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1. Tsimberidou AM, O'Brien S, Kantarjian HM, Koller C, Hagemeister FB, Fayad L, Lerner S, Bueso-Ramos CE, Keating MJ: Hodgkin transformation of chronic lymphocytic leukemia: the M. D. Anderson Cancer Center experience. Cancer; 2006 Sep 15;107(6):1294-302
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  • [Title] Hodgkin transformation of chronic lymphocytic leukemia: the M. D. Anderson Cancer Center experience.
  • BACKGROUND: Hodgkin transformation is a rare complication of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).
  • In this study, the authors assessed the incidence, presenting characteristics, and outcomes of patients with CLL/SLL who developed Hodgkin lymphoma (HL).
  • METHODS: An electronic database search of patients with CLL/SLL who presented at The University of Texas M. D.
  • Anderson Cancer Center Department of Leukemia between 1975 and 2005 was performed.
  • RESULTS: Among 4121 patients with CLL/SLL, 18 patients (0.4%) developed HL.
  • The median time from CLL to HL diagnosis was 4.6 years (range, 0-12.9 years).
  • Fourteen patients (78%) had been previously treated for CLL/SLL.
  • Ten patients (56%) had received >1 prior therapy.
  • Fourteen patients (78%) received chemotherapy.
  • CONCLUSIONS: The rates of response, survival, and FFS in patients with Hodgkin transformation of CLL/SLL were inferior to those reported in patients with de novo HL and were similar to those in patients with Richter syndrome.
  • [MeSH-major] Hodgkin Disease / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Female. Hospitals, University / statistics & numerical data. Humans. Male. Middle Aged. Prognosis. Remission Induction. Texas. Treatment Outcome

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  • [Copyright] (c) 2006 American Cancer Society.
  • (PMID = 16902984.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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2. Kalil N, Cheson BD: Management of chronic lymphocytic leukaemia. Drugs Aging; 2000 Jan;16(1):9-27
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  • [Title] Management of chronic lymphocytic leukaemia.
  • Chronic lymphocytic leukaemia (CLL) is the most common form of adult leukaemia in Western countries.
  • Cytogenetic abnormalities are frequent in patients with CLL, and may be associated with poor prognosis.
  • Aggressive transformation occurs in 10% of patients with CLL, most commonly prolymphocytic leukaemia (PLL) and Richter's syndrome.
  • PLL de novo must be differentiated from PLL of an aggressive transformation.
  • The incidences of autoimmune diseases and solid or haemopoietic secondary malignancies are increased in patients with CLL.
  • Clinical stage is the strongest prognostic factor in CLL.
  • The current recommendation to start treatment includes disease-related symptoms, massive and/or progressive hepatosplenomegaly or lymphadenopathy, increasing bone marrow failure, autoimmune disease, and recurrent infections.
  • Alkylating agents (e.g. chlorambucil) and nucleoside analogues (e.g. fludarabine) are the most active agents for CLL.
  • Fludarabine is the drug of choice for the majority of patients with CLL.
  • No drug combination is better than single agents.
  • For patients refractory to initial treatment, referral to a clinical trial is the best choice.
  • Other salvage therapy includes retreatment with the same initial agent (chlorambucil or fludarabine) if initial response was observed, or fludarabine for patients refractory to chlorambucil.
  • Promising new approaches include cycle-active agents, nelarabine, biological therapy such as anti-CD52 monoclonal antibody, bone marrow transplantation, including the use of submyeloablative preparative regimens ('minitransplant') to induce graft-versus-leukaemia effect, and gene therapy.
  • Assessment of response to therapy in CLL has been updated by the National Cancer Institute Working Group, and these guidelines are used worldwide for clinical trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Animals. Combined Modality Therapy. Humans. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / therapy

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  • (PMID = 10733261.001).
  • [ISSN] 1170-229X
  • [Journal-full-title] Drugs & aging
  • [ISO-abbreviation] Drugs Aging
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 236
  •  go-up   go-down


3. Narayan H, Bandyopadhyay D, Schmidt K, Chachlani N, Hughes M, Paneesha S, Rose P, Borg A: Successful treatment of a patient with chronic lymphocytic leukaemia (CLL) presenting with bony metastases with aggressive antibody and chemotherapy. Clin Lab Haematol; 2005 Dec;27(6):405-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of a patient with chronic lymphocytic leukaemia (CLL) presenting with bony metastases with aggressive antibody and chemotherapy.
  • Osteolytic lesions are rare in chronic lymphocytic leukaemia (CLL) and thought to result from Richter's transformation or metastatic disease from nonlymphoid malignancies.
  • We report a patient who presented with a large femoral metastatic lesion and hypercalcaemia caused by CLL itself.
  • Complete remission of CLL with resolution of the osteolytic lesion was achieved with rituximab and cyclophosphamide, adriamycin, oncovin and prednisolone [CHOP (R-CHOP)] combination chemotherapy.
  • [MeSH-major] Bone Neoplasms / secondary. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Aged, 80 and over. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Femur. Humans. Hypercalcemia / etiology. Male. Prednisolone / therapeutic use. Remission Induction / methods. Rituximab. Vincristine / therapeutic use

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  • [CommentIn] Int J Lab Hematol. 2007 Dec;29(6):478-9; author reply 479 [17988306.001]
  • (PMID = 16307545.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VAP-cyclo protocol
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4. Robak E, Góra-Tybor J, Kordek R, Wawrzyniak E, Bartkowiak J, Bednarek A, Constantinou M, Kałuzewski B, Robak T: Richter syndrome first manifesting as cutaneous B-cell lymphoma clonally distinct from primary B-cell chronic lymphocytic leukaemia. Br J Dermatol; 2005 Oct;153(4):833-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Richter syndrome first manifesting as cutaneous B-cell lymphoma clonally distinct from primary B-cell chronic lymphocytic leukaemia.
  • Richter syndrome (RS) is a transformation to high-grade non-Hodgkin lymphoma in patients with chronic lymphocytic leukaemia (CLL).
  • We present a 77-year-old woman who developed isolated diffuse large B-cell lymphoma (LBCL) in the skin of the nose without any other symptoms of RS.
  • The LBCL in the skin was clonally distinct from the original bone marrow CLL cells.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, B-Cell / pathology. Neoplastic Stem Cells / pathology. Nose Neoplasms / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / pathology. Prednisone / therapeutic use. Syndrome. Vincristine / therapeutic use

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  • (PMID = 16181471.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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5. Thornton PD, Bellas C, Santon A, Shah G, Pocock C, Wotherspoon AC, Matutes E, Catovsky D: Richter's transformation of chronic lymphocytic leukemia. The possible role of fludarabine and the Epstein-Barr virus in its pathogenesis. Leuk Res; 2005 Apr;29(4):389-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Richter's transformation of chronic lymphocytic leukemia. The possible role of fludarabine and the Epstein-Barr virus in its pathogenesis.
  • Transformation of CLL into a large cell lymphoma has an incidence of 3-5%.
  • We have studied 101 cases of CLL treated with fludarabine over a 10-year period (1990-2000) and observed a 12% incidence of transformation.
  • In six of 12 patients, transformation was documented within 4 months following treatment with fludarabine.
  • In two cases there was a different pattern of immunoglobulin gene rearrangement in the transformed cells assessed by PCR (FR3 fragment) compared to the original CLL clone.
  • The other seven cases, of which two were EBV positive, showed identical pattern of Ig gene rearrangement in both the CLL and the transformed cells.
  • We suggest that the relatively high incidence of transformation in this series may be due to immunosuppression mainly related to fludarabine, although other agents and prior therapies may have also contributed.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Herpesvirus 4, Human / isolation & purification. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / virology. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Transformation, Neoplastic. Disease Progression. Female. Humans. Kidney / pathology. Lymph Nodes / pathology. Male. Middle Aged. Reed-Sternberg Cells / parasitology. Treatment Outcome. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 15725472.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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6. Huh YO, Lin KI, Vega F, Schlette E, Yin CC, Keating MJ, Luthra R, Medeiros LJ, Abruzzo LV: MYC translocation in chronic lymphocytic leukaemia is associated with increased prolymphocytes and a poor prognosis. Br J Haematol; 2008 Jul;142(1):36-44
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  • [Title] MYC translocation in chronic lymphocytic leukaemia is associated with increased prolymphocytes and a poor prognosis.
  • Chromosomal translocations that involve MYC, characteristic of Burkitt lymphoma, are rare in chronic lymphocytic leukaemia (CLL).
  • We report the clinical, morphological, immunophenotypic, cytogenetic and molecular genetic features of eight CLL cases with MYC rearrangement.
  • Six cases were classified as CLL with increased prolymphocytes (CLL/PL; prolymphocytes 10-55%), and two were classified as CLL in prolymphocytic transformation (CLL/PT; prolymphocytes >55%).
  • All patients received combination chemotherapy.
  • Two developed Epstein-Barr virus (EBV)-associated diffuse large B-cell lymphomas (DLBCL) that were clonally unrelated to the CLL.
  • In summary, MYC rearrangement, which occurs rarely in CLL patients, is associated with increased prolymphocytes, complex cytogenetic abnormalities, and a poor prognosis.
  • [MeSH-major] Genes, myc / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Female. Humans. Immunophenotyping. Lymphoid Progenitor Cells / pathology. Male. Middle Aged. Mutation / genetics. Prognosis

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  • (PMID = 18477041.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] England
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7. O'Sullivan MJ, Kaleem Z, Bolger MJ, Swanson PE, Zutter MM: Composite prolymphocytoid and hodgkin transformation of chronic lymphocytic leukemia. Arch Pathol Lab Med; 2000 Jun;124(6):907-9
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  • [Title] Composite prolymphocytoid and hodgkin transformation of chronic lymphocytic leukemia.
  • The indolent course of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) is occasionally altered by transformation to a histologically distinct, rapidly progressive, and clinically unresponsive hematologic malignant neoplasm.
  • We report a case of CLL that, after 3 years of slowly progressive disease and treatment with single-agent chemotherapy (fludarabine phosphate), underwent a composite prolymphocytoid and classic Hodgkin lymphoma transformation.
  • The remainder of the lymph node and the peripheral blood showed increased numbers of prolymphocytes admixed with typical small CLL cells.
  • Recognition of such a transformation is of the utmost importance, since histologically similar Reed-Sternberg-like cells may be seen in Richter transformation.
  • In contrast to prolymphocytoid transformation of CLL, Richter syndrome is rapidly fatal, with a median survival of 4 to 5 months.
  • The patient pursued a clinical course similar to pure prolymphocytoid transformation and died with disease after 30 months following treatment with combination chemotherapy.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Hodgkin Disease / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Aged. Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bleomycin / administration & dosage. Dacarbazine / therapeutic use. Doxorubicin / administration & dosage. Fatal Outcome. Humans. Immunophenotyping. Male. Reed-Sternberg Cells / immunology. Reed-Sternberg Cells / pathology. Vinblastine / administration & dosage

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  • (PMID = 10835534.001).
  • [ISSN] 0003-9985
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD; 11056-06-7 / Bleomycin; 5V9KLZ54CY / Vinblastine; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin
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8. Schriever F, Huhn D: New directions in the diagnosis and treatment of chronic lymphocytic leukaemia. Drugs; 2003;63(10):953-69
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  • [Title] New directions in the diagnosis and treatment of chronic lymphocytic leukaemia.
  • Chronic lymphocytic leukaemia (CLL) is the most common leukaemia of adults in Western countries.
  • It is a systemic haematological malignancy that originates from B cells (B-CLL) in 95% of patients, while only a minority are derived through malignant transformation of T cells (T-CLL).
  • Although B-CLL is classified as a non-Hodgkin's lymphoma, several issues make this leukaemia a unique entity among malignant lymphoma.
  • Inhibition of the programmed cell death (apoptosis) and upregulation of the anti-apoptotic protein Bcl-2 are key elements of the pathophysiology of B-CLL cells and define clinical prognosis.
  • Furthermore, B-CLL cells are arrested in G0/G1 phase of the cell cycle.
  • Dysfunctional apoptosis and cell cycle are the main reasons for the clinical enigma, that CLL can not yet be cured with conventional chemotherapy.
  • However, the molecular pathways that are responsible for this characteristic feature of the B-CLL cells still need further definition.Recently, considerable progress has been made in defining the molecular basis for the pathogenesis of CLL and in finding new therapeutic options.
  • Recent studies indicate that B-CLL cells may be delineated from two main groups of normal B cells, i.e. pre- and postgerminal B cells, and can be distinguished through lack of or existence of mutations of the V heavy chain gene.
  • Modern cytogenetic methods such as fluorescence in situ hybridisation (FISH) have opened a new era in the molecular analysis of CLL cells.
  • The cytogenetic profile may soon help to define a clinical risk profile and guide the various treatment strategies.
  • Further progress has been made in the therapy of CLL.
  • Chimera of murine or rat monoclonal antibodies and human antibodies were designed to treat CLL.
  • Antibodies such as rituximab and alemtuzumab (Campath-1H), directed against CD20 and CD52, respectively, appear as attractive alternatives to conventional chemotherapy because of their lack of significant myelotoxicity.
  • Studies using myeloablative chemotherapy followed by autologous or allogeneic stem cell transplantation were initiated with the hope of finding a cure for CLL.
  • In conclusion, for many years CLL was considered as a chronic haematological malignancy that required only few diagnostic tools and for whom no hope of cure could be offered.
  • The current review focuses on recent improvements in diagnosis and treatment of CLL that have opened a new era in the management of patients with this systemic malignancy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / therapeutic use. Humans. Rituximab

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  • (PMID = 12699399.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 108
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9. Tsimberidou AM, Keating MJ: Richter's transformation in chronic lymphocytic leukemia. Semin Oncol; 2006 Apr;33(2):250-6
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  • [Title] Richter's transformation in chronic lymphocytic leukemia.
  • Richter's syndrome (RS) is characterized by the development of high-grade non-Hodgkin's lymphoma (NHL) in a patient with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma.
  • The large cells of RS may arise through transformation of the original CLL clone or represent a new neoplasm.
  • These abnormalities may cause CLL cells to proliferate and, by facilitating the acquisition of new genetic abnormalities, to transform into RS cells.
  • The therapeutic strategies for RS typically include therapies developed for NHL or acute lymphoblastic leukemia.
  • The reported response rates with these therapies are 5% to 43%, and the median survival duration ranges from 5 to 8 months.
  • Patients appear to benefit from cytoreductive therapy consisting of chemotherapy and immunotherapy, followed by allogeneic stem cell transplantation, as postremission therapy.
  • As part of a program aiming to cure RS, we are currently conducting a clinical trial of oxaliplatin, fludarabine, and cytarabine in combination with rituximab and recommend postremission therapy, including allogeneic stem cell transplantation in patients with available donors.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, Non-Hodgkin. Neoplasms, Multiple Primary
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Transformation, Neoplastic / pathology. Humans. Prognosis

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  • (PMID = 16616072.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 78
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10. Cohen Y, Da'as N, Libster D, Amir G, Berrebi A, Polliack A: Large-cell transformation of chronic lymphocytic leukemia and follicular lymphoma during or soon after treatment with fludarabine-rituximab-containing regimens: natural history- or therapy-related complication? Eur J Haematol; 2002 Feb;68(2):80-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large-cell transformation of chronic lymphocytic leukemia and follicular lymphoma during or soon after treatment with fludarabine-rituximab-containing regimens: natural history- or therapy-related complication?
  • Novel therapeutic regimens containing purine analogs and monoclonal antibodies have led to significant improvement in the course of indolent lymphoproliferative diseases (LPD).
  • Until now, attention has been paid mainly to opportunistic infection occurring as a result of the above drug-induced immunosuppression and less to other possible complications, such as malignancy or tumor progression in the immunocompromised host.
  • Here we briefly report nine patients with previously treated indolent LPD in whom the onset of large-cell transformation occurred during or shortly after the initiation of regimens containing these agents before transformation occurred.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunosuppressive Agents / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Follicular / drug therapy. Lymphoma, Large B-Cell, Diffuse / etiology. Vidarabine / adverse effects
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Murine-Derived. Cell Transformation, Neoplastic. Follow-Up Studies. Humans. Immunocompromised Host. Middle Aged. Neoplasms, Second Primary / etiology. Rituximab. Time Factors

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  • (PMID = 12038452.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Immunosuppressive Agents; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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11. Spell DW, Walker JE, Bueno CL: Hypercalcemia and Richter Syndrome of CLL. J Clin Oncol; 2004 Jul 15;22(14_suppl):6729

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hypercalcemia and Richter Syndrome of CLL.
  • However, severe hypercalcemia has not been reported with a Richter transformation of CLL.
  • METHODS: Case Report Results: A 51-year-old African-American woman with stage IV CLL diagnosed in 2001 was initiated on weekly rituximab in February 2003 due to worsening lymphadenopathy, anemia and thrombocytopenia.
  • Bone marrow aspirate and biopsy revealed nearly 100% cellularity with a prominent immature cell type.
  • The diagnosis of Richter syndrome was confirmed pathologically and the patient was started on salvage chemotherapy.
  • CONCLUSIONS: Proposed mechanisms for hypercalcemia in patients with CLL include concurrent primary hyperparathyroidism, secondary hyperparathyroidism related to tumor production of either calcitriol or parathyroid hormone-related peptide, or secondary osteolysis by an osteoclast activating factor such as TNF-α.
  • Hypercalcemia is usually associated with primary hyperparathyroidism in early stage CLL and with an osteolytic process in advanced CLL.
  • To our knowledge, this degree of hypercalcemia has not been previously reported with a Richter syndrome of CLL.

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  • (PMID = 28014668.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Yee KW, O'Brien SM, Giles FJ: Richter's syndrome: biology and therapy. Cancer J; 2005 May-Jun;11(3):161-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Richter's syndrome: biology and therapy.
  • Richter's syndrome, that is, transformation of chronic lymphocytic leukemia to a large cell or immunoblastic lymphoma, occurs in up to 10% of patients with chronic lymphocytic leukemia.
  • Median survival with conventional chemotherapy is less than 6 months.
  • Therapy with more recent therapeutic regimens, such as hyperCVXD (fractionated cyclophosphamide, vincristine, liposomal daunorubicin, and dexamethasone), augmented hyperCVXD, and yttrium-90 ibritumomab tiuxetan, has not produced major improvements in response rates or overall survival.
  • Improvement in the outcome of patients with Richter's syndrome may be aided by a more comprehensive understanding of the pathogenesis of Richter's syndrome; therapy could then be targeted against specific abnormalities.
  • Current data indicate that the transformation of chronic lymphocytic leukemia to a large-cell or immunoblastic lymphoma is associated with abnormalities in cell cycle regulation (e.g., loss of the cell cycle inhibitors p16(INK4a) and p27(KIP1) ) and DNA repair (e.g., mutations and/or deletions of the p53, ATM, and p14(ARF) genes and epigenetic silencing of the MLH1 gene).
  • However, the critical event leading to transformation is unclear.
  • [MeSH-major] Cell Transformation, Neoplastic. Leukemia, Lymphocytic, Chronic, B-Cell / physiopathology. Lymphoma, Large-Cell, Immunoblastic / physiopathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Cycle. Humans. Immunoconjugates / therapeutic use. Prognosis. Risk Factors. Stem Cell Transplantation. Survival. Syndrome

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  • (PMID = 16053658.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoconjugates
  • [Number-of-references] 113
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13. Rodriguez J, Keating MJ, O'Brien S, Champlin RE, Khouri IF: Allogeneic haematopoietic transplantation for Richter's syndrome. Br J Haematol; 2000 Sep;110(4):897-9
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  • This study evaluated the efficacy of allogeneic bone marrow transplantation (AlloBMT) in eight patients who had chronic lymphocytic leukaemia (CLL) in Richter's transformation.
  • These data suggest that, compared with conventional chemotherapy, AlloBMT improves the prognosis for patients with Richter's syndrome.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Lymphocytic, Chronic, B-Cell / therapy
  • [MeSH-minor] Adult. Disease-Free Survival. Female. Humans. Male. Middle Aged. Recurrence. Survival Rate. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 11054078.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
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14. Thornton PD, Matutes E, Bosanquet AG, Lakhani AK, Grech H, Ropner JE, Joshi R, Mackie PH, Douglas ID, Bowcock SJ, Catovsky D: High dose methylprednisolone can induce remissions in CLL patients with p53 abnormalities. Ann Hematol; 2003 Dec;82(12):759-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High dose methylprednisolone can induce remissions in CLL patients with p53 abnormalities.
  • Abnormalities of the p53 gene are known to confer detrimental effects in chronic lymphocytic leukaemia (CLL) and are associated with short survival.
  • We have used high dose methylprednisolone (HDMP) to treat 25 patients with advanced refractory CLL of whom 45% had p53 abnormalities shown by one or more methods: flow cytometry, fluorescent in situ hybridisation and direct DNA sequencing.
  • Fifteen were resistant to fludarabine and 16 were non-responders to their most recent therapy.
  • Methylprednisolone had a cytotoxic effect on lymphocytes from 95% of cases assessed by an ex vivo apoptotic drug sensitivity index (DSI).
  • HDMP was given alone or in combination with other drugs: vincristine, CCNU, Ara-C, doxorubicin, mitoxantrone and chlorambucil, according to the results of DSI.
  • Three patients were treated twice and each treatment was analysed separately.
  • Nine of the 22 evaluable patients (3 NR and 6 PR) have died from progressive disease or transformation.
  • This study demonstrates that HDMP alone or in combination with other agents is a useful treatment strategy in refractory CLL including patients with p53 abnormalities.
  • [MeSH-major] Genes, p53. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Methylprednisolone / administration & dosage
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Drug Screening Assays, Antitumor. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mutation. Remission Induction. Tumor Cells, Cultured

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  • (PMID = 14551737.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] X4W7ZR7023 / Methylprednisolone
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15. Castex MP, Bertozzi AI, Rubie H, Domenech B, Duchayne E, Selves J, Dastugue N, Danjoux M, Kulhein E, Galinier P, Robert A: [Testicular feminization, germinal tumor, NK lymphoma: what is the relationship?]. Arch Pediatr; 2001 Dec;8(12):1337-40
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  • CASE REPORT: The authors report the case of a ten-year-old girl, who had been treated for a malignant germinal tumour five years before, presenting with a leukaemia-like syndrome associating bone pain, liver and spleen nodules and bone marrow involvement.
  • The child received several subsequent lines of chemotherapy and ultimately died of the disease.
  • [MeSH-major] Androgen-Insensitivity Syndrome / genetics. Killer Cells, Natural. Leukemia / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Ovarian Neoplasms / genetics. Teratoma / genetics
  • [MeSH-minor] Antigens, CD56 / genetics. Bone Marrow / pathology. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Child. Female. Genotype. Humans. Liver / pathology. Male. S100 Proteins / genetics

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  • (PMID = 11811029.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / S100 Proteins
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16. Holománová D, Varga A, Mistrík M, Sakalová A, Kotoucek P, Plank L, Szépe P: [Richter's syndrome (bimorphologic malignant lymphoma)]. Vnitr Lek; 2002 Mar;48(3):259-63

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Two distinct morphological types of malignant lymphoma in the same patient occur mostly due to transformation of a low grade lymphoma (CLL) into a large--cell non-Hodgkin lymphoma (high-grade lymphoma).
  • Later reports have brough evidence of a clonal relationship between CLL and supervening NHL.
  • The Richter's syndrome was found to be more frequent in patients with CLL displaying either multiple chromosomal aberrations or monoclonal gammapaties.
  • In the last two decades reports have evidenced the existence of two types of the Richter's syndrome: one, the "classical" as a terminal event in a long evolving CLL, the other "variant" as the first clinical manifestation of a previously unrecognized subclinical CLL.
  • Aggressive chemotherapy of CLL play a role in transformation of CLL to Richter's syndrome.
  • [MeSH-minor] Cell Transformation, Neoplastic. Female. Humans. Middle Aged. Syndrome

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  • (PMID = 11968589.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] slo
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Czech Republic
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17. Denier C, Tertian G, Ribrag V, Lozeron P, Bilhou-Nabera C, Lazure T, Abbed K, Lacroix C, Adams D: Multifocal deficits due to leukemic meningoradiculitis in chronic lymphocytic leukemia. J Neurol Sci; 2009 Feb 15;277(1-2):130-2
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  • [Title] Multifocal deficits due to leukemic meningoradiculitis in chronic lymphocytic leukemia.
  • Symptomatic nervous system leukemic infiltration is rarely observed in CLL.
  • We report herein 2 CLL patients with unusual clinical presentations of nervous system invasion.
  • In both, CSF immunophenotyping analysis identified a majority of T cells (>90%), and less than 10% of B-CLL cells expressing CD5, CD19 and CD20.
  • Our analyses revealed the transformation of CLL into an aggressive B-cell lymphoma in one case (Richter's syndrome).
  • In the other case, CNS oriented chemotherapy led to remission and total neurological recovery.
  • In practice, the etiological diagnosis of neurological deficits in CLL patients is difficult.
  • Although rare, leptomeningeal leukemic localization has to be discussed, even in the absence of overt Richter syndrome, and may require an early therapeutic test.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Meningitis / etiology. Meningitis / pathology. Radiculopathy / etiology. Radiculopathy / pathology

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  • (PMID = 19100998.001).
  • [ISSN] 0022-510X
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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18. Turk N, Kusec R, Dominis M, Marusić-Vrsalović M, Jaksić B: [Occurrence of chronic B-cell lymphocytic leukemia in Hodgkin's disease: case report]. Lijec Vjesn; 2003 Jul-Aug;125(7-8):184-7
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  • [Title] [Occurrence of chronic B-cell lymphocytic leukemia in Hodgkin's disease: case report].
  • We present a case of a female patient (79 years) with pathohistologic diagnosis of Hodgkin's lymphoma (HL) (stage IIIB, histologic type MC) for which she was treated with chemotherapy according to LVPP protocol (6 cycles) with good therapeutic response.
  • Immunophenotype of these cells is typical for B-chronic lymphocytic leukemia (B-CLL) (CD5/CD19+, CD23-, CD38 +/-; with weak expression of monoclonal light chains lambda).
  • The diagnosis of B-CLL imposed the question of the connection between two neoplasms of lymphocytic origin.
  • Molecular analysis of lymph node biopsy taken at the time of lymphoma diagnosis revealed clonal population of B lymphocytes.
  • The latest PCR analysis of archive peripheral blood smears confirmed B lymphocyte clonality without diagnostic criteria for lymphoproliferative disease of CLL type.
  • This finding etiologically excludes secondary leukemia.
  • The possibility of untypical presentation of CLL in transformation to Richter's syndrome with morphologic characteristics of HL from the beginning stays unconfirmed.
  • [MeSH-major] Hodgkin Disease / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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  • (PMID = 14692092.001).
  • [ISSN] 0024-3477
  • [Journal-full-title] Lijec̆nic̆ki vjesnik
  • [ISO-abbreviation] Lijec Vjesn
  • [Language] hrv
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Croatia
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19. Hueber AJ, Kallert S, Aigner T, Rösler W, Kalden JR, Schulze-Koops H, Rech J: Early detection of Richter's transformation: stable disease with dose-reduced gemcitabine and local radiation. Onkologie; 2006 Nov;29(11):526-8
MedlinePlus Health Information. consumer health - Hodgkin Disease.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Early detection of Richter's transformation: stable disease with dose-reduced gemcitabine and local radiation.
  • BACKGROUND: The occurrence of Hodgkin's lymphoma (HL) as a second aggressive lymphoid malignancy (known as Hodgkin's disease variant of Richter's transformation) is rarely observed.
  • Response rates, even with highly aggressive therapy such as stem cell transplantation, are limited, ranging from 4 to 43%, and the medium survival time ranges from 5 to 8 months.
  • CASE REPORT: A 72-year-old patient with a history of chronic lymphatic leukemia (CLL) was admitted with thoracic back pain and assumed progression of the CLL.
  • A computed tomography (CT) scan confirmed the progression of axillary and cervical lymph nodes.
  • Infiltrates of small lymphocytes representing the pre-existing CLL (CD5-, CD20-, CD23-positive) coexisted with Reed-Sternberg Hodgkin's cells (CD30-, CD15-positive).
  • Chemotherapy was started, combined with palliative radiation of vertebrae Th7-Th10.
  • 12 months after diagnosis of Richter's transformation the patient is still alive without any progression of the underlying disease.
  • CONCLUSION: We present a unique case of a Hodgkin's disease variant of Richter's transformation and CLL in the same lymph node, which was detected early because of spinal infiltration and was subsequently stabilized with reduced-dosage gemcitabine and local radiation.
  • [MeSH-minor] Aged. Antimetabolites, Antineoplastic / administration & dosage. Humans. Radiation-Sensitizing Agents / administration & dosage. Treatment Outcome

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  • (PMID = 17068388.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Radiation-Sensitizing Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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20. Tsimberidou AM, O'Brien SM, Cortes JE, Faderl S, Andreeff M, Kantarjian HM, Keating MJ, Giles FJ: Phase II study of fludarabine, cytarabine (Ara-C), cyclophosphamide, cisplatin and GM-CSF (FACPGM) in patients with Richter's syndrome or refractory lymphoproliferative disorders. Leuk Lymphoma; 2002 Apr;43(4):767-72
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  • A phase II study was conducted to evaluate the safety and efficacy of fludarabine, cytarabine (ara-C), cyclophosphamide, cisplatin and GM-CSF (FACPGM) treatment in patients with Richter's syndrome (RS), refractory prolymphocytic leukemia (PLL) or refractory non-Hodgkin's lymphoma (NHL).
  • Histologic diagnosis was large cell NHL transformation in 15 patients with CLL, immunoblastic transformation of CLL in one, refractory PLL in three, and refractory NHL in three patients.
  • Treatment consisted of fludarabine 30mg/m2 (days 1-3), ara-C 0.5g/m2 (days 3-4), cyclophosphamide 250 mg/m2 (days 2-4), cisplatin 15 mg/m2 IV CI (days 1-4) with GM-CSF 250 microg/m2 from day 5 to recovery of neutrophils and antibiotic prophylaxis.
  • Patients with response were to receive a maximum of six cycles of therapy.
  • One (3%) patient developed cardiac failure.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoproliferative Disorders / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Aged. Cell Transformation, Neoplastic. Cisplatin / administration & dosage. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Female. Granulocyte-Macrophage Colony-Stimulating Factor / administration & dosage. Humans. Male. Middle Aged

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  • (PMID = 12153163.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; Q20Q21Q62J / Cisplatin
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