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1. Palena C, Foon KA, Panicali D, Yafal AG, Chinsangaram J, Hodge JW, Schlom J, Tsang KY: Potential approach to immunotherapy of chronic lymphocytic leukemia (CLL): enhanced immunogenicity of CLL cells via infection with vectors encoding for multiple costimulatory molecules. Blood; 2005 Nov 15;106(10):3515-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential approach to immunotherapy of chronic lymphocytic leukemia (CLL): enhanced immunogenicity of CLL cells via infection with vectors encoding for multiple costimulatory molecules.
  • Chronic lymphocytic leukemia (CLL) is a disease of CD5(+) B lymphocytes (designated as CLL cells) that are inefficient antigen-presenting cells.
  • We have investigated the ability of in vitro manipulated CLL cells, via hyperexpression of a triad of costimulatory molecules (B7-1, intercellular adhesion molecule 1 [ICAM-1], and leukocyte-function-associated antigen 3 [LFA-3], designated TRICOM), to stimulate effective antitumor T-cell responses.
  • A recombinant modified vaccinia virus strain Ankara (MVA), which is a highly attenuated, replication-impaired virus variant, was successfully used to infect and deliver the simultaneous expression of the 3 human costimulatory molecules in TRICOM on the surface of the CLL cells.
  • Proliferation of allogeneic and autologous T cells was observed when MVA-TRICOM-infected CLL cells were used as stimulators in proliferation assays.
  • Cytotoxic T lymphocytes, generated in vitro by stimulation of autologous T cells with MVA-TRICOM-infected CLL cells, showed cytotoxicity against unmodified/uninfected CLL cells.
  • Therefore, our findings suggest that the use of CLL cells infected ex vivo with MVA-TRICOM or direct injection of MVA-TRICOM in patients with CLL has potential for the immunotherapy of CLL.

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  • (PMID = 16081691.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / BC / Z01 BC010425-06; United States / NCI NIH HHS / BC / Z01 BC010427-06
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Cancer Vaccines
  • [Other-IDs] NLM/ PMC1895050
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2. Potter KN, Mockridge CI, Neville L, Wheatley I, Schenk M, Orchard J, Duncombe AS, Packham G, Stevenson FK: Structural and functional features of the B-cell receptor in IgG-positive chronic lymphocytic leukemia. Clin Cancer Res; 2006 Mar 15;12(6):1672-9
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  • [Title] Structural and functional features of the B-cell receptor in IgG-positive chronic lymphocytic leukemia.
  • PURPOSE: To determine the origin and relationship of the rare IgG+ variant of chronic lymphocytic leukemia (CLL) to the two common IgM+IgD+ subsets that are distinguished by expression of unmutated or mutated V(H) genes, with the former having a worse prognosis.
  • EXPERIMENTAL DESIGN: IgG+ CLL cells were characterized using phenotypic, functional, and immunogenetic analyses.
  • RESULTS: IgG+ CLL was phenotypically similar to mutated IgM+IgD+ CLL (M-CLL) and variably expressed CD38 (4 of 14).
  • ZAP-70, a tyrosine kinase preferentially expressed in unmutated CLL, was found in only 2 of 14 cases.
  • The ability to signal via surface IgM (sIgM) varies between the main subsets of CLL and is associated with expression of ZAP-70.
  • In IgG(+) CLL, 9 of 14 responded to engagement of sIgG with no apparent requirement for expression of CD38 or ZAP-70.
  • Derivation from a postgerminal center B cell is, therefore, likely, and a relationship with M-CLL is suggested.
  • However, conserved sequences detected in the CDR3 of V4-34-encoded gamma chains were not found M-CLL, indicating no direct path of isotype switch from M-CLL.
  • CONCLUSION: IgG+ CLL is likely to arise from an age-related expanded pool of B cells, on a path parallel to M-CLL, and perhaps with a similar clinical course.
  • [MeSH-major] Immunoglobulin G / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Antigen, B-Cell / immunology

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  • (PMID = 16551848.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin M; 0 / Immunoglobulin Variable Region; 0 / Receptors, Antigen, B-Cell; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; SY7Q814VUP / Calcium
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3. Jamroziak K, Szemraj Z, Grzybowska-Izydorczyk O, Szemraj J, Bieniasz M, Cebula B, Giannopoulos K, Balcerczak E, Jesionek-Kupnicka D, Kowal M, Kostyra A, Calbecka M, Wawrzyniak E, Mirowski M, Kordek R, Robak T: CD38 gene polymorphisms contribute to genetic susceptibility to B-cell chronic lymphocytic leukemia: evidence from two case-control studies in Polish Caucasians. Cancer Epidemiol Biomarkers Prev; 2009 Mar;18(3):945-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD38 gene polymorphisms contribute to genetic susceptibility to B-cell chronic lymphocytic leukemia: evidence from two case-control studies in Polish Caucasians.
  • Given the recent findings on the importance of CD38 signaling in the pathogenesis of B-cell chronic lymphocytic leukemia (B-CLL), we hypothesized that single nucleotide polymorphisms (SNP) in the CD38 gene may be related to B-CLL risk.
  • Genotyping was done using PCR-based assays in a total of 460 Polish Caucasian patients with B-CLL and 503 age-matched and gender-matched controls.
  • We found that frequencies of both variant alleles (rs6449182 G and rs1800561 T) were significantly higher in B-CLL.
  • In study A, logistic regression analysis revealed an association between B-CLL and genotypes: rs6449182 CG [odds ratio (OR), 3.57; 95% confidence interval (95% CI), 2.4-5.3], rs6449182 GG (OR, 5.2; 95% CI, 2.36-11.5), and rs1800561 CT (OR, 6.72; 95% CI, 1.5-30.1), although no homozygous rs1800561 TT genotype was detected in either study.
  • These results were confirmed in study B, which showed an association between B-CLL and genotypes rs6449182 CG (OR, 4.00; 95% CI, 2.7-6.0), rs6449182 GG (OR, 12.84; 95% CI, 4.3-38.7), and rs1800561 CT (OR, 10.12; 95% CI, 1.3-81.6), and in the combined analysis of both studies.
  • We also observed that rs6449182 G carriers had more advanced clinical stage (P=0.002) and tended to be younger at diagnosis (P=0.056).
  • In conclusion, our data show that CD38 SNPs may affect CD38 expression and contribute to the increased risk of B-CLL carcinogenesis.
  • [MeSH-major] Antigens, CD38 / genetics. Genetic Predisposition to Disease. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Single Nucleotide

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  • (PMID = 19240243.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.2.2.5 / Antigens, CD38
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4. Crowther-Swanepoel D, Qureshi M, Dyer MJ, Matutes E, Dearden C, Catovsky D, Houlston RS: Genetic variation in CXCR4 and risk of chronic lymphocytic leukemia. Blood; 2009 Nov 26;114(23):4843-6
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  • [Title] Genetic variation in CXCR4 and risk of chronic lymphocytic leukemia.
  • A genome-wide linkage scan has provided evidence for a chronic lymphocytic leukemia (CLL) susceptibility locus at 2q21 to which the chemokine receptor CXCR4 gene maps.
  • Recent data provide some evidence for common variation in CXCR4 according to the polymorphic variant rs2228014 defining CLL risk.
  • To examine the role of genetic variation in CXCR4 on CLL risk, we screened 188 familial CLL cases and 213 controls for germline mutations in the coding regions of CXCR4 and genotyped rs2228014 in 1058 CLL cases and 1807 controls.
  • No association between rs2228014 and risk of CLL was seen (P = .83).
  • Our analysis provides no evidence that common variation in CXCR4 defined by rs228014 influences the risk of CLL, but that functional coding mutations in CXCR4 may contribute to familial CLL.
  • [MeSH-major] Genetic Variation. Germ-Line Mutation. Leukemia, Lymphocytic, Chronic, B-Cell / epidemiology. Receptors, CXCR4 / genetics

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  • (PMID = 19812382.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCR4 protein, human; 0 / Codon, Nonsense; 0 / Receptors, CXCR4
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5. Cro L, Ferrario A, Lionetti M, Bertoni F, Zucal N N, Nobili L, Fabris S, Todoerti K, Cortelezzi A, Guffanti A, Goldaniga M, Marcheselli L, Neri A, Lambertenghi-Deliliers G, Baldini L: The clinical and biological features of a series of immunophenotypic variant of B-CLL. Eur J Haematol; 2010 Aug;85(2):120-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The clinical and biological features of a series of immunophenotypic variant of B-CLL.
  • OBJECTIVES: To describe the clinical and biological features of a series of immunophenotypic variant of B-CLL (v-CLL) characterised by intermediate RMH score, in the absence of t(11;14)(q13;q32) in FISH analysis in comparison with a series of typical CLL.
  • METHODS: We studied the clinical and biological features of 63 cases of v-CLL and 130 cases of CLL.
  • RESULTS: We observed significant differences in terms of age <70 yr (P < 0.001), lymphocytosis <20 x 10(9)/L (P < 0.001), lymphocyte doubling time <or=12 months (P = 0.02), high serum beta2-microglobulin levels (P < 0.001) and splenomegaly (P = 0.002); CD38, CD49d, CD1c were more expressed in v-CLL, CD43 in CLL (P < 0.001).
  • IgV(H) mutation and trisomy 12 were more frequent in v-CLL group (P = 0.001; P < 0.001); del13q14 in CLL (P = 0.008).
  • Gene expression profiling of nine v-CLL and 60 CLL indicated that the atypical group presented a specific molecular pattern.
  • After a median follow-up of respectively, 55 (4-196) and 60 months (6-180), 25/42 patients with v-CLL (48%) and 55/93 patients with CLL (59%) were treated.
  • Time to treatment was significantly shorter in IgV(H)-mutated v-CLL vs. mutated CLL (P = 0.006).
  • The median overall survival was worse in v-CLL-mutated cases (P = 0.062).
  • CONCLUSION: v-CLL should be identified and dealt with separately from classic CLL.
  • In particular, the prognostic markers that are routinely used to characterise classical B-CLL should not be interpreted as having the same meaning.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology

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  • (PMID = 20408870.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
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6. Tzankov A, Fong D: Hodgkin's disease variant of Richter's syndrome clonally related to chronic lymphocytic leukemia arises in ZAP-70 negative mutated CLL. Med Hypotheses; 2006;66(3):577-9
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  • [Title] Hodgkin's disease variant of Richter's syndrome clonally related to chronic lymphocytic leukemia arises in ZAP-70 negative mutated CLL.
  • Chronic lymphocytic leukemia (CLL) may derive from either immunoglobulin V(H) gene unmutated (naïve) or mutated (antigen-experienced) post-germinal center B-cells.
  • Richter's syndrome denotes the transformation of CLL into aggressive B-cell lymphoma.
  • Most Richter's syndrome cases are secondary diffuse large B-cell lymphomas, but some are Hodgkin's disease variants.
  • Taking into account CLL and Hodgkin's lymphoma histogenesis, hypothetically only CLL derived from V(H) mutated B-cells can clonally progress to Hodgkin's lymphoma variant of Richter's syndrome.
  • To test our hypothesis, we analyzed the CLL ZAP-70 status as a surrogate for the V(H) mutational status in four patients with subsequent Hodgkin's disease variants of Richter's syndrome.
  • In all three cases with proven or suspected clonal relationship between Hodgkin and Reed-Sternberg- and leukemia cells, the CLL samples remained negative for ZAP-70, corresponding to CLL histogenesis from V(H) mutated B-cells.
  • These empirical data suggest that the histological and clinical diversity of Richter's transformation could be to a part explained by the different origin of CLL, with Hodgkin's disease variants arising probably only in V(H) mutated CLL.
  • [MeSH-major] Hodgkin Disease / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Mutation. ZAP-70 Protein-Tyrosine Kinase / genetics
  • [MeSH-minor] Cell Transformation, Neoplastic. DNA Mutational Analysis. Disease Progression. Humans. Models, Biological. Models, Theoretical. Syndrome

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  • (PMID = 16223567.001).
  • [ISSN] 0306-9877
  • [Journal-full-title] Medical hypotheses
  • [ISO-abbreviation] Med. Hypotheses
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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7. Karsai S, Hou JS, Telang G, Kantor GR, Nowell PC, Vonderheid EC: Sézary syndrome coexisting with B-cell chronic lymphocytic leukemia: case report and review of the literature. Dermatology; 2008;216(1):68-75
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  • [Title] Sézary syndrome coexisting with B-cell chronic lymphocytic leukemia: case report and review of the literature.
  • INTRODUCTION: The simultaneous presentation of chronic B-cell lymphocytic leukemia (B-CLL) and cutaneous T-cell lymphoma (CTCL) is extremely rare.
  • CASE REPORT: We describe a patient with B-CLL and Sézary syndrome (SS), an erythrodermic and leukemic variant of CTCL.
  • This is the first reported case of SS coexisting with chronic lymphocytic leukemia in which an anti-V beta 13.6 antibody was used to serially track changes in circulating neoplastic T cells vis-à-vis neoplastic B cells and to detect neoplastic T cells in ascitic fluid near the end of the patient's life.
  • DISCUSSION: We speculate that the coexistence of B-CLL and CTCL is the result of an initiating genetic or epigenetic defect at the level of the common lymphoid stem cell that predisposes both B-cell and T-cell lineages to additional oncogenic changes at a more advanced stage of differentiation.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Sezary Syndrome / complications. Skin Neoplasms / complications
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, CD / analysis. B-Lymphocytes / metabolism. Fatal Outcome. Female. Humans. Male. Middle Aged. Receptors, Antigen, T-Cell, alpha-beta / analysis. Skin / pathology. T-Lymphocytes / metabolism

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  • [Copyright] (c) 2008 S. Karger AG, Basel.
  • (PMID = 18032903.001).
  • [ISSN] 1421-9832
  • [Journal-full-title] Dermatology (Basel, Switzerland)
  • [ISO-abbreviation] Dermatology (Basel)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Receptors, Antigen, T-Cell, alpha-beta
  • [Number-of-references] 59
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8. Lin K, Glenn MA, Harris RJ, Duckworth AD, Dennett S, Cawley JC, Zuzel M, Slupsky JR: c-Abl expression in chronic lymphocytic leukemia cells: clinical and therapeutic implications. Cancer Res; 2006 Aug 1;66(15):7801-9
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  • [Title] c-Abl expression in chronic lymphocytic leukemia cells: clinical and therapeutic implications.
  • c-Abl is important for normal B-cell development, but little is known about the function of this nonreceptor tyrosine kinase in chronic lymphocytic leukemia (CLL).
  • We show that the malignant cells of CLL predominantly express the type 1b splice variant of c-Abl and that the expression of c-Abl protein is higher in CLL cells than in normal peripheral blood B cells.
  • We also show that STI-571, an inhibitor of c-Abl kinase activity, induces apoptosis of CLL cells with high c-Abl expression levels through a mechanism involving inhibition of nuclear factor kappaB.
  • We conclude that overexpression of c-Abl is likely to play a pathogenetic role in CLL and that STI-571 may be of potential use in the treatment of this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Piperazines / pharmacology. Proto-Oncogene Proteins c-abl / biosynthesis. Pyrimidines / pharmacology

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  • (PMID = 16885384.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Immunoglobulin Variable Region; 0 / NF-kappa B; 0 / Piperazines; 0 / Protein Isoforms; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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9. Balogh Z, Reiniger L, Deák L, Bödör C, Csomor J, Szepesi A, Gagyi E, Kopper L, Matolcsy A: IgVH gene mutation status and genomic imbalances in chronic lymphocytic leukaemia with increased prolymphocytes (CLL/PL). Hematol Oncol; 2007 Jun;25(2):90-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgVH gene mutation status and genomic imbalances in chronic lymphocytic leukaemia with increased prolymphocytes (CLL/PL).
  • Chronic lymphocytic leukaemia (CLL) with increased prolymphocytes (CLL/PL) has been defined by the World Health Organization (WHO) classification and considered as a progressive and clinically aggressive variant of CLL.
  • To further characterize the biological features of this disease, we performed IgVH gene mutational status, FISH and high-resolution comparative genomic hybridization (HR-CGH) analysis in 17 cases of CLL/PL.
  • All CLL/PL utilized members of VH1, VH3 and VH4 families, with the highest prevalence of the VH1-69 gene.
  • The FISH and HR-CGH analyses showed frequent occurrence of trisomy 12, del(11)(q23), del(17)(p13) and genetic imbalances, but recurrent genetic lesion characteristic for CLL/PL was not found.
  • The follow-up HR-CGH analysis of two cases showed that increase of prolymphocytes in the course of CLL or CLL/PL are associated with clonal evolution and selection of the tumour clone.
  • In conclusion, this study suggests that CLL/PL is a relatively homogeneous disease regarding VH gene mutation, but heterogeneous regarding genetic lesions.
  • The heterogeneity and high number of genomic imbalances found in CLL/PL suggest that a genome-wide instability of the neoplastic cells may play a role in the development of the disease.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Mutation

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  • [Copyright] Copyright 2007 John Wiley & Sons, Ltd.
  • (PMID = 17410523.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region
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10. Fong D, Kaiser A, Spizzo G, Gastl G, Tzankov A: Hodgkin's disease variant of Richter's syndrome in chronic lymphocytic leukaemia patients previously treated with fludarabine. Br J Haematol; 2005 Apr;129(2):199-205
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  • [Title] Hodgkin's disease variant of Richter's syndrome in chronic lymphocytic leukaemia patients previously treated with fludarabine.
  • The transformation of chronic lymphocytic leukaemia (CLL) into large-cell lymphoma (Richter's syndrome, RS) is a well-documented phenomenon.
  • Only rarely does CLL transform into Hodgkin's lymphoma (HL).
  • To further analyse the clinico-pathological and genetic findings in the HL variant of RS, we performed a single-institution study in four patients, who developed HL within a mean of 107 months after diagnosis of CLL.
  • All patients presented with CLL treatment-resistant lymphadenopathies and B-symptoms.
  • In two of the MC cases, molecular analysis performed on CLL samples and microdissected Hodgkin and Reed-Sternberg cells (HRSC) suggested a clonal relationship, while in NS no indication of a clonal relationship was detected.
  • In summary, HL can occur in CLL patients at any site, up to 17 years after initial diagnosis, especially after treatment with fludarabine.
  • The majority present with B-symptoms and CLL treatment-resistant lymphadenopathy, are of the MC type, clonally related to CLL and might be triggered by an EBV infection.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hodgkin Disease / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use
  • [MeSH-minor] Cell Transformation, Viral. Clone Cells. Drug Resistance, Neoplasm. Epstein-Barr Virus Infections / immunology. Female. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Humans. Immunoglobulin Heavy Chains / genetics. Male. Micromanipulation. Middle Aged. Reed-Sternberg Cells / ultrastructure. Reed-Sternberg Cells / virology

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  • (PMID = 15813847.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunoglobulin Heavy Chains; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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11. Pekova S, Cmejla R, Smolej L, Kozak T, Spacek M, Prucha M: Identification of a novel, transactivation-defective splicing variant of p53 gene in patients with chronic lymphocytic leukemia. Leuk Res; 2008 Mar;32(3):395-400
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  • [Title] Identification of a novel, transactivation-defective splicing variant of p53 gene in patients with chronic lymphocytic leukemia.
  • p53 is implemented in many processes controlling cell fate.
  • In 109 out of 127 (86%) patients with chronic lymphocytic leukemia (CLL) we have identified a novel p53 splicing variant, lacking the whole coding sequence of exon 6.
  • This splicing p53 isoform ("delta ex6") is devoid of transactivational activity and is differentially expressed in CLL patients as compared to healthy controls.
  • The overexpression of "delta ex6" p53 variant in CLL patients supports the recent evidence on dysregulation of p53 splicing pattern in malignancies.
  • [MeSH-major] Alternative Splicing. Genes, p53. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

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  • (PMID = 17688945.001).
  • [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
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12. Broderick P, Sellick G, Fielding S, Catovsky D, Houlston R: Lack of a relationship between the common 18q24 variant rs12953717 and risk of chronic lymphocytic leukemia. Leuk Lymphoma; 2008 Feb;49(2):271-2
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  • [Title] Lack of a relationship between the common 18q24 variant rs12953717 and risk of chronic lymphocytic leukemia.
  • Linkage has implicated variation in 18q24 in genetic susceptibility to chronic lymphocytic leukemia (CLL).
  • Given that many polymorphic variants have pleiotropic effects we explore the relationship between polymorphic variation at rs12953717 and CLL we compared the frequency of genotypes in 984 cases and 4831 healthy controls.
  • There was therefore no evidence for an association between rs12953717 genotype and CLL; P = 0.40 (allelic test) with ORs of 0.99 (95% CI: 0.85 - 1.16) and 0.91 (95% CI: 0.74 - 1.11) for heterozygotes and TT homozygotes, respectively.
  • These data suggests variation at SMAD7 does not significantly contribute to an inherited susceptibility to CLL.
  • [MeSH-major] Genetic Predisposition to Disease. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Single Nucleotide. Smad7 Protein / genetics

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  • (PMID = 18231913.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / SMAD7 protein, human; 0 / Smad7 Protein
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13. Duhamel M, Arrouss I, Merle-Béral H, Rebollo A: The Aiolos transcription factor is up-regulated in chronic lymphocytic leukemia. Blood; 2008 Mar 15;111(6):3225-8
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  • [Title] The Aiolos transcription factor is up-regulated in chronic lymphocytic leukemia.
  • To assess Aiolos isoform role in humans' pathologies, we studied Aiolos variant distribution and expression in mature B lymphoproliferative disorders (chronic lymphocytic leukemia [CLL] and other B-cell lymphomas).
  • We demonstrated that more than 80% of expressed Aiolos in normal as well as in malignant B cells is of the hAio1 type, and we showed for the first time a homogeneous overexpression of the total amounts of Aiolos transcripts in the B cells of CLL patients, independently of ZAP-70 and IgV(H) mutational status prognosis factors.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Transcription Factors / metabolism. Up-Regulation

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  • (PMID = 18184862.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IKZF3 protein, human; 0 / Protein Isoforms; 0 / Transcription Factors; 148971-36-2 / Ikaros Transcription Factor
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14. Lahiri O, Harris S, Packham G, Howell M: p53 pathway gene single nucleotide polymorphisms and chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2007 Nov;179(1):36-44
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  • [Title] p53 pathway gene single nucleotide polymorphisms and chronic lymphocytic leukemia.
  • The p53 pathway plays a critical role in chronic lymphocytic leukemia (CLL).
  • The association between the single-nucleotide polymorphism (SNPs) within the p53 gene (R72P) and its downstream target/regulators, BAX (G125A) and MDM2 (SNP309), and clinical parameters/prognostic markers was investigated in 83 CLL patients.
  • Although the p53 R72P SNPs and MDM2 SNP309 did not associate with any of the parameters studied, the BAX G125A SNPs was associated with a more advanced Binet stage at diagnosis, supporting a potential role for this variant in CLL disease progression.
  • Further studies are required to understand the role of SNPs in the p53 pathway in CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Single Nucleotide. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 17981213.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Genetic Markers; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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15. Brickner AG, Evans AM, Mito JK, Xuereb SM, Feng X, Nishida T, Fairfull L, Ferrell RE, Foon KA, Hunt DF, Shabanowitz J, Engelhard VH, Riddell SR, Warren EH: The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL. Blood; 2006 May 1;107(9):3779-86
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  • [Title] The PANE1 gene encodes a novel human minor histocompatibility antigen that is selectively expressed in B-lymphoid cells and B-CLL.
  • Minor histocompatibility antigens (mHAg's) are peptides encoded by polymorphic genes that are presented by major histocompatibility complex (MHC) molecules and recognized by T cells in recipients of allogeneic hematopoietic cell transplants.
  • Sequencing of PANE1 alleles in mHAg-positive and mHAg-negative cells demonstrates that differential T-cell recognition is due to a single nucleotide polymorphism within the variant exon that replaces an arginine codon with a translation termination codon.
  • The PANE1 transcript that encodes the mHAg is expressed at high levels in resting CD19(+) B cells and B-lineage chronic lymphocytic leukemia (B-CLL) cells, and at significantly lower levels in activated B cells.
  • Activation of B-CLL cells through CD40 ligand (CD40L) stimulation decreases expression of the mHAg-encoding PANE1 transcript and reciprocally increases expression of PANE1 transcripts lacking the mHAg-encoding exon.
  • These studies suggest distinct roles for different PANE1 isoforms in resting compared with activated CD19(+) cells, and identify PANE1 as a potential therapeutic target in B-CLL.

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  • (PMID = 16391015.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA18029; United States / NIAID NIH HHS / AI / AI339933; United States / NIAID NIH HHS / AI / AI44134; United States / NIAID NIH HHS / AI / AI20963; United States / NCI NIH HHS / CA / CA106512
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Epitopes; 0 / HLA-A Antigens; 0 / HLA-A*03:01 antigen; 0 / HLA-A3 Antigen; 0 / Minor Histocompatibility Antigens; 0 / Nuclear Proteins; 0 / proliferation associated nuclear element protein 1, human; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC1895781
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16. Lan Q, Au WY, Chanock S, Tse J, Wong KF, Shen M, Siu LP, Yuenger J, Yeager M, Hosgood HD 3rd, Purdue MP, Liang R, Rothman N: Genetic susceptibility for chronic lymphocytic leukemia among Chinese in Hong Kong. Eur J Haematol; 2010 Dec;85(6):492-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic susceptibility for chronic lymphocytic leukemia among Chinese in Hong Kong.
  • The genetic basis of chronic lymphocytic leukemia (CLL) has not been fully elucidated to date.
  • A recent genome-wide scan of CLL in Caucasians, which was carried out in the UK, identified six variants showing strong association.
  • We attempted to replicate these findings in 71 patients with CLL and 1273 controls in Hong Kong Chinese.
  • Three of the six variants were significantly associated with CLL.
  • The rs872071 variant (Odds Ratio (95% Confidence Interval) = 1.78 (1.25-2.53), P = 0.0013) in the IRF4 gene region showed the strongest association, similar to that reported in the UK study.
  • Polymorphisms in SP140 and ACOXL were also associated with risk of CLL.
  • These results suggest that variants in three loci may contribute to risk of CLL among Chinese.
  • [MeSH-major] Genetic Predisposition to Disease. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

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  • [Copyright] © 2010 John Wiley & Sons A/S.
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  • (PMID = 20731705.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 CP010123-12
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Interferon Regulatory Factors; 0 / SP140 protein, human; 0 / Transcription Factors; 0 / interferon regulatory factor-4
  • [Other-IDs] NLM/ NIHMS246069; NLM/ PMC2980583
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17. Pulte D, Olson KE, Broekman MJ, Islam N, Ballard HS, Furman RR, Olson AE, Marcus AJ: CD39 activity correlates with stage and inhibits platelet reactivity in chronic lymphocytic leukemia. J Transl Med; 2007 May 04;5:23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD39 activity correlates with stage and inhibits platelet reactivity in chronic lymphocytic leukemia.
  • BACKGROUND: Chronic lymphocytic leukemia (CLL) is characterized by accumulation of mature appearing lymphocytes and is rarely complicated by thrombosis.
  • One possible explanation for the paucity of thrombotic events in these patients may be the presence of the ecto-nucleotidase CD39/NTDPase-1 on the surface of the malignant cells in CLL.
  • We hypothesize that if CD39 is observed on CLL cells, then patients with CLL may be relatively protected against platelet aggregation and recruitment and that CD39 may have other effects on CLL, including modulation of the disease, via its metabolism of ATP.
  • METHODS: Normal and malignant lymphocytes were isolated from whole blood from patients with CLL and healthy volunteers.
  • RESULTS: Functional assays demonstrated that ADPase and ATPase activities were much higher in CLL cells than in total lymphocytes from the normal population on a per cell basis (p-value < 0.00001).
  • CD39 activity was elevated in stage 0-2 CLL compared to stage 3-4 (p < 0.01).
  • RT-PCR showed increased full length CD39 and splice variant 1.5, but decreased variant 1.3 in CLL cells.
  • Platelet function tests showed inhibition of platelet activation and recruitment to ADP by CLL cells.
  • CONCLUSION: CD39 is expressed and active on CLL cells.
  • Enzyme activity is higher in earlier stages of CLL and decreased enzyme activity may be associated with worsening disease.
  • These results suggest that CD39 may play a role in the pathogenesis of malignancy and protect CLL patients from thrombotic events.

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  • (PMID = 17480228.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL046403; United States / NINDS NIH HHS / NS / R01 NS041462; United States / NHLBI NIH HHS / HL / R01 HL047073; United States / NHLBI NIH HHS / HL / HL 46403; United States / NHLBI NIH HHS / HL / R37 HL047073; United States / NHLBI NIH HHS / HL / HL 47073; United States / NINDS NIH HHS / NS / NS 41462
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 61D2G4IYVH / Adenosine Diphosphate; EC 3.6.1.5 / Apyrase; EC 3.6.1.5 / CD39 antigen
  • [Other-IDs] NLM/ PMC1885243
  • [General-notes] NLM/ Original DateCompleted: 20070813
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18. Vasilj A, Kojić-Katović S, Maricević I, Zokvić E, Kelcec IB, Tomas D, Curić-Jurić S: Hodgkin's lymphoma variant of Richter's syndrome. Coll Antropol; 2010 Mar;34(1):295-9
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  • [Title] Hodgkin's lymphoma variant of Richter's syndrome.
  • Chronic lymphocytic leukemia/small lymphocitic lymphoma (CLL/SLL) is low-grade malignant lymphoprolipheration, that has tendency to convert to a higher-grade neoplasm over time.
  • More common is the development of a diffuse large cell lymphoma or transformation into prolymphocytic cell population.
  • We present 65-year-old female with Hodgkin's variant of Richter's syndrome.
  • On the basis of clinical simptoms, cytological, hystological and immunohistological finding in April 2008 CLL/SLL were diagnosed.
  • The diagnosis was Hodgkin's disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Hodgkin Disease / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Reed-Sternberg Cells / pathology

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  • (PMID = 20437646.001).
  • [ISSN] 0350-6134
  • [Journal-full-title] Collegium antropologicum
  • [ISO-abbreviation] Coll Antropol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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19. Sellick GS, Lubbe SJ, Matutes E, Catovsky D, Houlston RS: Microsatellite instability indicative of defects in the major mismatch repair genes is rare in patients with B-cell chronic lymphocytic leukemia: Evaluation with disease stage and family history. Leuk Lymphoma; 2007 Jul;48(7):1320-2
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  • [Title] Microsatellite instability indicative of defects in the major mismatch repair genes is rare in patients with B-cell chronic lymphocytic leukemia: Evaluation with disease stage and family history.
  • A possible role for DNA mismatch repair defects and microsatellite instability (MSI) in the pathogenesis of a number of B-cell lymphoproliferative disorders has recently been debated.
  • To gain further insight into the impact of MSI on B-CLL, we evaluated samples from a series of 982 patients using the mono-satellite markers BAT25 and BAT26, which are highly sensitive in demonstrating classical mismatch repair (MMR) deficiency.
  • Only 1% of cases displayed MSI and this was not correlated with stage of disease or family history of B-CLL.
  • A sub-polymorphic germline variant of BAT25 was identified in one familial case, which was also detected in the patient's affected brother.
  • In conclusion, our study demonstrates that MSI does not have a prominent role in the pathogenesis of B-CLL.
  • [MeSH-major] DNA Mismatch Repair. DNA Repair / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Microsatellite Instability

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  • (PMID = 17613760.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BAT26 microsatellite DNA; 0 / Biomarkers, Tumor; 0 / Genetic Markers
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20. Sutton LA, Kostareli E, Hadzidimitriou A, Darzentas N, Tsaftaris A, Anagnostopoulos A, Rosenquist R, Stamatopoulos K: Extensive intraclonal diversification in a subgroup of chronic lymphocytic leukemia patients with stereotyped IGHV4-34 receptors: implications for ongoing interactions with antigen. Blood; 2009 Nov 12;114(20):4460-8
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  • [Title] Extensive intraclonal diversification in a subgroup of chronic lymphocytic leukemia patients with stereotyped IGHV4-34 receptors: implications for ongoing interactions with antigen.
  • Several studies indicate that the development of chronic lymphocytic leukemia (CLL) may be influenced by antigen recognition through the clonotypic B-cell receptors (BCRs).
  • However, it is still unclear whether antigen involvement is restricted to the malignant transformation phase or whether the putative antigen(s) may continuously trigger the CLL clone and affect not only the progenitor cell but also the leukemic cells themselves.
  • To address this issue, we conducted a large-scale subcloning study of rearranged immunoglobulin heavy variable (IGHV) genes of diverse mutational status from 71 CLL cases (total, 1496 subcloned sequences), belonging to both the common IgM/IgD variant and the rare IgG-positive variant.
  • [MeSH-major] Antigens / immunology. Genes, Immunoglobulin Heavy Chain / genetics. Genes, Immunoglobulin Heavy Chain / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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  • (PMID = 19713457.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens
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21. Ahmed SU, Meklat F, Shahriar M, Zhang J, Mastulov S, Giannakouros T, Jewell A, Zhang Y, Lim SH: SEMG-1 expression in early stage chronic lymphocytic leukemia. Cytotherapy; 2009;11(2):238-44
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  • [Title] SEMG-1 expression in early stage chronic lymphocytic leukemia.
  • BACKGROUND AIMS: Chronic lymphocytic leukemia (CLL) is an indolent disease.
  • It is currently recommended that patients with CLL stages 0 and I follow a watchful waiting strategy.
  • In this study, we investigated the expression of SEMG-1 in early CLL to determine the suitability of SEMG-1 as a target for further development of tumor vaccines for early CLL.
  • METHODS: A combination of reverse transcriptase (RT)-polymerase chain reaction (PCR) and immunocytochemistry was used to evaluate the expression of SEMG-1 in early CLL.
  • RESULTS: The SEMG-1 gene was expressed in 19/41 (46%) patients with early CLL.
  • Gene expression was associated with protein synthesis in CLL cells.
  • Only transcripts encoding the SEMG-1(50) variant and not SEMG-1(43) were detected.
  • High-titer SEMG-1 IgG but not IgM Ab were detected in some of these patients, suggesting that SEMG-1-reactive immune responses are intact within the immune repertoire of early CLL patients.
  • CONCLUSIONS: SEMG-1 is expressed in nearly half of patients with early CLL and may be a target for further investigations into its use for immunotherapy of early CLL.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Biomarkers, Tumor / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Seminal Vesicle Secretory Proteins / metabolism

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  • (PMID = 19241194.001).
  • [ISSN] 1477-2566
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 088434; United States / NCI NIH HHS / CA / R01 CA 106283
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cancer Vaccines; 0 / Immunoglobulin G; 0 / Immunoglobulin M; 0 / Seminal Vesicle Secretory Proteins; 0 / seminal vesicle-specific antigen; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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22. Wolf S, Mertens D, Pscherer A, Schroeter P, Winkler D, Gröne HJ, Hofele C, Hemminki K, Kumar R, Steineck G, Döhner H, Stilgenbauer S, Lichter P: Ala228 variant of trail receptor 1 affecting the ligand binding site is associated with chronic lymphocytic leukemia, mantle cell lymphoma, prostate cancer, head and neck squamous cell carcinoma and bladder cancer. Int J Cancer; 2006 Apr 1;118(7):1831-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ala228 variant of trail receptor 1 affecting the ligand binding site is associated with chronic lymphocytic leukemia, mantle cell lymphoma, prostate cancer, head and neck squamous cell carcinoma and bladder cancer.
  • Allelic loss of chromosome 8p21-22 is a frequent event in various human cancers including mantle cell lymphoma (MCL), prostate cancer, head and neck squamous cell carcinoma (HNSCC) and bladder cancer.
  • Since recent studies demonstrate that chronic lymphocytic leukemia (CLL) and prostate cells are TRAIL induced apoptosis, TRAIL-receptors are strong tumor suppressor candidate genes in human cancers exhibiting loss of chromosomal material in 8p21.3.
  • However, no mutation of the TRAIL receptor genes has been reported in CLL, MCL, prostate cancer, HNSCC so far.
  • In this study we analyzed the complete coding region of TNFRSF10A and TNFRSF10B in a series of 32 MCL and 101 CLL samples and detected a single nucleotide polymorphism (SNP) in TNFRSF10A (A683C) with tumor specific allele distribution.
  • We found the rare allele of TNFRSF10A is more frequent in CLL, MCL, prostate cancer, bladder cancer and HNSCC.
  • Thus screening for 683A-->C nucleotide exchanges may become important in diagnosis and/or treatment of these malignancies.


23. Martín-Subero JI, Ibbotson R, Klapper W, Michaux L, Callet-Bauchu E, Berger F, Calasanz MJ, De Wolf-Peeters C, Dyer MJ, Felman P, Gardiner A, Gascoyne RD, Gesk S, Harder L, Horsman DE, Kneba M, Küppers R, Majid A, Parry-Jones N, Ritgen M, Salido M, Solé F, Thiel G, Wacker HH, Oscier D, Wlodarska I, Siebert R: A comprehensive genetic and histopathologic analysis identifies two subgroups of B-cell malignancies carrying a t(14;19)(q32;q13) or variant BCL3-translocation. Leukemia; 2007 Jul;21(7):1532-44

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  • [Title] A comprehensive genetic and histopathologic analysis identifies two subgroups of B-cell malignancies carrying a t(14;19)(q32;q13) or variant BCL3-translocation.
  • The biologic and pathologic features of B-cell malignancies bearing a translocation t(14;19)(q32;q13) leading to a fusion of IGH and BCL3 are still poorly described.
  • Herein we report the results of a comprehensive cytogenetic, fluorescence in situ hybridization (FISH), molecular and histopathological survey of a large series of B-cell malignancies with t(14;19) or variant translocations.
  • A total of 56 B-cell malignancies with a FISH-proven BCL3 involvement were identified with the translocation partners being IGH (n=51), IGL (n=2), IGK (n=2) and a non-IG locus (n=1).
  • The first group included 26 B-cell malignancies of various histologic subtypes containing a relatively high number of chromosomal changes and mostly mutated IgVH genes.
  • The second group included 19 cases, mostly diagnosed as B-cell chronic lymphocytic leukemia (B-CLL), and characterized by few additional chromosomal changes (e.g. trisomy 12) and unmutated IgVH genes.
  • In conclusion, our study indicates that BCL3 translocations are not restricted to B-CLL but present in a heterogeneous group of B-cell malignancies.
  • [MeSH-major] Leukemia, B-Cell / genetics. Lymphoma, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Transcription Factors / genetics. Translocation, Genetic

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  • (PMID = 17495977.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / proto-oncogene protein bcl-3
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24. Johnson GG, Sherrington PD, Carter A, Lin K, Liloglou T, Field JK, Pettitt AR: A novel type of p53 pathway dysfunction in chronic lymphocytic leukemia resulting from two interacting single nucleotide polymorphisms within the p21 gene. Cancer Res; 2009 Jun 15;69(12):5210-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel type of p53 pathway dysfunction in chronic lymphocytic leukemia resulting from two interacting single nucleotide polymorphisms within the p21 gene.
  • The ATM-p53 pathway plays an important role in the biology of chronic lymphocytic leukemia (CLL).
  • Its functional integrity can be probed by exposing CLL cells to ionizing radiation (IR) and measuring levels of p53 protein and one of its transcriptional targets, the cyclin-dependent kinase inhibitor p21.
  • This so-called "type C" response was detected in 10.6% of unselected patients and was associated with resistance of CLL cells to p53-dependent killing by IR, with the clinically more aggressive variant of CLL characterized by unmutated immunoglobulin heavy-chain genes and with a single nucleotide polymorphism at codon 31 of the p21 gene in which Ser is replaced by Arg.
  • CLL samples with this allelic variant displayed impaired IR-induced up-regulation of total p21 mRNA and did not express the Arg-encoding transcript, except in those cases harboring an additional single nucleotide polymorphism (T instead of C) in the 3'-untranslated region of the same p21 allele.
  • Our data provide new insight into the importance of p21 in CLL biology.
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p21 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Single Nucleotide. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19491257.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MRC/ G9900432
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA Primers; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53
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25. Lin TS, Blum KA, Fischer DB, Mitchell SM, Ruppert AS, Porcu P, Kraut EH, Baiocchi RA, Moran ME, Johnson AJ, Schaaf LJ, Grever MR, Byrd JC: Flavopiridol, fludarabine, and rituximab in mantle cell lymphoma and indolent B-cell lymphoproliferative disorders. J Clin Oncol; 2010 Jan 20;28(3):418-23
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  • [Title] Flavopiridol, fludarabine, and rituximab in mantle cell lymphoma and indolent B-cell lymphoproliferative disorders.
  • PURPOSE: Flavopiridol downmodulates antiapoptotic proteins associated with resistance to fludarabine and rituximab and is effective against p53-mutated chronic lymphocytic leukemia (CLL).
  • We conducted a phase I study of flavopiridol, fludarabine, and rituximab (FFR) in patients with mantle-cell lymphoma (MCL), indolent B-cell non-Hodgkin's lymphomas (B-NHL), and CLL to determine the activity of FFR.
  • RESULTS: Thirty-eight patients (median age, 62 years) with MCL (n = 10); indolent B-NHL including follicular (n = 9), marginal zone (n = 4), lymphoplasmacytic (n = 1), or small lymphocytic lymphoma (n = 3); and CLL (n = 11), were enrolled.
  • Median PFS of patients with nonblastoid variant MCL (n = 8) was 35.9 months.
  • CONCLUSION: FFR was active in MCL, indolent B-NHL, and CLL and should be studied for older patients with MCL who are not candidates for aggressive chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes. Female. Flavonoids / administration & dosage. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoproliferative Disorders / drug therapy. Male. Middle Aged. Piperidines / administration & dosage. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 20008633.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / K23 CA102276-01A1; United States / NCI NIH HHS / CA / U01 CA076576; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / K23 CA102276; United States / NCI NIH HHS / CA / U01-CA76576
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Piperidines; 45AD6X575G / alvocidib; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2815704
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26. Setlur SR, Ihm C, Tchinda J, Shams S, Werner L, Cho EK, Thompson C, Phillips K, Rassenti LZ, Kipps TJ, Neuberg D, Freedman AS, Lee C, Brown JR: Comparison of familial and sporadic chronic lymphocytic leukaemia using high resolution array comparative genomic hybridization. Br J Haematol; 2010 Nov;151(4):336-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of familial and sporadic chronic lymphocytic leukaemia using high resolution array comparative genomic hybridization.
  • Approximately 10% of patients with chronic lymphocytic leukaemia (CLL) have a family history of the disease or a related lymphoproliferative disorder, yet the relationship of familial CLL to genomic abnormalities has not been characterized in detail.
  • We therefore studied 75 CLL patients, half familial and half sporadic, using high-resolution array comparative genomic hybridization (CGH), in order to better define the relationship of genomic abnormalities to familial disease and other biological prognostic factors.
  • Our results showed that the most common high-risk deletion in CLL, deletion 11q, was significantly associated with sporadic disease.
  • Comparison of familial to sporadic disease additionally identified a copy number variant region near the centromere on 14q, proximal to IGH@, in which gains were associated both with familial CLL, and with mutated IGHV and homozygous deletion of 13q.
  • This study is the first high resolution effort to investigate and report somatic genetic differences between familial and sporadic CLL.

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
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  • (PMID = 20812997.001).
  • [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 CA092625; United States / NCI NIH HHS / CA / R21 CA103244; United States / NCI NIH HHS / CA / K23 CA115682; United States / NCI NIH HHS / CA / R01 CA111560; United States / NCI NIH HHS / CA / P01 CA081534; United States / NCI NIH HHS / CA / P01-CA081534; United States / NCI NIH HHS / CA / CA-103244; United States / NCI NIH HHS / CA / 2P01CA092625; United States / NCI NIH HHS / CA / CA111560
  • [Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS442972; NLM/ PMC3584328
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27. Mao ZR, Rosenwald A, Zhang SJ, Zhou R, Mueller-Hermelink HK: [Clonality analysis and mutational status of IgVH gene in Hodgkin variant of Richter syndrome]. Zhonghua Bing Li Xue Za Zhi; 2008 Aug;37(8):523-8
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  • [Title] [Clonality analysis and mutational status of IgVH gene in Hodgkin variant of Richter syndrome].
  • OBJECTIVE: To detect the clonal relationship, the rearrangement, and the mutational status of IgVH gene; the influence of these molecular characteristics on the clinical outcome in Hodgkin variant of Richter syndrome; and the possible molecular pathogenesis in this transformation.
  • METHODS: The clonal rearrangements and mutational status of IgVH genes were analyzed in Hodgkin variant of Richter syndrome and B-CLL with Reed-Stemberg (R-S)-like cells by GeneScan analysis and sequencing.
  • Semi-nest PCR based on laser capture microdissection was utilized to compare the clonal relationship between B-CLL and R-S/R-Slike cells.
  • (1) 5/6 B-CLL cases transformed to Hodgkin lymphoma (HL)/R-S-like cells carried the mutated IgVH genes;.
  • (2) 2 cases of R-S cells and 1 case of R-S-like cells were clonally distinct from B-CLL clone and express LMP1, whereas 1 case of R-S-like cells was relating to the surrounding B-CLL cells and did not express LMP1;.
  • (3) 2/6 B-CLL cases transformed to HL convey VH4-34 and VH3-48 respectively. CONCLUSIONS:.
  • (1) Richter transformation to HL/R-S-like cells evolves from the B-CLL which originates from the germinal center or post germinal center B cells, indicating that different lymphoma cells of different subtypes in Richter syndrome come from different B cell lineage and possibly involve a different pathogenesis and pathway;.
  • (2) HL and R-S-like cells evolve from either the B-CLL clone or may develop as a clonally unrelated lymphoma, the independent secondary malignancies are appear to be EBV-positive, possibly as a consequence of the underlying immunodeficiency;.
  • (3) The biased usage of IgVH genes suggested a role of antigens involved in the HL variant of Richter syndrome.
  • [MeSH-major] Hodgkin Disease / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Reed-Sternberg Cells / pathology

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  • (PMID = 19094463.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region
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28. Ott G, Balague-Ponz O, de Leval L, de Jong D, Hasserjian RP, Elenitoba-Johnson KS: Commentary on the WHO classification of tumors of lymphoid tissues (2008): indolent B cell lymphomas. J Hematop; 2009 Jul;2(2):77-81
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  • [Title] Commentary on the WHO classification of tumors of lymphoid tissues (2008): indolent B cell lymphomas.
  • The 4th edition of the World Health Organization classification of tumors of hematopoietic and lymphoid tissues introduces many new items to the classification scheme of the so-called indolent B cell lymphomas.
  • New proposed entities, such as splenic B cell lymphoma/leukemia, unclassifiable, splenic diffuse red pulp small B cell lymphoma, hairy cell leukemia variant, pediatric follicular lymphoma, and pediatric marginal zone lymphoma have been coined, and some definitions of established diseases, such as chronic lymphocytic leukemia or Waldenström's macroglobulinemia have been revised.
  • One aspect of major importance is the recent description of small clonal B cell populations, in part with a CLL phenotype, and their relationship to B-CLL.

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  • (PMID = 19669189.001).
  • [ISSN] 1868-9256
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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29. Dujardin F, Lefrancq T, Bléchet C, Boni-Boka M, Sénecal D, Desmoulins I, Guyétant S: [Hodgkin's disease variant of Richter's syndrome. Two cases and literature review]. Ann Pathol; 2008 Sep;28(4):311-6
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  • [Title] [Hodgkin's disease variant of Richter's syndrome. Two cases and literature review].
  • [Transliterated title] Syndrome de Richter de type pseudohodgkinien. A propos de deux cas et revue de la littérature.
  • We report the clinical and immunohistological features of two cases of chronic lymphocytic leukaemia (CLL) with Hodgkin's transformation.
  • These cases occurred in a 70-year-old man with a three-year history of CLL and in a 76-year-old man with a few months history of CLL.
  • Microscopic examination showed the presence of large tumor cells with the morphological and immunophenotypic features of classical Hodgkin and Reed-Sternberg (R-S) cells, in a background of otherwise typical B-CLL.
  • The transformation of CLL into large B cell lymphoma (Richter's syndrome) is a well-documented phenomenon.
  • Only rarely does CLL transform into Hodgkin's lymphoma, but this diagnosis is often easy and offers few differential diagnoses.
  • The major points of interest lie in the pathogenetic relationship between CLL and Hodgkin's disease, and in the potential clinical implications of this peculiar condition.
  • Literature on the subject indicates that identical IgH gene rearrangements in micromanipulated R-S and CLL cells have been identified in 7/12 cases.
  • In these patients, the R-S and CLL cells belong to the same clonal population, suggesting a progression from the underlying CLL cells.
  • In other cases, the R-S cells were often Epstein-Barr virus (EBV) positive and did not share the clonal rearrangements identified in CLL cells, suggesting that Hodgkin's disease in these patients could represent a second malignancy, EBV-related and favored by immunosuppression, associated with a better prognosis.
  • [MeSH-major] Genetic Variation. Hodgkin Disease / genetics. Hodgkin Disease / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology

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  • (PMID = 18928873.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD; 0 / Antigens, CD15; 0 / Antigens, CD79
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30. Bentley G, Palutke M, Mohamed AN: Variant t(14;18) in malignant lymphoma: a report of seven cases. Cancer Genet Cytogenet; 2005 Feb;157(1):12-7
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  • [Title] Variant t(14;18) in malignant lymphoma: a report of seven cases.
  • Variant translocations leading to juxtaposing of the BCL2 with either the IGK or IGL gene have been recognized in B-cell malignant lymphoma, although they are rare.
  • We identified seven lymphoma cases that had variant translocations.
  • Morphologically, the lymphomas were categorized as B-cell follicular lymphoma in six cases and in the seventh case as diffuse large cell lymphoma (Richter syndrome) transformed from preexisting chronic lymphocytic leukemia (CLL).
  • In case 2, the variant t(18;22) was seen as a secondary aberration evolving from a trisomy 12 clone.
  • The findings revealed that BCL2 rearrangements in some malignant lymphomas occur through variant simple or complex chromosomal translocations, but always involving the IGH, IGK, or IGL chromosomal site.

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  • (PMID = 15676141.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Kardum-Skelin I, Planinc-Peraica A, Ostojić Kolonić S, Radić-Kristo D, Milas M, Vrhovac R, Sustercić D, Minigo H, Jaksić B: [Clinical and laboratory prognostic parameters for leukemic types of chronic lymphoproliferative diseases]. Acta Med Croatica; 2008 Oct;62(4):351-64

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  • [Title] [Clinical and laboratory prognostic parameters for leukemic types of chronic lymphoproliferative diseases].
  • AIM: The aim of the study was to identify the clinical and laboratory (hematologic, biochemical and morphological) prognostic parameters of chronic leukemic lymphoproliferative diseases (CLLPD).
  • Analysis was performed in the overall CLLPD population and separately in a subgroup of patients with B chronic lymphocytic leukemia with variants (B-CLL+V) including typical B chronic lymphocytic leukemia (B-CLL), mixed chronic lymphocytic leukemia and prolymphocytic leukemia (CLL/PLL), and a variant of chronic lymphocytic leukemia with lymphoplasmocytoid differentiation (CLL/IMC).
  • Analyis of sex distribution yielded an equal male to female ratio in the overall CLLPD population and B-CLL+V subgroup.
  • B-CLL+V patients and patients free from doubling of total tumor (DTM) or of absolute lymphocyte count (DTL) within 12 months had better survival than the overall CLLPD patient population.
  • Poorer prognosis was associated with red blood cell count <2.5 x 10(12)/L, leukocyte count >100 x 10(9)/L, reticulocyte count >5/10(3) E, hemoglobin <100 g/L and iron <15 mol/L.
  • Laboratory parameters (hematologic and biochemical) as objective quantitative parameters obtained by simple venipuncture, in contrast to the 'researcher-dependent' ones, increase the utilization of some of these parameters as risk factors in CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Prolymphocytic / pathology. Lymphoproliferative Disorders / pathology

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  • (PMID = 19205412.001).
  • [ISSN] 1330-0164
  • [Journal-full-title] Acta medica Croatica : c̆asopis Hravatske akademije medicinskih znanosti
  • [ISO-abbreviation] Acta Med Croatica
  • [Language] hrv
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Croatia
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32. Swords R, Bruzzi J, Giles F: Recent advances in the diagnosis and therapy of Richter's syndrome. Med Oncol; 2007;24(1):17-32
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  • [Title] Recent advances in the diagnosis and therapy of Richter's syndrome.
  • Richter's syndrome (RS) denotes the development of aggressive lymphoma that arises in patients with chronic lymphocytic leukemia (CLL).
  • Diagnostic biopsy of affected sites usually reveals large cell lymphomas; however, Hodgkin variant cases have been described.
  • Richter's transformation occurs in approx 5% of CLL patients and may be associated with infection with Epstein-Barr virus (EBV).
  • Treatment options for these patients are limited and include combination chemotherapy with or without the addition of monoclonal antibodies and stem cell transplantation.
  • More effective management for RS is needed as well as prognostic models that will identify CLL patients at risk of transformation.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Lymphoma, B-Cell / radionuclide imaging. Lymphoma, B-Cell / therapy

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  • (PMID = 17673808.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Citrates; 0 / Gallium Radioisotopes; 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18; 27905-02-8 / gallium citrate; CH46OC8YV4 / Gallium
  • [Number-of-references] 167
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33. Morabito F, Damle RN, Deaglio S, Keating M, Ferrarini M, Chiorazzi N: The CD38 ectoenzyme family: advances in basic science and clinical practice. Mol Med; 2006 Nov-Dec;12(11-12):342-4
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  • One aim of this session given at the Torino CD38 Meeting in June, 2006 was to review the role of CD38 in B-cell Chronic Lymphocytic Leukemia (B-CLL), and its potential as a therapeutic target.
  • CD38(high) B-CLL cases show activated phenotypic features as compared with CD38(low) cases.
  • Also, CD38 is not merely a negative prognostic marker in B-CLL, but also a key element in the pathogenetic network underlying the disease.
  • A large series of B-CLL cases investigating the CD38 expression on bone marrow B-cells identified CD38 value <10% as the cut-off predicting a longer time to treatment.
  • Transferring these findings into clinical ground, 3 groups of B-CLL cases were identified with significantly different clinical courses: i.e., low-risk (no negative prognostic factor), intermediate-risk (1 negative prognostic factor) and high-risk (2-3 negative prognostic factors) patients.
  • ii) CD38 contributes to controlling a signaling pathway that confers to B-CLL cells an increased proliferative potential, enhancing aggressiveness of this variant;.
  • iv) CD38 seems to independently contribute to prognostic stratification of B-CLL.
  • [MeSH-major] Antigens, CD38 / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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  • (PMID = 17380202.001).
  • [ISSN] 1076-1551
  • [Journal-full-title] Molecular medicine (Cambridge, Mass.)
  • [ISO-abbreviation] Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; EC 3.2.2.5 / Antigens, CD38
  • [Other-IDs] NLM/ PMC1829202
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34. Cabrini G, Falzoni S, Forchap SL, Pellegatti P, Balboni A, Agostini P, Cuneo A, Castoldi G, Baricordi OR, Di Virgilio F: A His-155 to Tyr polymorphism confers gain-of-function to the human P2X7 receptor of human leukemic lymphocytes. J Immunol; 2005 Jul 1;175(1):82-9
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  • The P2X(7)R is an ATP-gated cation channel expressed in hemopoietic cells that participates in both cell proliferation and apoptosis.
  • Expression and function of the P2X(7)R have been associated with the clinical course of patients affected by chronic lymphocytic leukemia (CLL).
  • Here we investigated other nonsynonymous polymorphisms located either in the extracellular portion of the receptor, such as the 489C>T (H155Y) variant, or in the long cytoplasmic tail of the receptor, such as the 1068G>A (A348T), 1096C>G (T357S), and 1405A>G (Q460R) variants.
  • P2X(7)R function was monitored by measuring ATP-induced Ca(2+) influx in PBL of patients affected by CLL and in recombinant human embryonic kidney (HEK) 293 cells stably transfected with each single P2X(7) allelic variant.
  • Significant Ca(2+) flux increase was observed in lymphocytes from CLL patients bearing the 489C/T and 489T/T genotypes in association with the 1513A/A genotype.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Polymorphism, Genetic. Receptors, Purinergic P2 / genetics. Receptors, Purinergic P2 / metabolism
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Alleles. Amino Acid Substitution. Base Sequence. Calcium Signaling. Case-Control Studies. Cell Line. DNA, Neoplasm / genetics. Gene Frequency. Genotype. Humans. Kinetics. Mutagenesis, Site-Directed. Polymorphism, Single Nucleotide. Receptors, Purinergic P2X7. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Transfection

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  • (PMID = 15972634.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / P2RX7 protein, human; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X7; 0 / Recombinant Proteins; 8L70Q75FXE / Adenosine Triphosphate
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35. Tyner JW, Fletcher LB, Wang EQ, Yang WF, Rutenberg-Schoenberg ML, Beadling C, Mori M, Heinrich MC, Deininger MW, Druker BJ, Loriaux MM: MET receptor sequence variants R970C and T992I lack transforming capacity. Cancer Res; 2010 Aug 1;70(15):6233-7
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  • We screened patients with chronic lymphocytic leukemia (CLL), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML), colorectal cancer, endometrial cancer, thyroid cancer, or melanoma, as well as individuals without cancer, and found these variants at low frequencies in most cohorts, including normal individuals.
  • No evidence of increased phosphorylation or transformative capacity by either sequence variant was found.

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  • (PMID = 20670955.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / CA146107-01; United States / NCI NIH HHS / CA / RC1 CA146107-01; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / 5 P30 CA069533; United States / NCI NIH HHS / CA / RC1 CA146107; United States / NCRR NIH HHS / RR / UL1 RR024140; United States / NCI NIH HHS / CA / 5P50CA069533; United States / NCI NIH HHS / CA / P30 CA069533
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Growth Factor; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  • [Other-IDs] NLM/ NIHMS211280; NLM/ PMC2913476
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36. Gustafsson K, Wang X, Severa D, Eriksson M, Kimby E, Merup M, Christensson B, Flygare J, Sander B: Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: growth inhibition by receptor activation. Int J Cancer; 2008 Sep 1;123(5):1025-33
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  • Endogenous and synthetic cannabinoids exert antiproliferative and proapoptotic effects in various types of cancer and in mantle cell lymphoma (MCL).
  • In this study, we evaluated the expression of cannabinoid receptors type 1 and type 2 (CB1 and CB2) in non-Hodgkin lymphomas of B cell type (n = 62).
  • Low levels of the splice variant CB1a, previously shown to have a different affinity for cannabinoids than CB1, were detected in 44% of the lymphomas, while CB1b expression was not detected.
  • In functional studies using MCL, Burkitt lymphoma (BL), chronic lymphatic leukemia (CLL) and plasma cell leukemia cell lines, the stable anandamide analog R(+)-methanandamide (R(+)-MA) induced cell death only in MCL and CLL cells, which overexpressed both cannabinoid receptors, but not in BL.
  • [MeSH-major] Antimitotic Agents / pharmacology. Arachidonic Acids / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Receptor, Cannabinoid, CB1 / metabolism. Receptor, Cannabinoid, CB2 / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / metabolism. Cell Proliferation / drug effects. DNA, Complementary / analysis. DNA, Neoplasm / analysis. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Leukemia, Plasma Cell / drug therapy. Leukemia, Plasma Cell / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Mitosis / drug effects. Mitotic Index. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous. Up-Regulation

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
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  • (PMID = 18546271.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimitotic Agents; 0 / Arachidonic Acids; 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / RNA, Messenger; 0 / Receptor, Cannabinoid, CB1; 0 / Receptor, Cannabinoid, CB2; 150314-39-9 / methanandamide
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37. Chaker L, Segeren CM, Bot FJ, Maartense E: Haemophagocytic syndrome and Hodgkin's disease variant of Richter's syndrome after fludarabine for CLL. Eur J Haematol; 2010 Jul;85(1):91-2
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Haemophagocytic syndrome and Hodgkin's disease variant of Richter's syndrome after fludarabine for CLL.
  • [MeSH-major] Hodgkin Disease / etiology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphohistiocytosis, Hemophagocytic / etiology. Vidarabine / analogs & derivatives

  • MedlinePlus Health Information. consumer health - Hodgkin Disease.
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  • (PMID = 20331737.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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