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1. Hofbauer SW, Piñón JD, Brachtl G, Haginger L, Wang W, Jöhrer K, Tinhofer I, Hartmann TN, Greil R: Modifying akt signaling in B-cell chronic lymphocytic leukemia cells. Cancer Res; 2010 Sep 15;70(18):7336-44
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modifying akt signaling in B-cell chronic lymphocytic leukemia cells.
  • Emerging evidence suggests that the survival of B-cell chronic lymphocytic leukemia (CLL) cells is dependent on microenvironmental influences such as antigenic stimulation and support by stromal cells.
  • We investigated the role of Akt and its modulation by the protooncogene T-cell leukemia 1a (Tcl1a) in the survival pathways of primary CLL samples and CLL-derived prolymphocytic cell lines MEC-1 and MEC-2.
  • Akt activation was increased by the protective presence of human bone marrow stromal cells and B-cell receptor mimicking signals but antagonized by direct Akt blockade with the novel specific inhibitor AiX, with preferential apoptosis induction in CLL cells with an unmutated immunoglobulin status, which predicts poor clinical outcome.
  • Confirming the critical role of Tcl1a in modulating Akt signaling, Akt activation was enhanced by overexpressing Tcl1a in CLL.
  • In contrast, decreasing Tcl1a levels by small interfering RNA reduced Akt activation in the fludarabine-insensitive CLL cell line MEC-2 and sensitized the malignant cells to fludarabine treatment.
  • In summary, our data reveal a significant role for the Akt-Tcl1a axis in CLL survival and propose a further evaluation of this interplay for targeting chemoresistance phenomena.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Humans. Oxazines / pharmacology. RNA, Small Interfering / genetics. Signal Transduction. Transfection

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  • [Copyright] ©2010 AACR.
  • (PMID = 20823161.001).
  • [ISSN] 1538-7445
  • [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 / Enzyme Inhibitors; 0 / Oxazines; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 0 / TCL1A protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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2. Prieto-Sánchez RM, Hernández JA, García JL, Gutiérrez NC, San Miguel J, Bustelo XR, Hernández JM: Overexpression of the VAV proto-oncogene product is associated with B-cell chronic lymphocytic leukaemia displaying loss on 13q. Br J Haematol; 2006 Jun;133(6):642-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of the VAV proto-oncogene product is associated with B-cell chronic lymphocytic leukaemia displaying loss on 13q.
  • The expression of the VAV proto-oncogene in 57 patients with chronic myeloproliferative disease (CMD), B-cell acute lymphoblastic leukaemia (B-ALL) and B-cell non-Hodgkin Lymphoma (B-NHL), and 61 with B-cell chronic lymphocytic leukaemia (B-CLL) was analysed.
  • Overexpression was not observed in B-ALL or CMD, but 13% of B-NHL and 34.4% of B-CLL patients (P = 0.002) overexpressed VAV.
  • The overexpression and phosphorylation of VAV was detected more frequently in 13q- chronic lymphocytic leukaemias (71.4%) versus other B-CLLs (23.4%, P = 0.001).
  • Overexpression of VAV protein is a frequent event in patients with B-CLL displaying loss of 13q sequences.

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  • [Cites] Mol Cell Biol. 2000 Mar;20(5):1461-77 [10669724.001]
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  • (PMID = 16704440.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA073735; United States / NCI NIH HHS / CA / 5R01-CA73735-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-vav
  • [Other-IDs] NLM/ NIHMS22208; NLM/ PMC1950221
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3. Ghosh AK, Secreto CR, Knox TR, Ding W, Mukhopadhyay D, Kay NE: Circulating microvesicles in B-cell chronic lymphocytic leukemia can stimulate marrow stromal cells: implications for disease progression. Blood; 2010 Mar 4;115(9):1755-64
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  • [Title] Circulating microvesicles in B-cell chronic lymphocytic leukemia can stimulate marrow stromal cells: implications for disease progression.
  • They can transfer various messages to target cells and may be critical to disease progression.
  • Here, we demonstrate that MVs circulating in plasma of B-cell chronic lymphocytic leukemia (CLL) patients exhibit a phenotypic shift from predominantly platelet derived in early stage to leukemic B-cell derived at advanced stage.
  • Furthermore, the total MV level in CLL was significantly greater compared with healthy subjects.
  • To understand the functional implication, we examined whether MVs can interact and modulate CLL bone marrow stromal cells (BMSCs) known to provide a "homing and nurturing" environment for CLL B cells.
  • We found that CLL-MV can activate the AKT/mammalian target of rapamycin/p70S6K/hypoxia-inducible factor-1alpha axis in CLL-BMSCs with production of vascular endothelial growth factor, a survival factor for CLL B cells.
  • This study demonstrates the existence of separate MV phenotypes during leukemic disease progression and underscores the important role of MVs in activation of the tumor microenvironment.
  • [MeSH-major] Bone Marrow Cells / pathology. Cell-Derived Microparticles / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Cell Line. Disease Progression. Glycogen Synthase Kinase 3 / metabolism. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Microscopy, Electron, Transmission. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. Stromal Cells / metabolism. Stromal Cells / pathology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A / metabolism. beta Catenin / metabolism


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4. Abramenko I, Bilous N, Kryachok I, Filonenko I, Pilipenko G, Chumak A, Bazyka D, Bebeshko V: IGHV3-21 gene expression in patients with B-cell chronic lymphocytic leukemia in Ukraine. Exp Oncol; 2007 Sep;29(3):226-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IGHV3-21 gene expression in patients with B-cell chronic lymphocytic leukemia in Ukraine.
  • THE AIM of the study was to evaluate the frequency of IGHV3-21 gene usage and its clinical significance for patients with B-cell chronic lymphocytic leukemia (CLL) in Ukraine.
  • PATIENTS AND METHODS: Immunoglobulin variable heavy chain (IGHV) gene repertoire was studied in 189 CLL patients using reverse transcribed polymerase chain reaction and direct sequence of amplified products.
  • RESULTS: IGHV3-21 gene expression was found in 11 cases (5.8%), and its frequency was intermediate between Scandinavian (11.7%) and Mediterranean CLL (2.9%) cohorts.
  • The differences in overall (OS), progression-free (PFS) and treatment-free survival (TFS) for IGHV3-21 positive patients in comparison with CLL patients expressing the other IGHV genes were statistically insignificant.
  • These survival parameters were comparable also for CLL patients with mutated IGHV3-21 gene usage and expression the others mutated IGHV genes.
  • Furthermore, in small group of 6 patients with mutated IGHV3-21 gene expression, 3 patients had solid tumors and one underwent Richter transformation.
  • Unmutated IGHV3-21 gene expressed patients had worse OS and PFS in comparison with CLL patients that expressed the others unmutated IGHV genes.
  • [MeSH-major] Gene Expression. Genes, Immunoglobulin Heavy Chain. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasms, Second Primary / genetics

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  • (PMID = 18004251.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
  • [Chemical-registry-number] 0 / Immunoglobulin Variable Region
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5. Richardson SJ, Matthews C, Catherwood MA, Alexander HD, Carey BS, Farrugia J, Gardiner A, Mould S, Oscier D, Copplestone JA, Prentice AG: ZAP-70 expression is associated with enhanced ability to respond to migratory and survival signals in B-cell chronic lymphocytic leukemia (B-CLL). Blood; 2006 May 1;107(9):3584-92
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  • [Title] ZAP-70 expression is associated with enhanced ability to respond to migratory and survival signals in B-cell chronic lymphocytic leukemia (B-CLL).
  • Molecular markers like IgV(H) mutational status, chromosomal abnormalities, and CD38 and ZAP-70 expression have prognostic value in B-cell chronic lymphocytic leukemia (B-CLL).
  • These may be pathogenetic because of the coincidental expression of ZAP-70 and increased B-cell receptor (BCR) signaling and the signaling function of CD38 in CLL.
  • This study shows that ZAP-70(+) CLL B cells respond in vitro more readily than ZAP-70(-) CLL and normal B cells to chemokine migratory signals through enhanced surface CCR7 expression (P = .009; P < .001) and increased responsiveness to its ligands CCL19 and CCL21, demonstrated by F-actin polymerization (P < .05) and cellular migration (P < .01).
  • In addition, ZAP-70(+) CLL cells exhibit sustained ERK phosphorylation/activation following stimulation with CXCL12 (SDF1-alpha, a survival factor produced by stromal cells) compared with ZAP-70(-) cells (P = .004).
  • Following coculture with nurse-like cells, the survival of ZAP-70(+) but not ZAP-70(-) CLL cells is significantly enhanced by the addition of CXCL12 (P < .05), an effect that is partially blocked by the MEK inhibitor PD98059.
  • These advantageous migratory and survival responses may promote easier access to and greater proliferation in pseudo-germinal centers and explain in part the more progressive nature of ZAP-70(+) disease.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Case-Control Studies. Cell Movement. Cell Survival. Chemokine CCL19. Chemokine CCL21. Chemokine CXCL12. Chemokines, CC / pharmacology. Chemokines, CXC / pharmacology. Genes, Immunoglobulin. Humans. In Vitro Techniques. MAP Kinase Signaling System / drug effects. Models, Biological. Mutation. Receptors, CCR7. Receptors, CXCR4 / metabolism. Receptors, Chemokine / metabolism. Signal Transduction

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  • (PMID = 16332969.001).
  • [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 / CCL19 protein, human; 0 / CCL21 protein, human; 0 / CCR7 protein, human; 0 / CXCL12 protein, human; 0 / Chemokine CCL19; 0 / Chemokine CCL21; 0 / Chemokine CXCL12; 0 / Chemokines, CC; 0 / Chemokines, CXC; 0 / Receptors, CCR7; 0 / Receptors, CXCR4; 0 / Receptors, Chemokine; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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6. Bagchi S: Alemtuzumab shows promise for CLL. Lancet Oncol; 2007 Dec;8(12):1060

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab shows promise for CLL.

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  • (PMID = 28581422.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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7. Hus I, Bojarska-Junak A, Dmoszyńska A, Wasik-Szczepanek E, Sieklucka M, Trześniewska W, Glazer M, Roliński J: ZAP-70 and CD38 expression are independent prognostic factors in patients with B-cell chronic lymphocytic leukaemia and combined analysis improves their predictive value. Folia Histochem Cytobiol; 2008;46(2):147-52

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 and CD38 expression are independent prognostic factors in patients with B-cell chronic lymphocytic leukaemia and combined analysis improves their predictive value.
  • Recently identified biological risk factors in B-cell chronic lymphocytic leukemia (B-CLL) include ZAP-70 and CD38 expression.
  • We examined the expression of ZAP-70 and CD38 by flow cytometry method in 217 newly diagnosed, consecutive, unselected and well characterized B-CLL patients in relation to laboratory parameters and clinical outcome.
  • We confirmed that both ZAP-70 as well as CD38 were independent of prognostic factors.

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  • (PMID = 18519230.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 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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8. Pérez-Chacón G, Contreras-Martín B, Cuní S, Rosado S, Martín-Donaire T, Losada-Fernández I, Vargas JA, Jordá J, Alvarez N, García-Marco J, Pérez-Aciego P: Polymorphism in the CD5 gene promoter in B-cell chronic lymphocytic leukemia and mantle cell lymphoma. Am J Clin Pathol; 2005 May;123(5):646-50
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  • [Title] Polymorphism in the CD5 gene promoter in B-cell chronic lymphocytic leukemia and mantle cell lymphoma.
  • Despite the low incidence of microsatellite instability (MSI) in lymphoid malignant neoplasms, it has been reported that the CD5 promoter MSI was relatively frequent among B-cell chronic lymphoproliferative disorders.
  • We studied the presence of MSI in the CD5 promoter in 134 cases of B-cell chronic lymphocytic leukemia (B-CLL) and 47 of mantle cell lymphoma (MCL) by comparing the pattern of microsatellite repeats on autologous germline and tumor DNA samples.
  • However, the allele distribution of this polymorphism showed a higher frequency of the 18 CA allele (0.585) in MCL cases (P = .026; odds ratio [OR], 1.75; 95% confidence interval [CI], 1.07-2.87) and of the 19 CA allele (0.179) in B-CLL cases (P = .005; OR, 2.26; 95% CI, 1.27-4.01) compared with control cases (0.442 and 0.087, respectively).
  • This suggests that although MSI seems not to be involved in the pathogenesis of these 2 lymphoid malignant neoplasms, the polymorphic CD5 promoter is associated with increased susceptibility to these disorders.
  • [MeSH-major] Antigens, CD5 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, Mantle-Cell / genetics. Polymorphism, Genetic. Promoter Regions, Genetic
  • [MeSH-minor] DNA, Neoplasm / analysis. Gene Frequency. Genetic Predisposition to Disease. Humans. Microsatellite Repeats / genetics. Odds Ratio

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  • (PMID = 15981803.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / DNA, Neoplasm
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9. Kern W, Haferlach T, Schnittger S, Schoch C: Detection of t(14;18)(q32;q21) in B-cell chronic lymphocytic leukemia. Arch Pathol Lab Med; 2005 Mar;129(3):410-1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of t(14;18)(q32;q21) in B-cell chronic lymphocytic leukemia.
  • Cytomorphologic testing and multiparameter flow cytometry are the mainstays in diagnosing B-cell chronic lymphocytic leukemia, whereas fluorescence in situ hybridization that targets the translocation t(14;18)(q32;q21) often is used to identify follicular lymphoma.
  • We describe a case with cytomorphologically and immunologically proven B-cell chronic lymphocytic leukemia in which t(14;18)(q32;q21) was found.
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Translocation, Genetic / genetics

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  • (PMID = 15737042.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. Smal C, Van Den Neste E, Maerevoet M, Poiré X, Théate I, Bontemps F: Positive regulation of deoxycytidine kinase activity by phosphorylation of Ser-74 in B-cell chronic lymphocytic leukaemia lymphocytes. Cancer Lett; 2007 Aug 8;253(1):68-73
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  • [Title] Positive regulation of deoxycytidine kinase activity by phosphorylation of Ser-74 in B-cell chronic lymphocytic leukaemia lymphocytes.
  • Here, we show that dCK from B-cell chronic lymphocytic leukaemia (B-CLL) lymphocytes can be detected by an anti-phospho-Ser-74 antibody and that interindividual variability in dCK activity is related to its phosphorylation level on Ser-74.
  • [MeSH-major] Deoxycytidine Kinase / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Serine / metabolism


11. Allen SL, Rai KR, Elstrom R, Negrea OG, Farber CM, Abbasi R, Teoh N, Horne H, Wegener WA, Goldenberg DM: Subcutaneous injections of low doses of veltuzumab (humanized anti-CD20 antibody): Objective responses in B-cell malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):8530

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcutaneous injections of low doses of veltuzumab (humanized anti-CD20 antibody): Objective responses in B-cell malignancies.
  • : 8530 Background: Low IV doses of veltuzumab, a second-generation anti-CD20 monoclonal antibody with structure-function differences from chimeric rituximab, have shown clinical activity, thus justifying subcutaneous (SC) injections.
  • METHODS: A phase I/II study was initiated in patients (pts) with previously untreated or relapsed CD20+ indolent NHL or CLL who received 4 SC injections of veltuzumab 2 weeks apart at dose levels of 80, 160, or 320 mg.
  • Efficacy was assessed by CT-based IWG (NHL) or hematology-based NCI/IWCLL (CLL) criteria 4 and 12 weeks later, with responding pts continuing follow-up.
  • Other evaluations included AEs, safety laboratories, B-cell blood levels (CD19), serum veltuzumab levels, and human anti-veltuzumab antibody (HAHA) titers.
  • RESULTS: Nineteen pts (8M/11F, median age 63), including 14 NHL pts (11 follicular, 3 other indolent NHL; 5 treatment naive) most with stage III or IV disease (11/14) and 5 CLL pts (4 treatment naïve) all with Rai stage II or III disease, have now received SC veltuzumab at 80 mg (3 NHL, 3 CLL), 160 mg (9 NHL, 2 CLL) or 320 mg (2 NHL) dose levels.
  • Pre-treatment with antihistamines or steroids has not been required, and SC veltuzumab was well tolerated with only mild, transient injection site reactions and tenderness.
  • In NHL pts, SC veltuzumab demonstrates good bio-availability, with a slow release pattern over several days and depletion of circulating B cells starting after 1<sup>st</sup> injection.
  • For 7 NHL pts, 4 weeks after treatment with 80 or 160 mg doses, 2 pts had partial responses, 3 pts showed stable disease, and 2 pts had disease progression.
  • For 3 CLL pts who received 80 mg doses, serum veltuzumab levels were lower, but all pts still achieved 65-75% decreases in circulating leukemic cells over the course of treatment.
  • CONCLUSIONS: SC administration of veltuzumab is well tolerated, achieves slow but efficient delivery into the blood, and is pharmacologically active.
  • The low doses currently evaluated in B-cell malignancies show evidence of therapeutic activity, achieving objective responses in NHL and notable reductions in circulating leukemic cells in CLL.

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  • (PMID = 27960927.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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12. Soliman HH, Antonia S, Sullivan D, Vanahanian N, Link C: Overcoming tumor antigen anergy in human malignancies using the novel indeolamine 2,3-dioxygenase (IDO) enzyme inhibitor, 1-methyl-D-tryptophan (1MT). J Clin Oncol; 2009 May 20;27(15_suppl):3004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3004 Background: The limited effect of cancer immunotherapy is due to the tumor's ability to induce host anergy towards its antigens.
  • The preclinical data support the activity of 1-MT in preventing T-cell anergy in TDLN, slowing growth of LLC mouse xenografts, and synergizing with chemotherapy in regression of autochthonous breast tumors in MMTV-Neu mice.
  • This led to a phase I first-in-man trial using 1-MT in solid tumors.
  • Correlative studies include serum kyn/trp levels, T-reg cell quantification by flow, tumor IDO expression by IHC, and humoral immune response using a proprietary tumor antigen microarray.
  • PK results show good bioavailability and a t1/2 of 2-4 hrs.
  • Attributable toxicities were 1 case of grade 1 fatigue and 2 cases of grade 2 hypophysitis.
  • CONCLUSIONS: 1-MT appears to be an active, orally bioavailable, and reasonably well tolerated immunomodulator at 200mg daily.
  • Development of hypophysitis in 2 patients indicates the drug can break tolerance resulting in autoimmunity.

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  • (PMID = 27962050.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Kurosumi M, Kobayashi Y, Takei H: The utility of a real-time RT-PCR assay for the detection of metastases greater than 0.2 mm in sentinel lymph nodes of breast cancer patients confirmed by detailed histological analysis. J Clin Oncol; 2009 May 20;27(15_suppl):628

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The utility of a real-time RT-PCR assay for the detection of metastases greater than 0.2 mm in sentinel lymph nodes of breast cancer patients confirmed by detailed histological analysis.
  • Our study confirms the reliability of the cutoff values of a real-time RT-PCR assay (GeneSearch, Veridex LLC) to detect metastases larger than 0.2 mm by detailed 0.2 mm frozen section histological diagnosis.
  • One half of each LN was used for routine intra-operative diagnosis.
  • These sections were then re-stained immunohistochemically using a pancytokeratin antibody (AE1/AE3) for detecting submicrometastses.
  • Cutoff values were pre-set in a large US study (n = 304).
  • RESULTS: Compared to the histological diagnosis using 0.2 mm interval frozen sections, the real-time RT-PCR results were as follows; sensitivity of 100.0% (34/34), specificity of 93.7% (89/95), and overall accuracy of 95.3% (123/129).

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  • (PMID = 27961430.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Hartmann BL, Winder T, Sandholzer M, Gasser K, Jäger I, Lang AH, Längle M, Hartmann G, Bartenstein C, Luger C: JC papovavirus leukencephalopathy in a patient with B-CLL receiving long-term chemotherapy in combination with an anti-CD20-antibody. J Clin Oncol; 2009 May 20;27(15_suppl):e18007

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] JC papovavirus leukencephalopathy in a patient with B-CLL receiving long-term chemotherapy in combination with an anti-CD20-antibody.
  • METHODS: Our patient was a 64-year-old woman with B-CLL diagnosed in 2000 in state B of Binet treated with 12 cycles of fludarabin until July 2007 in a B-cell and lymphoma-reducing manner.
  • For the reason of progressive disease 3 cycles of rituximab, fludarabin, mitoxantrone, and cyclophosphamide were added (dose reduced causing hematologic toxicity) until October 2007 continuing rituximab once a month up to Mai 2008.
  • RESULTS: In a CT scan mixed response was observed with progressive disease infradiafragmatic and regression supradiafragmatic.
  • Corticosteroids could stop B-symptoms and leads to a distinct shrinkage of the lymphomas within 2 weeks.
  • An MRI of the brain showed subcortical and periventricular lesions with increased signal on T2-weighted and fluid attentuated inversion recovery (FLAIR) suggestive of a vascular origin.
  • Her symptoms progressed by aphasia and weakness of the right leg corresponding to increased size and number of cerebral lesions.
  • CONCLUSIONS: Antibody deficiency syndrome corresponding to CLL under treatment with chemotherapy and rituximab lead to a severe immunosuppression enabling unusual viral infections such as PML.

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  • (PMID = 27963992.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Roberts AW, Wilson W, Gandhi L, O'Connor OA, Rudin CM, Brown JR, Xiong H, Chiu Y, Enschede S, Krivoshik AP: Ongoing phase I studies of ABT-263: Mitigating Bcl-X<sub>L</sub> induced thrombocytopenia with lead-in and continuous dosing. J Clin Oncol; 2009 May 20;27(15_suppl):3505

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ongoing phase I studies of ABT-263: Mitigating Bcl-X<sub>L</sub> induced thrombocytopenia with lead-in and continuous dosing.
  • Ongoing phase 1 studies of ABT-263 show anti-tumor activity in CLL and some lymphomas (Wilson W et al, ASH. 2008).
  • However, thrombocytopenia (TCP) due to on-target Bcl-X<sub>L</sub> inhibition-induced platelet apoptosis is also observed.
  • TCP was a dose limiting toxicity (DLT) in 3 patients (pts) in CLL study M06-873 (N = 15) where starting platelet counts tend to be low.
  • METHODS: CD with a 7 d lead-in dose was explored (150, 150 or 100 mg lead-in doses) with dosing at 200 and 275 mg, 225 and 325 mg, or 125 and 250 mg in studies M06-814 (NHL), M06-822 (SCLC), and M06 873 (CLL), respectively.
  • 2 DLTs were observed for CD, 1 pt per study M06-814 (275 mg) and M06-873 (200 mg) experienced grade 4 (TCP).
  • While CD enrollment and time on study is still limited, anti-tumor activity includes 1 unconfirmed partial response (68% CT regression) in a SLL pt at 275 mg and 3 CLL pts with ≥50% lymphocyte reduction for ≥2 months.

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  • (PMID = 27961281.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Cotter F, Smith DA, Boyd TE, Richards DA, Alemany C, Loesch D, Salogub G, Tidmarsh GF, Gammon GM, Gribben J: Single-agent activity of GCS-100, a first-in-class galectin-3 antagonist, in elderly patients with relapsed chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Single-agent activity of GCS-100, a first-in-class galectin-3 antagonist, in elderly patients with relapsed chronic lymphocytic leukemia.
  • GCS-100 has been shown to induce apoptosis of patient CLL cells ex vivo.
  • In addition, GCS-100 potentiates the in vitro activity of other agents commonly used to treat CLL, including rituximab.
  • This phase II clinical trial evaluated the potential of GCS-100 as a novel single-agent therapeutic for relapsed CLL.
  • METHODS: Patients with Rai Stage II or higher CLL who had relapsed after one or two prior therapies were eligible.
  • Patients received GCS-100 i.v. at 160 mg/m<sup>2</sup> for 5 days every 21 days until disease progression.
  • GCS-100 was well-tolerated.
  • There were no cases of drug-related grade 3 or 4 hematological toxicity or other serious AE.
  • CONCLUSIONS: GCS-100 has significant single-agent activity in relapsed CLL.
  • Its lack of myelosuppression and potential synergy with other agents makes GCS-100 a strong candidate for further development in CLL, particularly for elderly patients for whom there is a major need for less toxic agents.

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  • (PMID = 27961378.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Jones JA, Flynn J, Moran M, Lin T, Byrd J: Trends in pneumonia (PNA) hospitalization among patients (pts) with chronic lymphocytic leukemia (CLL). J Clin Oncol; 2009 May 20;27(15_suppl):e20500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trends in pneumonia (PNA) hospitalization among patients (pts) with chronic lymphocytic leukemia (CLL).
  • : e20500 Background: Despite recent therapeutic advances, PNA remains a significant source of morbidity and mortality among CLL pts.
  • Nationwide Inpatient Sample and ICD-9CM diagnosis codes, we identified all non-governmental hospitalizations of CLL pts for a primary dx of PNA in calendar years 1994 and 2004.
  • Admissions were described by pt demographics (age, gender, race) and comorbidity (Charlson index, presence of chronic lung disease).
  • Ten-year prevalence estimates for CLL were obtained from NCI SEER data and used as denominators in incidence calculations.
  • RESULTS: PNA was the primary dx for 7316 (13.1%) and 7651 (11.2%) CLL pt admissions in 1994 and 2004, respectively.
  • CLL pts admitted in 2004 were older (75.7 v. 74.2 years, p<0.001) and more likely to have at least one Charlson comorbidity (67.6% v. 56.2%, p<0.001) or comorbid chronic lung disease (40.6% v. 28.3%, p<0.001) than pts in 1994.
  • Intubation was rare in both cohorts (<1%) and did not significantly differ by year, but in-hospital mortality was significantly higher in 2004 (11.3% v. 8.2%, p=0.005).
  • However, LOS decreased significantly between 1994 and 2004 (9.2 v. 6.4 days, p<0.001).
  • CONCLUSIONS: PNA hospitalization rates for CLL pts have not significantly increased over the last decade despite more aggressive therapies, likely secondary to improved supportive care.
  • However, CLL pts hospitalized for PNA are now older, increasingly likely to suffer from chronic medical illness, and significantly more likely to die while in hospital.

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  • (PMID = 27960954.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Ganesan P, Raina V, Kumar R: A phase II pilot study of valproic acid in relapsed/refractory chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7081

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II pilot study of valproic acid in relapsed/refractory chronic lymphocytic leukemia.
  • : 7081 Background: Valproic acid (VA) has demonstrated cell-kill by triggering pro-apoptotic pathways in chronic lymphocytic leukemia (CLL) in preclinical studies.
  • We studied the safety and efficacy of VA in patients with relapsed and refractory CLL.
  • METHODS: Adult patients with CLL diagnosed by the NCI-WG criteria who had received at least one previous fludarabine-based therapy and subsequently progressed or relapsed with ECOG performance status (PS) ≤3 and normal organ functions were included.
  • RESULTS: Five patients have so far been included, age 48-70 years (mean 62 years); sex: 3 males/ 2 females; disease duration: 2-16 years (mean 5.4 years).
  • One patient had partial response and one had stable disease.
  • Grade 3 hypersensitivity skin rashes developed in one patient at one month and the therapy was discontinued.
  • Most patients had mild drowsiness and two patients had significant weight gain of grade 2.
  • CONCLUSIONS: VA produces very impressive palliation in advanced/ refractory CLL in terms of improvement of hemoglobin, ANC, platelets, PS, and a reduction in the number of infective episodes -apparently a sequel to significant rise in neutrophils.

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  • (PMID = 27961474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Cadoo KA, Lowery MA, Cumiskey J, McCaffrey J, Carney DN: Long term follow-up of primary B and T cell non-Hodgkin's lymphoma (NHL) of the gastrointestinal (GI) tract. J Clin Oncol; 2009 May 20;27(15_suppl):e19516

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long term follow-up of primary B and T cell non-Hodgkin's lymphoma (NHL) of the gastrointestinal (GI) tract.
  • : e19516 Background: Anthracycline based chemotherapy is the treatment of choice for aggressive primary lymphomas of the GI tract, with surgery reserved for management of complications.
  • We report long term follow up of 71 cases of primary GI NHL treated with chemotherapy and/or surgery.
  • Median age at diagnosis was 60 (15-83).
  • 52 (73%) were DLBCL, 11 (16%) were T-cell, 8 (11%) were MALT.
  • Of the aggressive lymphomas (63), all patients with T cell lymphoma had small bowel as primary site and histological evidence of celiac associated enteropathy, even in the absence of known celiac disease.
  • Primary sites of DLBCL were stomach 35 (67%), small bowel 11 (21%) & colon 6 (12%).
  • 39 (62%) patients underwent surgery at diagnosis due to acute presentation with perforation, bleeding or obstruction, or to obtain histology.
  • Following confirmed diagnosis, 61 patients received anthracycline based chemotherapy.
  • 2 patients with T cell lymphoma presented with perforation, were treated with surgery only and died of rapid disease progression.
  • Of the 63 patients with aggressive NHL, 37 (59%) remain alive & disease free at median follow up of 13 years (1-24).
  • 35 (67%) patients with DLBCL are alive & disease free.
  • Only 2 (18%) of the T cell lymphomas are alive & disease free.
  • All deaths in the T cell group were due to progressive disease.
  • CONCLUSIONS: Patients with aggressive primary B cell GI NHL have almost 70 % survival following anthracycline based chemotherapy.
  • However, in contrast, coeliac enteropathy associated T-cell lymphomas present with rapidly progressive disease & have a survival of < 20% with chemotherapy and/or surgery.

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  • (PMID = 27960953.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Ghosh J, Kumar L, Saxena R, Raina V, Sharma A, Gupta R, Vivekanandhan S, Sreenivas V, Verma R: A study of the prevalence and type of anemia in lymphoid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):e19556

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A study of the prevalence and type of anemia in lymphoid malignancies.
  • : e19556 Background: Anemia is a common and serious problem in patients with lymphoid malignancy.
  • METHODS: Newly diagnosed patients of lymphoid malignancy- non Hodgkins lymphoma (NHL), Hodgkins lymphoma (HL), and chronic lymphocytic leukemia (CLL) aged more than 15 years without renal failure and who had not received blood transfusion, iron, folic acid or vitamin B complex in the last 2 weeks were analyzed.
  • Of the anemic patients (hemoglobin <11gm/dl), 46 were studied for the type of anemia.
  • Anemia was categorized as due to either autoimmune hemolytic anemia (AIHA)-DCT positive with evidence of hemolysis on PBS, B12 and folate deficiency (<200 pgm/ml and < 4ngm/ml respectively), iron deficiency anemia (IDA)- psat <20% and SF315μgm/dl, anemia of chronic disease (ACD)-psat200μgm/L, a combination of IDA and ACD -psat <20%, SF -30-200 with TIBC ≤315 μgm/dl.
  • RESULTS: The prevalence of anemia in patients with lymphoid malignancy was 42.41% (134 /316, 95% CI-36.96% -47.85%).
  • CONCLUSIONS: Although anemia of chronic disease is the most common cause of anemia in patients with lymphoid malignancy, it is multifactorial in a large number of patients and hence it is important to rule out other causes of anemia like nutritional and AIHA in these patients.

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  • (PMID = 27961090.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Sola CB, Silva L, Saliba R, De Lima M, Giralt S, Qazilbash M, Champlin R, Khouri I, Popat U, Hosing C: Outcomes of autologous bone marrow transplantation in non-Hodgkin's lymphoma patients who failed peripheral blood stem cell mobilization. J Clin Oncol; 2009 May 20;27(15_suppl):7040

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes of autologous bone marrow transplantation in non-Hodgkin's lymphoma patients who failed peripheral blood stem cell mobilization.
  • : 7040 Background: Patients (pts) with relapsed/refractory non-Hodgkin's lymphoma (NHL) who fail to mobilize adequate peripheral blood stem cells (PBSC) often undergo bone marrow (BM) harvest for autologous transplantation.
  • METHODS: In this retrospective study (May 1996-September 2006), we identified 36 out of a total of 750 pts with advanced NHL, who failed to collect adequate PBSC and subsequently underwent BM harvest followed by ABMT.
  • Histology was intermediate grade in 31 (86%) patients and low grade in 5 (14%).
  • Twelve pts (35%) had history of BM involvement with lymphoma.
  • At the time of stem cell mobilization 18 (50%) were in complete remission (CR), 13 (37%) were in partial remission (PR) and 5 (13%) had progressive disease (PD).
  • RESULTS: The median total nucleated cell dose and CD34+ cell dose harvested/kg were 3.72 x 10<sup>8</sup> (range 0.25-58.0) and 1.6 x 10<sup>6</sup> (range 0.03-5.8), respectively.
  • After ABMT, 33 of 35 evaluable (94%) pts engrafted neutrophils with median time to ANC 0.5 x 10<sup>9</sup>/L of 23 days (range 8-47).
  • Median time to platelet count 20 x 10<sup>9</sup>/L was 63 days (range 11-375).
  • After ABMT, 25/36 (70%) pts achieved a CR.
  • After a median follow-up of 34 months (range 0.4-100), the 3-year OS and DFS were 47% and 35%, respectively.
  • Causes of death were: disease progression/relapse in 15 (60%), secondary malignancy in 3 (12%), multiorgan failure in 5 (20%), and unknown in 2 (8%).
  • Although the CR rate after transplant is high, the NRM is higher than expected.

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  • (PMID = 27961403.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Wilson W, O'Connor OO, Roberts AW, Czuczman M, Brown J, Xiong H, Xiong H, Chiu Y, Krivoshik A, Enschede S, Humerickhouse R: ABT-263 activity and safety in patients with relapsed or refractory lymphoid malignancies in particular chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL). J Clin Oncol; 2009 May 20;27(15_suppl):8574

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABT-263 activity and safety in patients with relapsed or refractory lymphoid malignancies in particular chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL).
  • : 8574 Background: ABT-263, a novel, orally bioavailable, BH3 mimetic, binds with high affinity (K<sub>i</sub> ≤ 1nM) and inhibits multiple antiapoptotic Bcl-2 family proteins.
  • ABT-263 displays activity (EC<sub>50</sub> ≤ 1μM) against human lymphoid and small cell lung cancer cell lines.
  • Mechanism based preclinical toxicities include reductions in circulating lymphocytes, apoptosis of circulating platelets, and decreased spermatogenesis, mediated by inhibition of Bcl-2, Bcl-X<sub>L</sub>, and Bcl-w, respectively.
  • METHODS: Safety and activity of ABT-263 in 2 enrolling phase I studies in relapsed/refractory lymphoid malignancies (M06-814) and CLL (M06-873) was evaluated.
  • Patients (pts) were dosed on days 1-14 of a 21 d cycle, 10-440mg (M06-814) or 10-250mg (M06-873).
  • Among 27 CLL/SLL pts, 3 have confirmed radiographic partial responses (PR) (99%, 92% and 72%) and 2 have unconfirmed regressions, 51% and 72%.
  • 6 pts maintained a ≥50% decrease in circulating lymphocytes for ≥ 2 months and 11 pts have stable disease; of these 5 experienced minor radiographic responses (range of 36% to 49%).
  • In addition, among 40 (M06-814) lymphoma pts, 3 with follicular lymphoma achieved PR and one had a minor response (49% regression).
  • With CD dosing (16 pts), activity includes 1 unconfirmed PR in SLL & and 3 CLL pts with ≥50% lymphocyte reduction for ≥2 months duration.
  • Pharmacodynamic toxicities included dose-dependent thrombocytopenia (TCP) resulting from on-target activity against Bcl-X<sub>L</sub>.
  • Dose limiting toxicities, 14/21 d dosing, in M06-814 occurred at 160mg (bronchitis), 315mg (elevated ALT and grade 4 TCP) and 440mg (worsening pleural effusion in a pt with underlying afib), and in M06-873 at 110mg (tumor lysis and grade 4 TCP) and 250mg (grade 4 TCP).
  • CONCLUSIONS: ABT-263 showed favorable PK and safety profiles with anti-tumor activity in relapsed/refractory CLL/SLL and follicular lymphoma.

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  • (PMID = 27962273.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Durbecq V, Majjaj S, Nogaret J, Sirtaine N, Schobbens J, Noterman D, Hertens D, Filipov V, Larsimont D, Veys I: Use of quantitative RT-PCR assay to predict metastases size of sentinel node from breast cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):621

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 621 Background: A RT-PCR Assay (GeneSearch, Veridex, LLC), FDA approved and CE marked to detect metastases > 0.2 mm in sentinel lymph nodes (SLNs) of breast cancer patients, has been in clinical use in our institute for 25 months.
  • An additional 74 patients were tested in a pilot study.
  • The marker Ct values are correlated with metastases size as determined by H&E on adjacent node pieces (r = -0.74 for MG and -0.77 for CK19, p < 0.001).
  • For example when CK19 and MG < 24 Cts, the non-SLN positivity rate jumps from 29% to 58%.

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  • (PMID = 27961419.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Baum PR, Cerveny C, Gordon B, Nilsson C, Wiens J, Rafiq S, Lapalombella R, Muthusamy N, Byrd JC, Wahl A: Evaluation of the effect of TRU-016, an anti-CD37 directed SMIP in combination with other therapeutic drugs in models of non-Hodgkin's lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8571

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the effect of TRU-016, an anti-CD37 directed SMIP in combination with other therapeutic drugs in models of non-Hodgkin's lymphoma.
  • : 8571 Background: TRU-016, a single chain anti-CD37 Fc fusion molecule has been shown to display pro-apoptotic and Fc-dependent cellular cytotoxicity activities against primary CLL cells and NHL cell lines.
  • The pro-apoptotic signal generated by TRU-016 binding to CD37 on CLL cells has been shown to be caspase-independent and distinct from the signal generated by many other therapeutics including rituximab.
  • We have tested drug combinations using the mantle cell lymphoma line Rec-1 and diffuse large B-cell lymphoma line SU-DHL-6 in vitro and extended these results to in vivo settings using the follicular lymphoma cell line DOHH2 treated with the combination of TRU-016 and bendamustine.
  • METHODS: To determine TRU-016 interactions with the established therapeutics rituximab, doxorubicin, rapamycin, and bendamustine, drugs were tested alone or in combination with TRU-016 and the anti-proliferative effects on cell lines measured after 96 hours.
  • To determine if in vitro synergy could be recapitulated in vivo, SCID mice were implanted with DOHH2 cells and therapeutic treatment was initiated when tumor volumes reached 200 mm<sup>3</sup>.
  • This demonstrates that the in vitro synergy results were extendable to a more complex in vivo disease model.
  • CONCLUSIONS: TRU-016 in combination with rituximab, rapamycin, or bendamustine increases cell killing of NHL cells.
  • Furthermore, the combination of TRU-016 and bendamustine displayed greater in vivo anti-tumor activity than either agent alone against a follicular lymphoma tumor model.

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  • (PMID = 27961015.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Ramaswamy B, Phelps M, Baiocchi R, Bekaii-Saab T, Wilkins D, Arbogast D, Campbell A, Doyle AL, Grever M, Shah M: A phase I study of flavopiridol using an alternative schedule in patients (pts) with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2580

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2580 Background: A phase I study of flavopiridol, a cyclin-dependent kinase inhibitor, using an alternative schedule was conducted in pts with solid tumors given its promising activity in pts with chronic lymphocytic leukemia (CLL).
  • DLT was defined as Gr 4 hematologic toxicity (HT) for > 7 days, > Gr 3 non-HT except Gr 3 fatigue or diarrhea resolving <4 days and cytokine release syndrome (CRS) > Gr 3 despite steroids.
  • Due to a grade 5 CRS/death in cohort 3, the protocol was amended to include 20 mg IV dexamethasone prior to flavopiridol to prevent CRS (cohorts 2B, 1B).
  • Of the 20 evaluable pts, 35% had stable- and 65% had progressive-disease.
  • CONCLUSIONS: There was a higher frequency of CRS, despite prophylactic steroids seen our pts with solid tumors compared to previous studies with CLL and this correlated with AUC.

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  • (PMID = 27961903.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Ramanarayanan J, Pahuja S, Elefante AN, Hernandez-Ilizaliturri FJ: Abrogation of tumor necrosis alpha (TNF-alpha) pathway by anti-TNF therapy in hematological malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7093

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: We reviewed the English literature by conducting systematic MEDLINE using the terms TNF-, infliximab, adalimumab, etanercept, cancer therapy, hematologic malignancies, myelodysplastic syndrome (MDS), multiple myeloma (MM), myeloproliferative disease (MPD), chronic lymphocytic leukemia (CLL), and lymphoma from January 2001 to August 2008.
  • RESULTS: Overall 11 phase I and II studies (n = 237; CLL n = 44, MM n = 10, MDS n = 109, MPD n = 51, HCL n = 3, TCL 13, FL 7) that involved anti-TNF- therapy in hematological malignancies were identified.
  • In conjunction with ATG or azacitidine in low-/intermediate-risk MDS, TNF inhibitors resulted in improvement in cytopenia.
  • No significant clinical benefit was seen among lymphoproliferative disorders, but treatment was well tolerated.

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  • (PMID = 27961263.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Kumar A, Mhaskar A, Vadaparampil S, Djulbegovic B, Quinn G, Moffitt Fertility Preservation Group: Fertility preservation and timing of cancer treatment. J Clin Oncol; 2009 May 20;27(15_suppl):e20629

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 3 RCTs assessed the efficacy of early versus deferred treatment in prostate cancer, 3 in multiple myeloma, and 1 each in lung cancer and chronic lymphocytic leukemia (CLL).
  • There was no survival difference between early and deferred treatment in multiple myeloma (HR=1.11,95%CI 0.67-1.84), CLL (HR=0.89,95%CI 0.49-1.59) or lung cancer (HR=0.95,95%CI 0.72-1.24).

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  • (PMID = 27961594.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Lu L, Schafer P, Bartlett JB: Inhibition by lenalidomide of growth factor and hypoxia-induced signaling in endothelial and epithelial tumor cells, and effects within the tumor cell microenvironment. J Clin Oncol; 2009 May 20;27(15_suppl):e14620

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition by lenalidomide of growth factor and hypoxia-induced signaling in endothelial and epithelial tumor cells, and effects within the tumor cell microenvironment.
  • Lenalidomide studies in CLL and MM suggest that it may also attenuate pro-survival signals generated by interaction of stroma with the malignant cell itself.
  • Ovarian cancer cell lines SKOV-3 and OVCAR-3 were treated with LPA and the effect of lenalidomide on invasiveness via enhanced p-Akt was investigated.
  • Treatment of ovarian tumor cells with LPA increased tumor cell invasiveness via enhanced p-Akt.
  • Lenalidomide strongly inhibited invasion and p-Akt (at S308 but not T473) in a dose-dependent manner.

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  • (PMID = 27964203.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Byrd JC, Lapalombella R, Ramanunni A, Andritsos LA, Flynn JM, Baum P, Thompson P, Muthusamy N: Effect of CD37 small modular immuno-pharmaceutical (SMIP) on direct apoptosis in chronic lymphocytic leukemia cells via transcriptional up-regulation of the BH3 family member BIM. J Clin Oncol; 2009 May 20;27(15_suppl):3035

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of CD37 small modular immuno-pharmaceutical (SMIP) on direct apoptosis in chronic lymphocytic leukemia cells via transcriptional up-regulation of the BH3 family member BIM.
  • A novel CD37<sup>SMIP</sup> was previously demonstrated to mediate superior direct apoptosis and NK-cell mediated killing of chronic lymphocytic leukemia (CLL) and other B-cell malignancies.
  • METHODS: Given the superior in vitro apoptosis observed with CD37<sup>SMIP</sup> treatment and early clinical activity observed in highly refractory CLL patients, we hypothesized that a unique mechanism of cell killing was utilized by CD37<sup>SMIP</sup>.
  • RESULTS: Unlike many other agents utilized to treat CLL, death mediated by CD37<sup>SMIP</sup> does not depend upon caspase activation.
  • Nonetheless, CD37<sup>SMIP</sup> treatment of CLL cells promotes time-dependent induction of mitochondrial membrane depolarization, mitochondrial translocation of Bax, and up-regulation of Bim protein.
  • CD37<sup>SMIP</sup> Bim protein induction occurred concomitantly with an increase in BIM mRNA levels.
  • Electrophoretic mobility shift assay using oligonucleotides of the BIM promoter demonstrated increased protein binding activity in nuclear extracts derived from CD37<sup>SMIP</sup> treated cells and the physical interaction of FoxO3a transcription factor with the FoxO3a responsive element in the BIM promoter was demonstrated using a "protein pull down" assay and confirmed by chromatin immunoprecipitation assays.
  • Furthermore, CD37<sup>SMIP</sup> treatment significantly increased BIM promoter regulated luciferase reporter expression in B-CLL cells.
  • Consistent with a primary role of Bim up-regulation in mitochondrial membrane destabilization and apoptosis, transfection of CLL cells with BIM siRNA resulted in inhibition of CD37<sup>SMIP</sup>-induced mitochondrial membrane depolarization and apoptosis.
  • CONCLUSIONS: These studies demonstrate CD37<sup>SMIP</sup> mediated apoptosis in CLL cells occurs via FoxO3a-dependent transcriptional up-regulation of BIM protein.
  • This distinct mechanism of apoptosis utilized by CD37<sup>SMIP</sup> contrasts it with other agents used for CLL treatment.
  • Additionally, it provides a mechanism for the promising clinical activity of TRU-016 (humanized CD37<sup>SMIP</sup>) observed to date in refractory CLL patients.

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  • (PMID = 27962079.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Wierda WG, Kipps T, Mayer J, Stilgenbauer S, Robak T, Williams CD, Furman R, Chan G, Russell C, Österborg A, 406 Study Investigators: Activity of ofatumumab, a novel CD20 mAb, and prior rituximab exposure in patients with fludarabine- and alemtuzumab-refractory or bulky fludarabine-refractory chronic lymphocytic leukemia (CLL). J Clin Oncol; 2009 May 20;27(15_suppl):7044

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of ofatumumab, a novel CD20 mAb, and prior rituximab exposure in patients with fludarabine- and alemtuzumab-refractory or bulky fludarabine-refractory chronic lymphocytic leukemia (CLL).
  • : 7044^ Background: Salvage therapy has limited activity (20-26% overall response rate [ORR]) in patients (pts) with CLL refractory to fludarabine and alemtuzumab (double-refractory, DR) or refractory to fludarabine with bulky (>5 cm) lymphadenopathy (bulky fludarabine-refractory, BFR).
  • Ofatumumab (OFA) is a fully human mAb that targets a unique small-loop epitope of CD20 close to the cell surface and elicits more potent in vitro complement-dependent cytotoxicity of B-cell lines and tumor cells vs rituximab (RTX).
  • To determine whether prior RTX exposure impacted activity of OFA in pts with DR or BFR CLL, an analysis was performed to assess efficacy by prior RTX exposure in pts treated with OFA in an international, pivotal study.
  • METHODS: Pts with DR or BFR CLL received 8 weekly infusions of OFA followed by 4 monthly infusions (Dose 1, 300 mg; Doses 2-12, 2,000 mg).
  • Secondary efficacy endpoints included progression-free survival (PFS) and overall survival (OS).
  • Median PFS (95% CI) was 5.7 mo (4.5, 8.0) and 5.9 mo (4.9, 6.4), and median OS (95% CI) was 13.7 mo (9.4, NYR) and 15.4 mo (10.2, 20.2), respectively.
  • CONCLUSIONS: Single-agent therapy with OFA is effective in pts with DR or BFR CLL, irrespective of prior CD20 mAb therapy with RTX.
  • Among the circumstances that might justify an exception are that the principal investigator (1) is a widely acknowledged expert in a particular therapeutic area;.
  • (2) is the inventor of a unique technology or treatment being evaluated in the clinical trial; or (3) is involved in international clinical oncology research and has acted consistently with recognized international standards of ethics in the conduct of clinical research.

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  • (PMID = 27961407.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Castro JE, Sandoval-Sus JD, Melo-Cardenas J, Darrah D, Urquiza M, Pakbaz RS, Prussak CE, Kipps TJ: Phase I study of intranodal direct injection of adenovirus encoding recombinant CD40-ligand (Ad-ISF35) in patients with chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):3003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of intranodal direct injection of adenovirus encoding recombinant CD40-ligand (Ad-ISF35) in patients with chronic lymphocytic leukemia.
  • : 3003 Background: Transduction of chronic lymphocytic leukemia (CLL) cells with replication-defective adenovirus (Ad) encoding a genetically engineered, membrane-stablized CD154 (ISF35) converts transduced, and "bystander" non-transduced, CLL cells into proficient antigen presenting cells that can induce immunity against autologous leukemia cells.
  • Preclinical studies demonstrated that direct injection of Ad-ISF35 into lymphoma nodules can induce potent anti-lymphoma immune responses in test animals, capable of eradicating lethal tumors at distal sites and protect against recurrent disease upon subsequent re-challenge with syngeneic tumor.
  • Pts, ages 45-71 yrs, with rapidly progressive disease (median CLL doubling time of 3.7 months) each received a single ultrasound guided IDI of 1 to 30 x 10<sup>10</sup> Ad-ISF35 viral particles in 4 different dose cohorts.
  • RESULTS: IDI of Ad-ISF35 was well-tolerated and effective in inducing systemic responses.
  • Some pts had grade ≤ 2 injection-site erythema, pain and/or swelling, or flu-like symptoms.
  • Some pts in the highest-dose cohorts had transient, asymptomatic grade 3/4 hypophosphatemia.
  • No long-term (≥ 6 wk) adverse effects were observed.
  • Although there was no evidence for dissemination of Ad-ISF35 beyond the injected lymph node, IDI of Ad-ISF35 induced blood CLL cells to express death receptors, pro-apoptotic proteins, and immune co-stimulatory molecules similar to those induced on "bystander" CLL cells co-cultured with Ad-ISF35 transduced cells in vitro.
  • Importantly, IDI of Ad-ISF35 resulted in significant reductions in blood leukemia cell counts and a median reduction of 53.2% (range 25-75.4%) in the size of lymph nodes and/or spleen, which was durable (≥ 4 months) in 9 pts.
  • Despite aggressive disease prior to treatment, the median treatment-free survival was 5.3 months and 3 pts have yet to require additional treatment after 1-year follow-up.
  • CONCLUSIONS: Single IDI of Ad-ISF35 was safe and effective in inducing systemic biologic and clinical responses in pts with CLL.
  • IDI of Ad-ISF35 might be effective in the treatment of CLL and related lymphomas.

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  • (PMID = 27962049.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Kipps TJ, Österborg A, Mayer J, Stilgenbauer S, Hellmann A, Williams CD, Furman R, Chan G, Russell C, Wierda WG, 406 Study Investigators: Clinical improvement with a novel CD20 mAb, ofatumumab, in fludarabine-refractory chronic lymphocytic leukemia (CLL) also refractory to alemtuzumab or with bulky lymphadenopathy. J Clin Oncol; 2009 May 20;27(15_suppl):7043

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical improvement with a novel CD20 mAb, ofatumumab, in fludarabine-refractory chronic lymphocytic leukemia (CLL) also refractory to alemtuzumab or with bulky lymphadenopathy.
  • : 7043 Background: Patients (pts) with CLL refractory tofludarabine and alemtuzumab (double-refractory, DR) or refractory to fludarabine with bulky (>5 cm) lymphadenopathy (bulky fludarabine-refractory, BFR) have a poor prognosis.
  • Ofatumumab is a human mAb specific for a distinctive small-loop epitope of CD20 that appears more potent than rituximab in eliciting complement-dependent lysis of B cells in vitro.
  • We report, for the first time, results from the planned interim analysis of the clinical benefit observed in pts with DR or BFR CLL treated with ofatumumab in an international pivotal clinical study.
  • METHODS: Pts with DR or BFR CLL received 8 weekly then 4 monthly ofatumumab infusions (Dose 1, 300 mg; Doses 2-12, 2,000 mg).
  • RESULTS: Of 138 treated pts (DR: N = 59; BFR: N = 79; median age 64 and 62 yrs, respectively), 63% had Rai stage III/IV disease at screening.
  • Resolution of disease symptoms (maintained for ≥2 mo) were observed in a large proportion of pts (Table), including in pts considered nonresponders by NCI-WG criteria.
  • Pts with thrombocytopenia at baseline (n = 73) experienced sustained increases in median platelet counts from 65 × 10<sup>9</sup>/L to over 100 × 10<sup>9</sup>/L by Wk 8; a similar pattern of rapid improvement was observed in Hgb values.
  • CONCLUSIONS: Ofatumumab as single-agent achieves high ORR, and improves disease symptoms and hematologic parameters in heavily pretreated pts with DR and BFR disease who lack standard treatment options.

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  • (PMID = 27961406.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Grubbs SS, Gonzalez M, Krasna M, Siegel R, Bryant D, Tschetter L, Hayenga L, Duggan B, St Germaine D, Denicoff A: Tracking clinical trial accrual strategies and barriers via a Web-based screening tool. J Clin Oncol; 2009 May 20;27(15_suppl):6586

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tracking clinical trial accrual strategies and barriers via a Web-based screening tool.
  • : 6586 Background: The National Cancer Institute Community Cancer Centers Program (NCCCP) has developed a web based tracking tool to monitor screening of patients for clinical trial participation.
  • METHODS: Seven NCCCP sites utilized the log during the 60 day open accrual period for the Wake Forrest WFU 07-02-03 cancer control trial (chronic lymphocytic leukemia COLD- fX) in Novermber 2008 and December 2008.
  • RESULTS: 327 chronic lymphocytic leukemia patients were screened mostly by chart review.

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  • (PMID = 27963861.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Colantuoni M, Matano E, Alfieri S, De Placido S, Carlomagno C: Guillain-Barre Syndrome Associated with Gastric Cancer: Paraneoplastic Syndrome or Immunological Disorder? World J Oncol; 2010 Dec;1(6):247-249

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Guillain-Barre Syndrome Associated with Gastric Cancer: Paraneoplastic Syndrome or Immunological Disorder?
  • Paraneoplastic Guillain-Barre syndrome has been described in association with some kinds of tumors (B-cell Lymphoma and small cell lung cancer).
  • We describe the case of a 74-year-old woman affected by gastric adenocarcinoma, treated with surgery and adjuvant chemotherapy, who developed simultaneously skin cancer relapse and severe Guillain-Barre syndrome.
  • Although the timing of clinical presentation suggests a paraneoplastic origin, other interesting features were present in this patient such as familial and personal anamnesis for autoimmune disease, HCV infection, and neurotoxic chemotherapy.

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  • (PMID = 29147216.001).
  • [ISSN] 1920-454X
  • [Journal-full-title] World journal of oncology
  • [ISO-abbreviation] World J Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Keywords] NOTNLM ; Gastric cancer / Guillain Barre syndrome / Paraneoplastic syndrome
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35. Samuel S, Tumilasci VF, Oliere S, Liên-Anh Nguyên T, Shamy A, Bell J, Hiscott J: VSV Oncolysis in Combination With the BCL-2 Inhibitor Obatoclax Overcomes Apoptosis Resistance in Chronic Lymphocytic Leukemia. Mol Ther; 2010 Dec;18(12):2094-2103

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] VSV Oncolysis in Combination With the BCL-2 Inhibitor Obatoclax Overcomes Apoptosis Resistance in Chronic Lymphocytic Leukemia.
  • In chronic lymphocytic leukemia (CLL), overexpression of antiapoptotic B-cell leukemia/lymphoma 2 (BCL-2) family members contributes to leukemogenesis by interfering with apoptosis; BCL-2 expression also impairs vesicular stomatitis virus (VSV)-mediated oncolysis of primary CLL cells.
  • In the effort to reverse resistance to VSV-mediated oncolysis, we combined VSV with obatoclax (GX15-070)'a small-molecule BCL-2 inhibitor currently in phase 2 clinical trials'and examined the molecular mechanisms governing the in vitro and in vivo antitumor efficiency of combining the two agents.
  • In combination with VSV, obatoclax synergistically induced cell death in primary CLL samples and reduced tumor growth in severe combined immunodeficient (SCID) mice-bearing A20 lymphoma tumors.
  • Combination treatment triggered the release of BAX from BCL-2 and myeloid cell leukemia-1 (MCL-1) from BAK, whereas VSV infection induced NOXA expression and increased the formation of a novel BAX-NOXA heterodimer.
  • These studies offer insight into the synergy between small-molecule BCL-2 inhibitors such as obatoclax and VSV as a combination strategy to overcome apoptosis resistance in CLL.

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  • [Copyright] Copyright © 2010 The American Society of Gene & Cell Therapy. Published by Elsevier Inc. All rights reserved.
  • (PMID = 28160637.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • : e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • To determine if cytogenetic abnormalities are present in MSC from CLL patients, we analyzed karyotypes of MSC from 13 CLL patients and 5 normal subjects.
  • METHODS: Stromal cells from marrow core biopsies of 13 CLL patients and 5 normal control subjects were isolated, cultured and confirmed as MSC based on their immunophenotype and capacity to differentiate into three lineages.
  • After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.
  • For each CLL patient, interphase FISH analysis to detect the common CLL-associated abnormalities was performed on freshly isolated peripheral blood mononuclear cells (PBMC).
  • RESULTS: Clonal cytogenetic abnormalities of the cultured MSC were observed in 6 of 13 CLL patients (46%) and 3 of 5 control subjects (60%).
  • The 6 CLL MSC had different clonal abnormalities than the PBMC CLL FISH studies.
  • One CLL MSC exhibited trisomy 5, one exhibited trisomy 8, and one had monosomy X clone.
  • There was no correlation of the chromosomal abnormalities in CLL MSC with clinical stage.
  • CONCLUSIONS: Marrow MSC derived from CLL patients and normal subjects do show an array of cytogenetic abnormalities including clonal chromosomal abnormalities.
  • However the genetic abnormalities found in both CLL and normal MSC could represent acquired genomic instability associated with advanced age, rather than oncogenesis associated with CLL.

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  • (PMID = 27963169.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Tsimberidou AM, Wierda WG, Plunkett WK, O'Brien S, Lerner S, Smith SC, Kantarjian HM, Keating MJ: Phase I/II study of oxaliplatin, fludarabine, cytarabine, and rituximab in patients (OFAR2) with Richter's syndrome (RS), and relapsed or refractory B-cell chronic lymphocytic leukemia (CLL). J Clin Oncol; 2009 May 20;27(15_suppl):7031

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of oxaliplatin, fludarabine, cytarabine, and rituximab in patients (OFAR2) with Richter's syndrome (RS), and relapsed or refractory B-cell chronic lymphocytic leukemia (CLL).
  • : 7031 Background: The first Phase I-II clinical trial of oxaliplatin, fluradabine, Ara-C, and rituximab (OFAR1) demonstrated significant activity in refractory CLL and RS (Tsimberidou et al, J Clin Oncol, 2008;26:196).
  • To enhance the response rate with a decrease in myelosuppression, the dose of oxaliplatin was increased to 30 mg daily, the dose of Ara-C was decreased to 0.5g/m<sup>2</sup> daily and the optimal number of days of fluradabine and Ara-C administration was explored (OFAR2).
  • METHODS: The OFAR2 regimen consisted of oxaliplatin 30mg/m<sup>2</sup>, D1-4; fludarabine 30mg/m<sup>2</sup>, Ara-C 0.5 g/m<sup>2</sup>; rituximab 375mg/m<sup>2</sup>, D3; and pelfigrastim 6mg D6.
  • DLTs were noted in 2/3 pts in dose level 3 (G4 diarrhea, 1; G4 neutropenic sepsis, 1), therefore level 2 was the MTD.
  • Forty-three pts were treated in the Phase II portion of the study (relapsed CLL, 35; RS, 8).
  • The median age was 64 yrs (range, 40- 81); 50 (91%) had β2-microglobulin > 3 mg/L; platelets were < 100 x10<sup>9</sup>/L in 22 pts; and 44 pts had > 1 prior therapies.
  • Eleven pts underwent stem cell transplantation as postremission or salvage therapy.

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  • (PMID = 27961393.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Goldman S, Coiffier B, Reiter A, Younes A, Cairo MS, International TLS Expert Panel: A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel. J Clin Oncol; 2009 May 20;27(15_suppl):e17575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Additionally, we recently reported an evidence based review of guidelines for the P and T of TLS (Coiffier et al, J Clin Oncol. 2008).
  • Rasburicase (R), a recombinant urate oxidase, results in a more rapid and total reduction of uric acid (UA) compared to allopurinol (A) in children at high-risk of TLS (Goldman/Cairo et al, Blood.
  • METHODS: We convened an international panel (N = 17) of experts in pediatric and adult hematological malignancies and solid tumors (ST) to develop a medical decision tree for the P and T of TLS based on the risk classification (low, medium, high) and management recommendations of Coiffier et al (J Clin Oncol.
  • 2008) Results: Patients without evidence of LTLS were assigned to either low-risk disease (LRD), medium-risk (MRD), or high-risk (HRD).
  • Risk factors included pathological classification stage, bulk, disease burden (WBC/LDH) and renal impairment/involvement.
  • HRD was assigned to patients with either B-ALL, ALL/AML ≥100K/mm<sup>3</sup>, BL/LL stage III/IV, and/or high LDH, DLBCL/PTCL/MCL/ATL with bulky and elevated LDH and patients with MRD with renal impairment/involvement.
  • MRD consisted of ALL ≤100K/mm<sup>3</sup>, AML 25-100K/mm<sup>3</sup>, BL/LL stage I/II and low LDH, childhood ALCL, DLBCL/PTCL/MCL/ATL non-bulky but elevated LDH, CLL treated with targeted therapy, and LRD with renal impairment/involvement.
  • LRD consisted of ST (except bulky sensitive to cytotoxic therapy [MRD]), CML, MM, HL, other NHL and AML <25K/mm<sup>3</sup>.
  • CONCLUSIONS: This medical decision tree will facilitate the practice of management of the P and T of TLS and hopefully improve the quality of care in a cost effective manner.

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  • (PMID = 27963935.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Townsend AR, Millward M, Price T, Mainwaring P, Spencer A, Longenecker A, Palladino MA, Lloyd GK, Spear MA, Padrik P: Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm). J Clin Oncol; 2009 May 20;27(15_suppl):3582

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm).
  • : 3582 Background: The novel structure (non-peptide based) of NPI-0052 (NPI) appears to lead to unique proteasome inhibition (PI), toxicology and signal transduction profiles.
  • Preclinical research suggests improvements in therapeutic ratio and activity in hematologic and solid tumor models, leading to clinical trials in patients with myeloma, lymphomas, leukemias, and solid tumors.
  • METHODS: Patients with solid tumor, lymphoma or leukemia diagnoses without standard treatment options were treated with IV NPI on Days 1, 8 and 15 of 28-day cycles in a 3+3 design dose escalation to a Recommended Phase 2 Dose (RP2D).
  • Enrollment then began in 10 patient lymphoma and CLL RP2D cohorts.
  • RESULTS: 30 patients were treated at doses ranging from 0.1 mg/m<sup>2</sup> to 0.9 mg/m<sup>2</sup>.
  • 0.7 mg/m<sup>2</sup> was selected as the RP2D secondary to DLT of transient "hallucinations" (visual imprints when eyes closed) and dizziness/unsteady gait at 0.9 mg/m<sup>2</sup>.
  • At the RP2D PK data showed: half-life = 31 ± 28 min; AUC<sub>total</sub> = 270 ± 219 ng/mL*min; Cmax = 33.4 ± 34.2 ng/mL; clearance = 7.17 ± 0.40 L/min; volume of distribution (Vz) = 223.3 ± 229.7 L.
  • Stable disease was induced in 31% of patients, including one each with mantle cell, Hodgkin's lymphoma, follicular lymphoma, sarcoma, prostate carcinoma, and two with melanoma.

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  • (PMID = 27961753.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e13506 Background: SJG-136 is a pyrrolobenzodiazepine dimer that forms covalent DNA crosslinks in a sequence-specific manner in the minor groove.
  • A phase I study in patients (pts) with solid tumors revealed clinical activity, defined MTD as 30 mg/m<sup>2</sup>/d administered on daily x 3 schedule, and confirmed manageable toxicity.
  • Here we report the results of a CTEP-sponsored phase I trial of SJG-136 administered on a daily x 5 schedule in pts with relapsed or refractory (R/R) leukemias.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • The starting dose level was 6 mcg/m<sup>2</sup> given intravenously daily x 5 days on a 21 day cycle.
  • Pts were sequentially enrolled in cohorts of 3 and the dose was escalated in a classic 3+3 schema at the dose levels: 6, 12, 24, and 36 mcg/m<sup>2</sup>.
  • Pts enrolled at each dose level (mcg/m<sup>2</sup>) were: 6 (3 pts), 12 (5 pts), 24 (4 pts), 36 (4 pts).
  • The dose of 36 mcg/m<sup>2</sup> was found to be above the MTD, with the DLT being grade 3 soft tissue edema.
  • Other manifestations of vascular leak including grade I, II hypoalbuminemia, edema, and pleural effusions were seen in a number of patients starting at dose level 24 mcg/m<sup>2</sup> and above.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.
  • CONCLUSIONS: SJG-136 is safe and active in patients with advanced leukemias.
  • 24 mcg/m<sup>2</sup> is the recommended phase II dose for the daily x 5 schedule.

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Tay K, Shapiro G, Disinski M, Chirieac LR, Pittaluga S, Jaffe ES, Janik JE, Wiestner A, Wilson WH, Dunleavy K: Phase I/II study of a hybrid schedule of flavopiridol in relapsed/refractory mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL). J Clin Oncol; 2009 May 20;27(15_suppl):8563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of a hybrid schedule of flavopiridol in relapsed/refractory mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL).
  • However, a pharmacologically derived hybrid schedule of administration is effective in refractory, genetically high-risk CLL, though life-threatening tumor lysis syndrome (TLS) may occur in patients with very high lymphocyte counts.
  • Because flavopiridol decreases cyclin D1 and mcl-1 and induces apoptosis in MCL cells, is significantly toxic for cell lines derived from the activated B-cell-like type of DLBCL (OCI-Ly3) and down-regulates NF-kappa B, we investigated the hybrid schedule in MCL and DLBCL.
  • Responses were PR in 2 (1 MCL; 1 DLBCL) pts (10%); SD in 5 (25%); and PD in 13 (65%).
  • DLTs were TLS and severe vomiting/diarrhea in 2 pts at DL3.
  • Other toxicities were grade 4 ANC (10 pts) requiring prophylactic G-CSF, TLS (1 pt) and bowel perforation (1 pt).
  • Analysis of cell cycle and transcriptional cdk targets is ongoing.

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  • (PMID = 27961020.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Andritsos L, Furman R, Flinn IW, Foreno-Torres A, Flynn JM, Stromatt SC, Byrd JC: A phase I trial of TRU-016, an anti-CD37 small modular immunopharmaceutical (SMIP) in relapsed and refractory CLL. J Clin Oncol; 2009 May 20;27(15_suppl):3017

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of TRU-016, an anti-CD37 small modular immunopharmaceutical (SMIP) in relapsed and refractory CLL.
  • Pre-clinical studies have demonstrated CD37 SMIP mediates significantly greater direct and NK-cell mediated killing of CLL cells as compared to other therapeutic antibodies used in CLL.
  • A phase I study with TRU-016 was initiated based upon these data.
  • METHODS: Patients with relapsed/refractory CLL or SLL who had adequate organ function, platelets > 30,000/mm<sup>3</sup> were eligible.
  • Dose escalation and de-escalation is based on CTC AE toxicity grades.
  • Mild (grade 1-2) infusion toxicity has been observed in 3 patients.
  • Two patients had partial clearing of leukemia cutis, and the other six had 27-94% reduction in peripheral lymphocyte count.
  • CONCLUSIONS: To date, TRU-016 is a well tolerated treatment with minimal infusional toxicity and no observed dose limiting toxicity.
  • Encouraging reduction in tumor lymphocyte blood counts, lymph node/spleen size and improvement in normal hematopoeitic function in patients with high risk genomic CLL have already been observed at low, non-saturating doses of CD37.
  • Future single agent and combination studies of Tru16 in CLL are warranted.

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  • (PMID = 27962057.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Witzig TE, Wiernik PH, Moore T, Reeder C, Cole C, Justice G, Kaplan H, Voralia M, Pietronigro D, Vose JM: Efficacy of lenalidomide oral monotherapy in relapsed or refractory indolent non-Hodgkin's lymphoma: Final results of NHL-001. J Clin Oncol; 2009 May 20;27(15_suppl):8560

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of lenalidomide oral monotherapy in relapsed or refractory indolent non-Hodgkin's lymphoma: Final results of NHL-001.
  • : 8560 Background: Lenalidomide has shown activity in a wide range of hematological malignancies.
  • We conducted a phase II trial of single-agent lenalidomide in indolent non-Hodgkin's lymphoma (NHL).
  • Oral lenalidomide 25 mg was self-administered once-daily on days 1-21 of every 28-day cycle for up to 52 weeks as tolerated, or until disease progression.
  • The ORR was 23% (10/43), including a complete response (CR) or unconfirmed CR (CRu) rate of 7%.
  • The median time to first response was 3.6 months (1.7-4.2) and the median time to CR or CRu was 4.2 months (1.9-11.1).
  • Twenty-seven percent (6/22) of patients with follicular lymphoma grade 1 or 2, and 22% (4/18) of patients with small lymphocytic lymphoma responded to therapy.
  • Adverse events were consistent with the known safety profile of lenalidomide and manageable; the most common grade 3 or 4 adverse events were neutropenia (30% and 16%, respectively) and thrombocytopenia (14% and 5%, respectively).

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  • (PMID = 27960983.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Melo-Cardenas J, Castro JE, Cox B, Sandoval-Sus JD, Darrah D, Urquiza M, Prussak CE, Kipps TJ: Ad-ISF35-transduced autologous cells promote in vitro and in vivo chemosensitization in patients with 17p-/P53-defective chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e14552

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ad-ISF35-transduced autologous cells promote in vitro and in vivo chemosensitization in patients with 17p-/P53-defective chronic lymphocytic leukemia.
  • : e14552 Background: Transduction of chronic lymphocytic leukemia (CLL) cells with a replication-defective adenovirus (Ad) encoding recombinant CD154 (Ad-ISF35) induces expression of death receptors and Bid via a P53-independent pathway involving induction of P73.
  • Induction of P73 significantly enhances the sensitivity of P53-defective CLL cells to "P53-dependent" drugs, such as Fludarabine (F-ara-A).
  • Patients with P53-defective CLL who received iv infusions of autologous Ad-ISF35-transduced CLL cells were observed to achieve complete remissions (CR) with subsequent treatment using F-ara-A based treatment regimens, suggesting Ad-ISF35 could sensitize P53-defective CLL to chemotherapy.
  • METHODS: We examined patients with drug-resistant and/or P53-defective CLL before and after iv infusions of autologous Ad-ISF35-transduced CLL cells who were enrolled in a phase I study examining whether such treatment could sensitize patients to a truncated fludarabine, cyclophosphamide and rituximab (FCR) regimen.
  • We examined CLL cells for sensitivity to F-ara-A in vitro, expression of CD95, DR5, Bid, and P73 and correlated these with the response to treatment in vivo.
  • RESULTS: P53-defective CLL cells were resistant to F-ara-A induced apoptosis with IC50 > 10μM prior to treatment.
  • CLL cells collected from patients≥24 hours after IV infusion of autologous Ad-ISF35-trasduced CLL cells became sensitive to the cytotoxic effects of F-ara-A, with IC50 0.3-1 μM.
  • Enhanced sensitivity to F-ara-A was associated with induced expression of Bid, DR5, CD95, and P73 by circulating CLL cells, an effect lasting≥2 weeks following iv infusion.
  • Consistent with this, we observed complete resolution in lymphocytosis, lymphadenopathy and splenomegaly following 1 cycle of FCR administered 2 weeks after 3 biweekly infusions of Ad-ISF35- transduced CLL cells.
  • CONCLUSIONS: IV infusion of autologous Ad-ISF35-transduced CLL cells can induce de novo, systemic expression of death receptors and Bid on bystander CLL cells, which is associated with enhanced sensitivity of P53-defective CLL to the cytotoxic effects of standard chemotherapy [Table: see text].

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  • (PMID = 27963590.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. McGregor BA, Gorrebeeck A, Struble E, Harroff A: The effects of sildenafil citrate on malignant B-cells in patients with chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7076

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effects of sildenafil citrate on malignant B-cells in patients with chronic lymphocytic leukemia.
  • : 7076 Background: Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in the Western Hemisphere, with over 10,000 cases diagnosed annually in the United States.
  • It is characterized by progressive accumulation of functionally incompetent long-lived lymphocytes, shown to be secondary to a defect in programmed cell death or apoptosis.
  • The phosphodiesterase inhibitor sildenafil induces capsase dependent apoptosis of malignant B lymphocytes in vitro.
  • This study will test the hypothesis that sildenafil reduces the expression of BCL-2 and increases the spontaneous apoptosis rate of malignant B-cells in patients with CLL.
  • METHODS: Thirteen patients with Rai Stage 0 CLL were enrolled.
  • RESULTS: The median age of patients enrolled in the study was 74 with a median white blood cell count of 18 x10<sup>3</sup>/mL.
  • While one patient withdrew due to blehparitis, not felt to be a side effect of sildenafil, all other patients tolerated the medication well without any adverse effects.
  • There was no significant decrease in white blood cell count or Bcl-2 expression; capsase 3 activity and apoptosis rates remained undetectable on presentation and throughout treatment.
  • CONCLUSIONS: At a dose of 25 to 50 mg weekly, sildenafil does not appear to have any effects on the malignant B cells in CLL.
  • While this dose may not produce a measurable clinical or cellular response, higher doses may still have an effect on the malignant B cells of CLL.
  • The dose of sildenafil was based on a case series of patients with Viagra who had decreases in IgM levels while taking sildenafil 25-50 mg weekly.

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  • (PMID = 27961459.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Cole J, Pantanowitz L, Aboulafia DM: Chronic lymphocytic leukemia (CLL) coexistent with HIV: An increasing association? J Clin Oncol; 2009 May 20;27(15_suppl):7078

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic lymphocytic leukemia (CLL) coexistent with HIV: An increasing association?
  • CLL is the most common leukemia in Western countries, yet very little has been published regarding HIV coexistent with CLL.
  • Therefore, the aim of this study was to evaluate the clinicopathological findings and outcome of HIV-associated CLL in a series of cases.
  • METHODS: Cases of HIV-associated CLL/small lymphocytic leukemia (SLL) were collected from the authors' archives and published case reports (using PubMed search).
  • Information regarding patient demographics (age, gender), mode of HIV acquisition, HAART use, immunosuppression (HIV Viral load [VL], CD4+ cell count), clinical presentation, pathology, and outcome were abstracted and analyzed.
  • Immunologic parameters available for 4 patients showed a median CD4+ count of 930 cells/mm3 (range, 396-1374) and mean HIV VL of 2,103 copies/ml (range, <75-5,297).
  • CLL/SLL was diagnosed by lymph node biopsy (n = 1) and/or flow cytometry (n = 5).
  • Two patients remained well without treatment and 4 required therapy due to either hemolytic anemia, CLL- induced renal failure, pancytopenia, or hypogammaglobulinemia with recurrent infections.
  • CONCLUSIONS: CLL/SLL may occur in association with HIV infection in the elderly without significant concomitant immunosuppression.
  • CLL-related complications in our small series were frequent (67%), including mortality (50%).
  • Additional cases of CLL/SLL are anticipated as HIV-infected patients in the HAART era are reported to be living longer.
  • The association between HIV and CLL is deserving of further attention and we encourage clinicians to report their findings.

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  • (PMID = 27961484.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. Hentrich M, Gerl A, Lutz L, Karthaus M, Schiel X: Unexpected toxicity (UT) and opportunistic infections (OI) after rituximab-containing therapy for non-Hodgkin's lymphoma (NHL). J Clin Oncol; 2009 May 20;27(15_suppl):e19546

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unexpected toxicity (UT) and opportunistic infections (OI) after rituximab-containing therapy for non-Hodgkin's lymphoma (NHL).
  • UT was considered as related to R if it could not be explained otherwise.
  • Pts received a median of 6 cycles (range 1 - 18) of R.
  • A total of 517 cycles of R were evaluable for OI or UT.
  • UT consisted of interstitial pneumonitis (IP) in 2 pts after 8 and 6 cycles of R-CHOP for diffuse large cell lymphoma (DLCL), a case of congestive heart failure (NYHA III°) after 6x R-CHOP + 2x R-M for follicular lymphoma (FL) and a case of grade 4 pancytopenia lasting for 22 days following 2x R-FC for chronic lymphocytic leukemia.
  • Congestive heart failure improved under appropriate therapy and the pt received 2 more cycles of R-M.
  • OI consisted of pneumocystis jirovecii pneumonia after 5x R-CHOP-14 for DLCL, Epstein-Barr-virus (EBV)-associated hepatitis after 5x R-CHOP-21 for relapsed FL and generalized herpes zoster following 6x R-bendamustine (RB) + 1x R-M for recurrent BALT-lymphoma.
  • Moreover, 2 pts were transferred to us for therapy of enterovirus-induced encephalitis after 6x R-CHOP-21 + 2x R-M for FL (n=1) and cerebral toxoplasmosis in a pt heavily pretreated with R-containing therapy for relapsed mantle cell lymphoma (n=1).
  • In selected cases reexposure of R may be feasible.

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  • (PMID = 27960975.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Chagpar AB, Blumencranz P, Whitworth PW, Deck KB, Rosenberg A, Simmons RM, Reintgen DS, Beitsch P, Saha S, Julian TB, GeneSearch Beta and Pivotal Investigators: Use of intraoperative breast cancer sentinel lymph node (SLN) assay to predict of ≥4 positive (+) lymph nodes (LN). J Clin Oncol; 2009 May 20;27(15_suppl):530

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We hypothesized that model s to predict the likelihood of ≥4+LN may be improved by incorporation of quantitative real time RT-PCR analysis of SLN.
  • METHODS: 728 patients were enrolled in 2 prospective studies of the GeneSearch BLN Assay (Veridex LLC) for SLN metastases.
  • Quantitative cycle times (CT) for mammaglobin (MG) and CK19 were correlated with finding ≥4+LN on final pathology.
  • Median CT for MG was 29.1 (interquartile range (IQR): 24.7-39.0) in patients with <4 +LN vs. 21.4 (IQR: 18.5-26.8) in those with ≥4 +LN, p<0.001.
  • Median CT for CK19 was 23.7 (IQR: 20.9-28.2) in patients with <4 +LN vs. 19.6 (IQR: 17.8-20.7) in those with ≥4 +LN, p<0.001.
  • Tumor size ≥2cm, proportion of SLN+ >50%, MG CT <25.8 and CK19 <20.8 were correlated with ≥4 +LN on final pathology.
  • A simplified CPR was created with 1 point given if tumor size was ≥2cm, 1 point if MG CT <25.8 and 2 points if CK19 CT<20.8.
  • Of the 24 patients (20.9%) with 0 points, only 1 (4.2%) had ≥4 +LN; of the 12 patients (10.4%) with 3 points, 8 (66.7%) had ≥4 +LN on final pathology, p<0.001.

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  • (PMID = 27960684.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies.
  • The PI3K p110δ isoform is highly expressed in cells of hematopoietic origin and plays a key role in B cell maturation and function.
  • CAL-101 is a potent inhibitor of PI3K p110δ (IC<sub>50</sub>=65 nM) with 40 to 300-fold selectivity compared to other PI3K isoforms.
  • In vitro studies of 0.1 to 10 μM CAL-101 showed inhibition of pAKT expression and/or apoptotic effects against primary chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) cells and against a range of leukemia and lymphoma cell lines.
  • METHODS: In an ongoing phase 1 dose escalation study in sequential cohorts of 3 patients with relapsed/refractory CLL or select B-cell non-Hodgkin's lymphoma, CAL-101 is administered orally twice daily for 28 days per cycle.
  • No treatment-related adverse events greater than grade 1 have been seen, with 2 patients treated for >5 cycles.
  • Two of 6 patients attained partial response and 4 have stable disease.
  • Partial responses were observed after 2 cycles of 50 mg in a patient with mantle cell lymphoma with 6 prior therapies, and after 1 cycle of 100 mg in a patient with follicular lymphoma with 6 prior therapies, including autologous stem cell transplant.
  • Disease specific cohort expansion will occur at the maximally tolerated dose, and patients with AML will be added.
  • CONCLUSIONS: Early results from a phase 1 study of the oral PI3K p110δ inhibitor CAL-101 show that it is well tolerated and has preliminary clinical activity in patients with B-cell malignancies.

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  • (PMID = 27961357.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. Faderl S, Ferrajoli A, Frankfurt O, Pettitt A: Treatment of B-cell chronic lymphocytic leukemia with nonchemotherapeutic agents: experience with single-agent and combination therapy. Leukemia; 2009 Mar;23(3):457-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of B-cell chronic lymphocytic leukemia with nonchemotherapeutic agents: experience with single-agent and combination therapy.
  • Recent advances in purine analog-based combination chemotherapy and chemoimmunotherapy have significantly improved response rates and progression-free survival in patients with B-cell chronic lymphocytic leukemia (CLL).
  • However, there are clinical scenarios in which purine analog-based treatment may not be appropriate, either because of the risk of toxicity in patients with comorbidity or because purine analog-based therapies are unlikely to achieve satisfactory responses.
  • Novel, nonchemotherapeutic treatment regimens are becoming increasingly important in these patients, as well as in patients in whom combination chemotherapy-based treatment has failed or resulted in relapse.
  • These agents use diverse mechanisms of action that may complement each other, therefore providing a scientific rationale to investigate combinations of these agents in the treatment of CLL.
  • In this review, we will discuss current knowledge of available nonchemotherapeutic agents, available clinical experience with their use alone and in combination and how these approaches may affect outcomes in patients with CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Immunotherapy. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
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  • (PMID = 18987653.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Cancer Vaccines; 0 / Glucocorticoids; 0 / Immunologic Factors; 0 / Immunosuppressive Agents
  • [Number-of-references] 70
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51. Jahrsdörfer B, Wooldridge JE, Blackwell SE, Taylor CM, Link BK, Weiner GJ: Good prognosis cytogenetics in B-cell chronic lymphocytic leukemia is associated in vitro with low susceptibility to apoptosis and enhanced immunogenicity. Leukemia; 2005 May;19(5):759-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Good prognosis cytogenetics in B-cell chronic lymphocytic leukemia is associated in vitro with low susceptibility to apoptosis and enhanced immunogenicity.
  • Chromosomal abnormalities in B-cell chronic lymphocytic leukemia (B-CLL) have been shown to correlate with prognosis.
  • Little is known about the relationship between chromosomal abnormalities and biological behavior of B-CLL cells in vitro.
  • The present study was designed to explore the impact of chromosomal abnormalities determined by interphase fluorescence in situ hybridization (FISH) on the in vitro survival and immunogenicity of B-CLL.
  • Considerable heterogeneity was noted in the in vitro survival and expression of costimulatory, adhesion, and antigen-presenting molecules by B-CLL cells.
  • Spontaneous apoptosis of B-CLL cells in vitro was significantly lower in samples with good prognosis cytogenetics when compared to samples with poor prognosis cytogenetics.
  • In contrast, B-CLL cells from samples with good prognosis cytogenetics exhibited higher basal expression of molecules involved in costimulation, cellular adhesion, and antigen presentation, and induced significantly more T-cell proliferation in mixed lymphocyte cultures.
  • We conclude that chromosomal aberrations of B-CLL cells correlate with the in vitro biological behavior of B-CLL.
  • These findings could have significant implications on the design of future therapeutic approaches in patients with CLL, and the likelihood of response based on cytogenetics.
  • [MeSH-major] Apoptosis / physiology. Cytogenetics. Leukemia, Lymphocytic, Chronic, B-Cell
  • [MeSH-minor] Aged. Cell Survival / physiology. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence / methods. L-Lactate Dehydrogenase / blood. Male. Middle Aged. Phenotype. Prognosis. Proto-Oncogene Proteins c-bcl-2 / genetics. Tumor Cells, Cultured

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  • (PMID = 15759034.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA97274; United States / NCI NIH HHS / CA / R01 CA77764
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; EC 1.1.1.27 / L-Lactate Dehydrogenase
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52. Gachard N, Salviat A, Boutet C, Arnoulet C, Durrieu F, Lenormand B, Leprêtre S, Olschwang S, Jardin F, Lafage-Pochitaloff M, Penther D, Sainty D, Reminieras L, Feuillard J, Béné MC, GEIL: Multicenter study of ZAP-70 expression in patients with B-cell chronic lymphocytic leukemia using an optimized flow cytometry method. Haematologica; 2008 Feb;93(2):215-23
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  • [Title] Multicenter study of ZAP-70 expression in patients with B-cell chronic lymphocytic leukemia using an optimized flow cytometry method.
  • BACKGROUND: Flow cytometry allows specific assessment of the expression of ZAP-70, a promising new prognostic factor in B-cell chronic lymphocytic leukemia (B-CLL), but suffers from a lack of multicenter standardization.
  • DESIGN AND METHODS: An optimized method for direct detection of ZAP-70 in flow cytometry was tested in a multicenter fashion.
  • ZAP-70 expression levels were assessed for 153 patients with typical B-cell chronic lymphocytic leukemia chronic lymphocytic leukemia.
  • Results were expressed as the ratio of ZAP-70 mean fluorescence intensity between B-CLL cells and normal B cells.
  • ZAP-70 was significantly expressed in 28%, 54% and 61% of patients with Binet stages A, B and C B-cell chronic lymphocytic leukemia, respectively (p=0.008).
  • The absence of ZAP-70 expression was associated with isolated del(13q14), a cytogenetic abnormality with a good prognosis, while most patients with the del(17p13) poor prognosis cytogenetic marker expressed ZAP-70 (p<10(-5)).
  • ZAP-70 expression was not related to the other poor prognosis cytogenetic abnormality del(11q22.3) nor to trisomy 12.
  • CONCLUSIONS: This new technique provides highly reliable results well correlated with the mutational status of IgVH genes, CD38 expression, Binet stage and cytogenetic abnormalities.
  • This robust discriminative technique appears of particular interest for routine diagnosis and assessment of ZAP-70 expression in large, prospective, multicenter therapeutic trials.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Blood Donors. Flow Cytometry. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. ZAP-70 Protein-Tyrosine Kinase / biosynthesis

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  • (PMID = 18223290.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Membrane Glycoproteins; 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; EC 3.2.2.5 / CD38 protein, human
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53. Dzietczenia J, Wróbel T, Jaźwiec B, Mazur G, Butrym A, Poręba R, Kuliczkowski K: Expression of bone morphogenetic proteins (BMPs) receptors in patients with B-cell chronic lymphocytic leukemia (B-CLL). Int J Lab Hematol; 2010 Dec;32(6 Pt 1):e217-21
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  • [Title] Expression of bone morphogenetic proteins (BMPs) receptors in patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • They regulate proliferation, differentiation, and apoptosis in a variety of cells including hematopoietic cells.
  • BMPs act because of binding to two types of serine/threonine kinase receptors: BMP type I receptors (IA and IB) and BMP type II receptor.
  • The aim of our study was to examine the percentage of expression of BMPs receptors on lymphocytes of patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • A total of 46 patients with B-CLL (27 men and 19 women) and 10 healthy persons were evaluated.
  • Freshly isolated mononuclear cells were incubated with antibodies against BMPs receptors: BMPRIA, BMPRIB, and BMPRII and examined in 2-color flow cytometry.
  • On cells of patients with B-CLL, the percentage of expression of BMP RIA, BMP RIB, and BMP RII was significantly higher than in normal cells of the control group.
  • The percentage of the expression of BMP RIA and BMP RIB was higher in patients with advanced stage of disease.
  • [MeSH-major] Bone Morphogenetic Protein Receptors, Type I / biosynthesis. Bone Morphogenetic Protein Receptors, Type II / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / physiopathology

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  • [Copyright] © 2010 Blackwell Publishing Ltd.
  • (PMID = 20491995.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.11.30 / Bone Morphogenetic Protein Receptors; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type I; EC 2.7.11.30 / Bone Morphogenetic Protein Receptors, Type II
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54. Takeshita A, Shinjo K, Yamakage N, Ono T, Hirano I, Matsui H, Shigeno K, Nakamura S, Tobita T, Maekawa M, Ohnishi K, Sugimoto Y, Kiyoi H, Naoe T, Ohno R: CMC-544 (inotuzumab ozogamicin) shows less effect on multidrug resistant cells: analyses in cell lines and cells from patients with B-cell chronic lymphocytic leukaemia and lymphoma. Br J Haematol; 2009 Jun;146(1):34-43
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  • [Title] CMC-544 (inotuzumab ozogamicin) shows less effect on multidrug resistant cells: analyses in cell lines and cells from patients with B-cell chronic lymphocytic leukaemia and lymphoma.
  • The effect of CMC-544, a calicheamicin-conjugated anti-CD22 monoclonal antibody, was analysed in relation to CD22 and P-glycoprotein (P-gp) in B-cell chronic lymphocytic leukaemia (CLL) and non-Hodgkin lymphoma (NHL) in vitro.
  • The cell lines used were CD22-positive parental Daudi and Raji, and their P-gp positive sublines, Daudi/MDR and Raji/MDR.
  • Cells obtained from 19 patients with B-cell CLL or NHL were also used.
  • The effect of CMC-544 was analysed by viable cell count, morphology, annexin-V staining, and cell cycle distribution.
  • A dose-dependent, selective cytotoxic effect of CMC-544 was observed in cell lines that expressed CD22.
  • In clinical samples, the cytotoxic effect of CMC-544 was inversely related to the amount of P-gp (P = 0.003), and to intracellular rhodamine-123 accumulation (P < 0.001).
  • Our findings will help to predict the clinical effectiveness of this drug on these B-cell malignancies, suggesting a beneficial effect with combined use of CMC-544 and MDR modifiers.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cell Count. Cell Line, Transformed. Cell Line, Tumor. Cyclosporins / therapeutic use. Dose-Response Relationship, Drug. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm. Flow Cytometry. Humans. Immunosuppressive Agents / therapeutic use. Jurkat Cells. P-Glycoprotein / analysis. P-Glycoprotein / antagonists & inhibitors. P-Glycoprotein / metabolism. Quinolines / therapeutic use. Sialic Acid Binding Ig-like Lectin 2 / analysis. Sialic Acid Binding Ig-like Lectin 2 / immunology. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 19388933.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Cyclosporins; 0 / Immunosuppressive Agents; 0 / Inotuzumab Ozogamicin; 0 / P-Glycoprotein; 0 / Quinolines; 0 / Sialic Acid Binding Ig-like Lectin 2; 0BJK6B565B / dofequidar; 121584-18-7 / valspodar
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55. Secchiero P, Barbarotto E, Tiribelli M, Zerbinati C, di Iasio MG, Gonelli A, Cavazzini F, Campioni D, Fanin R, Cuneo A, Zauli G: Functional integrity of the p53-mediated apoptotic pathway induced by the nongenotoxic agent nutlin-3 in B-cell chronic lymphocytic leukemia (B-CLL). Blood; 2006 May 15;107(10):4122-9
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  • [Title] Functional integrity of the p53-mediated apoptotic pathway induced by the nongenotoxic agent nutlin-3 in B-cell chronic lymphocytic leukemia (B-CLL).
  • Deletions and/or mutations of p53 are relatively rare and late events in the natural history of B-cell chronic lymphocytic leukemia (B-CLL).
  • However, it is unknown whether p53 signaling is functional in B-CLL and if targeted nongenotoxic activation of the p53 pathway by using nutlin-3, a small molecule inhibitor of the p53/MDM2 interaction, is sufficient to kill B-CLL cells.
  • In vitro treatment with nutlin-3 induced a significant cytotoxicity on primary CD19(+) B-CLL cells, but not on normal CD19(+) B lymphocytes, peripheral-blood mononuclear cells, or bone marrow hematopoietic progenitors.
  • Among 29 B-CLL samples examined, only one was resistant to nutlin-3-mediated cytotoxicity.
  • The induction of p53 by nutlin-3 in B-CLL samples was accompanied by alterations of the mitochondrial potential and activation of the caspase-dependent apoptotic pathway.
  • Moreover, nutlin-3 synergized with both fludarabine and chlorambucil in inducing B-CLL apoptosis.
  • Our data strongly suggest that nutlin-3 should be further investigated for clinical applications in the treatment of B-CLL.
  • [MeSH-major] Imidazoles / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Piperazines / pharmacology. Tumor Suppressor Protein p53 / blood


56. Bilban M, Heintel D, Scharl T, Woelfel T, Auer MM, Porpaczy E, Kainz B, Kröber A, Carey VJ, Shehata M, Zielinski C, Pickl W, Stilgenbauer S, Gaiger A, Wagner O, Jäger U, German CLL Study Group: Deregulated expression of fat and muscle genes in B-cell chronic lymphocytic leukemia with high lipoprotein lipase expression. Leukemia; 2006 Jun;20(6):1080-8
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  • [Title] Deregulated expression of fat and muscle genes in B-cell chronic lymphocytic leukemia with high lipoprotein lipase expression.
  • Lipoprotein lipase (LPL) is a prognostic marker in B-cell chronic lymphocytic leukemia (B-CLL) related to immunoglobulin V(H) gene (IgV(H))mutational status.
  • We determined gene expression profiles using Affymetrix U133A GeneChips in two groups of B-CLLs selected for either high ('LPL+', n=10) or low ('LPL-', n=10) LPL mRNA expression.
  • A total of 111 genes discriminated LPL+ from LPL- B-CLLs.
  • Of these, the top three genes associated with time to first treatment were Septin10, DMD and Gravin (P</=0.01).
  • The relationship of LPL+ and LPL- B-CLL gene expression signatures to 52 tissues was statistically analyzed.
  • The LPL+ B-CLL expression signature, represented by 64 genes was significantly related to fat, muscle and PB dendritic cells (P<0.001).
  • Exploration of microarray data to define functional alterations related to the biology of LPL+ CLL identified two functional modules, fatty acid degradation and MTA3 signaling, as being altered with higher statistical significance.
  • Our data show that LPL+ B-CLL cells have not only acquired gene expression changes in fat and muscle-associated genes but also in functional pathways related to fatty acid degradation and signaling which may ultimately influence CLL biology and clinical outcome.
  • [MeSH-major] Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Leukemic. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lipoprotein Lipase / genetics

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  • [CommentIn] Leukemia. 2008 Jan;22(1):224-6 [17657217.001]
  • (PMID = 16617321.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Dystrophin; 0 / Fatty Acids; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / RNA, Messenger; EC 3.1.1.34 / Lipoprotein Lipase; EC 3.6.1.- / GTP Phosphohydrolases; EC 3.6.1.- / SEPT10 protein, human; EC 3.6.1.- / Septins
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57. Krejcí M, Adam Z, Pour L, Brychtová Y, Mayer J, Vorlícek J: [B-cell chronic lymphocytic leukaemia and the similar states]. Vnitr Lek; 2009 Sep;55(9):746-65
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  • [Title] [B-cell chronic lymphocytic leukaemia and the similar states].
  • [Transliterated title] Chronická B-lymfatická leukemie a jí podobné stavy.
  • B-cell chronic lymphocytic leukaemia and the similar diseases are seen predominantly in patients above the age 50 years, i.e. at the age when the patients also have other co-morbidities.
  • The aim of the present review is to provide the medical community with the main information on this disease as patients with B-cell chronic lymphocytic leukaemia and similar disease states are of older age and very often suffer from a range of co-morbidities.
  • The aim of the following text is to present a clear overview of the basic information about this group of diseases that might be useful to all physicians who provide care to patients with B-cell chronic lymphocytic leukaemia and similar conditions.
  • Since monoclonal immunoglobulin is sometimes identified in patients with these diseases, it is important to consider these conditions in the differential diagnosis of the states with the presence of monoclonal immunoglobulin.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Humans. Leukemia, Hairy Cell / diagnosis. Leukemia, Prolymphocytic / diagnosis. Multiple Myeloma / diagnosis. Paraproteinemias / diagnosis

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  • (PMID = 19785372.001).
  • [ISSN] 0042-773X
  • [Journal-full-title] Vnitr̆ní lékar̆ství
  • [ISO-abbreviation] Vnitr Lek
  • [Language] cze
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Czech Republic
  • [Number-of-references] 41
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58. Van Den Neste E, Robin V, Francart J, Hagemeijer A, Stul M, Vandenberghe P, Delannoy A, Sonet A, Deneys V, Costantini S, Ferrant A, Robert A, Michaux L: Chromosomal translocations independently predict treatment failure, treatment-free survival and overall survival in B-cell chronic lymphocytic leukemia patients treated with cladribine. Leukemia; 2007 Aug;21(8):1715-22
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  • [Title] Chromosomal translocations independently predict treatment failure, treatment-free survival and overall survival in B-cell chronic lymphocytic leukemia patients treated with cladribine.
  • Chromosomal translocations represent an important prognostic indicator in B-cell chronic lymphocytic leukemia (B-CLL).
  • Sixty-five B-CLL patients were investigated using cytogenetics, interphase fluorescence in situ hybridization (FISH), analysis of IgV(H) and of TP53 mutational status before treatment with 2-chloro-2'-deoxyadenosine (CdA).
  • Patients with translocations were more heavily pretreated (P=0.05), presented with more complex karyotypes (P<0.001), 17p abnormalities and TP53 mutations, and had a higher failure rate (59 vs 21% in patients without translocations, P=0.004).
  • Patients with unbalanced translocations displayed a shorter median treatment-free survival (TFS, 6.9 vs 35.9 months, log rank 22.72, P<0.001) and overall survival (OS, 13.0 vs 68.0 months, log rank 16.51, P<0.001), as compared to patients without translocation.
  • In multivariate analysis, unbalanced translocations were independently associated with therapeutic failure, short TFS and short OS.
  • IgV(H) mutational status was independently associated with risk of failure and TFS, but not OS.
  • In B-CLL patients treated with CdA, translocations are strong predictors of outcome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cladribine / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / mortality. Translocation, Genetic


59. Suwalska K, Pawlak E, Karabon L, Tomkiewicz A, Dobosz T, Urbaniak-Kujda D, Kuliczkowski K, Wolowiec D, Jedynak A, Frydecka I: Association studies of CTLA-4, CD28, and ICOS gene polymorphisms with B-cell chronic lymphocytic leukemia in the Polish population. Hum Immunol; 2008 Mar;69(3):193-201
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  • [Title] Association studies of CTLA-4, CD28, and ICOS gene polymorphisms with B-cell chronic lymphocytic leukemia in the Polish population.
  • *642AT(8_33), CD28c.17+3T>C, and ICOSc.1554+4GT(8_15) and susceptibility to B-cell chronic lymphocytic leukemia (B-CLL) in the Polish population.
  • The study revealed increased frequency of the CTLA-4g.319C>T [T] allele and the CTLA-4g.319C>T [T] phenotype in B-CLL patients compared with healthy controls (p = 0.003, odds ratio [OR] = 1.73; and p = 0.009, OR = 1.74, respectively).
  • The presence of the CD28c.17+3T>C [C] allele and the CD28c.17+3T>C [C] phenotype increased the OR of B-CLL to 1.59 (p = 0.007) and 1.74 (p = 0.007), respectively.
  • Individuals possessing short alleles were 2.02 times more prone to B-CLL than others (p = 0.001), whereas carriers of long alleles were protected from B-CLL (p = 0.02, OR = 0.62).
  • The haplotype association study and multivariate analysis confirmed the association of CTLA-4g.319C>T and ICOSc.1554+4GT(8_15) gene polymorphisms with B-CLL.
  • *642AT(8_33) did not correlate with B-CLL.
  • Our results are the first in the literature to report that gene polymorphism of the costimulatory molecules CTLA-4, CD28, and ICOS contributes to susceptibility to B-CLL.
  • [MeSH-major] Antigens, CD / genetics. Antigens, CD28 / genetics. Antigens, Differentiation / genetics. Antigens, Differentiation, T-Lymphocyte / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Polymorphism, Genetic / genetics
  • [MeSH-minor] Aged. Alleles. CTLA-4 Antigen. Female. Gene Frequency. Genetic Predisposition to Disease / genetics. Genotype. Haplotypes. Humans. Inducible T-Cell Co-Stimulator Protein. Linkage Disequilibrium. Male. Middle Aged. Multivariate Analysis. Phenotype. Poland

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  • (PMID = 18396212.001).
  • [ISSN] 0198-8859
  • [Journal-full-title] Human immunology
  • [ISO-abbreviation] Hum. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD28; 0 / Antigens, Differentiation; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / CTLA-4 Antigen; 0 / CTLA4 protein, human; 0 / ICOS protein, human; 0 / Inducible T-Cell Co-Stimulator Protein
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60. Ziemer M, Bornkessel A, Hahnfeld S, Weyers W: 'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection. J Cutan Pathol; 2005 Sep;32(8):581-4
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  • [Title] 'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection.
  • BACKGROUND: Specific cutaneous infiltrates in patients with leukemia generally carry a grim prognosis.
  • METHODS: In a patient with B-cell chronic lymphocytic leukemia, a specific infiltrate developed at the site of a florid herpes simplex infection.
  • RESULTS: Histopathologically, the lesion was characterized by a dense, diffuse infiltrate of small hyperchromatic lymphocytes throughout the entire dermis.
  • Lymphocytes showed an aberrant CD20(+)/CD43(+)/CD5(+) phenotype of neoplastic B cells, and monoclonal rearrangement of immunoglobulin gamma genes could be demonstrated by polymerase chain reaction.
  • Although criteria for leukemia cutis were fulfilled, the patient did well.
  • CONCLUSIONS: The cutaneous infiltrate of neoplastic cells seemed to be part of a physiologic response to the antigenic stimulus, rather than indicating an exacerbation of leukemia.
  • 'Specific' cutaneous infiltrate of B-cell chronic lymphocytic leukemia at the site of a florid herpes simplex infection.
  • [MeSH-major] Herpes Zoster / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration / pathology. Skin Neoplasms / pathology


61. Moreton P, Kennedy B, Lucas G, Leach M, Rassam SM, Haynes A, Tighe J, Oscier D, Fegan C, Rawstron A, Hillmen P: Eradication of minimal residual disease in B-cell chronic lymphocytic leukemia after alemtuzumab therapy is associated with prolonged survival. J Clin Oncol; 2005 May 1;23(13):2971-9
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  • [Title] Eradication of minimal residual disease in B-cell chronic lymphocytic leukemia after alemtuzumab therapy is associated with prolonged survival.
  • PURPOSE: To test whether eradication of minimal residual disease (MRD) in B-cell chronic lymphocytic leukemia (CLL) by alemtuzumab is associated with a prolongation of treatment-free and overall survival.
  • PATIENTS AND METHODS: Ninety-one previously treated patients with CLL (74 men and 17 women; median age, 58 years [range, 32 to 75 years]; 44 were refractory to purine analogs) received a median of 9 weeks of alemtuzumab treatment between 1996 and 2003.
  • Regular bone marrow assessments by MRD flow cytometry were performed with the aim of eradicating detectable MRD (< 1 CLL cell in 10(5) normal cells).
  • RESULTS: Responses according to National Cancer Institute-sponsored working group response criteria were complete remission (CR) in 32 patients (36%), partial remission (PR) in 17 patients (19%), and no response (NR) in 42 patients (46%).
  • Detectable CLL was eradicated from the blood and marrow in 18 patients (20%).
  • Median survival was significantly longer in MRD-negative patients compared with those achieving an MRD-positive CR, PR, or NR.
  • Patients achieving an MRD-negative CR had a longer treatment-free survival than patients with MRD-positive CRs, PR, or NR: MRD-negative CRs, not reached; MRD-positive CRs, 20 months; PRs, 13 months; NR, 6 months (P < .0001).
  • CONCLUSION: MRD-negative remission in CLL is achievable with alemtuzumab, leading to an improved overall and treatment-free survival.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Neoplasm, Residual
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Bone Marrow / pathology. Disease-Free Survival. Female. Flow Cytometry. Humans. Male. Middle Aged

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  • [CommentIn] J Clin Oncol. 2005 May 1;23(13):2884-5 [15738532.001]
  • [CommentIn] J Clin Oncol. 2005 Nov 1;23(31):8122-3; author reply 8123-4 [16258114.001]
  • [CommentIn] J Clin Oncol. 2005 Oct 1;23(28):7240-1; author reply 7241-2 [16192616.001]
  • (PMID = 15738539.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
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62. Pourgheysari B, Bruton R, Parry H, Billingham L, Fegan C, Murray J, Moss P: The number of cytomegalovirus-specific CD4+ T cells is markedly expanded in patients with B-cell chronic lymphocytic leukemia and determines the total CD4+ T-cell repertoire. Blood; 2010 Oct 21;116(16):2968-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The number of cytomegalovirus-specific CD4+ T cells is markedly expanded in patients with B-cell chronic lymphocytic leukemia and determines the total CD4+ T-cell repertoire.
  • B-cell chronic lymphocytic leukemia is associated with immune suppression and an altered T-cell repertoire with expansion of memory cells.
  • Cytomegalovirus (CMV) is a common herpes virus that elicits a strong virus-specific T-cell immune response after infection.
  • We studied the CMV-specific CD4(+) T-cell response in 45 patients and 35 control subjects and demonstrated that it was markedly expanded in the patient group, averaging 11% of the CD4(+) pool compared with 4.7% in controls.
  • The magnitude of the CMV-specific CD4(+) immune response increased with disease stage and was particularly high in patients who received chemotherapy.
  • Within this group, the CMV-specific response comprised over 46% of the CD4(+) T-cell repertoire in some patients.
  • CMV-seropositive patients exhibited a markedly altered CD4(+) T-cell repertoire with increased numbers of CD45R0(+) T cells and a reduction in CD27, CD28, and CCR7 expression.
  • CLL patients therefore demonstrate an expansion of the CD4(+) CMV-specific immune response, which is likely to contribute to the immunological and clinical features of this disease.
  • [MeSH-major] CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / virology. Cytomegalovirus / immunology. Cytomegalovirus Infections / complications. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / immunology
  • [MeSH-minor] Aged. Aged, 80 and over. Antigens, CD3 / immunology. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / virology. Cell Count. Female. Humans. Male. Middle Aged

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  • [CommentIn] Blood. 2010 Oct 21;116(16):2869-70 [20966175.001]
  • (PMID = 20562332.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0800808; United Kingdom / Medical Research Council / / G9901249; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3
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63. Junevik K, Werlenius O, Hasselblom S, Jacobsson S, Nilsson-Ehle H, Andersson PO: The expression of NK cell inhibitory receptors on cytotoxic T cells in B-cell chronic lymphocytic leukaemia (B-CLL). Ann Hematol; 2007 Feb;86(2):89-94

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of NK cell inhibitory receptors on cytotoxic T cells in B-cell chronic lymphocytic leukaemia (B-CLL).
  • Reduced reactivity of CTL towards tumour cells could thus lead to disease progression and loss of tumour control.
  • In B-cell chronic lymphocytic leukaemia (B-CLL), the function of tumour-reactive CTL seems to correlate inversely to disease stage.
  • Inhibitory NK cell receptors are known to suppress the CTL response upon interaction with major histocompatibility complex (MHC) class I and increased expression of such receptors on CTL may inhibit the anti-tumour response.
  • So, the aim of this study was to investigate the expression of NK cell inhibitory receptors on CTL in B-CLL patients and if such expression correlated to disease stage.
  • CD8+ T cells from B-CLL patients in Binet stage A (n = 26) and stage C (n = 14) and healthy controls (n = 14) were analysed for the expression of killer immunoglobulin-like receptors (KIR) CD158a (KIR2DL1), CD158b (KIR2DL2), CD158e (KIR3DL1) and the C-type lectin receptor CD94, by flow cytometry analysis.
  • Patients with advanced disease (Binet stage C) had a significantly greater percentage of CTL expressing CD158b, CD158e and CD94 than patients with non-progressive disease (Binet stage A) and healthy controls.
  • Our results suggest that increased expression of KIR and CD94 on CTL in advanced stage B-CLL may potentially contribute to the impaired anti-tumour immune response in these patients.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Receptors, Immunologic / metabolism. T-Lymphocytes, Cytotoxic / metabolism

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  • (PMID = 17043777.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / KIR2DL2 protein, human; 0 / KIR3DL1 protein, human; 0 / Receptors, Immunologic; 0 / Receptors, KIR; 0 / Receptors, KIR2DL1; 0 / Receptors, KIR2DL2; 0 / Receptors, KIR2DL3; 0 / Receptors, KIR3DL1
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64. Kalla C, Nentwich H, Schlotter M, Mertens D, Wildenberger K, Döhner H, Stilgenbauer S, Lichter P: Translocation t(X;11)(q13;q23) in B-cell chronic lymphocytic leukemia disrupts two novel genes. Genes Chromosomes Cancer; 2005 Feb;42(2):128-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation t(X;11)(q13;q23) in B-cell chronic lymphocytic leukemia disrupts two novel genes.
  • Deletion of chromosome region 11q22-q23 defines a subgroup of patients with B-cell chronic lymphocytic leukemia (B-CLL) characterized by poor survival.
  • Although the tumor-suppressor gene ATM in the consensus deletion region was found to be biallelically inactivated in about one third of B-CLL cases, in the majority of those who have this deletion, inactivation of the remaining ATM allele was not observed.
  • To identify a second disease-associated gene, we investigated two B-CLL cases with translocation breakpoints in the critical 11q23 deletion region.
  • The rearrangement of ARHGAP20 and BRWD3 did not result in fusion transcripts, but it disrupted both genes.
  • Mutation analysis of 28 B-CLL samples with monoallelic deletions and two B-CLL samples with 11q23 translocations detected no deleterious mutation in the remaining copy of ARHGAP20.
  • Quantitative expression analysis in 22 B-CLLs revealed significant up-regulation of ARHGAP20 in CLL B cells, whereas BRWD3 was slightly down-regulated.
  • Thus, deregulation of ARHGAP20 by altered gene expression or by gene disruption (but not point mutation) might be a general molecular mechanism of B-CLL leukemogenesis.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, X / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Transcription Factors / genetics. Translocation, Genetic / genetics

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  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • [CommentIn] Genes Chromosomes Cancer. 2005 Sep;44(1):109-10; author reply 111-2 [15880590.001]
  • (PMID = 15543602.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY496263/ AY496264/ AY496265/ AY496266/ AY496267/ AY497046/ AY497047/ AY497048/ AY497049/ AY497050/ AY497051/ AY497052/ AY497053/ AY497054/ AY497055/ AY497056/ AY497057/ AY497058/ AY497059/ AY497060
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARHGAP20 protein, human; 0 / BRWD3 protein, human; 0 / DNA, Neoplasm; 0 / GTPase-Activating Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA Splice Sites; 0 / Transcription Factors
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65. Hadj Tahar A: Alemtuzumab for B-cell chronic lymphocytic leukemia. Issues Emerg Health Technol; 2005 Mar;(66):1-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab for B-cell chronic lymphocytic leukemia.
  • Alemtuzumab, a humanized monoclonal antibody, is thought to destroy cancer cells through immune system stimulation or apoptosis induction (programmed cell death).
  • In case series studies using alemtuzumab as salvage therapy, about a third of patients with B-cell chronic lymphocytic leukemia (B-CLL), who were otherwise refractory to chemotherapy, improved.
  • Anti-tumour activity was also observed when the drug was used as first-line therapy or to treat minimal residual disease.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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  • (PMID = 15806747.001).
  • [ISSN] 1488-6316
  • [Journal-full-title] Issues in emerging health technologies
  • [ISO-abbreviation] Issues Emerg Health Technol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm
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66. El-Khoury V, Moussay E, Janji B, Palissot V, Aouali N, Brons NH, Van Moer K, Pierson S, Van Dyck E, Berchem G: The histone deacetylase inhibitor MGCD0103 induces apoptosis in B-cell chronic lymphocytic leukemia cells through a mitochondria-mediated caspase activation cascade. Mol Cancer Ther; 2010 May;9(5):1349-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The histone deacetylase inhibitor MGCD0103 induces apoptosis in B-cell chronic lymphocytic leukemia cells through a mitochondria-mediated caspase activation cascade.
  • In this study, we found that MGCD0103 was substantially more toxic in neoplastic B cells relative to normal cells, and we described the death pathways activated by MGCD0103 in B-cell chronic lymphocytic leukemia (CLL) cells from 32 patients.
  • MGCD0103 decreased the expression of Mcl-1 and induced translocation of Bax to the mitochondria, mitochondrial depolarization, and release of cytochrome c in the cytosol.
  • Thus, MGCD0103 induced the intrinsic pathway of apoptosis in CLL cells.
  • Moreover, MGCD0103 treatment resulted in the activation of a caspase cascade downstream of caspase-9, caspase-dependent amplification of mitochondrial depolarization, activation of calpain, and Bax cleavage.
  • We propose a model whereby the intrinsic pathway of apoptosis triggered by MGCD0103 in CLL is associated with a mitochondrial death amplification loop.
  • [MeSH-major] Apoptosis / drug effects. Benzamides / pharmacology. Caspases / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Pyrimidines / pharmacology

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  • (PMID = 20406947.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [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 / Histone Deacetylase Inhibitors; 0 / Pyrimidines; A6GWB8T96J / mocetinostat; EC 3.4.22.- / Caspases
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67. Kiewe P, Dallenbach FE, Fischer L, Hoecht S, Kombos T, Thiel E, Korfel A: Isolated B-cell lymphoproliferative disorder at the dura mater with B-cell chronic lymphocytic leukemia immunophenotype. Clin Lymphoma Myeloma; 2007 Nov;7(9):594-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Isolated B-cell lymphoproliferative disorder at the dura mater with B-cell chronic lymphocytic leukemia immunophenotype.
  • Lymphoma manifestations of the dura mater are extremely rare and have mostly been attributed to extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) type.
  • We report a patient with an isolated meningeal tumor, identified as a B-cell lymphoproliferative disorder with typical B-cell chronic lymphocytic leukemia immunophenotype.
  • Because of the subclinical detection of trisomy 3 in the bone marrow by cytogenetic analysis and interphase fluorescence in situ hybridization, CD5(+) MALT is an important differential diagnosis; however, to our knowledge, this entity has never been reported in the context of dural lymphoma.
  • [MeSH-major] Brain Neoplasms / pathology. Leukemia, Large Granular Lymphocytic / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Immunophenotyping. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / immunology. Lymphoma, B-Cell, Marginal Zone / pathology. Male


68. Cailliod R, Quantin C, Carli PM, Jooste V, Le Teuff G, Binquet C, Maynadie M: A population-based assessment of the prognostic value of the CD19 positive lymphocyte count in B-cell chronic lymphocytic leukemia using Cox and Markov models. Eur J Epidemiol; 2005;20(12):993-1001
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A population-based assessment of the prognostic value of the CD19 positive lymphocyte count in B-cell chronic lymphocytic leukemia using Cox and Markov models.
  • No population-based study has assessed the prognostic impact on survival of the CD19 positive lymphocyte count, evaluated by immunophenotyping at diagnosis, in B-cell chronic lymphocytic leukemia (B-CLL).
  • Aiming at addressing this issue, we investigated the clinical outcome of a well-defined population of B-CLL patients.
  • Survival of B-CLL patients, diagnosed between 1990 and 1999 and recorded by the Registry of Hematological Malignancies of the Côte d'Or, was analysed applying Cox's regression model to the 237 included cases and to the 195 Binet stage A patients.
  • To assess simultaneously the predictive value of each parameter on the risk of disease progression and on the risk of death, we completed this analysis by applying a three-states homogeneous Markov model to the whole study population.
  • Analysis of the entire population showed that age (p < 0.001), Binet stage (p = 0.008) and CD19 positive lymphocyte count (p = 0.038) were three independent prognostic factors.
  • However, in stage A patients, only progression into a more advanced stage, analysed as a time-dependent variable, and age had a clear impact on survival (p < 0.001 for both).
  • Markov model revealed that an increased CD19 positive lymphocyte count increased the risk of disease progression in stage A patients (p = 0.002) but did not have direct impact on survival of either stage A patients with stable disease or stage B or C patients.
  • An increased CD19 positive lymphocyte count at diagnosis is a marker of an increased risk of disease progression in stage A patients.
  • [MeSH-major] Antigens, CD19 / blood. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Leukemia, Lymphocytic, Chronic, B-Cell / mortality
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Female. Humans. Immunophenotyping. Lymphocyte Count. Male. Markov Chains. Middle Aged. Prognosis. Proportional Hazards Models. Survival Analysis

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  • (PMID = 16331430.001).
  • [ISSN] 0393-2990
  • [Journal-full-title] European journal of epidemiology
  • [ISO-abbreviation] Eur. J. Epidemiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD19
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69. Bojarska-Junak A, Giannopoulos K, Kowal M, Dmoszyńska A, Roliński J: Comparison of methods for determining zeta-chain associated protein - 70 (ZAP-70) expression in patients with B-cell chronic lymphocytic leukemia (B-CLL). Cytometry B Clin Cytom; 2006 Jul 15;70(4):293-301
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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 methods for determining zeta-chain associated protein - 70 (ZAP-70) expression in patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • BACKGROUND: Zeta-chain associated protein of 70kDa (ZAP-70) is the most promising surrogate marker for the immunoglobulin heavy chain variable region (IgV(H)) mutation status in B-cell chronic lymphocytic leukemia (B-CLL).
  • METHODS: We compared different staining methods utilizing monoclonal antibodies (moAb) against ZAP-70: anti-ZAP-70 PE, clone 1E7.2, anti-ZAP-70 PE, clone 17A/P-ZAP70 directly stained with flourochrome as well as anti-ZAP-70 antibody, clone 2F3.2 stained with Zenontrade mark Alexa Fluor(R) 488 Labeling Kit.
  • Additionally different reagents for permeabilization such as IntraPrep, FIX & PERM, Perm/Wash and 70% ethanol/paraformaldehyde were used to find the most clinically relevant and easy assay to determine ZAP-70 expression in B-CLL.
  • RESULTS: Anti-ZAP-70 moAb clone 17A/P-ZAP70 gave elevated results for all B-CLL patients as well as healthy controls.
  • [MeSH-major] Antibodies, Monoclonal / chemistry. Flow Cytometry / methods. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Staining and Labeling / methods. Tissue Fixation / methods. ZAP-70 Protein-Tyrosine Kinase / analysis. ZAP-70 Protein-Tyrosine Kinase / biosynthesis
  • [MeSH-minor] Aged. Aged, 80 and over. Antigen-Antibody Reactions. Biomarkers, Tumor / analysis. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / immunology. Cell Membrane Permeability. Female. Humans. Male. Middle Aged. Reproducibility of Results

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  • [Copyright] (c) 2006 International Society for Analytical Cytology.
  • (PMID = 16906577.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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70. Kokhaei P, Palma M, Hansson L, Osterborg A, Mellstedt H, Choudhury A: Telomerase (hTERT 611-626) serves as a tumor antigen in B-cell chronic lymphocytic leukemia and generates spontaneously antileukemic, cytotoxic T cells. Exp Hematol; 2007 Feb;35(2):297-304
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase (hTERT 611-626) serves as a tumor antigen in B-cell chronic lymphocytic leukemia and generates spontaneously antileukemic, cytotoxic T cells.
  • In B-cell chronic lymphocytic leukemia (B-CLL), telomerase activity is increased in about 75% of patients.
  • The aim of this study was to analyze whether B-CLL patients with telomerase-positive leukemic cells had naturally occurring, telomerase-specific T cells that might be utilized for immune-mediated lysis of autologous tumor cells.
  • METHODS: Spontaneous T-cell immunity and cytotoxicity against hTERT was explored in B-CLL.
  • Nineteen of 25 B-CLL patients (76%) expressed hTERT (reverse transcriptase polymerase chain reaction) and 10 were selected for specific T-cell analysis against hTERT.
  • DC pulsed with the hTERT-peptide generated MHC class I-restricted, hTERT-specific cytotoxic T lymphocytes in six of seven telomerase-positive patients; mean cytotoxicity of hTERT-stimulated T cells was 49.8% +/- 9.3% vs 13.1 +/- 2.9% for Ras-stimulated T cells (p < 0.05).
  • In three of three telomerase-negative patients, no hTERT-specific cytotoxic T lymphocytes could be expanded.
  • CONCLUSION: Telomerase-positive B-CLL patients have spontaneously occurring cytotoxic hTERT-specific T cells.
  • This antigen might be explored as a therapeutic vaccine in B-CLL.
  • [MeSH-major] Antigens, Neoplasm / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Peptide Fragments / immunology. T-Lymphocytes, Cytotoxic / immunology. Telomerase / immunology

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  • (PMID = 17258078.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Histocompatibility Antigens Class I; 0 / Peptide Fragments; EC 2.7.7.- / GV1001 peptide; EC 2.7.7.49 / Telomerase
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71. Plaza JA, Comfere NI, Gibson LE, Colgan M, Davis DM, Pittelkow MR, Colgan JP: Unusual cutaneous manifestations of B-cell chronic lymphocytic leukemia. J Am Acad Dermatol; 2009 May;60(5):772-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual cutaneous manifestations of B-cell chronic lymphocytic leukemia.
  • BACKGROUND: B-cell chronic lymphocytic leukemia (B-CLL) is a low-grade lymphoproliferative disorder with characteristic histomorphologic features and an identifiable immunophenotype.
  • The skin can be involved in the context of known disease, but cutaneous signs are rarely the presenting findings.
  • OBJECTIVE: Evaluation of unusual clinical cutaneous presentations of B-CLL.
  • METHODS: We conducted a retrospective case series analysis of 3 patients with unusual cutaneous clinicopathologic presentations of B-cell chronic lymphocytic leukemia, including erythematous plaques, angiomatosis/telangiectasia, and erosive skin changes, respectively, without a previous clinical history of chronic lymphocytic lymphoma.
  • Main outcome measures were clinical cutaneous presentations and histopathologic results in the diagnosis of underlying disease.
  • Histomorphologic testing showed mild to dense perivascular and periadnexal lymphoid aggregates throughout the dermis and extending into the panniculus, consistent with B-CLL.
  • The diagnosis was confirmed with immunohistochemical studies that showed coexpression of CD5 and CD20 in the neoplastic lymphocytic infiltrate.
  • CONCLUSION: Cutaneous manifestations are an uncommon presentation of subclinical B-CLL.
  • Cutaneous changes were the presenting features of underlying lymphoma in all 3 cases, highlighting the importance of maintaining a high index of suspicion for a lymphoproliferative process in cases with unusual or atypical clinicopathologic features.
  • Additional investigations into the behavior of B-CLL in the skin may elucidate further the evolution of cutaneous lesions in this disease.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Skin / pathology. Skin Diseases / pathology


72. Robak T: Alemtuzumab for B-cell chronic lymphocytic leukemia. Expert Rev Anticancer Ther; 2008 Jul;8(7):1033-51
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  • [Title] Alemtuzumab for B-cell chronic lymphocytic leukemia.
  • Alemtuzumab (Campath, MabCampath) is a humanized therapeutic monoclonal antibody (mAb) that recognizes the CD52 antigen expressed on normal and neoplastic lymphoid cells.
  • This mAb is active in previously treated patients with B-cell chronic lymphocytic leukemia (B-CLL) refractory to alkylating agents and purine nucleoside analogs.
  • Alemtuzumab is also investigated in previously untreated patients with this leukemia.
  • The results of a prospective randomized Phase III study (CAM307 trial) comparing chlorambucil with alemtuzumab in the first-line treatment of progressive B-CLL were recently published.
  • Moreover, elimination of minimal residual disease occurred in one third of complete responders to alemtuzumab and none to chlorambucil.
  • In 2001, alemtuzumab was approved in the USA and Europe as a third-line therapy for patients with B-CLL who had been treated with alkylating agents and failed fludarabine therapy.
  • In September 2007, the US FDA, on the basis of CAM307 results, approved alemtuzumab for the treatment of previously untreated patients with B-CLL.
  • Moreover, the European Commission recently granted marketing authorization to alemtuzumab for the treatment of patients with B-CLL for whom fludarabine combination monotherapy is not appropriate.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Anemia, Hemolytic / drug therapy. Anemia, Hemolytic / etiology. Antibodies, Monoclonal, Humanized. Humans. Neoplasm, Residual. Neutropenia / drug therapy. Neutropenia / etiology. Purpura, Thrombocytopenic, Idiopathic / drug therapy. Purpura, Thrombocytopenic, Idiopathic / etiology. Red-Cell Aplasia, Pure / drug therapy. Red-Cell Aplasia, Pure / etiology

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  • (PMID = 18588450.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  • [Number-of-references] 139
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73. Coll-Mulet L, Iglesias-Serret D, Santidrián AF, Cosialls AM, de Frias M, Castaño E, Campàs C, Barragán M, de Sevilla AF, Domingo A, Vassilev LT, Pons G, Gil J: MDM2 antagonists activate p53 and synergize with genotoxic drugs in B-cell chronic lymphocytic leukemia cells. Blood; 2006 May 15;107(10):4109-14
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  • [Title] MDM2 antagonists activate p53 and synergize with genotoxic drugs in B-cell chronic lymphocytic leukemia cells.
  • B-cell chronic lymphocytic leukemia (B-CLL) is characterized by the accumulation of long-lived CD5(+) B lymphocytes.
  • Several drugs currently used in the therapy of B-CLL act, at least partially, through activation of the p53 pathway.
  • Recently, nongenotoxic small-molecule activators of p53, the nutlins, have been developed that inhibit p53-MDM2 binding.
  • We have investigated the antitumor potential of nutlin-3 in B-CLL and find that it can activate the p53 pathway and effectively induce apoptosis in cells with wild-type p53, including cells with dysfunctional ataxia telangiectasia mutated, but not mutant p53.
  • Normal human T cells showed lower sensitivity to nutlin-3 than B-CLL cells and no synergism with the genotoxic drugs.
  • These results suggest that MDM2 antagonists alone or in combination with chemotherapeutic drugs may offer a new treatment option for B-CLL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Lymphoma, B-Cell / drug therapy. Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Antigens, CD. Antigens, CD5. Apoptosis. Cell Line, Tumor. Flow Cytometry. Humans. Imidazoles / pharmacology. Piperazines / pharmacology

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  • (PMID = 16439685.001).
  • [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 / Antigens, CD; 0 / Antigens, CD5; 0 / Antineoplastic Agents; 0 / Imidazoles; 0 / Piperazines; 0 / Tumor Suppressor Protein p53; 0 / nutlin 3; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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74. Süss A, Wetzig T, Sticherling M, Tannapfel A, Simon JC: [Mycosis fungoides and B-cell chronic lymphocytic leukemia: an extremely rare coincidence]. Hautarzt; 2006 Oct;57(10):888-92
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  • [Title] [Mycosis fungoides and B-cell chronic lymphocytic leukemia: an extremely rare coincidence].
  • [Transliterated title] Mycosis fungoides und chronisch lymphatische B-zell-leukämie: eine äusserst seltene koinzidenz.
  • The simultaneous appearance of mycosis fungoides (MF) and B-cell chronic lymphocytic leukemia (B-CLL) in the same patient is extremely rare.
  • A 72-year-old patient was diagnosed with coincident MF, stage Ib, and B-CLL, Binet stage A.
  • Hypotheses on simultaneous occurrence of B- and T-cell malignancies as well as a new therapeutic option are discussed.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Mycosis Fungoides / diagnosis. Neoplasms, Multiple Primary / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Aged. Humans. Male. Rare Diseases / diagnosis


75. Baskar S, Suschak JM, Samija I, Srinivasan R, Childs RW, Pavletic SZ, Bishop MR, Rader C: A human monoclonal antibody drug and target discovery platform for B-cell chronic lymphocytic leukemia based on allogeneic hematopoietic stem cell transplantation and phage display. Blood; 2009 Nov 12;114(20):4494-502
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  • [Title] A human monoclonal antibody drug and target discovery platform for B-cell chronic lymphocytic leukemia based on allogeneic hematopoietic stem cell transplantation and phage display.
  • Allogeneic hematopoietic stem cell transplantation (alloHSCT) is the only potentially curative treatment available for patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • Here, we show that post-alloHSCT antibody repertoires can be mined for the discovery of fully human monoclonal antibodies to B-CLL cell-surface antigens.
  • Sera collected from B-CLL patients at defined times after alloHSCT showed selective binding to primary B-CLL cells.
  • To identify post-alloHSCT serum antibodies and subsequently B-CLL cell-surface antigens they recognize, we generated a human antibody-binding fragment (Fab) library from post-alloHSCT peripheral blood mononuclear cells and selected it on primary B-CLL cells by phage display.
  • A panel of Fab with B-CLL cell-surface reactivity was strongly enriched.
  • One Fab was converted to immunoglobulin G1 and analyzed for reactivity with peripheral blood mononuclear cells from B-CLL patients and healthy volunteers.
  • Cell-surface antigen expression was restricted to primary B cells and up-regulated in primary B-CLL cells.
  • Mining post-alloHSCT antibody repertoires offers a novel route to discover fully human monoclonal antibodies and identify antigens of potential therapeutic relevance to B-CLL and possibly other cancers.
  • Trials described herein were registered at www.clinicaltrials.gov as nos.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antigens, Neoplasm / immunology. Hematopoietic Stem Cell Transplantation. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Peptide Library

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  • (PMID = 19667400.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00003838/ NCT00055744
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Neoplasm; 0 / Antigens, Neoplasm; 0 / Immunoglobulin Fab Fragments; 0 / Peptide Library
  • [Other-IDs] NLM/ PMC2777128
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76. de Viron E, Knoops L, Connerotte T, Smal C, Michaux L, Saussoy P, Vannuffel P, Beert E, Vekemans MC, Hermans C, Bontemps F, Van Den Neste E: Impaired up-regulation of polo-like kinase 2 in B-cell chronic lymphocytic leukaemia lymphocytes resistant to fludarabine and 2-chlorodeoxyadenosine: a potential marker of defective damage response. Br J Haematol; 2009 Dec;147(5):641-52
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  • [Title] Impaired up-regulation of polo-like kinase 2 in B-cell chronic lymphocytic leukaemia lymphocytes resistant to fludarabine and 2-chlorodeoxyadenosine: a potential marker of defective damage response.
  • The functional evaluation of ataxia telangiectasia mutated (ATM) and p53 was recently developed in B-cell chronic lymphocytic leukaemia (B-CLL), a disease in which the response to DNA damage is frequently altered.
  • We identified a novel biomarker of chemosensitivity based on the induction of DNA damage by the purine nucleoside analogues (PNA) fludarabine and 2-chlorodeoxyadenosine (CdA).
  • Using a quantitative real time polymerase chain reaction, we confirmed that PNA dose- and time-dependently increased PLK2 expression in chemosensitive but not chemoresistant B-CLL samples.
  • Analysis of a larger cohort of B-CLL patients showed that cytotoxicity induced by PNA correlated well with PLK2 mRNA induction.
  • In conclusion, we propose that testing PLK2 activation after a 24-h incubation with PNA could be used to investigate the functional integrity of DNA damage-response pathways in B-CLL cells, and predict clinical sensitivity to these drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Protein-Serine-Threonine Kinases / biosynthesis. Up-Regulation / drug effects
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Death / drug effects. Cladribine / pharmacology. Cohort Studies. DNA Damage. DNA, Neoplasm / genetics. Drug Resistance, Neoplasm. Female. Gene Expression Profiling / methods. Gene Expression Regulation, Enzymologic / drug effects. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis / methods. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured. Vidarabine / analogs & derivatives. Vidarabine / pharmacology

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  • (PMID = 19764992.001).
  • [ISSN] 1365-2141
  • [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 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 47M74X9YT5 / Cladribine; EC 2.7.11.- / PLK2 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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77. Giannopoulos K, Schmitt M, Kowal M, Własiuk P, Bojarska-Junak A, Roliński J, Dmoszyńska A: The significance of soluble HLA-G plasma levels as well as messenger HLA-G for B-cell chronic lymphocytic leukemia (B-CLL). Leuk Res; 2008 Dec;32(12):1815-9
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  • [Title] The significance of soluble HLA-G plasma levels as well as messenger HLA-G for B-cell chronic lymphocytic leukemia (B-CLL).
  • The immunosuppression accompanies B-cell chronic lymphocytic leukemia (B-CLL) but might be also responsible for disease progression by enabling CLL cells to escape from the immunosurveillance.
  • Some particles involved in the regulation of an immune system might represent prognostic value for B-CLL.
  • To confront this hypothesis we characterized soluble HLA-G (sHLA-G) by the prognostic factors in the first cohort of 34 CLL patients.
  • No correlation was observed between sHLA-G levels in ZAP-70(+) and ZAP-70(-) CLL as well as in CD38(+) CLL and CD38(-) CLL patients.
  • Next, we wondered whether gene expression of HLA-G, which represent the whole HLA-G pool in the cell, posses prognostic value for CLL.
  • In the second cohort of 41 CLL patients we assessed messenger levels of HLA-G by the strongest prognostic factors in CLL including cytogenetics, IgVH mutational status, ZAP-70 as well as CD38.
  • No changes of HLA-G expression levels were found in different CLL groups characterized by IgVH gene mutational status, ZAP-70 as well as CD38.
  • We observed no differences in expression of HLA-G in various cytogenetic groups of CLL including del17p, del13q, del11q, +8q, +3q, del14q and del6q when compared to those with normal karyotype or with 12+.
  • Both, mRNA expression of HLA-G and levels of its soluble form in plasma bring no additional prognostic value for B-CLL patients.
  • [MeSH-major] HLA Antigens / blood. HLA Antigens / genetics. Histocompatibility Antigens Class I / blood. Histocompatibility Antigens Class I / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. RNA, Messenger / genetics

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  • (PMID = 18499249.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I; 0 / RNA, Messenger
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78. Jablonska E, Kiersnowska-Rogowska B, Rogowski F, Parfienczyk A, Puzewska W, Bukin M: TNF family molecules in the serum of patients with B-cell chronic lymphocytic leukemia (B-CLL). Leuk Lymphoma; 2005 Sep;46(9):1307-12
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  • [Title] TNF family molecules in the serum of patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • In the present study levels of TNF-alpha, sTNFRp55, sTNFRp75 and sCD40 and sCD40L in the serum of patients with B-CLL before and after treatment were measured.
  • Results obtained suggest that the relationships between examined soluble form of TNF family proteins may influence the development of B-cell chronic lymphocytic leukemia.
  • The used therapy with 2CdA and CMC led to a favorable effect for host through changes in the relations between sCD40 and sCD40L.
  • It was also found that sCD40 and sCD40L serum concentrations, which are dependent on the clinical stage and used therapy, are more sensitive tumor markers than TNF-alpha and its soluble receptor in patients with B-CLL treated with 2CdA and CMC.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / blood. Tumor Necrosis Factors / blood

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  • (PMID = 16109608.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Necrosis Factors; 147205-72-9 / CD40 Ligand
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79. Catherwood MA, Wall JP, Morris TC, Alexander HD: Detection of tumor-derived antigen receptor DNA by polymerase chain reaction in the serum of patients with B-cell chronic lymphocytic leukemia. Haematologica; 2005 Jul;90(7):992-4
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  • [Title] Detection of tumor-derived antigen receptor DNA by polymerase chain reaction in the serum of patients with B-cell chronic lymphocytic leukemia.
  • In this study, tumor derived and mononuculear cell DNA from 50 patients with B-cell chronic lymphocytic leukemia (B-CLL) was amplified by polymerase chain reaction (PCR) and analyzed using polyacrylamide electrophoressis and Genescan analysis.
  • [MeSH-major] DNA, Neoplasm / analysis. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Polymerase Chain Reaction / methods
  • [MeSH-minor] Antigens, Neoplasm / genetics. Cell Separation. Flow Cytometry. Gene Rearrangement. Humans. Immunoglobulin Heavy Chains / genetics. Leukocytes, Mononuclear / metabolism. Sensitivity and Specificity

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  • (PMID = 15996944.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA, Neoplasm; 0 / Immunoglobulin Heavy Chains
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80. Giannopoulos K, Schmitt M: Targets and strategies for T-cell based vaccines in patients with B-cell chronic lymphocytic leukemia. Leuk Lymphoma; 2006 Oct;47(10):2028-36
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  • [Title] Targets and strategies for T-cell based vaccines in patients with B-cell chronic lymphocytic leukemia.
  • T-cell based immunotherapies might be a novel option for the treatment of B-cell chronic lymphocytic leukemia (B-CLL), a disease characterized by a prolonged natural course.
  • Different strategies of active immunotherapy have been tested in vitro to enhance a specific T-cell response against tumor cells and an anti-leukemic effect has been observed in B-CLL patients after allogenic stem cell transplantation.
  • Several antigens have been characterized as tumor/leukemia associated antigens (T/LAAs) in B-CLL with the potential to elicit specific anti-tumor response encompassing idiotype immunoglobulin, oncofetal antigen-immature laminin receptor protein (OFAiLRP), survivin, as well as fibromodulin, the receptor for hyaluronic acid mediated motility (RHAMM/CD168) and the murine double-minute 2 oncoprotein (MDM2).
  • This study presents an overview of possible targets and genetherapeutical maneuvers for future immunotherapies of B-CLL patients and summarizes recent clinical vaccination trials with dendritic cells (DCs) for B-CLL.
  • [MeSH-major] Cancer Vaccines. Leukemia, Lymphocytic, Chronic, B-Cell / prevention & control. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. T-Lymphocytes / metabolism


81. Mao Z, Quintanilla-Martinez L, Raffeld M, Richter M, Krugmann J, Burek C, Hartmann E, Rudiger T, Jaffe ES, Müller-Hermelink HK, Ott G, Fend F, Rosenwald A: IgVH mutational status and clonality analysis of Richter's transformation: diffuse large B-cell lymphoma and Hodgkin lymphoma in association with B-cell chronic lymphocytic leukemia (B-CLL) represent 2 different pathways of disease evolution. Am J Surg Pathol; 2007 Oct;31(10):1605-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgVH mutational status and clonality analysis of Richter's transformation: diffuse large B-cell lymphoma and Hodgkin lymphoma in association with B-cell chronic lymphocytic leukemia (B-CLL) represent 2 different pathways of disease evolution.
  • Approximately 5% of B-cell chronic lymphocytic leukemia (B-CLL) patients develop a secondary aggressive lymphoma, usually of diffuse large B-cell type (DLBCL), termed Richter's transformation (RT).
  • Rarely, classic Hodgkin lymphoma (HL) is observed.
  • Published small series suggest that tumor cells in DLBCL and HL can be clonally identical to the B-CLL clone or arise as an independent, secondary lymphoma.
  • We describe the morphology, immunophenotype, and clinical features of 34 classic RT patients with DLBCL, 6 cases of B-CLL with HL, and 8 cases with scattered CD30-positive Hodgkin and Reed-Sternberg (HRS)-like cells.
  • In classic RT, 18/23 B-CLL cases (78%) showed clonal progression to DLBCL with identical IgVH sequences in both lymphoma components, whereas in 5 cases (22%) the DLBCL was clonally unrelated.
  • Immunophenotypically, most cases of DLBCL irrespective of clonal relatedness showed significant differences in phenotype compared with the B-CLL, with common loss of CD5 and CD23.
  • Using immuno-laser capture microdissection, sequencing of the IgVH CDR3 region of isolated HRS cells showed that 2/2 cases with HL were clonally unrelated, whereas they were clonally identical in 1/2 cases of B-CLL with scattered HRS-like cells.
  • Of interest, 5/6 cases of B-CLL with HL, and 5/6 cases of B-CLL with HRS cells showed mutated IgVH genes.
  • [MeSH-major] Hodgkin Disease / genetics. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Transformation, Neoplastic. Clone Cells. DNA Mutational Analysis. DNA, Neoplasm / analysis. Female. Gene Rearrangement, B-Lymphocyte. Humans. Lasers. Male. Microdissection. Middle Aged. Polymerase Chain Reaction. Somatic Hypermutation, Immunoglobulin


82. Joshi AD, Dickinson JD, Hegde GV, Sanger WG, Armitage JO, Bierman PJ, Bociek RG, Devetten MP, Vose JM, Joshi SS: Bulky lymphadenopathy with poor clinical outcome is associated with ATM downregulation in B-cell chronic lymphocytic leukemia patients irrespective of 11q23 deletion. Cancer Genet Cytogenet; 2007 Jan 15;172(2):120-6
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  • [Title] Bulky lymphadenopathy with poor clinical outcome is associated with ATM downregulation in B-cell chronic lymphocytic leukemia patients irrespective of 11q23 deletion.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common B-cell leukemia among older populations in Western countries.
  • The clinical course of B-CLL is heterogeneous: in some patients the disease course is indolent, in others it is aggressive.
  • The B-CLL subgroups with chromosome 11q23 deletion have been associated with aggressive disease course involving ATM deletion, extensive bulky lymphadenopathy (BLA), and inferior clinical outcome.
  • Using real-time reverse transcriptase-polymerase chain reaction, we found that ATM was consistently underexpressed in B-CLL patients with BLA, irrespective of 11q23 deletion status.
  • In addition, B-CLL patients who presented with BLA had a significantly shorter time to treatment (2 months) than did patients without BLA (74 months).
  • Moreover, gene expression analysis in B-CLL patients with and without BLA revealed differences in expression for genes involved in apoptosis, cell cycle, and cell adhesion.
  • These results indicate an association between BLA and reduced expression of ATM, suggesting a role for ATM in disease progression in B-CLL.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Down-Regulation / genetics. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphatic Diseases / genetics. Protein-Serine-Threonine Kinases / biosynthesis. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / biosynthesis. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Cell Adhesion / genetics. Cell Cycle / genetics. Female. Humans. Male. Middle Aged. Prognosis

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  • (PMID = 17213020.001).
  • [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
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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83. Battle TE, Arbiser J, Frank DA: The natural product honokiol induces caspase-dependent apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) cells. Blood; 2005 Jul 15;106(2):690-7
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  • [Title] The natural product honokiol induces caspase-dependent apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) cells.
  • B-cell chronic lymphocytic leukemia (B-CLL) remains an incurable disease that requires innovative new approaches to improve therapeutic outcome.
  • We examined whether honokiol can overcome apoptotic resistance in primary tumor cells derived from B-CLL patients.
  • Honokiol induced caspase-dependent cell death in all of the B-CLL cells examined and was more toxic toward B-CLL cells than to normal mononuclear cells, suggesting greater susceptibility of the malignant cells.
  • Exposure of B-CLL cells to honokiol resulted in up-regulation of Bcl2-associated protein (Bax) and down-regulation of the expression of the key survival protein myeloid-cell leukemia sequence 1 (Mcl-1), which is associated with response to treatment in B-CLL patients.
  • In addition, B-CLL cells pretreated with interleukin-4 (IL-4), a cytokine known to support B-CLL survival, underwent apoptosis when subsequently incubated with honokiol, indicating that honokiol could also overcome the prosurvival effects of IL-4.
  • These data indicate that honokiol is a potent inducer of apoptosis in B-CLL cells and should be examined for further clinical application either as a single agent or in combination with other anticancer agents.
  • [MeSH-major] Apoptosis / drug effects. Biphenyl Compounds / pharmacology. Drugs, Chinese Herbal / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lignans / pharmacology. Phytotherapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Caspases / metabolism. Chlorambucil / administration & dosage. Cladribine / administration & dosage. Dose-Response Relationship, Drug. Humans. In Vitro Techniques. Interleukin-4 / pharmacology. Magnolia. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism

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  • (PMID = 15802533.001).
  • [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 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Drugs, Chinese Herbal; 0 / Lignans; 0 / MCL1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 11513CCO0N / honokiol; 18D0SL7309 / Chlorambucil; 207137-56-2 / Interleukin-4; 47M74X9YT5 / Cladribine; EC 3.4.22.- / Caspases; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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84. Terrin L, Trentin L, Degan M, Corradini I, Bertorelle R, Carli P, Maschio N, Bo MD, Noventa F, Gattei V, Semenzato G, De Rossi A: Telomerase expression in B-cell chronic lymphocytic leukemia predicts survival and delineates subgroups of patients with the same igVH mutation status and different outcome. Leukemia; 2007 May;21(5):965-72
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  • [Title] Telomerase expression in B-cell chronic lymphocytic leukemia predicts survival and delineates subgroups of patients with the same igVH mutation status and different outcome.
  • Activation of telomerase reverse transcriptase (hTERT) is essential for unlimited cell growth and plays a critical role in tumorigenesis.
  • We investigated hTERT gene expression in 134 B-cell chronic lymphocytic leukemia (B-CLL) cases and evaluated its prognostic value with other prognostic markers (IgVH mutation status, CD38 and ZAP-70 expression).
  • Real-time PCR assays to quantify either all hTERT transcripts (AT) or only the full length (FL) transcript encoding the functional protein were developed. hTERT-AT levels strongly correlated with hTERT-FT levels (r=0.743, P<0.0001); both inversely correlated with the percentage of IgVH mutation (P<0.005) and were significantly higher in unmutated than in mutated cases (P=0.004 and P=0.001, respectively).
  • Using these cut-off values, there was a significant difference in the survival of patients with high or low hTERT levels (P<0.0001).
  • Unmutated cases with low hTERT levels had an overall survival close to mutated cases with high hTERT levels.
  • Thus, this work identifies hTERT-RNA level as a new prognostic marker in B-CLL, and may be used to identify previously unrecognized patient groups with the same IgVH mutation status and different disease outcomes.
  • [MeSH-major] Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Mutation. Telomerase / genetics
  • [MeSH-minor] Adult. Aged. Antigens, CD38 / analysis. B-Lymphocytes / enzymology. Female. Humans. Male. Middle Aged. ZAP-70 Protein-Tyrosine Kinase / analysis

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  • (PMID = 17344921.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [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; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 3.2.2.5 / Antigens, CD38
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85. Sanchez-Aguilera A, Rattmann I, Drew DZ, Müller LU, Summey V, Lucas DM, Byrd JC, Croce CM, Gu Y, Cancelas JA, Johnston P, Moritz T, Williams DA: Involvement of RhoH GTPase in the development of B-cell chronic lymphocytic leukemia. Leukemia; 2010 Jan;24(1):97-104
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  • [Title] Involvement of RhoH GTPase in the development of B-cell chronic lymphocytic leukemia.
  • RhoH is a hematopoietic-specific, GTPase-deficient member of the Rho GTPase family that functions as a regulator of thymocyte development and T-cell receptor signaling by facilitating localization of zeta-chain-associated protein kinase 70 (ZAP70) to the immunological synapse.
  • Here we investigated the function of RhoH in the B-cell lineage.
  • B-cell receptor (BCR) signaling was intact in Rhoh(-/-) mice.
  • Because RhoH interacts with ZAP70, which is a prognostic factor in B-cell chronic lymphocytic leukemia (CLL), we analyzed the mRNA levels of RhoH in primary human CLL cells and showed a 2.3-fold higher RhoH expression compared with normal B cells.
  • RhoH expression in CLL positively correlated with the protein levels of ZAP70.
  • Deletion of Rhoh in a murine model of CLL (Emu-TCL1(Tg) mice) significantly delayed the accumulation of CD5(+)IgM(+) leukemic cells in peripheral blood and the leukemic burden in the peritoneal cavity, bone marrow and spleen of Rhoh(-/-) mice compared with their Rhoh(+/+) counterparts.
  • These data suggest that RhoH has a function in the progression of CLL in a murine model and show RhoH expression is altered in human primary CLL samples.

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  • (PMID = 19847197.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113969; United States / NCI NIH HHS / CA / R01 CA113969-05; United States / NIDDK NIH HHS / DK / R01 DK062757; United States / NCI NIH HHS / CA / CA113969
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, B-Cell; 0 / RhoH protein, human; 0 / RhoH protein, mouse; 0 / Transcription Factors; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 2.7.10.2 / Zap70 protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ NIHMS158682; NLM/ PMC3869226
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86. Quiney C, Billard C, Faussat AM, Salanoubat C, Ensaf A, Naït-Si Y, Fourneron JD, Kolb JP: Pro-apoptotic properties of hyperforin in leukemic cells from patients with B-cell chronic lymphocytic leukemia. Leukemia; 2006 Mar;20(3):491-7
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  • [Title] Pro-apoptotic properties of hyperforin in leukemic cells from patients with B-cell chronic lymphocytic leukemia.
  • The effects of the hyperforin (HF), a natural phloroglucinol purified from Hypericum perforatum, were investigated ex vivo on leukemic cells from patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • HF was found to promote apoptosis of B-CLL cells, as shown by time- and dose-dependent stimulation of phosphatidylserine externalization and DNA fragmentation, by disruption of the mitochondrial transmembrane potential, caspase-3 activation and cleavage of the caspase substrate PARP-1.
  • HF also downregulated two proteins which are overexpressed by B-CLL patients' cells, the cell cycle inhibitor p27kip1 through caspase-dependent cleavage into a p23 form, and the nitric oxid (NO) synthase of type 2 (inducible NO synthase).
  • This latter was accompanied by reduction in the production of NO known to be antiapoptotic in B-CLL cells.
  • Preventing effects of the general caspase inhibitor z-VAD-fmk indicated that HF-promoted apoptosis of B-CLL cells was mostly caspase dependent.
  • Furthermore, normal B lymphocytes purified from healthy donors appeared less sensitive to HF-induced apoptosis than B-CLL cells.
  • These results indicate that HF may be of interest in the development of new therapies for B-CLL based on the induction of apoptosis and combination with cell cycle-dependent antitumor drugs.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Phloroglucinol / analogs & derivatives. Terpenes / pharmacology
  • [MeSH-minor] Bicyclo Compounds / pharmacology. Blotting, Western. Caspases / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Humans. Nitric Oxide / antagonists & inhibitors. Nitric Oxide / biosynthesis. Nitric Oxide Synthase Type II / antagonists & inhibitors

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  • (PMID = 16424868.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bicyclo Compounds; 0 / Terpenes; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 31C4KY9ESH / Nitric Oxide; DHD7FFG6YS / Phloroglucinol; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 3.4.22.- / Caspases; RM741E34FP / hyperforin
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87. Pozdnyakova O, Stachurski D, Hutchinson L, Ramakrishnan S, Miron PM: Trisomy 8 in B-cell chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2008 May;183(1):49-52
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  • [Title] Trisomy 8 in B-cell chronic lymphocytic leukemia.
  • Association between trisomy 8 and myeloid disorders/malignancies has been well documented.
  • We report on two patients with a known history of B-cell chronic lymphocytic leukemia (B-CLL) with bone marrow involvement.
  • In addition to the classic B-CLL cytogenetic abnormalities in one of the patients, both showed a trisomy 8 clone in their bone marrow specimens.
  • We believe that this finding signifies the development of myelodysplastic syndrome (de novo or therapy related), rather than progression of B-CLL with the occurrence of a new clone, and that in general, it has implications for the finding of trisomy 8 in CLL.
  • [MeSH-major] Chromosomes, Human, Pair 8. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Trisomy

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  • (PMID = 18474297.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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88. Ghiotto F, Fais F, Tenca C, Tomati V, Morabito F, Casciaro S, Mumot A, Zoppoli G, Ciccone E, Parodi S, Bruno S: Apoptosis of B-cell chronic lymphocytic leukemia cells induced by a novel BH3 peptidomimetic. Cancer Biol Ther; 2009 Feb;8(3):263-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Apoptosis of B-cell chronic lymphocytic leukemia cells induced by a novel BH3 peptidomimetic.
  • B-cell chronic lymphocytic leukemia (B-CLL) is the most common leukemia in human adults of the Western world and no definitive cure is yet available.
  • The disease is characterized by accumulation of clonal malignant B lymphocytes resistant to apoptosis.
  • Strategies to hit the anti-apoptotic drift of the Bcl-2 family in B-CLL cells are being explored.
  • A novel peptidomimetic based on the BH3 domain of the pro-apoptotic protein Bim and recently shown to exert significant apoptotic activity on acute myeloid leukemia cells, both in vitro and in vivo, was assayed on ex-vivo derived leukemic cells from untreated B-CLL patients (n = 7).
  • We found that this peptide, named 072RB, induced apoptosis of B-CLL samples at a concentration that does not affect viability of peripheral and bone marrow derived lymphocytes from healthy donors.
  • The negative control peptide 072RBL94A was ineffective for B-CLL cells, supporting the sequence specificity of 072RB activity.
  • No relationship was found between responsiveness to 072RB and Mcl-1/Bcl-X(L) basal levels or decrease magnitude, possibly because of the limited sample size of the study.
  • Altogether, we demonstrate that 072RB induces significant apoptosis of B-CLL cells subsequent to Bcl-X(L) and Mcl-1 downregulation.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Peptides / pharmacology
  • [MeSH-minor] Biomarkers / analysis. Cell Culture Techniques. Down-Regulation. Flow Cytometry. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Phosphatidylserines / analysis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. bcl-2 Homologous Antagonist-Killer Protein / biosynthesis. bcl-2-Associated X Protein / biosynthesis. bcl-X Protein / biosynthesis

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  • (PMID = 19164937.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 072RB peptide; 0 / BAK1 protein, human; 0 / BCL2L1 protein, human; 0 / Biomarkers; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Peptides; 0 / Phosphatidylserines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein
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89. Catherwood MA, Matthews C, Niblock R, Dobbin E, Morris TC, Alexander HD: ZAP-70 mRNA quantification in B-cell chronic lymphocytic leukaemia. Eur J Haematol; 2006 Apr;76(4):294-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 mRNA quantification in B-cell chronic lymphocytic leukaemia.
  • OBJECTIVE: The mutational status of the immunoglobulin (Ig) V(H) gene in B-cell chronic lymphocytic leukaemia (B-CLL) identifies two subgroups of patients with significantly different outcomes.
  • We investigated the association of ZAP-70 expression with IgVH mutational status in B-CLL by quantifying ZAP-70 mRNA, to evaluate its use as a surrogate marker for mutational status.
  • The aim of this study was to develop a quantitative reverse transcriptase-polymerase chain reaction (RQ-PCR) assay for the detection of ZAP-70 expression in a group of patients whose mutational status and cytogenetics had been determined previously.
  • METHODS: RQ-PCR was used to analyse ZAP-70 expression from 42 B-CLL patients.
  • CONCLUSION: This paper describes an RQ-PCR assay for the detection of ZAP-70 expression and confirms that IgV(H) unmutated CLL cells have a high expression of ZAP-70 in comparison with IgVH mutated CLL.
  • This robust method acts as a surrogate marker for IgVH mutational status albeit with <100% concordance.
  • [MeSH-major] Gene Expression Regulation, Leukemic / genetics. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Mutation. ZAP-70 Protein-Tyrosine Kinase / genetics

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  • (PMID = 16519700.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / RNA, Messenger; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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90. Perez-Chacon G, Rosado S, Rebolleda N, Losada-Fernandez I, Vargas JA, Morado M, Jorda J, Perez-Aciego P: Prognostic irrelevance of HLA-G in B-cell chronic lymphocytic leukemia. Int J Lab Hematol; 2009 Jun;31(3):327-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic irrelevance of HLA-G in B-cell chronic lymphocytic leukemia.
  • Recently, positive HLA-G surface expression has been associated with a poor prognosis in a small group of patients with B-cell chronic lymphocytic leukemia (B-CLL), a lymphoproliferative disorder characterized by a heterogeneous clinical course.
  • In the present work, 169 patients suffering from B-CLL were analyzed for the expression of HLA-G by flow cytometry in order to verify its prognostic value in a larger cohort.
  • We observed a low expression of this molecule on leukemic B cells and no significant relation to clinical data or progression-free survival time, indicating that this molecule is not as good immunologic prognostic marker for B-CLL as suggested.
  • [MeSH-major] B-Lymphocytes / immunology. HLA Antigens / analysis. Histocompatibility Antigens Class I / analysis. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis

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  • (PMID = 18241213.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I
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91. Barcellini W, Capalbo S, Agostinelli RM, Mauro FR, Ambrosetti A, Calori R, Cortelezzi A, Laurenti L, Pogliani EM, Pedotti P, Liso V, Girelli G, Mandelli F, Zanella A, GIMEMA Chronic Lymphocytic Leukemia Group: Relationship between autoimmune phenomena and disease stage and therapy in B-cell chronic lymphocytic leukemia. Haematologica; 2006 Dec;91(12):1689-92
Archivio Istituzionale della Ricerca Unimi. Full text from AIR - Univ. Milan .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship between autoimmune phenomena and disease stage and therapy in B-cell chronic lymphocytic leukemia.
  • The aim of this multicenter GIMEMA study was to correlate autoimmune complications (AIC) in B-cell chronic lymphocytic leukemia (B-CLL) with stage and therapy.
  • Autoimmune hemolytic anemia (129/194 cases) and autoimmune thrombocytopenia (35/194 cases) were typically present in advanced and multi-treated disease.
  • In contrast, non-hematologic AIC (30/194 cases) and the presence of serological markers of autoimmunity were mostly observed in early B-CLL, suggesting different pathogenic mechanisms underlying hematologic and non-hematologic autoimmune phenomena in B-CLL.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Purpura, Thrombocytopenic, Idiopathic / immunology

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  • (PMID = 17145607.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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92. Nückel H, Switala M, Sellmann L, Horn PA, Dürig J, Dührsen U, Küppers R, Grosse-Wilde H, Rebmann V: The prognostic significance of soluble NKG2D ligands in B-cell chronic lymphocytic leukemia. Leukemia; 2010 Jun;24(6):1152-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic significance of soluble NKG2D ligands in B-cell chronic lymphocytic leukemia.
  • Soluble or membrane-anchored ligands of NKG2D and their receptor have a critical role in the elimination of tumor cells and disease progression.
  • Plasma samples of 98 patients with B-cell chronic lymphocytic leukemia (CLL) were analyzed with specific ELISA systems for soluble major histocompatibility complex class I-related chains (sMICA and sMICB) and UL-16-binding proteins (ULBP1, 2, and 3).
  • The flow cytometric analysis of MICA on CLL cells and natural killer group 2 member D (NKG2D) receptors on NK cells was performed after thawing of frozen peripheral blood lymphocytes of CLL patients (N=51).
  • Levels of sMICA, sMICB, and sULBP2 were significantly increased (P<0.001) compared with 48 controls, whereas sULBP1 3 were not detectable in patients and controls.
  • Levels of sMICA>990 pg/ml (P=0.014), sMICB>200 pg/ml (P=0.0001), and sULBP2>105 pg/ml (P<0.0001) were associated with poor treatment-free survival (TFS).
  • Our data show that soluble but not membrane-anchored NKG2D ligands or receptors are of prognostic significance in CLL.
  • Moreover, sULBP2 seems to be useful to identify early-stage patients with risk of disease progression.
  • [MeSH-major] Histocompatibility Antigens Class I / blood. Intercellular Signaling Peptides and Proteins / blood. Leukemia, Lymphocytic, Chronic, B-Cell / blood

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  • (PMID = 20428196.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Histocompatibility Antigens Class I; 0 / Intercellular Signaling Peptides and Proteins; 0 / MHC class I-related chain A; 0 / MICB antigen; 0 / ULBP2 protein, human; 0 / ULBP3 protein, human
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93. Molica S, Vitelli G, Cutrona G, Todoerti K, Mirabelli R, Digiesi G, Giannarelli D, Sperduti I, Molica M, Gentile M, Morabito F, Neri A, Ferrarini M: Prognostic relevance of serum levels and cellular expression of adiponectin in B-cell chronic lymphocytic leukemia. Int J Hematol; 2008 Nov;88(4):374-80
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic relevance of serum levels and cellular expression of adiponectin in B-cell chronic lymphocytic leukemia.
  • The correlation between well-established biological parameters of prognostic relevance in B-cell chronic lymphocytic leukaemia (CLL) [i.e., mutational status of the immunoglobulin heavy chain variable region (IgV(H)), ZAP-70- and CD38-expression] and adiponectin serum concentration was evaluated in a cohort of 69 previously untreated Binet stage A CLL patients.
  • Adiponectin levels inversely correlated with absolute peripheral blood lymphocyte count (r = -0.254; P = 0.03), CD38-positive CLL cells (r = -0.294; P = 0.04) and ZAP-70 (r = -0.285; P = 0.03).
  • The levels of adiponectin in CLL were evaluated in 60 patients from an independent cohort investigated by gene expression profiling.
  • Adiponectin gene expression was invariably low suggesting a limited (if any) role of leukemic cells in the production of circulating adiponectin levels.
  • In contrast, both adiponectin receptor 1 (AdipoR1) and AdipoR2 mRNA were highly expressed by CLL cells with a degree of inter-patient variability.
  • [MeSH-major] Adipocytes / secretion. Adiponectin / blood. Biomarkers, Tumor / blood. Bone Marrow Cells / secretion. Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / blood

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  • (PMID = 18818986.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / ADIPOR1 protein, human; 0 / ADIPOR2 protein, human; 0 / Adiponectin; 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Receptors, Adiponectin; 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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94. Molica S, Vitelli G, Mirabelli R, Digiesu G, Giannarelli D, Cuneo A, Ribatti D, Vacca A: Serum insulin-like growth factor is not elevated in patients with early B-cell chronic lymphocytic leukemia but is still a prognostic factor for disease progression. Eur J Haematol; 2006 Jan;76(1):51-7
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum insulin-like growth factor is not elevated in patients with early B-cell chronic lymphocytic leukemia but is still a prognostic factor for disease progression.
  • OBJECTIVES: Insulin-like growth factor 1 (IGF-1) is an important growth and anti-apoptotic factor for the cancer cells in several malignancies and in multiple myeloma recent studies support the hypothesis of a role for IGF-1 in disease progression; however, clinico-biological relevance of IGF-1 was never studied in B-cell chronic lymphocytic leukemia (CLL).
  • PATIENTS AND METHODS: Using a quantitative sandwich immunoassay technique (ELISA) (Quantikine, Human IGF-1 and IGFBP-3, R&D Systems), we measured the concentration of IGF-1 and its major binding protein IGF-binding protein 3 (IGFBP-3) in serum drawn at the time of diagnosis from 77 Binet stage A CLL patients.
  • RESULTS: Either IGF-1 or IGFBP-3 were significantly decreased compared with healthy age- and sex-matched controls (P < 0.0001 for both; Mann-Whitney test).
  • When correlation were attempted with circulating levels of angiogenic cytokines such as vascular endothelial growth factor (P = 0.971), basic fibroblastic growth factor (P = 0.695), angiogenin (P = 0.282) or adhesion molecules such as vascular cell adhesion molecule-1 (P = 0.318), intercellular adhesion molecule-1 (P = 0.883) and platelet endothelial cell adhesion molecule-1 (P = 0.772) similar results were found.
  • Serum levels of IGF-1 were further evaluated as a dichotomous variable with respect to progression-free survival (PFS), an endpoint surrogate for overall survival in early B-cell CLL.
  • Median PFS was 63 months in the patient group with low IGF-1, compared with a median PFS of 40 months in the remaining patients (P = 0.03).
  • However, after removing from analysis LDT (only six of 77 had an LDT < 12 months), either IGF-1 or Rai substage entered the model at a significant level (P = 0.03 and P = 0.01, respectively).
  • CONCLUSIONS: IGF-1 did not correlate with markers of tumor burden or clinical status in CLL thus suggesting that levels of this cytokine do not reflect the intrinsic malignancy of disease.
  • Results of the present study highlight, however, its involvement in mechanisms of disease progression in early CLL.
  • [MeSH-major] Biomarkers, Tumor / blood. Insulin-Like Growth Factor I / analysis. Leukemia, Lymphocytic, Chronic, B-Cell / blood
  • [MeSH-minor] Age Factors. Aged. Aged, 80 and over. Disease Progression. Disease-Free Survival. Female. Growth Substances / blood. Humans. Hydro-Lyases / blood. Insulin-Like Growth Factor Binding Protein 3 / blood. Leukocyte Count. Male. Middle Aged. Multiple Myeloma / blood. Multiple Myeloma / mortality. Multiple Myeloma / pathology. Predictive Value of Tests. Prognosis. Tumor Burden. beta 2-Microglobulin / blood

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  • (PMID = 16343271.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Growth Substances; 0 / Insulin-Like Growth Factor Binding Protein 3; 0 / beta 2-Microglobulin; 67763-96-6 / Insulin-Like Growth Factor I; EC 4.2.1.- / Hydro-Lyases; EC 4.2.1.54 / lactate dehydratase
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95. Fabris S, Mosca L, Todoerti K, Cutrona G, Lionetti M, Intini D, Matis S, Colombo M, Agnelli L, Gentile M, Spriano M, Callea V, Festini G, Molica S, Lambertenghi Deliliers G, Morabito F, Ferrarini M, Neri A: Molecular and transcriptional characterization of 17p loss in B-cell chronic lymphocytic leukemia. Genes Chromosomes Cancer; 2008 Sep;47(9):781-93
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  • [Title] Molecular and transcriptional characterization of 17p loss in B-cell chronic lymphocytic leukemia.
  • Distinct genetic abnormalities, such as TP53 deletion at 17p13.1, have been identified as having adverse prognostic relevance in B-cell chronic lymphocytic leukemia (B-CLL), and conventional cytogenetic studies have shown that TP53 deletion in B-CLL is mainly associated with the loss of 17p due to complex chromosomal rearrangements.
  • We used an integrative genomic approach to investigate the significance of 17p loss in 18 B-CLLs in Binet stage A, carrying a TP53 monoallelic deletion detected by means of fluorescence in situ hybridization (FISH).
  • FISH analysis confirmed these findings and revealed 17p loss in a small fraction of leukemic cells in the remaining TP53-deleted case, and it also indicated 17p loss in the six cases not investigated by means of SNP arrays.
  • Gene-expression profiling of 60 B-CLLs, including seven patients with 17p loss, identified 40 differentially expressed genes in 17p- versus 17p normal samples, 35 of which were downregulated in 17p-tumors.
  • Our data provide evidence that 17p loss may play an additional pathogenetic role in B-CLL and suggest that the concomitant loss of multiple tumor suppressor genes could be responsible for the highly adverse prognostic relevance associated with TP53 loss.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 17. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Transcription, Genetic

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  • [Copyright] 2008 Wiley-Liss, Inc.
  • (PMID = 18521849.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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96. Gryshchenko I, Hofbauer S, Stoecher M, Daniel PT, Steurer M, Gaiger A, Eigenberger K, Greil R, Tinhofer I: MDM2 SNP309 is associated with poor outcome in B-cell chronic lymphocytic leukemia. J Clin Oncol; 2008 May 10;26(14):2252-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MDM2 SNP309 is associated with poor outcome in B-cell chronic lymphocytic leukemia.
  • PURPOSE: A single nucleotide polymorphism (SNP) at position 309 in the promoter region of MDM2 leading to increased expression of MDM2 and attenuated function of p53 has been negatively associated with onset and outcome of disease in solid tumors.
  • Because inactivation of p53 by deletion and/or mutations also impacts on the clinical course of B-cell chronic lymphocytic leukemia (B-CLL), we assessed the role of the SNP309 genotype in B-CLL.
  • PATIENTS AND METHODS: The frequency of SNP309 T/T, T/G, or G/G genotypes and the p53 status (wild type, mutated, or deleted) were assessed and correlated with clinical outcome in 140 B-CLL patients and a second independent cohort.
  • In addition, the correlation of the MDM2 SNP309 genotype with the MDM2 protein expression level in B-CLL cells was evaluated by immunoblotting.
  • RESULTS: A significant negative association of the SNP309 T/G and G/G genotypes with overall survival was seen (T/G genotype, relative risk = 3.7; 95% CI, 1.2 to 11.5; P = .02; G/G genotype, relative risk = 9.1; 95% CI, 2.4 to 35.1; P = .001), but no correlation with incidence or onset of B-CLL was observed.
  • The influence of the heterozygous SNP309 T/G genotype on treatment-free survival depended on the p53 status but not on the CD38, Zap-70, or IgVH mutational status or Rai stage of B-CLL patients.
  • CONCLUSION: The MDM2 SNP309 genotype influencing MDM2 expression levels was identified as an additional independent risk factor in B-CLL.
  • Targeting MDM2-p53 interactions might emerge as a successful treatment strategy for B-CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Proto-Oncogene Proteins c-mdm2 / genetics

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  • [CommentIn] J Clin Oncol. 2008 May 10;26(14):2244-5 [18467712.001]
  • (PMID = 18467716.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Membrane Glycoproteins; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; EC 6.3.2.19 / MDM2 protein, human; EC 6.3.2.19 / Proto-Oncogene Proteins c-mdm2
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97. Gamberale R, Fernández-Calotti P, Sánchez-Avalos J, Alberto MF, Geffner J, Giordano M: The effect of fludarabine on interferon-gamma production by lymphoid cells from healthy donors and patients with B-cell chronic lymphocytic leukemia. Haematologica; 2006 Apr;91(4):574-6
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of fludarabine on interferon-gamma production by lymphoid cells from healthy donors and patients with B-cell chronic lymphocytic leukemia.
  • Fludarabine treatment in patients with B-cell chronic lymphocytic leukemia (B-CLL) can trigger or exacerbate the development of autoimmune hemolytic anemia (AHA) through a currently ill-defined mechanism.
  • We here show that exposure of peripheral blood lymphocytes from healthy donors and B-CLL patients to fludarabine increases in vitro production of interferon-gamma, a key cytokine in the pathogenesis of AHA.
  • [MeSH-major] Interferon-gamma / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Anemia, Hemolytic, Autoimmune / chemically induced. Anemia, Hemolytic, Autoimmune / etiology. Case-Control Studies. Humans. Lymphocytes / drug effects

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  • (PMID = 16533725.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 82115-62-6 / Interferon-gamma; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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98. Bojarska-Junak A, Hus I, Chocholska S, Wasik-Szczepanek E, Sieklucka M, Dmoszyńska A, Roliński J: BAFF and APRIL expression in B-cell chronic lymphocytic leukemia: correlation with biological and clinical features. Leuk Res; 2009 Oct;33(10):1319-27
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BAFF and APRIL expression in B-cell chronic lymphocytic leukemia: correlation with biological and clinical features.
  • B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) are involved in normal B cell survival and differentiation.
  • We analyzed BAFF and APRIL plasma levels in patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • We also tested intracellular BAFF and APRIL expression in B-CLL and evaluated their prognostic relevance.
  • Moreover, we found a close relationship between LPL protein expression or LPL/ADAM29 MFI ratio and proportion of B-CLL cells with intracellular BAFF or APRIL expression.
  • Furthermore, patients with a low percentage of leukemic cells with intracellular BAFF or APRIL expression had a significantly longer overall survival than those with a high proportion of APRIL or BAFF positive leukemic cells.
  • [MeSH-major] B-Cell Activating Factor / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Tumor Necrosis Factor Ligand Superfamily Member 13 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. B-Lymphocytes / pathology. Female. Humans. Male. Middle Aged. Neoplasm Staging. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction. Survival Analysis. Survivors

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  • [CommentIn] Leuk Res. 2009 Oct;33(10):1306-7 [19464058.001]
  • (PMID = 19395025.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / RNA, Neoplasm; 0 / TNFSF13 protein, human; 0 / TNFSF13B protein, human; 0 / Tumor Necrosis Factor Ligand Superfamily Member 13
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99. Jablonska E, Kiersnowska-Rogowska B, Aleksandrowicz-Bukin M, Rogowski F, Sawicka-Powierza J: TRAIL receptors in the serum of patients with B-cell chronic lymphocytic leukemia. Neoplasma; 2008;55(1):51-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TRAIL receptors in the serum of patients with B-cell chronic lymphocytic leukemia.
  • Great importance in the course of chronic B-cell lymphocytic leukemia (B-CLL) has been ascribed to cytokines belonging to the superfamily of the tumor necrosis factor (TNF), including TRAIL (TNF-related apoptosis inducing ligand) and its specific receptors: TRAIL receptor 1 (TRAIL-R1), TRAIL receptor 2 (TRAIL-R2), TRAIL receptor 3 (TRAIL-R3), TRAIL receptor 4 (TRAIL-R4) and osteoprotegerin (OPG).
  • The aim of the study was to assess the levels of sTRAIL molecule and soluble TRAIL receptors - sTRAIL-R2 and OPG in the serum of patients with B-CLL.
  • The relationships between TRAIL and its natural regulators in the serum of BCLL patients prior to treatment may impair apoptosis of leukemic B cells.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / blood. Osteoprotegerin / blood. Receptors, TNF-Related Apoptosis-Inducing Ligand / blood


100. Malcikova J, Smardova J, Pekova S, Cejkova S, Kotaskova J, Tichy B, Francova H, Doubek M, Brychtova Y, Janek D, Pospisilova S, Mayer J, Dvorakova D, Trbusek M: Identification of somatic hypermutations in the TP53 gene in B-cell chronic lymphocytic leukemia. Mol Immunol; 2008 Mar;45(5):1525-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of somatic hypermutations in the TP53 gene in B-cell chronic lymphocytic leukemia.
  • Abnormalities of the TP53 gene are associated with a particularly severe prognosis in patients with B-cell chronic lymphocytic leukemia (B-CLL).
  • This tumor-suppressor is mostly inactivated by the deletion of one and point mutation of the other allele and has not been previously shown to be hypermutated in B-CLL.
  • We identified two patients whose lymphocytes showed repeatedly an extensive proportion of TP53 mutated cells by FASAY analysis (the yeast functional assay) and harbored various TP53 mutations, mostly single-base substitutions, in individual cells.
  • In the first patient (harboring the unmutated IgVH locus) a significant bias to point mutations at CG pairs (21/25; P=0.009), their remarkable preference for the RGYW/WRCY motives (28%) and the highest expression of the activation-induced cytidine deaminase (AID) mRNA among the 34 tested B-CLL samples.
  • Our findings add a new aspect to the mosaic of the p53 mutability in B-CLL.
  • [MeSH-major] Genes, p53. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Mutation
  • [MeSH-minor] Cytidine Deaminase / genetics. Humans. Lymphocytes / pathology. Point Mutation. Somatic Hypermutation, Immunoglobulin

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  • (PMID = 17920683.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.5.4.5 / Cytidine Deaminase
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