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Items 1 to 63 of about 63
1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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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3. 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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4. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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5. 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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6. 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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  • [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.
  • [Cites] Hum Mol Genet. 2010 May 1;19(9):1840-5 [20123861.001]
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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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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. 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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9. 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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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. 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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12. 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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13. Alexopoulou A, Dourakis SP, Pandelidaki H, Archimandritis AJ, Karayiannis P: Detection of a hepatitis B surface antigen variant emerging in a patient with chronic lymphocytic leukaemia treated with fludarabine. J Med Virol; 2006 Aug;78(8):1043-6
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  • [Title] Detection of a hepatitis B surface antigen variant emerging in a patient with chronic lymphocytic leukaemia treated with fludarabine.
  • Fludarabine is used widely for the treatment of chronic lymphocytic leukaemia, but not as yet implicated in the emergence of hepatitis B surface antigen (HBsAg) variants following hepatitis B virus (HBV) reactivation.
  • Such a variant was detected in a 78-year-old female who was HBsAg(-)/anti-HBc(+)/anti-HBs(+)/anti-HBe(+), and with normal ALT levels, who developed HBV reactivation after fludarabine treatment.
  • It is concluded that a surface variant emerged in an HBsAg(-)/anti-HBs(+) patient with chronic lymphocytic leukaemia following fludarabine treatment, with an unprecedented number of amino-acid substitutions in the alpha determinant region of HBsAg, including a subtype switch.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hepatitis B / complications. Hepatitis B / virology. Hepatitis B Surface Antigens / genetics. Hepatitis B Surface Antigens / isolation & purification. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Vidarabine / analogs & derivatives

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  • [Copyright] 2006 Wiley-Liss, Inc.
  • (PMID = 16789016.001).
  • [ISSN] 0146-6615
  • [Journal-full-title] Journal of medical virology
  • [ISO-abbreviation] J. Med. Virol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hepatitis B Surface Antigens; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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14. 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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  • [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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15. 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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16. Almhanna K, Wongchaowart N, Sweetenham J: Intracerebral Hodgkin's lymphoma in a patient with chronic lymphocytic leukemia/small lymphocytic lymphoma: a case report and literature review. Cancer Invest; 2009 Feb;27(2):215-20
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  • [Title] Intracerebral Hodgkin's lymphoma in a patient with chronic lymphocytic leukemia/small lymphocytic lymphoma: a case report and literature review.
  • Richter's syndrome is defined as the transformation of low grade lymphoma to more aggressive high grade malignant form, usually diffuse large B cell lymphoma.
  • Primary or metastatic cerebral Hodgkin's lymphoma and Hodgkin's lymphoma variant of Richter transformation are extremely rare.
  • We report a case of 65-year old man who developed isolated intracerebral Hodgkin's lymphoma almost 8 years after the diagnosis of chronic lymphocytic leukemia/small lymphocytic lymphoma, and we reviewed the related literature.
  • [MeSH-major] Brain Neoplasms / therapy. Hodgkin Disease / therapy. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Neoplasms, Second Primary / therapy

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  • (PMID = 19235595.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 27
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17. 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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  • [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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18. 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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19. 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.


20. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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21. 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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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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23. Biswas A, Hamid B, Coupland SE, Franks A, Leonard N: Multiple periocular adult onset xanthogranulomas in a patient with chronic lymphocytic leukaemia. Eur J Dermatol; 2010 Mar-Apr;20(2):211-3
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  • [Title] Multiple periocular adult onset xanthogranulomas in a patient with chronic lymphocytic leukaemia.
  • Unlike the juvenile variant, systemic disorders including haematological malignancies have only rarely been reported in association with adult xanthogranuloma.
  • We report a case of multiple periocular xanthogranulomas arising in a 43 year old man with chronic lymphocytic leukaemia.
  • Also highlighted is the fact that some patients with periocular cutaneous xanthogranulomas of adult onset can have co-existing orbital xanthogranulomatous disease and appropriate clinical and radiological investigations may be needed for accurate diagnosis.
  • [MeSH-major] Eyelid Diseases / diagnosis. Granuloma / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Paraneoplastic Syndromes / diagnosis. Xanthomatosis / diagnosis

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  • (PMID = 19919911.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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24. 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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25. 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

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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26. 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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27. Wanko SO, de Castro C: Hairy cell leukemia: an elusive but treatable disease. Oncologist; 2006 Jul-Aug;11(7):780-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hairy cell leukemia: an elusive but treatable disease.
  • Hairy cell leukemia (HCL) is a unique chronic lymphoproliferative disorder that can mimic or coexist with other clonal hematologic disorders and has been associated with autoimmune disorders.
  • It should be entertained as an alternative diagnosis in patients with cytopenias being assigned the diagnosis of aplastic anemia, hypoplastic myelodysplastic syndrome, atypical chronic lymphocytic leukemia, B-prolymphocytic leukemia, or idiopathic myelofibrosis.
  • A variant subtype exists and is frequently associated with a poor response.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Hairy Cell / pathology. Leukemia, Hairy Cell / therapy

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  • (PMID = 16880237.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 395575MZO7 / Pentostatin; 47M74X9YT5 / Cladribine; 4F4X42SYQ6 / Rituximab; 9008-11-1 / Interferons
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28. 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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29. 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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30. Hashimoto Y, Tsukamoto N, Nakahashi H, Yokohama A, Saitoh T, Handa H, Matsushima T, Murakami H, Nojima Y, Karasawa M: Hairy cell leukemia-related disorders consistently show low CD27 expression. Pathol Oncol Res; 2009 Dec;15(4):615-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hairy cell leukemia-related disorders consistently show low CD27 expression.
  • In Japan, typical hairy cell leukemia (HCL) is rare, and HCL-Japanese variant (HCL-JV) is more common.
  • Hairy B-cell lymphoproliferative disorder (HBLD) is another unusual disorder of polyclonal B-lymphocytosis of hairy cell appearance.
  • As compared with other B-cell lymphoproliferative disorders, CD27 expression on B cells was significantly lower in all patients, ranging from 0.3% to 23.4%.
  • [MeSH-major] Antigens, CD27 / metabolism. Leukemia, Hairy Cell / ethnology. Leukemia, Hairy Cell / metabolism. Lymphoproliferative Disorders / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers / metabolism. Case-Control Studies. Female. HLA-DR Antigens / metabolism. HLA-DRB1 Chains. Humans. Immunoglobulin Heavy Chains / metabolism. Japan. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma / metabolism. Lymphoma, Follicular / metabolism. Male. Middle Aged

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  • (PMID = 19301150.001).
  • [ISSN] 1532-2807
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Biomarkers; 0 / HLA-DR Antigens; 0 / HLA-DRB1 Chains; 0 / HLA-DRB1*04 antigen; 0 / Immunoglobulin Heavy Chains
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31. 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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32. 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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33. Medeiros LJ, Estrov Z, Rassidakis GZ: Z-138 cell line was derived from a patient with blastoid variant mantle cell lymphoma. Leuk Res; 2006 Apr;30(4):497-501
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  • [Title] Z-138 cell line was derived from a patient with blastoid variant mantle cell lymphoma.
  • The Z-138 cell line, reported in the journal in 1998, was derived from a patient who developed a leukemia initially classified as chronic lymphocytic leukemia in 1987.
  • Splenectomy for massive involvement was required in 1998 and the neoplasm subsequently transformed to an aggressive, mature B-cell leukemia 2 years later.
  • According to the criteria of the current World Health Organization lymphoma classification, this neoplasm is best classified as mantle cell lymphoma, with blastoid transformation present in the terminal phase of disease.
  • [MeSH-major] Lymphoma, Mantle-Cell / pathology
  • [MeSH-minor] Aged. Cell Line, Tumor. Humans. Immunohistochemistry. Male


34. 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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35. Lin P, Jetly R, Lennon PA, Abruzzo LV, Prajapati S, Medeiros LJ: Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature. Hum Pathol; 2008 Nov;39(11):1664-72
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  • [Title] Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature.
  • Variant translocations that juxtapose the BCL-2 gene with the immunoglobulin kappa (2p11) and lambda (22q11) light chain genes are rare.
  • We report 4 cases of B-cell lymphoma/leukemia associated with t(18;22)(q21;q11).
  • Three cases were classified as chronic lymphocytic leukemia, and one as follicular lymphoma based on morphology and immunophenotype.
  • These cases illustrate that t(18;22)(q21;q11) is more commonly observed in chronic lymphocytic leukemia and may represent either an initial or secondary genetic event.
  • [MeSH-major] Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 22. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics

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  • (PMID = 18656237.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 25
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36. Ishibashi M, Yamamoto K, Kudo S, Chen KR: Mantle cell lymphoma with skin invasion characterized by the common variant in the subcutis and blastoid transformation in the overlying dermis. Am J Dermatopathol; 2010 Apr;32(2):180-2
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  • [Title] Mantle cell lymphoma with skin invasion characterized by the common variant in the subcutis and blastoid transformation in the overlying dermis.
  • We report a case of common mantle cell lymphoma (MCL) with subcutis infiltration and transformation to blastoid MCL in the overlying dermis.
  • The patient was initially diagnosed as having chronic lymphocytic leukemia and treated with chemotherapy.
  • Eight months after the diagnosis of MCL with bone marrow involvement, subcutaneous nodules developed on the patient's left thigh and forearm.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Dermis / pathology. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / pathology. Skin Neoplasms / diagnosis. Skin Neoplasms / pathology

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  • (PMID = 20010283.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 136601-57-5 / Cyclin D1
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37. 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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38. 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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39. Kobayashi G, Fujita N, Noda Y, Ito K, Horaguchi J, Takasawa O, Obana T, Nakahara K, Uzuki M, Sawai T: Lymphoplasmacytic sclerosing pancreatitis forming a localized mass: a variant form of autoimmune pancreatitis. J Gastroenterol; 2007 Aug;42(8):650-6
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  • [Title] Lymphoplasmacytic sclerosing pancreatitis forming a localized mass: a variant form of autoimmune pancreatitis.
  • In group B, histological findings typical of chronic pancreatitis with dilated branch ducts and protein plugs were observed.
  • [MeSH-major] Antibodies, Anti-Idiotypic / immunology. Autoimmune Diseases / etiology. Immunoglobulin G / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Pancreatitis / etiology
  • [MeSH-minor] Adult. Aged. CD4-CD8 Ratio. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Cholangiopancreatography, Endoscopic Retrograde. Diagnosis, Differential. Female. Humans. Magnetic Resonance Imaging. Male. Middle Aged. Prognosis. Retrospective Studies. Tomography, X-Ray Computed


40. Camacho E, Beà S, Salaverría I, López-Guillermo A, Puig X, Benavente Y, de Sanjosé S, Campo E, Hernández L: Analysis of Aurora-A and hMPS1 mitotic kinases in mantle cell lymphoma. Int J Cancer; 2006 Jan 15;118(2):357-63
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  • [Title] Analysis of Aurora-A and hMPS1 mitotic kinases in mantle cell lymphoma.
  • Aurora-A and hMPS1 are kinases involved in spindle checkpoint and centrosome duplication regulation and whose alterations have been associated with cell transformation and chromosome instability in different tumor models.
  • In this study, we have examined the possible alterations of these genes in 58 mantle cell lymphomas (MCLs) and 4 MCL-related cell lines.
  • Aurora-A was also examined in 46 diffuse large B-cell lymphomas (DLBCLs).
  • No Aurora-A gene amplifications were detected in any tumor or cell line, whereas hemizygous hMPS1 gene deletions were observed in 23% of MCLs and 3 of the 4 cell lines.
  • The Aurora-A proposed cancer susceptibility polymorphic variant (P31I) was observed with a similar frequency in MCL, DLBCL, chronic lymphocytic leukemia and in the 431 healthy controls.
  • However, the 3 MCLs and 4 DLBCLs with the homozygous variant of this polymorphism had particular clinical characteristics with an unusual early-age presentation and second epithelial malignancies in MCL and extranodal origin in DLBCL.
  • Although the Aurora-A P31I polymorphic variant is not directly involved in a genetic predisposition to these lymphomas, it may modulate the clinical presentation of these tumors.
  • [MeSH-major] Cell Cycle Proteins / genetics. Genetic Predisposition to Disease. Lymphoma, Mantle-Cell / genetics. Protein-Serine-Threonine Kinases / genetics
  • [MeSH-minor] Aurora Kinases. Case-Control Studies. DNA Mutational Analysis. Gene Expression Profiling. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Polymorphism, Genetic. Prognosis. Protein-Tyrosine Kinases. Tumor Cells, Cultured

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16080195.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.1 / TTK protein, human
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41. 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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42. Ruoppolo M, Pezzica E, Milesi R, Corti D, Mercurio P, Fragapane G: [Neuroendocrine small-cell bladder cancer: our experience]. Urologia; 2010 Oct-Dec;77 Suppl 17:64-71
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  • [Title] [Neuroendocrine small-cell bladder cancer: our experience].
  • The small-cell carcinoma represents the most frequent histologic variant described.
  • Small-cell carcinoma is an epithelial tumor associated with a more aggressive behavior and poorer prognosis than transitional cell bladder carcinoma.
  • PATIENTS AND METHODS: We report three cases of pure neuroendocrine small-cell bladder cancer.
  • CONCLUSIONS: In the absence of a prospective study, and because of the rarity of the disease, the best treatment for small-cell bladder cancer remains uncertain.
  • [MeSH-major] Carcinoma, Neuroendocrine / pathology. Carcinoma, Small Cell / pathology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Combined Modality Therapy. Cystectomy. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Disease Progression. Fatal Outcome. Gastrointestinal Hemorrhage / etiology. Hematuria / etiology. Humans. Intestinal Neoplasms / complications. Intestinal Neoplasms / secondary. Leukemia, Lymphocytic, Chronic, B-Cell. Liver Neoplasms / secondary. Lymph Node Excision. Male. Middle Aged. Neoplasms, Second Primary. Peritoneal Neoplasms / secondary. Prostatic Neoplasms. Stomach Neoplasms. Survival Rate

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  • (PMID = 21308678.001).
  • [ISSN] 0391-5603
  • [Journal-full-title] Urologia
  • [ISO-abbreviation] Urologia
  • [Language] ita
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
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43. 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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44. Lee S, Huang H, Niu Y, Tommasino M, Lenoir G, Sylla BS: Dok1 expression and mutation in Burkitt's lymphoma cell lines. Cancer Lett; 2007 Jan 8;245(1-2):44-50
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  • [Title] Dok1 expression and mutation in Burkitt's lymphoma cell lines.
  • We have previously reported a frameshift mutation of this gene and the down-regulation of its expression in chronic lymphocytic leukemia.
  • In this study, we have determined the expression levels of Dok1 in Burkitt's lymphoma (BL) cell lines, lymphoblastoid cell lines from patients with X-linked lymphoproliferative (XLP-LCL), or from control healthy donors.
  • Dok1 expression was down-regulated in all BL and XLP-LCL cell lines in comparison to the control cells.
  • Interestingly, the C(89487)T variant is associated with a significantly lower level of Dok1 expression compared to the control samples.
  • [MeSH-minor] Base Sequence. Burkitt Lymphoma / genetics. Burkitt Lymphoma / pathology. Cell Line, Tumor. DNA Mutational Analysis. DNA, Neoplasm / chemistry. DNA, Neoplasm / genetics. Heteroduplex Analysis. Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16338067.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / DOK1 protein, human; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / RNA-Binding Proteins
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45. Nishimura H, Akiyama T, Monobe Y, Matsubara K, Igarashi Y, Abe M, Sugihara T, Sadahira Y: Expression of sphingosine-1-phosphate receptor 1 in mantle cell lymphoma. Mod Pathol; 2010 Mar;23(3):439-49
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  • [Title] Expression of sphingosine-1-phosphate receptor 1 in mantle cell lymphoma.
  • Microarray-based immunohistochemistry with tissue samples from 85 lymphoid malignancy cases demonstrated that sphingosine-1-phosphate receptor 1 was expressed on the surface of mantle cell lymphoma cells.
  • Strong expression was observed in all classical mantle cell lymphoma cases involving the lymph node (19 out of 19), gastrointestinal tract (10 out of 10), bone marrow (9 out of 9), and orbita (1 out of 1).
  • One aggressive variant of mantle cell lymphoma displayed a weaker membranous staining than classical mantle cell lymphoma in the lymph node and bone marrow.
  • In a cyclin D1-negative mantle cell lymphoma of the orbita, no conclusive result was obtained.
  • No cases of follicular lymphoma, marginal zone lymphoma, B lymphoblastic leukemia/lymphoma, or Burkitt's lymphoma showed any significant expression, whereas 2 out of 6 chronic lymphocytic leukemia/small lymphocytic lymphomas in bone marrow, 1 out of 3 lymphoplasmacytic lymphomas in the lymph node, and 2 out of 37 diffuse large B-cell lymphomas exhibited staining.
  • A quantitative reverse transcription polymerase chain reaction-based analysis of mantle cell lymphoma lines revealed the sphingosine-1-phosphate receptor 1 mRNA expression level to be well correlated with the results of immunocytochemistry, flow cytometry, and western blotting.
  • Thus, sphingosine-1-phosphate receptor 1 immunohistochemistry may be useful in the histological diagnosis of mantle cell lymphoma with formalin-fixed and paraffin-embedded sections.
  • [MeSH-major] Lymphoma, Mantle-Cell / metabolism. Receptors, Lysosphingolipid / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Line, Tumor. Cyclin D1 / metabolism. Female. Humans. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymphocytes / metabolism. Lymphocytes / pathology. Male. Middle Aged. Tissue Array Analysis

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  • (PMID = 20081804.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CCND1 protein, human; 0 / Receptors, Lysosphingolipid; 0 / S1PR1 protein, human; 136601-57-5 / Cyclin D1
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46. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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  • [Cites] Blood. 2001 Jul 1;98(1):181-6 [11418478.001]
  • [Cites] Blood. 2002 Jun 1;99(11):4087-93 [12010811.001]
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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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47. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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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48. Cummins DL, Mimouni D, Tzu J, Owens N, Anhalt GJ, Meyerle JH: Lichenoid paraneoplastic pemphigus in the absence of detectable antibodies. J Am Acad Dermatol; 2007 Jan;56(1):153-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Paraneoplastic pemphigus (PNP) has been described as an antibody-mediated mucocutaneous disease occurring almost exclusively in patients with lymphocytic neoplasms.
  • We describe 4 patients with the clinical features of the lichenoid variant of PNP in the absence of detectable autoantibodies.
  • [MeSH-minor] Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antibody Formation / drug effects. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. B-Lymphocytes / drug effects. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Esophageal Diseases / diagnosis. Esophageal Diseases / etiology. Esophageal Diseases / immunology. Etoposide / administration & dosage. Female. Hematopoietic Stem Cell Transplantation. Humans. Immunity, Cellular. Interleukin-2 / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / radiotherapy. Leukemia, Lymphocytic, Chronic, B-Cell / surgery. Lymphoma, Follicular / complications. Lymphoma, Follicular / drug therapy. Lymphoma, Follicular / radiotherapy. Lymphoma, Non-Hodgkin / complications. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / radiotherapy. Male. Middle Aged. Mucositis / complications. Prednisone / administration & dosage. Recurrence. Rituximab. T-Lymphocytes / immunology. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives. Vincristine / administration & dosage

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  • [CommentIn] J Am Acad Dermatol. 2007 Dec;57(6):1094-5 [18021856.001]
  • (PMID = 17097371.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Autoantibodies; 0 / Interleukin-2; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; VB0R961HZT / Prednisone; CHOP protocol; EPOCH protocol
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49. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

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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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50. Chen TY, Chen JS, Su WC, Wu MS, Tsao CJ: Expression of DNA repair gene Ku80 in lymphoid neoplasm. Eur J Haematol; 2005 Jun;74(6):481-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PATIENTS AND METHODS: Competitive reverse transcription-polymerase chain reaction assays were performed and the expression levels of Ku80 were measured in normal peripheral blood mononuclear cells (n = 9) and malignant cells from 25 patients with acute lymphoblastic leukemia (ALL) (14 children, 11 adults), and chronic lymphoproliferative disorders (n = 6).
  • RESULTS: No mutation or Ku80 variant at the RNA level was seen in any patient samples or in the Raji or CCRF-CEM cell lines.
  • In Ku80 expression, 8.8-, 1.9-, and 6.2-fold mean increases were seen in adult, pediatric ALL, and chronic lymphoid malignancies compared with the control.
  • The amount of Ku80 expression in ALL was moderately correlated with peripheral white blood cell counts, but not with Ki67 labeling index.
  • [MeSH-major] Antigens, Nuclear / biosynthesis. DNA Repair / genetics. DNA-Binding Proteins / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Cell Line, Tumor. Child. Child, Preschool. Humans. Infant. Ki-67 Antigen / biosynthesis. Ki-67 Antigen / genetics. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Prognosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15876251.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Ku autoantigen; 0 / RNA, Messenger
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51. 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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52. Tefferi A, Gotlib J, Pardanani A: Hypereosinophilic syndrome and clonal eosinophilia: point-of-care diagnostic algorithm and treatment update. Mayo Clin Proc; 2010 Feb;85(2):158-64
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  • The World Health Organization classification system for hematologic malignancies recognizes 2 distinct subcategories of clonal eosinophilia: chronic eosinophilic leukemia, not otherwise specified and myeloid/lymphoid neoplasms with eosinophilia and mutations involving platelet-derived growth factor receptor alpha/beta or fibroblast growth factor receptor 1.
  • Clonal eosinophilia might also accompany other World Health Organization-defined myeloid malignancies, including chronic myelogenous leukemia, myelodysplastic syndromes, chronic myelomonocytic leukemia, and systemic mastocytosis.
  • The presence of the latter defines lymphocytic variant hyper eosinophilia, which is best classified under secondary eosinophilia.
  • [MeSH-major] Algorithms. Eosinophilia / diagnosis. Eosinophilia / drug therapy. Hypereosinophilic Syndrome / diagnosis. Hypereosinophilic Syndrome / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Benzamides. Causality. Decision Trees. Diagnosis, Differential. Humans. Imatinib Mesylate. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / complications. Leukemia, Myelomonocytic, Chronic / complications. Mastocytosis / complications. Mutation / genetics. Myelodysplastic Syndromes / complications. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Receptors, Platelet-Derived Growth Factor / genetics. mRNA Cleavage and Polyadenylation Factors / genetics

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  • (PMID = 20053713.001).
  • [ISSN] 1942-5546
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / FIP1L1 protein, human; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 0 / mepolizumab; 3A189DH42V / alemtuzumab; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  • [Number-of-references] 77
  • [Other-IDs] NLM/ PMC2813824
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53. Natsume A, Shimizu-Yokoyama Y, Satoh M, Shitara K, Niwa R: Engineered anti-CD20 antibodies with enhanced complement-activating capacity mediate potent anti-lymphoma activity. Cancer Sci; 2009 Dec;100(12):2411-8
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  • Various biological factors relating to the host's immune system or tumor cells have been suggested to reduce the efficacy of anti-CD20 therapy in B-cell malignancies.
  • Anti-CD20 antibodies having a variant heavy constant region of mixed IgG1/IgG3 isotype, which have previously been found to enhance CDC, were investigated for their in vitro CDC against lymphoma cells and whole blood B-cell depletion activity.
  • Use of the variant constant region greatly increased the CDC of an anti-CD20 antibody having variable regions identical to those of rituximab to the level shown by an IgG1 antibody of ofatumumab.
  • Although the whole blood assay showed different cytotoxicity patterns among individual blood donors, the CDC-enhancing variant of rituximab showed higher activity than the parent IgG1 and consistently showed maximized activity when further combined with antibody-dependent cellular cytotoxicity (ADCC)-enhancing modification by fucose removal from Fc-linked oligosaccharides.
  • In addition, the rituximab variant showed potent CDC against transfectant cells with lower CD20 expression and chronic lymphocytic leukemia-derived cell lines with higher complement regulatory proteins.
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Murine-Derived. Antibody-Dependent Cell Cytotoxicity. CHO Cells. Complement System Proteins / immunology. Cricetinae. Cricetulus. Humans. Protein Engineering. Rituximab

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  • (PMID = 19758394.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab; 9007-36-7 / Complement System Proteins
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54. Lux H, Flammann H, Hafner M, Lux A: Genetic and molecular analyses of PEG10 reveal new aspects of genomic organization, transcription and translation. PLoS One; 2010;5(1):e8686

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Overexpression or reinduced PEG10 expression was seen in malignancies, like hepatocellular carcinoma or B-cell acute and chronic lymphocytic leukemia.
  • Experimental evidence suggests that the PEG10-RF1 protein is an inhibitor of apoptosis and mediates cell proliferation.
  • Here we present new data on the genomic organization of PEG10 by identifying the major transcription start site, a new splice variant and report the cloning and analysis of 1.9 kb of the PEG10 promoter.
  • In summary, our study provides new data on the genomic organization as well as expression and translation of PEG10, a prerequisite in order to study and understand the role of PEG10 in cancer, embryonic development and normal cell homeostasis.
  • [MeSH-minor] Adipocytes / metabolism. Alternative Splicing. Base Sequence. Cell Differentiation / physiology. Codon. DNA. Frameshift Mutation. Humans. Molecular Sequence Data. Promoter Regions, Genetic. Sequence Homology, Nucleic Acid

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  • (PMID = 20084274.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Codon; 0 / PEG10 protein, human; 0 / Proteins; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2800197
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55. Aamot HV, Bjørnslett M, Delabie J, Heim S: t(14;22)(q32;q11) in non-Hodgkin lymphoma and myeloid leukaemia: molecular cytogenetic investigations. Br J Haematol; 2005 Sep;130(6):845-51
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  • [Title] t(14;22)(q32;q11) in non-Hodgkin lymphoma and myeloid leukaemia: molecular cytogenetic investigations.
  • Two non-Hodgkin lymphomas (NHL), one chronic lymphocytic leukaemia/small lymphocytic lymphoma and one diffuse large B-cell lymphoma and three cases of myeloid leukaemia, two chronic (CML) and one acute (AML), showed, by G-banding analysis, apparently identical chromosomal translocations t(14;22)(q32;q11), in three of the cases as the sole abnormality.
  • A three-way variant translocation of the classical t(9;22)(q34;q11), t(9;22;14)(q34;q11;q32), involving both BCR and ABL, was unravelled by the molecular cytogenetic investigations in the three myeloid leukaemia cases; a similar variant translocation has previously been reported in seven CML.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Myeloid / genetics. Lymphoma, Non-Hodgkin / genetics. Translocation, Genetic

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  • (PMID = 16156854.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. 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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56. Solini A, Cuccato S, Ferrari D, Santini E, Gulinelli S, Callegari MG, Dardano A, Faviana P, Madec S, Di Virgilio F, Monzani F: Increased P2X7 receptor expression and function in thyroid papillary cancer: a new potential marker of the disease? Endocrinology; 2008 Jan;149(1):389-96
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  • Nucleotides are increasingly recognized as nonredundant extracellular signals for chemotaxis, cell growth, and cytokine release.
  • Effects of extracellular nucleotides are mediated by P2 receptors, among which the P2X(7) subtype is attracting increasing attention for its involvement in apoptosis, cell growth, and cytokine release.
  • Recent studies showed that P2X(7) is overexpressed in chronic lymphocytic leukemia and breast and prostate cancer.
  • P2X(7) receptor message and protein expression and functional activity were tested in two cell lines (FB1 and FB2) established from either anaplastic or papillary primary thyroid cancer and in several histological samples of human papillary cancer.
  • We show here that human thyroid papillary carcinoma, whether of the classical or follicular variant, expresses the P2X(7) receptor (P2X(7)R) to a much higher level than normal thyroid tissue.
  • The P2X(7)R was similarly up-regulated in FB1 and FB2 cell lines.
  • In contrast to normal thyroid cells, both cell lines responded to extracellular nucleotide stimulation with a large increase in intracellular Ca(2+) and secretion of IL-6.
  • Finally, the thyroid carcinoma cell lines had at least a 3-fold higher intracellular ATP concentration and maintained at least a 3-fold higher extracellular ATP level, compared with control cells.
  • [MeSH-minor] Adenosine Triphosphate / analysis. Adenosine Triphosphate / pharmacology. Cell Line, Tumor. Gene Expression Regulation, Neoplastic. Humans. Interleukin-6 / secretion. Receptors, Purinergic P2X7. Thyroid Gland / metabolism. Up-Regulation

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  • (PMID = 17947359.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Grant] Italy / Telethon / / TI/ GGP06070
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-6; 0 / P2RX7 protein, human; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X7; 8L70Q75FXE / Adenosine Triphosphate
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57. Zhang Y, Lan Q, Rothman N, Zhu Y, Zahm SH, Wang SS, Holford TR, Leaderer B, Boyle P, Zhang B, Zou K, Chanock S, Zheng T: A putative exonic splicing polymorphism in the BCL6 gene and the risk of non-Hodgkin lymphoma. J Natl Cancer Inst; 2005 Nov 2;97(21):1616-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have shown that the B-cell lymphoma 6 gene (BCL6) is an oncogene that contributes to lymphomagenesis.
  • Higher risks were observed for two NHL subtypes, namely B-cell chronic lymphatic leukemia/prolymphocytic leukemia/small lymphocytic lymphoma (OR = 3.5, 95% CI = 1.6 to 7.8) and T-cell lymphoma (OR = 5.2, 95% CI = 2.0 to 13.3).
  • Our results support the hypothesis that a genetic variant that could alter mRNA transcripts of BCL6 may contribute to the etiology of NHL and suggest that this variant warrants further investigation.

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  • (PMID = 16264183.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62006
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins
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58. Said JW: Immunodeficiency-related Hodgkin lymphoma and its mimics. Adv Anat Pathol; 2007 May;14(3):189-94
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  • Topics under review include: (a) CHL posttransplant lymphoproliferative disorders, (b) CHL in HIV/AIDS, (c) Hodgkin variant of Richter syndrome in chronic lymphocytic leukemia in association with fludarabine therapy, (d) CHL in other immunodeficiency states including methotrexate-associated lymphoproliferative disorder in patients with rheumatoid arthritis and primary immune deficiencies, and (e) Hodgkin-like lymphoid proliferations including senile Epstein-Barr virus+ B-cell lymphoproliferative disorder.

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  • (PMID = 17452815.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 21
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59. Quintás-Cardama A, Cortes J: Therapeutic options for patients with clonal and idiopathic hypereosinophia. Expert Opin Investig Drugs; 2008 Jul;17(7):1039-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The hypereosinophilic syndrome (HES) comprises a heterogeneous group of disorders characterized by chronic, unexplained hypereosinophilia with organ involvement.
  • Moreover, the elucidation of the role of interleukin-5 in the pathogenesis of the lymphocytic variant of HES and the fact that CD52 is expressed on the surface of eosinophils and T cells have led to the clinical use of monoclonal antibodies such as mepolizumab, reslizumumab, and alemtuzumab for the treatment of different forms of hypereosinophilia.
  • [MeSH-minor] Algorithms. Animals. Eosinophilia / diagnosis. Eosinophilia / metabolism. Humans. Immunotherapy. Stem Cell Transplantation

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  • (PMID = 18549340.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 101
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60. Wahner-Roedler DL, Kyle RA: Heavy chain diseases. Best Pract Res Clin Haematol; 2005;18(4):729-46
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  • Heavy chain diseases (HCDs) are rare B-cell lymphoplasma-cell proliferative disorders characterized by production of truncated monoclonal immunoglobulin heavy chains without associated light chains.
  • HCDs can be thought of as variant types of non-Hodgkin lymphoma: alpha-HCD presents as an extranodal marginal-zone lymphoma of mucosa-associated lymph-node tissue, gamma-HCD as lymphoplasmacytoid non-Hodgkin lymphoma, and mu-HCD as small lymphocytic non-Hodgkin lymphoma or chronic lymphocytic leukemia.
  • Diagnosis of HCD requires documentation of a deleted immunoglobulin heavy chain without a bound light chain in the serum or urine.
  • [MeSH-major] Heavy Chain Disease / diagnosis

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  • (PMID = 16026747.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
  • [Number-of-references] 38
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61. Sellick GS, Broderick P, Fielding S, Catovsky D, Houlston RS: Lack of a relationship between the common 8q24 variant rs6983267 and risk of chronic lymphocytic leukemia. Leukemia; 2008 Feb;22(2):438-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of a relationship between the common 8q24 variant rs6983267 and risk of chronic lymphocytic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 8. Genetic Predisposition to Disease. Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Polymorphism, Single Nucleotide

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  • (PMID = 17713544.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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62. Allan JM, Sunter NJ, Bailey JR, Pettitt AR, Harris RJ, Pepper C, Fegan C, Hall AG, Deignan L, Bacon CM, Pointon JC, Houlston RS, Broderick P, Mainou-Fowler T, Jackson GH, Summerfield G, Evans PA, Strefford JC, Parker A, Oscier D, Pratt G, Allsup DJ: Variant IRF4/MUM1 associates with CD38 status and treatment-free survival in chronic lymphocytic leukaemia. Leukemia; 2010 Apr;24(4):877-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variant IRF4/MUM1 associates with CD38 status and treatment-free survival in chronic lymphocytic leukaemia.
  • [MeSH-major] Antigens, CD38 / genetics. Genetic Variation / physiology. Interferon Regulatory Factors / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / mortality

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  • (PMID = 20090783.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38
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63. 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
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  • [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

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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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