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10.1056\u002FNEJMoa064601\nHutchings, 2005, Prognostic value of interim FDG-PET after two or three cycles of chemotherapy in Hodgkin lymphoma, Ann Oncol, 16, 1160, 10.1093\u002Fannonc\u002Fmdi200\nGallamini, 2007, Early interim 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography is prognostically superior to international prognostic score in advanced-stage Hodgkin lymphoma: a report from a joint Italian-Danish study, J Clin Oncol, 25, 3746, 10.1200\u002FJCO.2007.11.6525\nCheson, 2007, Revised response criteria for malignant lymphoma, J Clin Oncol, 25, 579, 10.1200\u002FJCO.2006.09.2403\nJuweid, 2007, Use of positron emission tomography for response assessment of lymphoma: consensus of the imaging subcommittee of international harmonization project in lymphoma, J Clin Oncol, 25, 571, 10.1200\u002FJCO.2006.08.2305\nMeignan, 2009, Report on the First International Workshop on Interim-PET-Scan in Lymphoma, Leuk Lymphoma, 50, 1257, 10.1080\u002F10428190903040048\nEvens, 2014, The role of FDG-PET in defining prognosis of Hodgkin lymphoma for early-stage disease, Blood, 124, 3356, 10.1182\u002Fblood-2014-05-577627\nMesguich, 2016, Hodgkin lymphoma: a negative interim-PET cannot circumvent the need for end-of-treatment-PET evaluation, Br J Haematol, 175, 652, 10.1111\u002Fbjh.14292\nFilippi, 2013, Interim positron emission tomography and clinical outcome in patients with early stage Hodgkin lymphoma treated with combined modality therapy, Leuk Lymphoma, 54, 1183, 10.3109\u002F10428194.2012.735667\nBarnes, 2011, End-of-treatment but not interim PET scan predicts outcome in nonbulky limited-stage Hodgkin lymphoma, Ann Oncol, 22, 910, 10.1093\u002Fannonc\u002Fmdq549\nSher, 2009, Prognostic significance of mid- and post-ABVD PET imaging in Hodgkin lymphoma: the importance of involved-field radiotherapy, Ann Oncol, 20, 1848, 10.1093\u002Fannonc\u002Fmdp071\nCerci, 2010, 18F-FDG PET after 2 cycles of ABVD predicts event-free survival in early and advanced Hodgkin lymphoma, J Nucl Med, 51, 1337, 10.2967\u002Fjnumed.109.073197\nHutchings, 2006, FDG-PET after two cycles of chemotherapy predicts treatment failure and progression-free survival in Hodgkin lymphoma, Blood, 107, 52, 10.1182\u002Fblood-2005-06-2252\nRadford, 2015, Results of a trial of PET-directed therapy for early-stage Hodgkin lymphoma, N Engl J Med, 372, 1598, 10.1056\u002FNEJMoa1408648\nRaemaekers, 2014, Omitting radiotherapy in early positron emission tomography-negative stage I\u002FII Hodgkin lymphoma is associated with an increased risk of early relapse: clinical results of the preplanned interim analysis of the randomized EORTC\u002FLYSA\u002FFIL H10 trial, J Clin Oncol, 32, 1188, 10.1200\u002FJCO.2013.51.9298\nBakhshi, 2017, Post-treatment PET-CT rather than interim PET-CT using Deauville criteria predicts outcome in pediatric Hodgkin lymphoma: a prospective study comparing PET-CT versus conventional imaging, J Nucl Med, 58, 577, 10.2967\u002Fjnumed.116.176511\nAdams, 2016, Proportion of false-positive lesions at interim and end-of-treatment FDG-PET in lymphoma as determined by histology: systematic review and meta-analysis, Eur J Radiol, 85, 1963, 10.1016\u002Fj.ejrad.2016.08.011\nCheson, 1999, Report of an international workshop to standardize response criteria for non-Hodgkin lymphomas, J Clin Oncol, 17, 1244, 10.1200\u002FJCO.1999.17.4.1244\nCerci, 2010, Cost Effectiveness of positron emission tomography in patients with Hodgkin lymphoma in unconfirmed complete remission or partial remission after first-line therapy, J Clin Oncol, 28, 1415, 10.1200\u002FJCO.2009.25.4367\nGanesan, 2015, Phase II study of interim PET–CT-guided response-adapted therapy in advanced Hodgkin lymphoma, Ann Oncol, 26, 1170, 10.1093\u002Fannonc\u002Fmdv077\nSavage, 2015, Advanced stage classical Hodgkin lymphoma patients with a negative PET-scan following treatment with ABVD have excellent outcomes without the need for consolidative radiotherapy regardless of disease bulk at presentation, Blood, 126, 579, 10.1182\u002Fblood.V126.23.579.579\nEngert, 2012, Reduced-intensity chemotherapy and PET-guided radiotherapy in patients with advanced stage Hodgkin lymphoma (HD15 trial): a randomised, open-label, phase 3 non-inferiority trial, Lancet, 379, 1791, 10.1016\u002FS0140-6736(11)61940-5\nAdvani, 2007, Impact of positive positron emission tomography on prediction of freedom from progression after Stanford V chemotherapy in Hodgkin disease, J Clin Oncol, 25, 3902, 10.1200\u002FJCO.2007.11.9867\nKobe, 2014, Assessment of tumor size reduction improves outcome prediction of positron emission tomography\u002Fcomputed tomography after chemotherapy in advanced-stage Hodgkin lymphoma, J Clin Oncol, 32, 1776, 10.1200\u002FJCO.2013.53.2507\nDhakal, 2009, Patterns and timing of initial relapse in patients subsequently undergoing transplantation for Hodgkin lymphoma, Int J Radiat Oncol Biol Phys, 75, 188, 10.1016\u002Fj.ijrobp.2008.10.048\nvon Tresckow, 2011, The role of autologous transplantation in Hodgkin lymphoma, Curr Hematol Malig Rep, 6, 172, 10.1007\u002Fs11899-011-0091-0\nLinch, 1993, Dose intensification with autologous bone-marrow transplantation in relapsed and resistant Hodgkin disease: results of a BNLI randomised trial, Lancet, 341, 1051, 10.1016\u002F0140-6736(93)92411-L\nSchmitz, 2002, Aggressive conventional chemotherapy compared with high-dose chemotherapy with autologous haemopoietic stem-cell transplantation for relapsed chemosensitive Hodgkin disease: a randomised trial, Lancet, 359, 2065, 10.1016\u002FS0140-6736(02)08938-9\nMoskowitz, 2010, Pretransplantation functional imaging predicts outcome following autologous stem cell transplantation for relapsed and refractory Hodgkin lymphoma, Blood, 116, 4934, 10.1182\u002Fblood-2010-05-282756\nEroglu, 2015, Contribution of involved-field radiotherapy to survival in patients with relapsed or refractory Hodgkin lymphoma undergoing autologous stem cell transplantation, Am J Clin Oncol, 38, 68, 10.1097\u002FCOC.0b013e3182880b9f\nShafer, 2010, Outcome of hematopoietic stem cell transplant as salvage therapy for Hodgkin lymphoma in adolescents and young adults at a single institution, Leuk Lymphoma, 51, 664, 10.3109\u002F10428190903580410\nPoen, 1996, High-dose therapy and autologous bone marrow transplantation for relapsed\u002Frefractory Hodgkin disease: the impact of involved field radiotherapy on patterns of failure and survival, Int J Radiat Oncol Biol Phys, 36, 3, 10.1016\u002FS0360-3016(96)00277-5\nWendland, 2006, The impact of involved field radiation therapy for patients receiving high-dose chemotherapy followed by hematopoietic progenitor cell transplant for the treatment of relapsed or refractory Hodgkin disease, Am J Clin Oncol, 29, 189, 10.1097\u002F01.coc.0000209370.61355.8e\nLevis, 2017, Potential benefit of involved-field radiotherapy for patients with relapsed-refractory Hodgkin lymphoma with incomplete response before autologous stem cell transplantation, Clin Lymphoma Myeloma Leuk, 17, 14, 10.1016\u002Fj.clml.2016.09.008\nGentzler, 2014, F-18 FDG-PET predicts outcomes for patients receiving total lymphoid irradiation and autologous blood stem-cell transplantation for relapsed and refractory Hodgkin lymphoma, Br J Haematol, 165, 793, 10.1111\u002Fbjh.12824\nJabbour, 2007, Pretransplant positive positron emission tomography\u002Fgallium scans predict poor outcome in patients with recurrent\u002Frefractory Hodgkin lymphoma, Cancer, 109, 2481, 10.1002\u002Fcncr.22714\nMoskowitz, 2012, Normalization of pre-ASCT, FDG-PET imaging with second-line, non-cross-resistant, chemotherapy programs improves event-free survival in patients with Hodgkin lymphoma, Blood, 119, 1665, 10.1182\u002Fblood-2011-10-388058\nSucak, 2011, Early post-transplantation positron emission tomography in patients with Hodgkin lymphoma is an independent prognostic factor with an impact on overall survival, Ann Hematol, 90, 1329, 10.1007\u002Fs00277-011-1209-0\nAdams, 2016, Prognostic value of pretransplant FDG-PET in refractory\u002Frelapsed Hodgkin lymphoma treated with autologous stem cell transplantation: systematic review and meta-analysis, Ann Hematol, 95, 695, 10.1007\u002Fs00277-016-2619-9\nOkeley, 2010, Intracellular activation of SGN-35, a potent anti-CD30 antibody-drug conjugate, Clin Cancer Res, 16, 888, 10.1158\u002F1078-0432.CCR-09-2069\nYounes, 2012, Results of a pivotal phase II study of brentuximab vedotin for patients with relapsed or refractory Hodgkin lymphoma, J Clin Oncol, 30, 2183, 10.1200\u002FJCO.2011.38.0410\nGreen, 2010, Integrative analysis reveals selective 9p24.1 amplification, increased PD-1 ligand expression, and further induction via JAK2 in nodular sclerosing Hodgkin lymphoma and primary mediastinal large B-cell lymphoma, Blood, 116, 3268, 10.1182\u002Fblood-2010-05-282780\nAnsell, 2015, PD-1 blockade with nivolumab in relapsed or refractory Hodgkin lymphoma, N Engl J Med, 372, 311, 10.1056\u002FNEJMoa1411087\nArmand P, Shipp MA, Ribrag V, et al. 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J Clin Oncol http:\u002F\u002Fdx.doi.org\u002F10.1200\u002FJCO.2016.67.3467, accessed April 8, 2017.",{"EN":1431},"How to Approach a Patient With Limited Stage Hodgkin Lymphoma Who Remains PET Positive at the End of Chemotherapy: Radiation Therapy?",{"VOID":1433},"10.1016\u002Fj.clml.2017.06.019","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS2152265017306596",[1436,1453],{"id":1437,"sortIndex":165,"researcher":24,"roles":1438,"affiliations":1439,"properties":1450},"a145714d-8bdf-41a5-b40f-b32012f657d8",[167],[1440],{"id":24,"sortIndex":119,"affiliation":1441,"properties":24},{"id":1442,"createTime":1443,"updateTime":1444,"relativeEntities":1445,"slug":1446,"properties":1447,"entityType":61,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":119},"794f9ee2-4cbc-4191-82c1-d7fd1bbce4c7","2024-01-12T01:40:40.035+00:00","2025-02-06T11:51:50.299+00:00",[],"Department-of-Medical-Oncology-Dana-Farber-Cancer-Institute-Boston-MA",{"title":1448},{"VI":1449},"Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA",{"title":1451},{"VI":1452},"Ann S. 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2016, The 2016 revision of the World Health Organization classification of lymphoid neoplasms, Blood, 127, 2375, 10.1182\u002Fblood-2016-01-643569\nRiedell, 2018, Double hit and double expressors in lymphoma: definition and treatment, Cancer, 124, 4622, 10.1002\u002Fcncr.31646\nGreen, 2012, Immunohistochemical double-hit score is a strong predictor of outcome in patients with diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone, J Clin Oncol, 30, 3460, 10.1200\u002FJCO.2011.41.4342\nJohnson, 2012, Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone, J Clin Oncol, 30, 3452, 10.1200\u002FJCO.2011.41.0985\nHorn, 2013, MYC status in concert with BCL2 and BCL6 expression predicts outcome in diffuse large B-cell lymphoma, Blood, 121, 2253, 10.1182\u002Fblood-2012-06-435842\nHu, 2013, MYC\u002FBCL2 protein coexpression contributes to the inferior survival of activated B-cell subtype of diffuse large B-cell lymphoma and demonstrates high-risk gene expression signatures: a report from The International DLBCL Rituximab-CHOP Consortium Program, Blood, 121, 4021, 10.1182\u002Fblood-2012-10-460063\nAlexandra, 2013, MYC protein expression and genetic alterations have prognostic impact in patients with diffuse large B-cell lymphoma treated with immunochemotherapy, Haematologica, 98, 1554, 10.3324\u002Fhaematol.2013.086173\nPerry, 2014, MYC and BCL2 protein expression predicts survival in patients with diffuse large B-cell lymphoma treated with rituximab, Br J Haematol, 165, 382, 10.1111\u002Fbjh.12763\nStaiger, 2017, clinical impact of the cell-of-origin classification and the MYC\u002FBCL2 dual expresser status in diffuse large b-cell lymphoma treated within prospective clinical trials of the german high-grade non-hodgkin's lymphoma study group, J Clin Oncol, 35, 2515, 10.1200\u002FJCO.2016.70.3660\nSehn, 2021, Diffuse large B-Cell lymphoma, N Engl J Med, 384, 842, 10.1056\u002FNEJMra2027612\nZelenetz, 2021, NCCN Guidelines® insights: b-cell lymphomas, version 5.2021: featured updates to the nccn guidelines, J Natl Compr Canc Netw, 19, 1218, 10.6004\u002Fjnccn.2021.0054\nPhilip, 1995, Autologous bone marrow transplantation as compared with salvage chemotherapy in relapses of chemotherapy-sensitive non-hodgkin's lymphoma, N Engl J Med, 333, 1540, 10.1056\u002FNEJM199512073332305\nHerrera, 2017, Relapsed or refractory double-expressor and double-hit lymphomas have inferior progression-free survival after autologous stem-cell transplantation, J Clin Oncol, 35, 24, 10.1200\u002FJCO.2016.68.2740\nBartlett, 2019, Dose-adjusted epoch-r compared with r-chop as frontline therapy for diffuse large b-cell lymphoma: clinical outcomes of the phase iii intergroup trial alliance\u002Fcalgb 50303, J Clin Oncol, 37, 1790, 10.1200\u002FJCO.18.01994\nAggarwal, 2016, Outcome of patients with Double-Expressor Lymphomas (DELs) treated with R-CHOP or DA-EPOCH-R, Blood, 128, 5396, 10.1182\u002Fblood.V128.22.5396.5396\nZhang, 2019, DA-EPOCH-R improves the outcome over that of R-CHOP regimen for DLBCL patients below 60 years, GCB phenotype, and those with high-risk IPI, but not for double expressor lymphoma, J Cancer Res Clin Oncol, 145, 117, 10.1007\u002Fs00432-018-2771-9\nDodero, 2019, Dose-adjusted EPOCH plus rituximab improves the clinical outcome of young patients affected by double expressor diffuse large B-cell lymphoma, Leukemia, 33, 1047, 10.1038\u002Fs41375-018-0320-9\nHardefeldt, 2019, Dose Adjusted DA-EPOCH-R does not improve outcomes in high grade b cell lymphoma with double expressor status or gain of MYC\u002FBCL2, Blood, 134, 5336, 10.1182\u002Fblood-2019-125154\nD'Angelo, 2021, Impact of initial chemotherapy regimen on outcomes for patients with double-expressor lymphoma: a multi-center analysis, Hematol Oncol, 39, 473, 10.1002\u002Fhon.2902\nDevi, 2021, Outcomes of patients with double\u002Ftriple expressor diffuse large b-cell lymphoma (dlbcl) treated with r-da-epoch\u002Fr-chop: a single-center experience, Leuk Res Rep, 16\nHans, 2004, Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray, Blood, 103, 275, 10.1182\u002Fblood-2003-05-1545\nCheson, 2014, Recommendations for initial evaluation, staging, and response assessment of Hodgkin and non-Hodgkin lymphoma: the Lugano classification, J Clin Oncol, 32, 3059, 10.1200\u002FJCO.2013.54.8800\nThe R Project for Statistical Computing. 2021, Available at: https:\u002F\u002Fwww.r-project.org\u002F. 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A phase II study conducted by the Spanish PETHEMA Group, Br J Haematol, 169, 188, 10.1111\u002Fbjh.13273\nWyndham, 2012, A Cancer and Leukemia Group B multi-center study of DA-EPOCH-rituximab in untreated diffuse large B-cell lymphoma with analysis of outcome by molecular subtype, Haematologica, 97, 758, 10.3324\u002Fhaematol.2011.056531\nGutierrez, 2000, Role of a doxorubicin-containing regimen in relapsed and resistant lymphomas: an 8-year follow-up study of EPOCH, J Clin Oncol, 18, 3633, 10.1200\u002FJCO.2000.18.21.3633\nWeis, 2019, Dosing vincristine in dose-adjusted EPOCH-R: to cap or not to cap?, J Clin Oncol, 37, 2952, 10.1200\u002FJCO.19.01259",{"EN":1516},"R-CHOP Vs DA-EPOCH-R for Double-Expressor Lymphoma: A University of California Hematologic Malignancies Consortium Retrospective 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2007, Chronic lymphocytic leukaemia and small lymphocytic lymphoma: overview of the descriptive epidemiology, Br J Haematol, 139, 809, 10.1111\u002Fj.1365-2141.2007.06856.x\nSmith, 2011, Incidence of haematological malignancy by sub-type: a report from the haematological malignancy research network, Br J Cancer, 105, 1684, 10.1038\u002Fbjc.2011.450\nWu, 2010, The incidence of chronic lymphocytic leukemia in Taiwan, 1986-2005: a distinct increasing trend with birth-cohort effect, Blood, 116, 4430, 10.1182\u002Fblood-2010-05-285221\nDighiero, 2008, Chronic lymphocytic leukaemia, Lancet, 371, 1017, 10.1016\u002FS0140-6736(08)60456-0\nDamle, 1999, Ig V gene mutation status and CD38 expression as novel prognostic indicators in chronic lymphocytic leukemia, Blood, 94, 1840, 10.1182\u002Fblood.V94.6.1840\nHamblin, 1999, Unmutated Ig V(H) genes are associated with a more aggressive form of chronic lymphocytic leukemia, Blood, 94, 1848, 10.1182\u002Fblood.V94.6.1848\nCrespo, 2003, ZAP-70 expression as a surrogate for immunoglobulin-variable-region mutations in chronic lymphocytic leukemia, N Engl J Med, 348, 1764, 10.1056\u002FNEJMoa023143\nKröber, 2002, V(H) mutation status, CD38 expression level, genomic aberrations, and survival in chronic lymphocytic leukemia, Blood, 100, 1410, 10.1182\u002Fblood.V100.4.1410.h81602001410_1410_1416\nDöhner, 2000, Genomic aberrations and survival in chronic lymphocytic leukemia, N Engl J Med, 343, 1910, 10.1056\u002FNEJM200012283432602\nDuke, 2003, VH gene usage differs in germline and mutated B-cell chronic lymphocytic leukemia, Haematologica, 88, 1259\nMauerer, 2005, Immunoglobulin gene segment usage, location and immunogenicity in mutated and unmutated chronic lymphocytic leukaemia, Br J Haematol, 129, 499, 10.1111\u002Fj.1365-2141.2005.05480.x\nDonisi, 2006, Pattern and distribution of immunoglobulin VH gene usage in a cohort of B-CLL patients from a northeastern region of Italy, Diagn Mol Pathol, 15, 206, 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molecular and cytogenetic characteristics, IgV gene restriction and hypermutation patterns, Leuk Res, 33, 1599, 10.1016\u002Fj.leukres.2008.12.021\nGhia, 2005, Geographic patterns and pathogenetic implications of IGHV gene usage in chronic lymphocytic leukemia: the lesson of the IGHV3-21 gene, Blood, 105, 1678, 10.1182\u002Fblood-2004-07-2606\nCahill, 2012, IGHV3-21 gene frequency in Swedish cohort of patients with newly diagnosed chronic lymphocytic leukemia, Clin Lymphoma Myeloma Leuk, 12, 201, 10.1016\u002Fj.clml.2012.01.009\nRuiz-Argüelles, 1999, Chronic lymphocytic leukemia is infrequent in Mexican mestizos, Int J Hematol, 69, 253\nMoro I, Foren L, Guillermo C, et al. 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chronic lymphocytic leukemia, Blood, 46, 219, 10.1182\u002Fblood.V46.2.219.219\nPritsch, 1993, V gene usage by seven hybrids derived from CD5+ B-cell chronic lymphocytic leukemia and displaying autoantibody activity, Blood, 82, 3103, 10.1182\u002Fblood.V82.10.3103.3103\nCampbell, 1992, Use of family specific leader region primers for PCR amplification of the human heavy chain variable region gene repertoire, Mol Immunol, 29, 193, 10.1016\u002F0161-5890(92)90100-C\nBrochet, 2008, IMGT\u002FV-QUEST: the highly customized and integrated system for IG and TR standardized V-J and V-D-J sequence analysis, Nucleic Acids Res, 36, 503, 10.1093\u002Fnar\u002Fgkn316\nMurray, 2008, Stereotyped patterns of somatic hypermutation in subsets of patients with chronic lymphocytic leukemia: implications for the role of antigen selection in leukemogenesis, Blood, 111, 1524, 10.1182\u002Fblood-2007-07-099564\nMessmer, 2009, Computational identification of CDR3 sequence archetypes among immunoglobulin sequences in chronic lymphocytic leukemia, Leuk Res, 33, 368, 10.1016\u002Fj.leukres.2008.05.022\nChenna, 2003, Multiple sequence alignment with the Clustal series of programs, Nucleic Acids Res, 31, 3497, 10.1093\u002Fnar\u002Fgkg500\nMessmer, 2004, The pattern and distribution of immunoglobulin VH gene mutations in chronic lymphocytic leukemia B cells are consistent with the canonical somatic hypermutation process, Blood, 103, 3490, 10.1182\u002Fblood-2003-10-3407\nFais, 1998, Chronic lymphocytic leukemia B cells express restricted sets of mutated and unmutated antigen receptors, J Clin Invest, 102, 1515, 10.1172\u002FJCI3009\nHaferlach, 2007, Comprehensive genetic characterization of CLL: a study on 506 cases analyzed with chromosome banding analysis, interphase FISH, IgV(J) status and immunophenotype, Leukemia, 21, 2442, 10.1038\u002Fsj.leu.2404935\nWidhopf, 2004, Chronic lymphocytic leukemia B cells of more than 1% of patients express virtually identical immunoglobulins, Blood, 104, 2499, 10.1182\u002Fblood-2004-03-0818\nIkematsu, 1994, Surface phenotype and Ig heavy-chain gene usage in chronic B cell leukemias: expression of myelomonocytic surface markers in CD5-chronic B-cell leukemia, Blood, 83, 2602, 10.1182\u002Fblood.V83.9.2602.2602\nChen, 2008, Distinctive IgVH gene segments usage and mutation status in Chinese patients with chronic lymphocytic leukemia, Leuk Res, 32, 1491, 10.1016\u002Fj.leukres.2008.02.005\nHojjat-Farsangi, 2007, Analysis of the immunoglobulin heavy chain variable region gene expression in Iranian patients with chronic lymphocytic leukemia, Leuk Lymphoma, 48, 109, 10.1080\u002F10428190601043310\nAvena, 2012, Heterogeneity in genetic admixture across different regions of Argentina, PLoS ONE, 7, e34695, 10.1371\u002Fjournal.pone.0034695\nHidalgo, 2005, Genetic admixture estimate in the Uruguayan population based on the loci LDLR, GYPA, HBGG, GC and D7S8, Int J Hum Genet, 5, 217, 10.1080\u002F09723757.2005.11885929\nGiolo, 2012, Brazilian population genetic structure reveals a high degree of admixture, Eur J Hum Genet, 20, 111, 10.1038\u002Fejhg.2011.144\nMaloum, 2000, Expression of unmutated VH genes is a detrimental prognostic factor in chronic lymphocytic leukemia, Blood, 96, 377, 10.1182\u002Fblood.V96.1.377\nCapello, 2004, Evidence of biased immunoglobulin variable gene usage in highly stable B-cell chronic lymphocytic leukemia, Leukemia, 18, 1941, 10.1038\u002Fsj.leu.2403537\nWeinberg, 2007, Clinical and molecular predictors of disease severity and survival in chronic lymphocytic leukemia, Am J Hematol, 82, 1063, 10.1002\u002Fajh.20987\nNardini, 2003, Thymic function and immunoglobulin mutation genotype in B-cell chronic lymphocytic leukemia patients, Int J Cancer, 107, 958, 10.1002\u002Fijc.11482\nHojjat-Farsangi, 2009, Immunoglobulin heavy chain variable region gene usage and mutational status of the leukemic B cells in Iranian patients with chronic lymphocytic leukemia, Cancer Sci, 100, 2346, 10.1111\u002Fj.1349-7006.2009.01341.x\nAbramenko, 2007, IGHV3-21 gene expression in patients with B-cell chronic lymphocytic leukemia in Ukraine, Exp Oncol, 29, 226\nBomben, 2010, Expression of mutated IGHV3-23 genes in chronic lymphocytic leukemia identifies a disease subset with peculiar clinical and biological features, Clin Cancer Res, 16, 620, 10.1158\u002F1078-0432.CCR-09-1638\nPotter, 2003, Features of the overexpressed V1-69 genes in the unmutated subset of chronic lymphocytic leukemia are distinct from those in the healthy elderly repertoire, Blood, 101, 3082, 10.1182\u002Fblood-2002-08-2432\nNakahashi, 2009, Characterization of immunoglobulin heavy and light chain expression in chronic lymphocytic leukemia and related disorders, Cancer Sci, 100, 671, 10.1111\u002Fj.1349-7006.2009.01092.x\nTobin, 2004, Subsets with restricted immunoglobulin gene rearrangement features indicate a role for antigen selection in the development of chronic lymphocytic leukemia, Blood, 104, 2879, 10.1182\u002Fblood-2004-01-0132\nHadzidimitriou, 2011, Is there a role for antigen selection in mantle cell lymphoma?, Blood, 118, 3088, 10.1182\u002Fblood-2011-03-343434\nTschumper, 2008, Immunoglobulin diversity gene usage predicts unfavorable outcome in a subset of chronic lymphocytic leukemia patients, J Clin Invest, 118, 306, 10.1172\u002FJCI32625\nMarincevic, 2010, Distinct gene expression profiles in subsets of chronic lymphocytic leukemia expressing stereotyped IGHV4-34 B-cell receptors, Haematologica, 95, 2072, 10.3324\u002Fhaematol.2010.028639\nMaura, 2011, Relevance of stereotyped B-cell receptors in the context of the molecular, cytogenetic and clinical features of chronic lymphocytic leukemia, PLoS ONE, 6, e24313, 10.1371\u002Fjournal.pone.0024313\nMaura, 2012, B-cell receptor configuration and adverse cytogenetics are associated with autoimmune hemolytic anemia in chronic lymphocytic leukemia, Am J Hematol, 88, 32, 10.1002\u002Fajh.23342\nGhiotto, 2004, Remarkable similar antigen receptors among a subset of patients with chronic lymphocytic leukemia, J Clin Invest, 113, 1008, 10.1172\u002FJCI19399\nChu, 2008, Chronic lymphocytic leukemia antibodies with a common stereotypic rearrangement recognize nonmuscle myosin heavy chain IIA, Blood, 112, 5122, 10.1182\u002Fblood-2008-06-162024\nChu, 2010, Many chronic lymphocytic leukemia antibodies recognize apoptotic cells with exposed nonmuscle myosin heavy chain IIA: implications for patient outcome and cell of origin, Blood, 115, 3907, 10.1182\u002Fblood-2009-09-244251\nMauerer, 2005, Immunoglobulin gene segment usage, location and immunogenicity in mutated and unmutated chronic lymphocytic leukemia, Br J Haematol, 129, 499, 10.1111\u002Fj.1365-2141.2005.05480.x\nWeinberg, 2007, Clinical and molecular predictors of disease severity and survival in chronic lymphocytic leukemia, Am J Hematol, 82, 1063, 10.1002\u002Fajh.20987\nMessmer, 2004, The pattern and distribution of immunoglobulin VH gene mutations in chronic lymphocytic leukemia B cells are consistent with the canonical somatic hypermutation process, Blood, 103, 3490, 10.1182\u002Fblood-2003-10-3407\nPasqualucci, 2000, BCL-6 mutations are associated with immunoglobulin variable heavy chain mutations in B-cell chronic lymphocytic leukemia, Cancer Res, 60, 5644\nTobin, 2004, Subsets with restricted immunoglobulin gene rearrangement features indicate a role for antigen selection in the development of chronic lymphocytic leukemia, Blood, 104, 2879, 10.1182\u002Fblood-2004-01-0132\nPritsch, 1993, V gene usage by seven hybrids derived from CD5+ B-cell chronic lymphocytic leukemia and displaying autoantibody activity, Blood, 82, 3103, 10.1182\u002Fblood.V82.10.3103.3103\nBomben, 2009, Molecular and clinical features of chronic lymphocytic leukemia with stereotyped B cell receptor: results from Italian multicentre study, Br J Haematol, 144, 492, 10.1111\u002Fj.1365-2141.2008.07469.x\nNardini, 2003, Thymic function and immunoglobulin mutation genotype in B-cell chronic lymphocytic leukemia patients, Int J Cancer, 107, 958, 10.1002\u002Fijc.11482\nCrespo, 2003, ZAP-70 expression as a surrogate for immunoglobulin-variable-region mutations in chronic lymphocytic leukemia, N Engl J Med, 348, 1764, 10.1056\u002FNEJMoa023143\nMaloum, 2000, Expression of unmutated VH genes is a detrimental prognostic factor in chronic lymphocytic leukemia, Blood, 96, 377, 10.1182\u002Fblood.V96.1.377\nStamatopoulos, 2007, Over 20% of patients with chronic lymphocytic leukemia carry stereotyped receptors: pathogenetic implications and clinical correlations, Blood, 109, 259, 10.1182\u002Fblood-2006-03-012948\nGhia, 2005, Geographic patterns and pathogenetic implications of IGHV gene usage in chronic lymphocytic leukemia: Lesson of the IGHV3-21 gene, Blood, 105, 1678, 10.1182\u002Fblood-2004-07-2606\nHamblin, 1999, Unmutated Ig V(H) genes are associated with a more aggressive form of chronic lymphocytic leukemia, Blood, 94, 1848, 10.1182\u002Fblood.V94.6.1848\nDuke, 2003, VH gene usage differs in germline and mutated B-cell chronic lymphocytic leukemia, Haematologica, 88, 1259\nAbramenko, 2007, IGHV3-21 gene expression in patients with B-cell chronic lymphocytic leukemia in Ukraine, Exp Oncol, 29, 226\nKoiso, 2006, Distinctive immunoglobulin VH gene usage in Japanese patients with CLL, Leukemia Res, 30, 272, 10.1016\u002Fj.leukres.2005.07.007\nNakahashi, 2009, Characterization of immunoglobulin heavy and light chain expression in chronic lymphocytic leukemia and related disorders, Cancer Sci, 100, 671, 10.1111\u002Fj.1349-7006.2009.01092.x\nChen, 2008, Distinctive IgVH gene segments usage and mutation status in Chinese patients with chronic lymphocytic leukemia, Leuk Res, 32, 1491, 10.1016\u002Fj.leukres.2008.02.005\nIrons, 2009, Characterization of chronic lymphocytic leukemia\u002Fsmall lymphocytic lymphoma (CLL\u002FSLL) in Shanghai, China: molecular and cytogenetic characteristics, IgV gene restriction and 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