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2019, B and T cell prolymphocytic leukaemia, Best Pract. Res. Clin. Haematol., 32, 217, 10.1016\u002Fj.beha.2019.06.001\nChaar, 2007, Complete response to alemtuzumab in a patient with B prolymphocytic leukemia [7], Am. J. Hematol., 82, 417, 10.1002\u002Fajh.20843\nEyre, 2019, Idelalisib-rituximab induces durable remissions in TP53 disrupted B-PLL but results in significant toxicity: updated results of the UK-wide compassionate use programme, Br. J. Haematol., 184, 667, 10.1111\u002Fbjh.15151\nEyre, 2019, Efficacy of venetoclax monotherapy in patients with relapsed chronic lymphocytic leukaemia in the post-BCR inhibitor setting: a UK wide analysis, Br. J. Haematol., 185, 656, 10.1111\u002Fbjh.15802\nJ. Swerdlow, S.H.; Campo, E.; Harris, N.L.; Jaffe, E.S.; Pileri, S.A.; Stein, H.; Thiele, J.; Vardiman, WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues, 4th ed., 2008.\nRavandi, 2005, Chronic lymphoid leukemias other than chronic lymphocytic leukemia: diagnosis and treatment, Mayo Clin. Proc., 80, 1660, 10.4065\u002F80.12.1660\nShvidel, 1999, B-Cell prolymphocytic leukemia: a survey of 35 patients emphasizing heterogeneity, prognostic factors and evidence for a group with an indolent course, Leuk. Lymphoma., 33, 169, 10.3109\u002F10428199909093739\nDearden, 2012, How I treat prolymphocytic leukemia, Blood, 120, 538, 10.1182\u002Fblood-2012-01-380139\nDel Giudice, 2006, IgVH genes mutation and usage, ZAP-70 and CD38 expression provide new insights on B-cell prolymphocytic leukemia (B-PLL), Leukemia, 20, 1231, 10.1038\u002Fsj.leu.2404238\nDavi, 1996, High frequency of somatic mutations in the VH genes expressed in prolymphocytic leukemia, Blood, 88, 3953, 10.1182\u002Fblood.V88.10.3953.bloodjournal88103953\nPut, 2012, Chronic lymphocytic leukemia and prolymphocytic leukemia with MYC translocations: a subgroup with an aggressive disease course, Ann. Hematol., 91, 863, 10.1007\u002Fs00277-011-1393-y\nFlatley, 2014, Aberrations of MYC are a common event in B-cell prolymphocytic leukemia, Am. J. Clin. Pathol., 142, 347, 10.1309\u002FAJCPUBHM8U7ZFLOB\nChapiro, 2019, Genetic characterization of B-cell prolymphocytic leukemia: a prognostic model involving MYC and TP53, Blood, 134, 1821\nDöhner, 1993, Pentostatin in prolymphocytic leukemia: phase II trial of the European organization for research and treatment of cancer leukemia cooperative study group, J. Natl. Cancer Inst., 85, 658, 10.1093\u002Fjnci\u002F85.8.658\nTempescul, 2009, A combination therapy with fludarabine, mitoxantrone and rituximab induces complete immunophenotypical remission in B-cell prolymphocytic leukaemia, Ann. Hematol., 88, 85, 10.1007\u002Fs00277-008-0541-5\nChow, 2011, Clinical efficacy of immunochemotherapy with fludarabine, epirubicin and rituximab in the treatment for chronic lymphocytic leukaemia and prolymphocytic leukaemia, Eur. J. Haematol., 87, 426, 10.1111\u002Fj.1600-0609.2011.01680.x\nMcCune, 2002, Alemtuzumab in relapsed or refractory chronic lymphocytic leukemia and prolymphocytic leukemia, Leuk. Lymphoma., 43, 1007, 10.1080\u002F10428190290021597\nCoelho, 2017, Sequential kinase inhibition (idelalisib\u002Fibrutinib) induces clinical remission in b-cell prolymphocytic leukemia harboring a 17p deletion, Case Rep. Hematol., 2017, 1, 10.1155\u002F2017\u002F8563218\nGordon, 2017, Ibrutinib is an effective treatment for B-cell prolymphocytic leukaemia, Br. J. Haematol., 179, 501, 10.1111\u002Fbjh.14224\nBindra, 2019, B-cell prolymphocytic leukemia: case report and challenges on a diagnostic and therapeutic forefront, Cureus., 11\nOka, 2020, Effective upfront treatment with low-dose ibrutinib for a patient with B cell prolymphocytic leukemia, Invest. New Drugs., 38, 1598, 10.1007\u002Fs10637-020-00902-9\nJain, 2019, Ibrutinib and Venetoclax for First-Line Treatment of CLL, N. Engl. J. 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2019, Chronic lymphocytic leukemia: 2020 update on diagnosis, risk stratification and treatment, Am. J. Hematol., 94, 1266, 10.1002\u002Fajh.25595\nHerndon, 2017, Direct in vivo evidence for increased proliferation of CLL cells in lymph nodes compared to bone marrow and peripheral blood, Leuk., 31, 1340, 10.1038\u002Fleu.2017.11\nZent, 2011, FISHing for answers in proliferation centers of chronic lymphocytic leukemia lymph nodes, Leuk Lymphoma, 52, 946, 10.3109\u002F10428194.2011.565099\nHerishanu, 2011, The lymph node microenvironment promotes B-cell receptor signaling, NF-kappaB activation, and tumor proliferation in chronic lymphocytic leukemia, Blood, 117, 563, 10.1182\u002Fblood-2010-05-284984\nSwerdlow, 2017\nPugh, 1988, Paraimmunoblastic variant of small lymphocytic lymphoma\u002Fleukemia, Am J Surg Pathol, 12, 907, 10.1097\u002F00000478-198812000-00002\nGine, 2010, Expanded and highly active proliferation centers identify a histological subtype of chronic lymphocytic leukemia (“accelerated” chronic lymphocytic leukemia) with aggressive clinical behavior, Haematologica, 95, 1526, 10.3324\u002Fhaematol.2010.022277\nBoyd, 2013, Selective immunophenotyping for diagnosis of B-cell neoplasms: immunohistochemistry and flow cytometry strategies and results, Appl. Immunohistochem. Mol. Morphol., 21, 116, 10.1097\u002FPAI.0b013e31825d550a\nJain, 2012, Chronic lymphocytic leukemia with deletion 17p: emerging treatment options, Oncol. (Williston Park), 26, 1070\nMatutes, 2000, Morphological and immunophenotypic features of chronic lymphocytic leukemia, Rev. Clin. Exp. Hematol., 4, 22, 10.1046\u002Fj.1468-0734.2000.00002.x\nGarces, 2018, Chronic lymphocytic leukemia with proliferation centers in bone marrow is associated with younger age at initial presentation, complex karyotype, and TP53 disruption, Hum. Pathol., 82, 215, 10.1016\u002Fj.humpath.2018.07.030\nLiu, 2020, Chronic lymphocytic leukemia with TP53 gene alterations: a detailed clinicopathologic analysis, Mod. Pathol., 33, 344, 10.1038\u002Fs41379-019-0356-z\nCiccone, 2012, Proliferation centers in chronic lymphocytic leukemia: correlation with cytogenetic and clinicobiological features in consecutive patients analyzed on tissue microarrays, Leuk., 26, 499, 10.1038\u002Fleu.2011.247\nWoyach, 2019, Treatment-naive CLL: lessons from phase 2 and phase 3 clinical trials, Blood, 134, 1796, 10.1182\u002Fblood.2019001321\nEichhorst, 2019, Relapsed disease and aspects of undetectable MRD and treatment discontinuation, Hematol. Am. Soc. Hematol. Educ. Prog., 2019, 482, 10.1182\u002Fhematology.2019000070\nTsang, 2015, The efficacy of ibrutinib in the treatment of richter syndrome, Blood, 125, 1676, 10.1182\u002Fblood-2014-12-610782\nFischer, 2018, Ibrutinib-induced rapid response in chemotherapy-refractory richter's syndrome, Hematol. Oncol., 36, 370, 10.1002\u002Fhon.2464\nAllan, 2018, Current trends in the management of richter's syndrome, Int. J. Hematol. Oncol., 7, 10.2217\u002Fijh-2018-0010\nKhan, 2018, Approach to richter transformation of chronic lymphocytic leukemia in the era of novel therapies, Ann. Hematol., 97, 1, 10.1007\u002Fs00277-017-3149-9\nRossi, 2011, The genetics of richter syndrome reveals disease heterogeneity and predicts survival after transformation, Blood, 117, 3391, 10.1182\u002Fblood-2010-09-302174\nMaddocks, 2015, Etiology of ibrutinib therapy discontinuation and outcomes in patients with chronic lymphocytic leukemia, JAMA Oncol, 1, 80, 10.1001\u002Fjamaoncol.2014.218\nMunir, 2019, Final analysis from RESONATE: up to six years of follow-up on ibrutinib in patients with previously treated chronic lymphocytic leukemia or small lymphocytic lymphoma, Am. J. 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