copy-number and gene-expression profiles of\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>were assessed in a cohort of 159 FL patients from the PRIMA trial. Immunohistochemical (IHC) EZH2 expression (\u003Cjats:italic>n\u003C\u002Fjats:italic>=55) and H3K27 methylation (\u003Cjats:italic>n\u003C\u002Fjats:italic>=63) profiles were also evaluated. In total, 37% of patients (59\u002F159) harbored an alteration in the\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>gene (mutation\u003Cjats:italic>n\u003C\u002Fjats:italic>=46, gain\u003Cjats:italic>n\u003C\u002Fjats:italic>=23). Both types of alterations were associated with highly similar transcriptional changes, with increased proliferation programs. An H3K27me3\u002Fme2 IHC score fully distinguished mutated from wild-type samples, showing its applicability as surrogate for\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>mutation analysis. However, this score did not predict the presence of gains at the\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>locus. The presence of an\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>genetic alteration was an independent factor associated with a longer progression-free survival (hazard ratio 0.58, 95% confidence interval 0.36–0.93,\u003Cjats:italic>P\u003C\u002Fjats:italic>=0.025). We propose that the copy-number status of\u003Cjats:italic>EZH2\u003C\u002Fjats:italic>should also be considered when evaluating patient stratification and selecting patients for EZH2 inhibitor-targeted therapies.\u003C\u002Fjats:p>",{"EN":671},"EZH2 alterations in follicular lymphoma: biological and clinical 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Coordinated activities of wild-type plus mutant EZH2 drive tumor-associated hypertrimethylation of lysine 27 on histone H3 (H3K27) in human B-cell lymphomas. Proc Natl Acad Sci USA 2010; 107: 20980–20985.",{"doi":1160},"10.1073\u002Fpnas.1012525107",{"id":23,"text":1162,"url":23,"identifiers":1163},"Yap DB, Chu J, Berg T, Schapira M, Cheng S-WG, Moradian A et al. Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. Blood 2011; 117: 2451–2459.",{"doi":1164},"10.1182\u002Fblood-2010-11-321208",{"id":23,"text":1166,"url":23,"identifiers":1167},"McCabe MT, Ott HM, Ganji G, Korenchuk S, Thompson C, Van Aller GS et al. EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations. Nature 2012; 492: 108–112.",{"doi":1168},"10.1038\u002Fnature11606",{"id":23,"text":1170,"url":23,"identifiers":1171},"Béguelin W, Popovic R, Teater M, Jiang Y, Bunting KL, Rosen M et al. EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. Cancer Cell 2013; 23: 677–692.",{"doi":1172},"10.1016\u002Fj.ccr.2013.04.011",{"id":23,"text":1174,"url":23,"identifiers":1175},"Souroullas GP, Jeck WR, Parker JS, Simon JM, Liu J-Y, Paulk J et al. An oncogenic Ezh2 mutation induces tumors through global redistribution of histone 3 lysine 27 trimethylation. Nat Med 2016; 22: 632–640.",{"doi":1176},"10.1038\u002Fnm.4092",{"id":23,"text":1178,"url":23,"identifiers":1179},"Caganova M, Carrisi C, Varano G, Mainoldi F, Zanardi F, Germain P-L et al. Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis. J Clin Invest 2013; 123: 5009–5022.",{"doi":1180},"10.1172\u002FJCI70626",{"id":23,"text":1182,"url":23,"identifiers":1183},"Knutson SK, Kawano S, Minoshima Y, Warholic NM, Huang K-C, Xiao Y et al. Selective inhibition of EZH2 by EPZ-6438 leads to potent antitumor activity in EZH2-mutant non-Hodgkin lymphoma. Mol Cancer Ther 2014; 13: 842–854.",{"doi":1184},"10.1158\u002F1535-7163.MCT-13-0773",{"id":23,"text":1186,"url":23,"identifiers":1187},"Qi W, Chan H, Teng L, Li L, Chuai S, Zhang R et al. Selective inhibition of Ezh2 by a small molecule inhibitor blocks tumor cells proliferation. Proc Natl Acad Sci USA 2012; 109: 21360–21365.",{"doi":1188},"10.1073\u002Fpnas.1210371110",{"id":23,"text":1190,"url":23,"identifiers":1191},"Dubois S, Mareschal S, Picquenot J-M, Viailly P-J, Bohers E, Cornic M et al. Immunohistochemical and genomic profiles of diffuse large B-cell lymphomas: implications for targeted EZH2 inhibitor therapy? Oncotarget 2015; 6: 16712–16724.",{"doi":1192},"10.18632\u002Foncotarget.3154",{"id":23,"text":1194,"url":23,"identifiers":1195},"Zhou Z, Gao J, Popovic R, Wolniak K, Parimi V, Winter JN et al. 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J R Stat Soc Ser B 1995; 57: 289–300.",{"doi":1232},"10.1111\u002Fj.2517-6161.1995.tb02031.x",{"id":23,"text":1234,"url":23,"identifiers":1235},"Subramanian A, Tamayo P, Mootha VK, Mukherjee S, Ebert BL, Gillette MA et al. Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles. Proc Natl Acad Sci USA 2005; 102: 15545–15550.",{"doi":1236},"10.1073\u002Fpnas.0506580102",{"id":23,"text":1238,"url":23,"identifiers":1239},"Casulo C, Byrtek M, Dawson KL, Zhou X, Farber CM, Flowers CR et al. Early relapse of follicular lymphoma after rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone defines patients at high risk for death: an analysis from the National LymphoCare Study. J Clin Oncol 2015; 33: 2516–2522.",{"doi":1240},"10.1200\u002FJCO.2014.59.7534",{"id":23,"text":1242,"url":23,"identifiers":1243},"Maurer MJ, Bachy E, Ghesquières H, Ansell SM, Nowakowski GS, Thompson CA et al. 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Genome-wide analysis of pediatric-type follicular lymphoma reveals low genetic complexity and recurrent alterations of TNFRSF14 gene. Blood 2016; 128: 1101–1111.",{"doi":1256},"10.1182\u002Fblood-2016-03-703819",{"id":23,"text":1258,"url":23,"identifiers":1259},"Jurinovic V, Kridel R, Staiger AM, Szczepanowski M, Horn H, Dreyling MH et al. Clinicogenetic risk models predict early progression of follicular lymphoma after first-line immunochemotherapy. Blood 2016; 128: 1112–1120.",{"doi":1260},"10.1182\u002Fblood-2016-05-717355",{"id":23,"text":1262,"url":23,"identifiers":1263},"Sarkozy C, Seymour JF, Ferme C, Caballero D, Ghesquieres H, Leppa S et al. Rituximab maintenance obviates the poor prognosis associated with circulating lymphoma cells in patients with follicular lymphoma. Blood 2014; 123: 2740–2742.",{"doi":1264},"10.1182\u002Fblood-2014-02-553693",{"id":1266,"createTime":1267,"updateTime":1267,"relativeEntities":1268,"slug":1269,"properties":1270,"entityType":132,"verifyStatus":133,"verifyTime":1267,"verifyNote":135,"syncStatus":22,"languages":1286,"translateLanguages":23,"viewCount":24,"primaryUrl":1287,"fullTextUrl":23,"authors":1288,"publicationType":264,"publisherRelationship":1508,"citationCount":1540,"citationInfo":1541,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":1543,"isForceReanalyzing":352},"aaee609f-39b8-4076-84b9-0d5cdd6444f4","2024-12-05T19:19:19.003+00:00",[],"IL-10-induces-the-development-of-immunosuppressive-CD14-HLA-DRlow-monocytes-in-B-cell-non-Hodgkin-lymphoma",{"mag":1271,"keywords":1273,"pmc":1274,"openalex":1276,"abstract":1278,"title":1280,"pm":1282,"doi":1284},{"VOID":1272},"2402627636",{},{"VOID":1275},"4526782",{"VOID":1277},"W2402627636",{"EN":1279},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The biological role of monocytes and macrophages in B-cell non-Hodgkin lymphoma (NHL) is not fully understood. We have previously reported that monocytes from patients with B-cell NHL have an immunosuppressive CD14\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> phenotype that correlates with a poor prognosis. However, the underlying mechanism by which CD14\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> monocytes develop in lymphoma is unknown. In the present study, we found that interleukin (IL)-10, which is increased in the serum of patients with B-cell NHL, induced the development of the CD4\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> population. Using peripheral blood samples from patients with B-cell NHL, we found that absolute numbers of CD14\u003Cjats:sup>+\u003C\u002Fjats:sup> monocytic cells with an HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> phenotype were higher than healthy controls and correlated with a higher International Prognostic Index score. IL-10 serum levels were elevated in lymphoma patients compared with controls and were associated with increased peripheral monocyte counts. Treatment of monocytes with IL-10 \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> significantly decreased HLA-DR expression and resulted in the expansion of CD14\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> population. We found that lymphoma B cells produce IL-10 and supernatants from cultured lymphoma cells increased the CD14\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> population. Furthermore, we found that IL-10-induced CD14\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> monocytes inhibited the activation and proliferation of T cells. Taken together, these results suggest that elevated IL-10 serum levels contribute to increased numbers of immunosuppressive CD14\u003Cjats:sup>+\u003C\u002Fjats:sup>HLA-DR\u003Cjats:sup>low\u002F−\u003C\u002Fjats:sup> monocytes in B-cell NHL.\u003C\u002Fjats:p>",{"EN":1281},"IL-10 induces the development of immunosuppressive CD14+HLA-DRlow\u002F− monocytes in B-cell non-Hodgkin lymphoma",{"VOID":1283},"26230952",{"VOID":1285},"10.1038\u002Fbcj.2015.56",[137],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fbcj201556",[1289,1308,1328,1350,1365,1382,1399,1414,1429,1444,1459,1476,1491],{"id":1290,"sortIndex":554,"researcher":23,"roles":1291,"affiliations":1292,"properties":1303},"dea30833-44ab-4af5-ac60-28afd6ca847a",[],[1293],{"id":1294,"sortIndex":24,"affiliation":1295,"properties":23},"48e4edbe-4ba3-48cd-9d11-3abc6bc5bbfb",{"id":1296,"createTime":1297,"updateTime":1297,"relativeEntities":1298,"slug":1299,"properties":1300,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"a0b25c39-b8bc-477e-9534-1d933c9302cf","2024-12-05T19:19:19.032+00:00",[],"Department-of-Hematology-Tongji-Hospital-Tongji-University-Shanghai-China",{"title":1301},{"EN":1302},"Department of Hematology, Tongji Hospital, Tongji University, Shanghai, China",{"openalex":1304,"title":1306},{"VOID":1305},"A5108585605",{"EN":1307},"A-B Liang",{"id":1309,"sortIndex":553,"researcher":23,"roles":1310,"affiliations":1311,"properties":1323},"adb7c40f-1fef-4add-974d-3e4765d704bf",[],[1312],{"id":1313,"sortIndex":24,"affiliation":1314,"properties":23},"e21da54a-a1d3-48cb-b176-2e31ec5092cb",{"id":1315,"createTime":1316,"updateTime":1317,"relativeEntities":1318,"slug":1319,"properties":1320,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"5421f93c-ea59-487e-bf03-6840aee71ceb","2023-12-05T11:39:47.046+00:00","2024-12-05T19:19:19.022+00:00",[],"Division-of-Hematology-and-Internal-Medicine-Mayo-Clinic-Rochester-MN-USA",{"title":1321},{"VI":1322},"Division of Hematology and Internal Medicine, Mayo Clinic, Rochester, MN, USA",{"openalex":1324,"title":1326},{"VOID":1325},"A5102226858",{"EN":1327},"Z-Z Yang",{"id":1329,"sortIndex":299,"researcher":23,"roles":1330,"affiliations":1331,"properties":1343},"30900eac-6e1e-4b26-afec-d7e1f733a463",[],[1332],{"id":1333,"sortIndex":24,"affiliation":1334,"properties":23},"4e4a515b-e080-495c-b23b-1caa2d50ca94",{"id":1335,"createTime":1336,"updateTime":1337,"relativeEntities":1338,"slug":1339,"properties":1340,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"c3150a88-d92b-49c5-a0c1-bcf18f0b886a","2023-12-31T03:30:47.236+00:00","2024-12-05T19:19:19.066+00:00",[],"Division-of-Transfusion-Medicine-Mayo-Clinic-Rochester-MN-USA",{"title":1341},{"VI":1342},"Division of Transfusion Medicine, Mayo Clinic, Rochester, MN, USA",{"openalex":1344,"orcid":1346,"title":1348},{"VOID":1345},"A5027942310",{"VOID":1347},"https:\u002F\u002Forcid.org\u002F0000-0003-3410-9621",{"EN":1349},"Allan B. 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Absolute lymphocyte count predicts therapeutic efficacy and survival at the time of radioimmunotherapy in patients with relapsed follicular lymphomas. Leukemia 2007; 21: 2554–2556.",{"doi":1574},"10.1038\u002Fsj.leu.2404819",{"id":23,"text":1576,"url":23,"identifiers":1577},"Farinha P, Masoudi H, Skinnider BF, Shumansky K, Spinelli JJ, Gill K et al. Analysis of multiple biomarkers shows that lymphoma-associated macrophage (LAM) content is an independent predictor of survival in follicular lymphoma (FL). Blood 2005; 106: 2169–2174.",{"doi":1578},"10.1182\u002Fblood-2005-04-1565",{"id":23,"text":1580,"url":23,"identifiers":1581},"Canioni D, Salles G, Mounier N, Brousse N, Keuppens M, Morchhauser F et al. High numbers of tumor-associated macrophages have an adverse prognostic value that can be circumvented by rituximab in patients with follicular lymphoma enrolled onto the GELA-GOELAMS FL-2000 trial. J Clin Oncol 2008; 26: 440–446.",{"doi":1582},"10.1200\u002FJCO.2007.12.8298",{"id":23,"text":1584,"url":23,"identifiers":1585},"Clear AJ, Lee AM, Calaminici M, Ramsay AG, Morris KJ, Hallam S et al. Increased angiogenic sprouting in poor prognosis FL is associated with elevated numbers of CD163+ macrophages within the immediate sprouting microenvironment. Blood 2010; 115: 5053–5056.",{"doi":1586},"10.1182\u002Fblood-2009-11-253260",{"id":23,"text":1588,"url":23,"identifiers":1589},"Marchesi F, Cirillo M, Bianchi A, Gately M, Olimpieri OM, Cerchiara E et al. High density of CD68+\u002FCD163+ tumour-associated macrophages (M2-TAM) at diagnosis is significantly correlated to unfavorable prognostic factors and to poor clinical outcomes in patients with diffuse large B-cell lymphoma. Hematol Oncol 2014; 33: 110–112.",{"doi":1590},"10.1002\u002Fhon.2142",{"id":23,"text":1592,"url":23,"identifiers":1593},"Yamamoto W, Nakamura N, Tomita N, Takeuchi K, Ishii Y, Takahashi H et al. Human leukocyte antigen-DR expression on flow cytometry and tumor-associated macrophages in diffuse large B-cell lymphoma treated by rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone therapy: retrospective cohort study. Leuk Lymphoma 2014; 55: 2721–2727.",{"doi":1594},"10.3109\u002F10428194.2014.893311",{"id":23,"text":1596,"url":23,"identifiers":1597},"Lin Y, Gustafson MP, Bulur PA, Gastineau DA, Witzig TE, Dietz AB . Immunosuppressive CD14+HLA-DR(low)\u002F− monocytes in B-cell non-Hodgkin lymphoma. Blood 2011; 117: 872–881.",{"doi":1598},"10.1182\u002Fblood-2010-05-283820",{"id":23,"text":1600,"url":23,"identifiers":1601},"Khalifa KA BH, Radwan WM, Shehata MA, Bassuoni MA . CD14+HLA-DRlow\u002F− monocytes as indicator of disease aggressiveness in B-cell non-Hodgkin lymphoma. Int J Lab Hematol 2014; 36: 650–655.",{"doi":1602},"10.1111\u002Fijlh.12203",{"id":23,"text":1604,"url":23,"identifiers":1605},"Asadullah K, Sterry W, Volk HD . Interleukin-10 therapy–review of a new approach. Pharmacol Rev 2003; 55: 241–269.",{"doi":1606},"10.1124\u002Fpr.55.2.4",{"id":23,"text":1608,"url":23,"identifiers":1609},"de Waal Malefyt R, Abrams J, Bennett B, Figdor CG, de Vries JE . Interleukin 10(IL-10) inhibits cytokine synthesis by human monocytes: an autoregulatory role of IL-10 produced by monocytes. J Exp Med 1991; 174: 1209–1220.",{"doi":1610},"10.1084\u002Fjem.174.5.1209",{"id":23,"text":1612,"url":23,"identifiers":1613},"Fiorentino DF, Zlotnik A, Vieira P, Mosmann TR, Howard M, Moore KW et al. IL-10 acts on the antigen-presenting cell to inhibit cytokine production by Th1 cells. J Immunol 1991; 146: 3444–3451.",{"doi":1614},"10.4049\u002Fjimmunol.146.10.3444",{"id":23,"text":1616,"url":23,"identifiers":1617},"Mocellin S, Marincola FM, Young HA . Interleukin-10 and the immune response against cancer: a counterpoint. J Leukoc Biol 2005; 78: 1043–1051.",{"doi":1618},"10.1189\u002Fjlb.0705358",{"id":23,"text":1620,"url":23,"identifiers":1621},"Sharma S, Stolina M, Lin Y, Gardner B, Miller PW, Kronenberg M et al. T cell-derived IL-10 promotes lung cancer growth by suppressing both T cell and APC function. J Immunol 1999; 163: 5020–5028.",{"doi":1622},"10.4049\u002Fjimmunol.163.9.5020",{"id":23,"text":1624,"url":23,"identifiers":1625},"Charbonneau B, Maurer MJ, Ansell SM, Slager SL, Fredericksen ZS, Ziesmer SC et al. Pretreatment circulating serum cytokines associated with follicular and diffuse large B-cell lymphoma: a clinic-based case-control study. Cytokine 2012; 60: 882–889.",{"doi":1626},"10.1016\u002Fj.cyto.2012.08.028",{"id":23,"text":1628,"url":23,"identifiers":1629},"Gupta M, Han JJ, Stenson M, Maurer M, Wellik L, Hu G et al. Elevated serum IL-10 levels in diffuse large B-cell lymphoma: a mechanism of aberrant JAK2 activation. Blood 2012; 119: 2844–2853.",{"doi":1630},"10.1182\u002Fblood-2011-10-388538",{"id":23,"text":1632,"url":23,"identifiers":1633},"Conroy SM, Maskarinec G, Morimoto Y, Franke AA, Cooney RV, Wilkens LR et al. Non-hodgkin lymphoma and circulating markers of inflammation and adiposity in a nested case-control study: the multiethnic cohort. Cancer Epidemiol Biomarkers Prev 2013; 22: 337–347.",{"doi":1634},"10.1158\u002F1055-9965.EPI-12-0947",{"id":23,"text":1636,"url":23,"identifiers":1637},"Gustafson MP, Lin Y, Maas ML, Van Keulen VP, Johnston PB, Peikert T et al. A method for identification and analysis of non-overlapping myeloid immunophenotypes in humans. PLoS One 2015; 10: e0121546.",{"doi":1638},"10.1371\u002Fjournal.pone.0121546",{"id":23,"text":1640,"url":23,"identifiers":1641},"Ziegler-Heitbrock L, Ancuta P, Crowe S, Dalod M, Grau V, Hart DN et al. Nomenclature of monocytes and dendritic cells in blood. Blood 2010; 116: e74–e80.",{"doi":1642},"10.1182\u002Fblood-2010-02-258558",{"id":23,"text":1644,"url":23,"identifiers":1645},"Dave SS, Wright G, Tan B, Rosenwald A, Gascoyne RD, Chan WC et al. Prediction of survival in follicular lymphoma based on molecular features of tumor-infiltrating immune cells. N Engl J Med 2004; 351: 2159–2169.",{"doi":1646},"10.1056\u002FNEJMoa041869",{"id":23,"text":1648,"url":23,"identifiers":1649},"Filipazzi P, Valenti R, Huber V, Pilla L, Canese P, Iero M et al. Identification of a new subset of myeloid suppressor cells in peripheral blood of melanoma patients with modulation by a granulocyte-macrophage colony-stimulation factor-based antitumor vaccine. J Clin Oncol 2007; 25: 2546–2553.",{"doi":1650},"10.1200\u002FJCO.2006.08.5829",{"id":23,"text":1652,"url":23,"identifiers":1653},"Hoechst B, Ormandy LA, Ballmaier M, Lehner F, Kruger C, Manns MP et al. A new population of myeloid-derived suppressor cells in hepatocellular carcinoma patients induces CD4(+)CD25(+)Foxp3(+) T cells. Gastroenterology 2008; 135: 234–243.",{"doi":1654},"10.1053\u002Fj.gastro.2008.03.020",{"id":23,"text":1656,"url":23,"identifiers":1657},"Chikamatsu K, Sakakura K, Toyoda M, Takahashi K, Yamamoto T, Masuyama K . Immunosuppressive activity of CD14+ HLA-DR cells in squamous cell carcinoma of the head and neck. Cancer Sci 2012; 103: 976–983.",{"doi":1658},"10.1111\u002Fj.1349-7006.2012.02248.x",{"id":23,"text":1660,"url":23,"identifiers":1661},"Gustafson MP, Lin Y, New KC, Bulur PA, O'Neill BP, Gastineau DA et al. Systemic immune suppression in glioblastoma: the interplay between CD14+HLA-DRlo\u002Fneg monocytes, tumor factors, and dexamethasone. Neuro Oncol 2010; 12: 631–644.",{"doi":1662},"10.1093\u002Fneuonc\u002Fnoq001",{"id":23,"text":1664,"url":23,"identifiers":1665},"Vuk-Pavlovic S, Bulur PA, Lin Y, Qin R, Szumlanski CL, Zhao X et al. Immunosuppressive CD14+HLA-DRlow\u002F− monocytes in prostate cancer. Prostate 2010; 70: 443–455.",{"doi":1666},"10.1002\u002Fpros.21078",{"id":23,"text":1668,"url":23,"identifiers":1669},"Gustafson MP, Abraham RS, Lin Y, Wu W, Gastineau DA, Zent CS et al. Association of an increased frequency of CD14+ HLA-DR lo\u002Fneg monocytes with decreased time to progression in chronic lymphocytic leukaemia (CLL). Br J Haematol 2012; 156: 674–676.",{"doi":1670},"10.1111\u002Fj.1365-2141.2011.08902.x",{"id":23,"text":1672,"url":23,"identifiers":1673},"Jitschin R, Braun M, Buttner M, Dettmer-Wilde K, Bricks J, Berger J et al. CLL-cells induce IDOhi CD14+HLA-DRlo myeloid-derived suppressor cells that inhibit T-cell responses and promote TRegs. Blood 2014; 124: 750–760.",{"doi":1674},"10.1182\u002Fblood-2013-12-546416",{"id":23,"text":1676,"url":23,"identifiers":1677},"Arihara F, Mizukoshi E, Kitahara M, Takata Y, Arai K, Yamashita T et al. Increase in CD14+HLA-DR−\u002Flow myeloid-derived suppressor cells in hepatocellular carcinoma patients and its impact on prognosis. Cancer Immunol Immunother 2013; 62: 1421–1430.",{"doi":1678},"10.1007\u002Fs00262-013-1447-1",{"id":23,"text":1680,"url":23,"identifiers":1681},"Huang A, Zhang B, Wang B, Zhang F, Fan KX, Guo YJ . Increased CD14(+)HLA-DR (-\u002Flow) myeloid-derived suppressor cells correlate with extrathoracic metastasis and poor response to chemotherapy in non-small cell lung cancer patients. Cancer Immunol Immunother 2013; 62: 1439–1451.",{"doi":1682},"10.1007\u002Fs00262-013-1450-6",{"id":23,"text":1684,"url":23,"identifiers":1685},"Vari F, Gandhi MK . Broad-spectrum immunosuppression by classless monocytes in non-Hodgkin's lymphoma. Immunotherapy 2011; 3: 723–726.",{"doi":1686},"10.2217\u002Fimt.11.56",{"id":23,"text":1688,"url":23,"identifiers":1689},"Gustafson MP, Lin Y, LaPlant B, Liwski CJ, Maas ML, League SC et al. Immune monitoring using the predictive power of immune profiles. J Immunother Cancer 2013; 1: 7.",{"doi":1690},"10.1186\u002F2051-1426-1-7",{"id":1692,"createTime":1693,"updateTime":1693,"relativeEntities":1694,"slug":1695,"properties":1696,"entityType":132,"verifyStatus":133,"verifyTime":1693,"verifyNote":135,"syncStatus":22,"languages":1712,"translateLanguages":23,"viewCount":24,"primaryUrl":1713,"fullTextUrl":23,"authors":1714,"publicationType":264,"publisherRelationship":1858,"citationCount":550,"citationInfo":1889,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":1891,"isForceReanalyzing":352},"f1e8109f-a841-4b47-ab91-f349db41c190","2024-11-29T18:03:20.677+00:00",[],"NPM-ALK-mediates-phosphorylation-of-MSH2-at-tyrosine-238-creating-a-functional-deficiency-in-MSH2-and-the-loss-of-mismatch-repair",{"mag":1697,"keywords":1699,"pmc":1700,"openalex":1702,"abstract":1704,"title":1706,"pm":1708,"doi":1710},{"VOID":1698},"344822596",{},{"VOID":1701},"4476014",{"VOID":1703},"W344822596",{"EN":1705},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The vast majority of anaplastic lymphoma kinase-positive anaplastic large cell lymphoma (ALK+ALCL) tumors express the characteristic oncogenic fusion protein NPM-ALK, which mediates tumorigenesis by exerting its constitutive tyrosine kinase activity on various substrates. We recently identified MSH2, a protein central to DNA mismatch repair (MMR), as a novel binding partner and phosphorylation substrate of NPM-ALK. Here, using liquid chromatography–mass spectrometry, we report for the first time that MSH2 is phosphorylated by NPM-ALK at a specific residue, tyrosine 238. Using GP293 cells transfected with NPM-ALK, we confirmed that the MSH2\u003Cjats:sup>Y238F\u003C\u002Fjats:sup> mutant is not tyrosine phosphorylated. Furthermore, transfection of MSH2\u003Cjats:sup>Y238F\u003C\u002Fjats:sup> into these cells substantially decreased the tyrosine phosphorylation of endogenous MSH2. Importantly, gene transfection of MSH2\u003Cjats:sup>Y238F\u003C\u002Fjats:sup> abrogated the binding of NPM-ALK with endogenous MSH2, re-established the dimerization of MSH2:MSH6 and restored the sensitivity to DNA mismatch-inducing drugs, indicative of MMR return. Parallel findings were observed in two ALK+ALCL cell lines, Karpas 299 and SUP-M2. In addition, we found that enforced expression of MSH2\u003Cjats:sup>Y238F\u003C\u002Fjats:sup> into ALK+ALCL cells alone was sufficient to induce spontaneous apoptosis. In conclusion, our findings have identified NPM-ALK-induced phosphorylation of MSH2 at Y238 as a crucial event in suppressing MMR. Our studies have provided novel insights into the mechanism by which oncogenic tyrosine kinases disrupt MMR.\u003C\u002Fjats:p>",{"EN":1707},"NPM-ALK mediates phosphorylation of MSH2 at tyrosine 238, creating a functional deficiency in MSH2 and the loss of mismatch repair",{"VOID":1709},"25978431",{"VOID":1711},"10.1038\u002Fbcj.2015.35",[137],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fbcj201535",[1715,1737,1759,1774,1789,1809,1824,1841],{"id":1716,"sortIndex":248,"researcher":23,"roles":1717,"affiliations":1718,"properties":1730},"c3323af4-8286-4bbf-9a2d-5f16f6c561e9",[],[1719],{"id":1720,"sortIndex":24,"affiliation":1721,"properties":23},"f961cdaa-a107-46f6-b9b5-7d1260e2b485",{"id":1722,"createTime":1723,"updateTime":1724,"relativeEntities":1725,"slug":1726,"properties":1727,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"26eb134c-4426-46c6-80b1-bc516ffad26e","2023-11-24T23:46:54.169+00:00","2024-12-10T10:43:07.021+00:00",[],"Department-of-Laboratory-Medicine-and-Pathology-University-of-Alberta-Edmonton-Alberta-Canada",{"title":1728},{"VI":1729},"Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, Canada",{"openalex":1731,"orcid":1733,"title":1735},{"VOID":1732},"A5101672255",{"VOID":1734},"https:\u002F\u002Forcid.org\u002F0000-0003-0975-811X",{"EN":1736},"Fang Wu",{"id":1738,"sortIndex":299,"researcher":23,"roles":1739,"affiliations":1740,"properties":1752},"5824fbe3-9ef2-401a-a20c-568313519f4c",[],[1741],{"id":1742,"sortIndex":24,"affiliation":1743,"properties":23},"46beca85-20ee-4e8a-803c-112c9121cee9",{"id":1744,"createTime":1745,"updateTime":1746,"relativeEntities":1747,"slug":1748,"properties":1749,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"1f6bec2c-a935-4b4b-a882-edb26ed9f031","2024-01-01T10:22:34.916+00:00","2024-11-29T18:03:20.930+00:00",[],"Department-of-Oncology-University-of-Alberta-Edmonton-Alberta-Canada",{"title":1750},{"VI":1751},"Department of Oncology, University of Alberta, Edmonton, Alberta, Canada",{"openalex":1753,"orcid":1755,"title":1757},{"VOID":1754},"A5114377244",{"VOID":1756},"https:\u002F\u002Forcid.org\u002F0000-0001-5608-6921",{"EN":1758},"Rai‐Hua Lai",{"id":1760,"sortIndex":187,"researcher":23,"roles":1761,"affiliations":1762,"properties":1769},"1daa4b46-2d56-4495-bce2-c90ad8712e89",[],[1763],{"id":1764,"sortIndex":24,"affiliation":1765,"properties":23},"7f3df572-9cde-4093-9a92-7c312dc25614",{"id":1722,"createTime":1723,"updateTime":1724,"relativeEntities":1766,"slug":1726,"properties":1767,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":1768},{"VI":1729},{"openalex":1770,"title":1772},{"VOID":1771},"A5006164186",{"EN":1773},"L Li",{"id":1775,"sortIndex":142,"researcher":23,"roles":1776,"affiliations":1777,"properties":1784},"be74b3f8-b356-44e0-bdd3-5539c43d5741",[],[1778],{"id":1779,"sortIndex":24,"affiliation":1780,"properties":23},"f212ecc7-7a25-4a90-8f8a-af8e0ee29243",{"id":1722,"createTime":1723,"updateTime":1724,"relativeEntities":1781,"slug":1726,"properties":1782,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":1783},{"VI":1729},{"openalex":1785,"title":1787},{"VOID":1786},"A5010503467",{"EN":1788},"Julinor Bacani",{"id":1790,"sortIndex":64,"researcher":23,"roles":1791,"affiliations":1792,"properties":1804},"f5ce644d-dacc-4864-b47f-0d9f7d008981",[],[1793],{"id":1794,"sortIndex":24,"affiliation":1795,"properties":23},"9817b9b3-d324-4dc7-a97a-e7f80bb3f08d",{"id":1796,"createTime":1797,"updateTime":1798,"relativeEntities":1799,"slug":1800,"properties":1801,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"66255b70-dbf6-411d-be21-bb9ac8604af5","2024-02-02T11:39:48.393+00:00","2024-11-29T18:03:20.901+00:00",[],"Department-of-Medical-Genetics-University-of-Alberta-Edmonton-Alberta-Canada",{"title":1802},{"VI":1803},"Department of Medical Genetics, University of Alberta, Edmonton, Alberta, Canada",{"openalex":1805,"title":1807},{"VOID":1806},"A5110253025",{"EN":1808},"Susan E. 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Oncogenic tyrosine kinases and the DNA-damage response. Nat Rev Cancer 2002; 2: 351–360.",{"doi":2096},"10.1038\u002Fnrc799",{"id":23,"text":2098,"url":23,"identifiers":2099},"Hallberg B, Palmer RH . Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology. Nat Rev Cancer 2013; 13: 685–700.",{"doi":2100},"10.1038\u002Fnrc3580",{"id":23,"text":2102,"url":23,"identifiers":2103},"Drummond JT, Genschel J, Wolf E, Modrich P . DHFR\u002FMSH3 amplification in methotrexate-resistant cells alters the hMutSalpha\u002FhMutSbeta ratio and reduces the efficiency of base-base mismatch repair. Proc Natl Acad Sci USA 1997; 94: 10144–10149.",{"doi":2104},"10.1073\u002Fpnas.94.19.10144",{"id":23,"text":2106,"url":23,"identifiers":2107},"Shcherbakova PV, Kunkel TA . Mutator phenotypes conferred by MLH1 overexpression and by heterozygosity for mlh1 mutations. Mol Cell Biol 1999; 19: 3177–3183.",{"doi":2108},"10.1128\u002FMCB.19.4.3177",{"id":2110,"createTime":2111,"updateTime":2111,"relativeEntities":2112,"slug":2113,"properties":2114,"entityType":132,"verifyStatus":133,"verifyTime":2130,"verifyNote":135,"syncStatus":22,"languages":2131,"translateLanguages":23,"viewCount":24,"primaryUrl":2132,"fullTextUrl":23,"authors":2133,"publicationType":264,"publisherRelationship":2209,"citationCount":2238,"citationInfo":2239,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":2241,"isForceReanalyzing":352},"b850e0e0-c360-41f9-bf0e-057e023f0dca","2024-09-26T15:50:46.622+00:00",[],"Myelofibrosis-Treatment-Algorithm-2018",{"mag":2115,"keywords":2117,"pmc":2118,"openalex":2120,"abstract":2122,"title":2124,"pm":2126,"doi":2128},{"VOID":2116},"2885153903",{},{"VOID":2119},"6068139",{"VOID":2121},"W2885153903",{"EN":2123},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Two novel prognostic systems for primary myelofibrosis (PMF) were recently unveiled: GIPSS (genetically inspired prognostic scoring system) and MIPSS70 (mutation-enhanced international prognostic scoring system for transplant-age patients). GIPSS is based exclusively on genetic markers: mutations and karyotype. MIPSS70 includes mutations and clinical risk factors. In its most recent adaptation, the prognostic value of MIPSS70 has been bolstered by the inclusion of a three-tiered cytogenetic risk stratification and use of hemoglobin thresholds that are adjusted for sex and severity (MIPSS70+ version 2.0). GIPSS features four, MIPSS70 three, and MIPSS70+ version 2.0 five risk categories. MIPSS70 is most useful in the absence of cytogenetic information. MIPSS70+ version 2.0 is more comprehensive than MIPSS70 and is the preferred model in the presence of cytogenetic information. Both MIPSS70 and MIPSS70+ version 2.0 require an online score calculator (\u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" ext-link-type=\"uri\" xlink:href=\"http:\u002F\u002Fwww.mipss70score.it\">http:\u002F\u002Fwww.mipss70score.it\u003C\u002Fjats:ext-link>). GIPPS offers a lower complexity prognostic tool that reliably identifies candidates for allogeneic stem cell transplant (GIPSS high-risk disease) or long-term observation with little or no therapeutic intervention (GIPSS low-risk disease). Ultimately, we favor a step-wise prognostication approach that starts with GIPSS but also considers MIPSS70+ version 2.0 for confirming the most appropriate treatment approach for the individual patient.\u003C\u002Fjats:p>",{"EN":2125},"Myelofibrosis Treatment Algorithm 2018",{"VOID":2127},"30065290",{"VOID":2129},"10.1038\u002Fs41408-018-0109-0","2024-09-26T15:50:46.621+00:00",[137],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fs41408-018-0109-0",[2134,2156,2175,2192],{"id":2135,"sortIndex":24,"researcher":23,"roles":2136,"affiliations":2137,"properties":2149},"55e24629-0058-40cd-88c3-34049e3b9b74",[],[2138],{"id":2139,"sortIndex":24,"affiliation":2140,"properties":23},"e0eefc03-f090-44e7-acce-e4737a51c8e4",{"id":2141,"createTime":2142,"updateTime":2143,"relativeEntities":2144,"slug":2145,"properties":2146,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"15627d91-9fbf-4184-a4a9-3be340480132","2023-12-07T16:39:26.155+00:00","2024-10-13T05:13:55.331+00:00",[],"Division-of-Hematology-Department-of-Internal-Medicine-Mayo-Clinic-Rochester-MN-USA",{"title":2147},{"VI":2148},"Division of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA",{"openalex":2150,"orcid":2152,"title":2154},{"VOID":2151},"A5016216479",{"VOID":2153},"https:\u002F\u002Forcid.org\u002F0000-0003-4605-3821",{"EN":2155},"Ayalew Tefferi",{"id":2157,"sortIndex":232,"researcher":23,"roles":2158,"affiliations":2159,"properties":2171},"a0d48a86-afa8-49bf-b060-16b50974f264",[],[2160],{"id":2161,"sortIndex":24,"affiliation":2162,"properties":23},"4c814dfe-72ef-496c-bcdd-b82e35b4bb75",{"id":2163,"createTime":2164,"updateTime":2165,"relativeEntities":2166,"slug":2167,"properties":2168,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"be483a7d-ffca-4380-9d57-968d8acf06c6","2024-04-11T16:14:19.132+00:00","2024-09-26T15:50:49.130+00:00",[],"Department-of-Experimental-and-Clinical-Medicine-CRIMM-Center-Research-and-Innovation-of-Myeloproliferative-Neoplasms-Azienda-Ospedaliera-Universitaria-Careggi-University-of-Florence-Florence-Italy",{"title":2169},{"EN":2170},"Department of Experimental and Clinical Medicine, CRIMM, Center Research and Innovation of Myeloproliferative Neoplasms, Azienda Ospedaliera Universitaria Careggi, University of Florence, Florence, Italy",{"openalex":2172,"orcid":2173,"title":2174},{"VOID":158},{"VOID":160},{"EN":162},{"id":2176,"sortIndex":248,"researcher":23,"roles":2177,"affiliations":2178,"properties":2185},"70f360d3-8ca3-40ec-b473-ba8119443422",[],[2179],{"id":2180,"sortIndex":24,"affiliation":2181,"properties":23},"c70f8e9e-1982-4da9-a53e-75b5f141f086",{"id":2141,"createTime":2142,"updateTime":2143,"relativeEntities":2182,"slug":2145,"properties":2183,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":2184},{"VI":2148},{"openalex":2186,"orcid":2188,"title":2190},{"VOID":2187},"A5024612499",{"VOID":2189},"https:\u002F\u002Forcid.org\u002F0000-0002-9084-4148",{"EN":2191},"Animesh Pardanani",{"id":2193,"sortIndex":209,"researcher":23,"roles":2194,"affiliations":2195,"properties":2202},"d7670c1d-e416-4687-ae17-ce2b1df3bed5",[],[2196],{"id":2197,"sortIndex":24,"affiliation":2198,"properties":23},"a49c06d7-1c95-4117-96b8-2a88c7abcc59",{"id":2163,"createTime":2164,"updateTime":2165,"relativeEntities":2199,"slug":2167,"properties":2200,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":2201},{"EN":2170},{"openalex":2203,"orcid":2205,"title":2207},{"VOID":2204},"A5013539196",{"VOID":2206},"https:\u002F\u002Forcid.org\u002F0000-0003-1809-284X",{"EN":2208},"Paola Guglielmelli",{"url":23,"publisher":2210,"properties":2235},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2211,"slug":10,"properties":2212,"entityType":21,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24,"subjectFields":2218,"manageAffiliations":2219,"indexDatabases":2220,"url":107,"thumbnailPath":23,"statistic":23,"gsStatistic":23,"type":23,"analyzePriority":23},[],{"country":2213,"issn":2214,"introduce":2215,"eissn":2216,"title":2217},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":15},{"EN":20},[],[],[2221,2228],{"id":68,"indexDatabase":2222,"url":83,"indexYears":23,"academicFieldIds":2227,"indexDatabaseRanking":23},{"id":70,"createTime":71,"updateTime":72,"relativeEntities":2223,"label":2224,"description":2225,"key":79,"publicationTags":2226,"standard":23},[],{"EN":75,"VI":75},{"VI":77,"EN":78},[81,82],[85,86],{"id":88,"indexDatabase":2229,"url":101,"indexYears":102,"academicFieldIds":2234,"indexDatabaseRanking":106},{"id":90,"createTime":91,"updateTime":92,"relativeEntities":2230,"label":2231,"description":2232,"key":98,"publicationTags":2233,"standard":23},[],{"EN":95,"VI":95},{"EN":95,"VI":97},[100],[104,105],{"volume":2236,"issue":2237},{"VOID":293},{"VOID":293},37,{"total":2238,"publishYear":23,"statisticByYear":2240},{"2018":248,"2019":187,"2020":299,"2021":552,"2022":142,"2023":187,"2024":248},[2242,2246,2250,2254,2258,2262,2266,2270,2274,2278,2282,2286,2290,2294,2298,2302,2306,2310,2314,2318,2322,2326,2330,2334,2338,2342,2346,2350,2354,2358,2362,2366,2370,2374,2378,2382,2386,2390],{"id":23,"text":2243,"url":23,"identifiers":2244},"Barbui, T. et al. 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Epidemiology and clinical relevance of mutations in postpolycythemia vera and postessential thrombocythemia myelofibrosis: a study on 359 patients of the AGIMM group. Am. J. Hematol. 91, 681–686 (2016).",{"doi":2297},"10.1002\u002Fajh.24377",{"id":23,"text":2299,"url":23,"identifiers":2300},"Tefferi, A. et al. The prognostic advantage of calreticulin mutations in myelofibrosis might be confined to type 1 or type 1-like CALR variants. Blood 124, 2465–2466 (2014).",{"doi":2301},"10.1182\u002Fblood-2014-07-588426",{"id":23,"text":2303,"url":23,"identifiers":2304},"Li, B. et al. The different prognostic impact of type-1 or type-1 like and type-2 or type-2 like CALR mutations in patients with primary myelofibrosis. Am. J. Hematol. 91, E320–E321 (2016).",{"doi":2305},"10.1002\u002Fajh.24378",{"id":23,"text":2307,"url":23,"identifiers":2308},"Guglielmelli, P. et al. Validation of the differential prognostic impact of type 1\u002Ftype 1-like versus type 2\u002Ftype 2-like CALR mutations in myelofibrosis. Blood Cancer J. 5, e360 (2015).",{"doi":2309},"10.1038\u002Fbcj.2015.90",{"id":23,"text":2311,"url":23,"identifiers":2312},"Vannucchi, A. M. et al. Mutations and prognosis in primary myelofibrosis. Leukemia 27, 1861–1869 (2013).",{"doi":2313},"10.1038\u002Fleu.2013.119",{"id":23,"text":2315,"url":23,"identifiers":2316},"Tefferi A., et al. U2AF1 mutation types in primary myelofibrosis: phenotypic and prognostic distinctions. Leukemia. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41375-018-0078-0 (2018).",{"doi":2317},"10.1038\u002Fs41375-018-0078-0",{"id":23,"text":2319,"url":23,"identifiers":2320},"Vaidya, R. et al. Monosomal karyotype in primary myelofibrosis is detrimental to both overall and leukemia-free survival. Blood 117, 5612–5615 (2011).",{"doi":2321},"10.1182\u002Fblood-2010-11-320002",{"id":23,"text":2323,"url":23,"identifiers":2324},"Tefferi A, et al. Revised cytogenetic risk stratification in primary myelofibrosis: analysis based on 1002 informative patients. Leukemia. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41375-018-0018-z (2018).",{"doi":2325},"10.1038\u002Fs41375-018-0018-z",{"id":23,"text":2327,"url":23,"identifiers":2328},"Mudireddy M, et al. Prefibrotic versus overtly fibrotic primary myelofibrosis: clinical, cytogenetic, molecular and prognostic comparisons. Br. J. Haematol. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fbjh.14838 (2017).",{"doi":2329},"10.1111\u002Fbjh.14838",{"id":23,"text":2331,"url":23,"identifiers":2332},"Guglielmelli, P. et al. Presentation and outcome of patients with 2016 WHO diagnosis of prefibrotic and overt primary myelofibrosis. Blood 129, 3227–3236 (2017).",{"doi":2333},"10.1182\u002Fblood-2017-01-761999",{"id":23,"text":2335,"url":23,"identifiers":2336},"Guglielmelli, P., Vannucchi, A. M. & Investigators, A. The prognostic impact of bone marrow fibrosis in primary myelofibrosis. Am. J. Hematol. 91, E454–E455 (2016).",{"doi":2337},"10.1002\u002Fajh.24482",{"id":23,"text":2339,"url":23,"identifiers":2340},"Tefferi A, et al. Monocytosis is a powerful and independent predictor of inferior survival in primary myelofibrosis. Br. J. Haematol. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fbjh.15061 (2017).",{"doi":2341},"10.1111\u002Fbjh.15061",{"id":23,"text":2343,"url":23,"identifiers":2344},"Shah, S. et al. Marked elevation of serum lactate dehydrogenase in primary myelofibrosis: clinical and prognostic correlates. Blood Cancer J. 7, 657 (2017).",{"doi":2345},"10.1038\u002Fs41408-017-0024-9",{"id":23,"text":2347,"url":23,"identifiers":2348},"Tefferi, A. et al. JAK2 germline genetic variation affects disease susceptibility in primary myelofibrosis regardless of V617F mutational status: nullizygosity for the JAK2 46\u002F1 haplotype is associated with inferior survival. Leukemia 24, 105–109 (2010).",{"doi":2349},"10.1038\u002Fleu.2009.225",{"id":23,"text":2351,"url":23,"identifiers":2352},"Tefferi, A. et al. Low JAK2V617F allele burden in primary myelofibrosis, compared to either a higher allele burden or unmutated status, is associated with inferior overall and leukemia-free survival. Leukemia 22, 756–761 (2008).",{"doi":2353},"10.1038\u002Fsj.leu.2405097",{"id":23,"text":2355,"url":23,"identifiers":2356},"Guglielmelli, P. et al. Identification of patients with poorer survival in primary myelofibrosis based on the burden of JAK2V617F mutated allele. Blood 114, 1477–1483 (2009).",{"doi":2357},"10.1182\u002Fblood-2009-04-216044",{"id":23,"text":2359,"url":23,"identifiers":2360},"Tefferi, A. et al. Circulating interleukin (IL)-8, IL-2R, IL-12, and IL-15 levels are independently prognostic in primary myelofibrosis: a comprehensive cytokine profiling study. J. Clin. Oncol. 29, 1356–1363 (2011).",{"doi":2361},"10.1200\u002FJCO.2010.32.9490",{"id":23,"text":2363,"url":23,"identifiers":2364},"Pardanani, A., Begna, K., Finke, C., Lasho, T. & Tefferi, A. Circulating levels of MCP-1, sIL-2R, IL-15, and IL-8 predict anemia response to pomalidomide therapy in myelofibrosis. Am. J. Hematol. 86, 343–345 (2011).",{"doi":2365},"10.1002\u002Fajh.21972",{"id":23,"text":2367,"url":23,"identifiers":2368},"Pardanani, A., Finke, C., Abdelrahman, R. A., Lasho, T. L. & Tefferi, A. Associations and prognostic interactions between circulating levels of hepcidin, ferritin and inflammatory cytokines in primary myelofibrosis. Am. J. Hematol. 88, 312–316 (2013).",{"doi":2369},"10.1002\u002Fajh.23406",{"id":23,"text":2371,"url":23,"identifiers":2372},"Guglielmelli, P. et al. MIPSS70: Mutation-Enhanced International Prognostic Score System for Transplantation-Age Patients With Primary Myelofibrosis. J. Clin. Oncol. 36, 310–318 (2018).",{"doi":2373},"10.1200\u002FJCO.2017.76.4886",{"id":23,"text":2375,"url":23,"identifiers":2376},"Tefferi A et al. MIPSS70+ version 2.0: mutation and karyotype enhanced international prognostic scoring system for primary myelofibrosis. J. Clin. Oncol. (2018, in press).",{"doi":2377},"10.1200\u002FJCO.2018.78.9867",{"id":23,"text":2379,"url":23,"identifiers":2380},"Tefferi, A. et al. GIPSS: genetically-inspired prognostic scoring system for primary myelofibrosis. Leukemia 32, 1631–1642 (2018).",{"doi":2381},"10.1038\u002Fs41375-018-0107-z",{"id":23,"text":2383,"url":23,"identifiers":2384},"Cervantes, F. & Pereira, A. Does ruxolitinib prolong the survival of patients with myelofibrosis? Blood 129, 832–837 (2017).",{"doi":2385},"10.1182\u002Fblood-2016-11-731604",{"id":23,"text":2387,"url":23,"identifiers":2388},"Verstovsek, S. et al. Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis. N. Engl. J. Med. 363, 1117–1127 (2010).",{"doi":2389},"10.1056\u002FNEJMoa1002028",{"id":23,"text":2391,"url":23,"identifiers":2392},"Tefferi, A. et al. Risk factors and a prognostic model for postsplenectomy survival in myelofibrosis. Am. J. Hematol. 92, 1187–1192 (2017).",{"doi":2393},"10.1002\u002Fajh.24881",{"id":2395,"createTime":2396,"updateTime":2396,"relativeEntities":2397,"slug":2398,"properties":2399,"entityType":132,"verifyStatus":133,"verifyTime":2414,"verifyNote":135,"syncStatus":22,"languages":2415,"translateLanguages":23,"viewCount":24,"primaryUrl":2416,"fullTextUrl":23,"authors":2417,"publicationType":264,"publisherRelationship":2569,"citationCount":2601,"citationInfo":2602,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":2604,"isForceReanalyzing":352},"bd64af63-ea26-4f0d-9ad2-decba2f2f341","2024-09-25T14:52:42.972+00:00",[],"Investigating-heredity-in-cutaneous-T-cell-lymphoma-in-a-unique-cohort-of-Danish-twins",{"mag":2400,"keywords":2402,"pmc":2403,"openalex":2405,"abstract":2407,"title":2408,"pm":2410,"doi":2412},{"VOID":2401},"2576944938",{},{"VOID":2404},"5301035",{"VOID":2406},"W2576944938",{},{"EN":2409},"Investigating heredity in cutaneous T-cell lymphoma in a unique cohort of Danish twins",{"VOID":2411},"28106877",{"VOID":2413},"10.1038\u002Fbcj.2016.128","2024-09-25T14:52:42.971+00:00",[137],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fbcj2016128",[2418,2440,2462,2479,2501,2518,2535,2552],{"id":2419,"sortIndex":24,"researcher":23,"roles":2420,"affiliations":2421,"properties":2433},"27e17f28-8e22-4738-8cc0-d8c876a6faec",[],[2422],{"id":2423,"sortIndex":24,"affiliation":2424,"properties":23},"16e6ec07-5f35-4f3f-9943-fa7056b89743",{"id":2425,"createTime":2426,"updateTime":2427,"relativeEntities":2428,"slug":2429,"properties":2430,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"8ffd0106-142b-432a-9c69-67127789e956","2024-01-14T02:16:41.825+00:00","2024-10-16T08:10:59.517+00:00",[],"Department-of-Immunology-and-Microbiology-University-of-Copenhagen-Copenhagen-Denmark",{"title":2431},{"VI":2432},"Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark",{"openalex":2434,"orcid":2436,"title":2438},{"VOID":2435},"A5004078001",{"VOID":2437},"https:\u002F\u002Forcid.org\u002F0000-0003-3135-5624",{"EN":2439},"Niels Ødum",{"id":2441,"sortIndex":187,"researcher":23,"roles":2442,"affiliations":2443,"properties":2455},"009fd7e6-968b-4844-a22d-64d003758a0b",[],[2444],{"id":2445,"sortIndex":24,"affiliation":2446,"properties":23},"ca5ec28b-81c3-4597-a0cb-8865383b0e8b",{"id":2447,"createTime":2448,"updateTime":2449,"relativeEntities":2450,"slug":2451,"properties":2452,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"99db8e0c-2d39-4fc9-adff-a75ad4519dc3","2023-12-06T01:49:36.780+00:00","2024-09-25T14:52:43.016+00:00",[],"The-Danish-Twin-Registry-Institute-of-Public-Health-University-of-Southern-Denmark-Odense-Denmark",{"title":2453},{"VI":2454},"The Danish Twin Registry, Institute of Public Health, University of Southern Denmark, Odense, Denmark",{"openalex":2456,"orcid":2458,"title":2460},{"VOID":2457},"A5024136724",{"VOID":2459},"https:\u002F\u002Forcid.org\u002F0000-0002-8629-4913",{"EN":2461},"Axel Skytthe",{"id":2463,"sortIndex":232,"researcher":23,"roles":2464,"affiliations":2465,"properties":2472},"907383ec-dad1-4d9d-a28f-70b72c447301",[],[2466],{"id":2467,"sortIndex":24,"affiliation":2468,"properties":23},"3d04e9c7-fd85-4e5d-9016-e36be83dcf43",{"id":2425,"createTime":2426,"updateTime":2427,"relativeEntities":2469,"slug":2429,"properties":2470,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},[],{"title":2471},{"VI":2432},{"openalex":2473,"orcid":2475,"title":2477},{"VOID":2474},"A5020760826",{"VOID":2476},"https:\u002F\u002Forcid.org\u002F0000-0001-6350-1150",{"EN":2478},"Thorbjørn Krejsgaard",{"id":2480,"sortIndex":209,"researcher":23,"roles":2481,"affiliations":2482,"properties":2494},"4dc6ca5a-4f2f-4c19-a096-b2da3e594360",[],[2483],{"id":2484,"sortIndex":24,"affiliation":2485,"properties":23},"5396e1a9-1e11-4b6e-a23e-6ac661ef9ade",{"id":2486,"createTime":2487,"updateTime":2488,"relativeEntities":2489,"slug":2490,"properties":2491,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"1962a171-423b-42f4-b0db-dc54822f5a12","2024-02-10T00:03:52.149+00:00","2024-11-25T05:25:36.685+00:00",[],"Department-of-Dermatology-Aarhus-University-Hospital-Aarhus-Denmark",{"title":2492},{"VI":2493},"Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark",{"openalex":2495,"orcid":2497,"title":2499},{"VOID":2496},"A5014191622",{"VOID":2498},"https:\u002F\u002Forcid.org\u002F0000-0003-3768-4146",{"EN":2500},"Lise M. 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The pathogenesis of mycosis fungoides. N Engl J Med 2004; 350: 1978–1988.",{"doi":2608},"10.1056\u002FNEJMra032810",{"id":23,"text":2610,"url":23,"identifiers":2611},"Willemze R, Jaffe ES, Burg G, Cerroni L, Berti E, Swerdlow SH et al. WHO-EORTC classification for cutaneous lymphomas. Blood 2005; 105: 3768–3785.",{"doi":2612},"10.1182\u002Fblood-2004-09-3502",{"id":23,"text":2614,"url":23,"identifiers":2615},"Hodak E, Lapidoth M, Kohn K, David D, Brautbar B, Kfir K et al. Mycosis fungoides: HLA class II associations among Ashkenazi and non-Ashkenazi Jewish patients. Br J Dermatol 2001; 145: 974–980.",{"doi":2616},"10.1046\u002Fj.1365-2133.2001.04496.x",{"id":23,"text":2618,"url":23,"identifiers":2619},"Jackow CM, McHam JB, Friss A, Alvear J, Reveille JR, Duvic M . HLA-DR5 and DQB1*03 class II alleles are associated with cutaneous T-cell lymphoma. J Invest Dermatol 1996; 107: 373–376.",{"doi":2620},"10.1111\u002F1523-1747.ep12363352",{"id":23,"text":2622,"url":23,"identifiers":2623},"Naji AA, Waiz MM, Sharquie KE . Mycosis fungoides in identical twins. J Am Acad Dermatol 2001; 44: 532–533.",{"doi":2624},"10.1067\u002Fmjd.2001.110655",{"id":23,"text":2626,"url":23,"identifiers":2627},"Schneider BF, Christian M, Hess CE, Williams ME . Familial occurrence of cutaneous T cell lymphoma: a case report of monozygotic twin sisters. Leukemia 1995; 9: 1979–1981.",{},{"id":23,"text":2629,"url":23,"identifiers":2630},"Bradford PT, Devesa SS, Anderson WF, Toro JR . Cutaneous lymphoma incidence patterns in the United States: a population-based study of 3884 cases. Blood 2009; 113: 5064–5073.",{"doi":2631},"10.1182\u002Fblood-2008-10-184168",{"id":23,"text":2633,"url":23,"identifiers":2634},"Kim YH, Liu HL, Mraz-Gernhard S, Varghese A, Hoppe RT . Long-term outcome of 525 patients with mycosis fungoides and Sezary syndrome: clinical prognostic factors and risk for disease progression. Arch Dermatol 2003; 139: 857–866.",{},{"id":23,"text":2636,"url":23,"identifiers":2637},"Lindahl LM, Fenger-Gron M, Iversen L . Subsequent cancers, mortality and causes of death in patients with mycosis fungoides and parapsoriasis: a danish nationwide population-based cohort study. J Am Acad Dermatol 2014; 71: 529–535.",{"doi":2638},"10.1016\u002Fj.jaad.2014.03.044",{"id":23,"text":2640,"url":23,"identifiers":2641},"Willerslev-Olsen A, Krejsgaard T, Lindahl LM, Bonefeld CM, Wasik MA, Koralov SB et al. Bacterial toxins fuel disease progression in cutaneous T-cell lymphoma. Toxins 2013; 5: 1402–1421.",{"doi":2642},"10.3390\u002Ftoxins5081402",{"id":23,"text":2644,"url":23,"identifiers":2645},"Axelrod PI, Lorber B, Vonderheid EC . Infections complicating mycosis fungoides and Sezary syndrome. JAMA 1992; 267: 1354–1358.",{"doi":2646},"10.1001\u002Fjama.1992.03480100060031",{"id":23,"text":2648,"url":23,"identifiers":2649},"Posner LE, Fossieck BE, Eddy JL, Bunn PA . Septicemic complications of the cutaneous T-cell lymphomas. Am J Med 1981; 71: 210–216.",{"doi":2650},"10.1016\u002F0002-9343(81)90107-8",{"id":23,"text":2652,"url":23,"identifiers":2653},"Berger CL, Tigelaar R, Cohen J, Mariwalla K, Trinh J, Wang N et al. Cutaneous T-cell lymphoma: malignant proliferation of T-regulatory cells. Blood 2005; 105: 1640–1647.",{"doi":2654},"10.1182\u002Fblood-2004-06-2181",{"id":2656,"createTime":2657,"updateTime":2657,"relativeEntities":2658,"slug":2659,"properties":2660,"entityType":132,"verifyStatus":133,"verifyTime":2657,"verifyNote":135,"syncStatus":22,"languages":2676,"translateLanguages":23,"viewCount":24,"primaryUrl":2677,"fullTextUrl":23,"authors":2678,"publicationType":264,"publisherRelationship":3092,"citationCount":3122,"citationInfo":3123,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":3125,"isForceReanalyzing":352},"39b54c5d-a291-4400-be8f-61e27704cc96","2024-09-25T14:52:42.722+00:00",[],"Staphylococcus-aureus-enterotoxins-induce-FOXP3-in-neoplastic-T-cells-in-S%C3%A9zary-syndrome",{"mag":2661,"keywords":2663,"pmc":2664,"openalex":2666,"abstract":2668,"title":2670,"pm":2672,"doi":2674},{"VOID":2662},"3024544545",{},{"VOID":2665},"7225173",{"VOID":2667},"W3024544545",{"EN":2669},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Sézary syndrome (SS) is a heterogeneous leukemic subtype of cutaneous T-cell lymphoma (CTCL) with generalized erythroderma, lymphadenopathy, and a poor prognosis. Advanced disease is invariably associated with severe immune dysregulation and the majority of patients die from infectious complications caused by microorganisms such as,\u003Cjats:italic>Staphylococcus aureus\u003C\u002Fjats:italic>, rather than from the lymphoma per se. Here, we examined if staphylococcal enterotoxins (SE) may shape the phenotype of malignant SS cells, including expression of the regulatory T-cell-associated marker FOXP3. Our studies with primary and cultured malignant cells show that SE induce expression of FOXP3 in malignant cells when exposed to nonmalignant cells. Mutations in the MHC class II binding domain of SE-A (SEA) largely block the effect indicating that the response relies at least in part on the MHC class II-mediated antigen presentation. Transwell experiments show that the effect is induced by soluble factors, partly blocked by anti-IL-2 antibody, and depends on STAT5 activation in malignant cells. 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A humanised anti-IGF-1R monoclonal antibody (AVE1642) enhances Bortezomib-induced apoptosis in myeloma cells lacking CD45. Br J Cancer 2009; 100: 366–369.",{"doi":3810},"10.1038\u002Fsj.bjc.6604839",{"id":23,"text":3812,"url":23,"identifiers":3813},"Kuhn DJ, Berkova Z, Jones RJ, Woessner R, Bjorklund CC, Ma W et al. Targeting the insulin-like growth factor-1 receptor to overcome bortezomib resistance in preclinical models of multiple myeloma. Blood 2012; 120: 3260–3270.",{"doi":3814},"10.1182\u002Fblood-2011-10-386789",{"id":3816,"createTime":3817,"updateTime":3817,"relativeEntities":3818,"slug":3819,"properties":3820,"entityType":132,"verifyStatus":133,"verifyTime":3836,"verifyNote":135,"syncStatus":22,"languages":3837,"translateLanguages":23,"viewCount":24,"primaryUrl":3838,"fullTextUrl":23,"authors":3839,"publicationType":264,"publisherRelationship":3883,"citationCount":3912,"citationInfo":3913,"publishDate":23,"publishYear":23,"citationAnalyzeStatus":22,"lastCitationAnalyze":23,"indexDatabases":23,"openAccess":23,"references":3919,"isForceReanalyzing":352},"d141a3a2-bb7a-447a-b909-06091edb713f","2024-09-24T09:52:29.833+00:00",[],"CAR-T-cell-therapy-current-limitations-and-potential-strategies",{"mag":3821,"keywords":3823,"pmc":3824,"openalex":3826,"abstract":3828,"title":3830,"pm":3832,"doi":3834},{"VOID":3822},"3148729173",{},{"VOID":3825},"8024391",{"VOID":3827},"W3148729173",{"EN":3829},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Chimeric antigen receptor (CAR)-T cell therapy is a revolutionary new pillar in cancer treatment. Although treatment with CAR-T cells has produced remarkable clinical responses with certain subsets of B cell leukemia or lymphoma, many challenges limit the therapeutic efficacy of CAR-T cells in solid tumors and hematological malignancies. Barriers to effective CAR-T cell therapy include severe life-threatening toxicities, modest anti-tumor activity, antigen escape, restricted trafficking, and limited tumor infiltration. In addition, the host and tumor microenvironment interactions with CAR-T cells critically alter CAR-T cell function. Furthermore, a complex workforce is required to develop and implement these treatments. In order to overcome these significant challenges, innovative strategies and approaches to engineer more powerful CAR-T cells with improved anti-tumor activity and decreased toxicity are necessary. In this review, we discuss recent innovations in CAR-T cell engineering to improve clinical efficacy in both hematological malignancy and solid tumors and strategies to overcome limitations of CAR-T cell therapy in both hematological malignancy and solid tumors.\u003C\u002Fjats:p>",{"EN":3831},"CAR-T cell therapy: current limitations and potential strategies",{"VOID":3833},"33824268",{"VOID":3835},"10.1038\u002Fs41408-021-00459-7","2024-09-24T09:52:29.832+00:00",[137],"https:\u002F\u002Fwww.nature.com\u002Farticles\u002Fs41408-021-00459-7",[3840,3861],{"id":3841,"sortIndex":24,"researcher":23,"roles":3842,"affiliations":3843,"properties":3854},"80f87faf-2cae-47aa-b34b-d9f63514bf15",[],[3844],{"id":3845,"sortIndex":24,"affiliation":3846,"properties":23},"d1c88c40-38e4-49bd-a02d-f2a7e5fe9a63",{"id":3847,"createTime":3848,"updateTime":3848,"relativeEntities":3849,"slug":3850,"properties":3851,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"e077c1ed-b491-4f69-b1a2-9d85191b6c05","2024-09-24T09:52:29.850+00:00",[],"Medical-Scientist-Training-Program-University-of-Wisconsin-Madison-School-of-Medicine-and-Public-Health-Madison-WI-USA",{"title":3852},{"EN":3853},"Medical Scientist Training Program, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI, USA",{"openalex":3855,"orcid":3857,"title":3859},{"VOID":3856},"A5033812946",{"VOID":3858},"https:\u002F\u002Forcid.org\u002F0000-0001-8195-4970",{"EN":3860},"Robert C. Sterner",{"id":3862,"sortIndex":209,"researcher":23,"roles":3863,"affiliations":3864,"properties":3876},"e9cf853a-74b2-4834-b40c-f9ec4c7677bb",[],[3865],{"id":3866,"sortIndex":24,"affiliation":3867,"properties":23},"c10cba94-30bb-4e0a-b59a-e7029a31e5f5",{"id":3868,"createTime":3869,"updateTime":3870,"relativeEntities":3871,"slug":3872,"properties":3873,"entityType":52,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24},"d07943a5-cdcf-4526-83c1-c0c4d801244b","2024-09-24T09:52:29.861+00:00","2024-10-14T04:24:21.351+00:00",[],"Department-of-Surgery-Mayo-Clinic-Rochester-MN-USA",{"title":3874},{"EN":3875},"Department of Surgery, Mayo Clinic, Rochester, MN, USA",{"openalex":3877,"orcid":3879,"title":3881},{"VOID":3878},"A5032681443",{"VOID":3880},"https:\u002F\u002Forcid.org\u002F0000-0002-9323-3625",{"EN":3882},"Rosalie M. Sterner",{"url":23,"publisher":3884,"properties":3909},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":3885,"slug":10,"properties":3886,"entityType":21,"verifyStatus":22,"verifyTime":23,"verifyNote":23,"syncStatus":22,"languages":23,"translateLanguages":23,"viewCount":24,"subjectFields":3892,"manageAffiliations":3893,"indexDatabases":3894,"url":107,"thumbnailPath":23,"statistic":23,"gsStatistic":23,"type":23,"analyzePriority":23},[],{"country":3887,"issn":3888,"introduce":3889,"eissn":3890,"title":3891},{"VOID":13},{"VOID":15},{"EN":17},{"VOID":15},{"EN":20},[],[],[3895,3902],{"id":68,"indexDatabase":3896,"url":83,"indexYears":23,"academicFieldIds":3901,"indexDatabaseRanking":23},{"id":70,"createTime":71,"updateTime":72,"relativeEntities":3897,"label":3898,"description":3899,"key":79,"publicationTags":3900,"standard":23},[],{"EN":75,"VI":75},{"VI":77,"EN":78},[81,82],[85,86],{"id":88,"indexDatabase":3903,"url":101,"indexYears":102,"academicFieldIds":3908,"indexDatabaseRanking":106},{"id":90,"createTime":91,"updateTime":92,"relativeEntities":3904,"label":3905,"description":3906,"key":98,"publicationTags":3907,"standard":23},[],{"EN":95,"VI":95},{"EN":95,"VI":97},[100],[104,105],{"volume":3910,"issue":3911},{"VOID":546},{"VOID":1113},1288,{"total":3912,"publishYear":23,"statisticByYear":3914},{"2021":3915,"2022":3916,"2023":3917,"2024":3918},30,266,501,444,[3920,3924,3928,3932,3936,3940,3944,3947,3951,3955,3959,3963,3967,3971,3975,3979,3983,3987,3991,3995,3999,4003,4007,4011,4015,4019,4023,4027,4031,4035,4039,4043,4047,4051,4055,4059,4063,4067,4071,4075,4079,4083,4087,4091,4095,4099,4103,4107,4111,4115,4119,4123,4127,4131,4135,4139,4143,4147,4151,4155,4158,4162,4166,4170,4174,4178,4182,4186,4190,4194,4198,4202,4206,4210,4214,4218,4222,4226,4230,4234,4238,4242,4245,4248,4252,4256,4260,4264,4268,4272,4276,4280,4284,4288,4292,4296,4300,4304,4308,4311,4315,4319,4323,4327,4331,4335,4339],{"id":23,"text":3921,"url":23,"identifiers":3922},"June, C. 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