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1. Tyner JW, Fletcher LB, Wang EQ, Yang WF, Rutenberg-Schoenberg ML, Beadling C, Mori M, Heinrich MC, Deininger MW, Druker BJ, Loriaux MM: MET receptor sequence variants R970C and T992I lack transforming capacity. Cancer Res; 2010 Aug 1;70(15):6233-7
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  • We screened patients with chronic lymphocytic leukemia (CLL), acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML), colorectal cancer, endometrial cancer, thyroid cancer, or melanoma, as well as individuals without cancer, and found these variants at low frequencies in most cohorts, including normal individuals.
  • No evidence of increased phosphorylation or transformative capacity by either sequence variant was found.
  • Because small-molecule inhibitors for MET are currently in development, it will be important to distinguish between oncogenic sequence variants and rare single-nucleotide polymorphisms to avoid the use of unnecessary, and potentially toxic, cancer therapy agents.

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  • (PMID = 20670955.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / CCR NIH HHS / RC / CA146107-01; United States / NCI NIH HHS / CA / RC1 CA146107-01; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / 5 P30 CA069533; United States / NCI NIH HHS / CA / RC1 CA146107; United States / NCRR NIH HHS / RR / UL1 RR024140; United States / NCI NIH HHS / CA / 5P50CA069533; United States / NCI NIH HHS / CA / P30 CA069533
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Growth Factor; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  • [Other-IDs] NLM/ NIHMS211280; NLM/ PMC2913476
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2. Potter KN, Mockridge CI, Neville L, Wheatley I, Schenk M, Orchard J, Duncombe AS, Packham G, Stevenson FK: Structural and functional features of the B-cell receptor in IgG-positive chronic lymphocytic leukemia. Clin Cancer Res; 2006 Mar 15;12(6):1672-9
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  • [Title] Structural and functional features of the B-cell receptor in IgG-positive chronic lymphocytic leukemia.
  • PURPOSE: To determine the origin and relationship of the rare IgG+ variant of chronic lymphocytic leukemia (CLL) to the two common IgM+IgD+ subsets that are distinguished by expression of unmutated or mutated V(H) genes, with the former having a worse prognosis.
  • EXPERIMENTAL DESIGN: IgG+ CLL cells were characterized using phenotypic, functional, and immunogenetic analyses.
  • RESULTS: IgG+ CLL was phenotypically similar to mutated IgM+IgD+ CLL (M-CLL) and variably expressed CD38 (4 of 14).
  • ZAP-70, a tyrosine kinase preferentially expressed in unmutated CLL, was found in only 2 of 14 cases.
  • The ability to signal via surface IgM (sIgM) varies between the main subsets of CLL and is associated with expression of ZAP-70.
  • In IgG(+) CLL, 9 of 14 responded to engagement of sIgG with no apparent requirement for expression of CD38 or ZAP-70.
  • Derivation from a postgerminal center B cell is, therefore, likely, and a relationship with M-CLL is suggested.
  • However, conserved sequences detected in the CDR3 of V4-34-encoded gamma chains were not found M-CLL, indicating no direct path of isotype switch from M-CLL.
  • CONCLUSION: IgG+ CLL is likely to arise from an age-related expanded pool of B cells, on a path parallel to M-CLL, and perhaps with a similar clinical course.
  • [MeSH-major] Immunoglobulin G / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Receptors, Antigen, B-Cell / immunology
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Anti-Idiotypic / pharmacology. Antigens, CD38 / immunology. Calcium / metabolism. DNA Mutational Analysis. Female. Humans. Immunoglobulin Heavy Chains / genetics. Immunoglobulin M / immunology. Immunoglobulin Variable Region / genetics. Immunophenotyping. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / metabolism. Male. Middle Aged. Mutation / genetics. Signal Transduction / immunology. ZAP-70 Protein-Tyrosine Kinase / immunology

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  • (PMID = 16551848.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Anti-Idiotypic; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin M; 0 / Immunoglobulin Variable Region; 0 / Receptors, Antigen, B-Cell; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; SY7Q814VUP / Calcium
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3. Pulte D, Olson KE, Broekman MJ, Islam N, Ballard HS, Furman RR, Olson AE, Marcus AJ: CD39 activity correlates with stage and inhibits platelet reactivity in chronic lymphocytic leukemia. J Transl Med; 2007 May 04;5:23
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  • [Title] CD39 activity correlates with stage and inhibits platelet reactivity in chronic lymphocytic leukemia.
  • BACKGROUND: Chronic lymphocytic leukemia (CLL) is characterized by accumulation of mature appearing lymphocytes and is rarely complicated by thrombosis.
  • One possible explanation for the paucity of thrombotic events in these patients may be the presence of the ecto-nucleotidase CD39/NTDPase-1 on the surface of the malignant cells in CLL.
  • We hypothesize that if CD39 is observed on CLL cells, then patients with CLL may be relatively protected against platelet aggregation and recruitment and that CD39 may have other effects on CLL, including modulation of the disease, via its metabolism of ATP.
  • METHODS: Normal and malignant lymphocytes were isolated from whole blood from patients with CLL and healthy volunteers.
  • RESULTS: Functional assays demonstrated that ADPase and ATPase activities were much higher in CLL cells than in total lymphocytes from the normal population on a per cell basis (p-value < 0.00001).
  • CD39 activity was elevated in stage 0-2 CLL compared to stage 3-4 (p < 0.01).
  • RT-PCR showed increased full length CD39 and splice variant 1.5, but decreased variant 1.3 in CLL cells.
  • Platelet function tests showed inhibition of platelet activation and recruitment to ADP by CLL cells.
  • CONCLUSION: CD39 is expressed and active on CLL cells.
  • Enzyme activity is higher in earlier stages of CLL and decreased enzyme activity may be associated with worsening disease.
  • These results suggest that CD39 may play a role in the pathogenesis of malignancy and protect CLL patients from thrombotic events.

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  • (PMID = 17480228.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / P01 HL046403; United States / NINDS NIH HHS / NS / R01 NS041462; United States / NHLBI NIH HHS / HL / R01 HL047073; United States / NHLBI NIH HHS / HL / HL 46403; United States / NHLBI NIH HHS / HL / R37 HL047073; United States / NHLBI NIH HHS / HL / HL 47073; United States / NINDS NIH HHS / NS / NS 41462
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 61D2G4IYVH / Adenosine Diphosphate; EC 3.6.1.5 / Apyrase; EC 3.6.1.5 / CD39 antigen
  • [Other-IDs] NLM/ PMC1885243
  • [General-notes] NLM/ Original DateCompleted: 20070813
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4. Lin TS, Blum KA, Fischer DB, Mitchell SM, Ruppert AS, Porcu P, Kraut EH, Baiocchi RA, Moran ME, Johnson AJ, Schaaf LJ, Grever MR, Byrd JC: Flavopiridol, fludarabine, and rituximab in mantle cell lymphoma and indolent B-cell lymphoproliferative disorders. J Clin Oncol; 2010 Jan 20;28(3):418-23
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  • [Title] Flavopiridol, fludarabine, and rituximab in mantle cell lymphoma and indolent B-cell lymphoproliferative disorders.
  • PURPOSE: Flavopiridol downmodulates antiapoptotic proteins associated with resistance to fludarabine and rituximab and is effective against p53-mutated chronic lymphocytic leukemia (CLL).
  • We conducted a phase I study of flavopiridol, fludarabine, and rituximab (FFR) in patients with mantle-cell lymphoma (MCL), indolent B-cell non-Hodgkin's lymphomas (B-NHL), and CLL to determine the activity of FFR.
  • PATIENTS AND METHODS: Therapy included fludarabine 25 mg/m(2) intravenously (IV) days 1 to 5 and rituximab 375 mg/m(2) day 1 every 28 days for 6 cycles.
  • We administered flavopiridol 50 mg/m(2) by 1-hour IV bolus (IVB) day 1 (n = 15); day 1 to 2 (n = 6); 20 mg/m(2) 30-minute IVB + 20 mg/m(2) 4-hour IV infusion (n = 3); or 30 mg/m(2) + 30 mg/m(2) (n = 14).
  • RESULTS: Thirty-eight patients (median age, 62 years) with MCL (n = 10); indolent B-NHL including follicular (n = 9), marginal zone (n = 4), lymphoplasmacytic (n = 1), or small lymphocytic lymphoma (n = 3); and CLL (n = 11), were enrolled.
  • Median PFS of patients with nonblastoid variant MCL (n = 8) was 35.9 months.
  • CONCLUSION: FFR was active in MCL, indolent B-NHL, and CLL and should be studied for older patients with MCL who are not candidates for aggressive chemotherapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes. Female. Flavonoids / administration & dosage. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Lymphoproliferative Disorders / drug therapy. Male. Middle Aged. Piperidines / administration & dosage. Rituximab. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 20008633.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA102276-01A1; United States / NCI NIH HHS / CA / U01 CA076576; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NCI NIH HHS / CA / K23 CA102276; United States / NCI NIH HHS / CA / U01-CA76576
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Piperidines; 45AD6X575G / alvocidib; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC2815704
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5. Gustafsson K, Wang X, Severa D, Eriksson M, Kimby E, Merup M, Christensson B, Flygare J, Sander B: Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: growth inhibition by receptor activation. Int J Cancer; 2008 Sep 1;123(5):1025-33
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  • [Title] Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: growth inhibition by receptor activation.
  • Endogenous and synthetic cannabinoids exert antiproliferative and proapoptotic effects in various types of cancer and in mantle cell lymphoma (MCL).
  • In this study, we evaluated the expression of cannabinoid receptors type 1 and type 2 (CB1 and CB2) in non-Hodgkin lymphomas of B cell type (n = 62).
  • Low levels of the splice variant CB1a, previously shown to have a different affinity for cannabinoids than CB1, were detected in 44% of the lymphomas, while CB1b expression was not detected.
  • In functional studies using MCL, Burkitt lymphoma (BL), chronic lymphatic leukemia (CLL) and plasma cell leukemia cell lines, the stable anandamide analog R(+)-methanandamide (R(+)-MA) induced cell death only in MCL and CLL cells, which overexpressed both cannabinoid receptors, but not in BL.
  • [MeSH-major] Antimitotic Agents / pharmacology. Arachidonic Acids / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Receptor, Cannabinoid, CB1 / metabolism. Receptor, Cannabinoid, CB2 / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / metabolism. Cell Proliferation / drug effects. DNA, Complementary / analysis. DNA, Neoplasm / analysis. Enzyme-Linked Immunosorbent Assay. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Leukemia, Plasma Cell / drug therapy. Leukemia, Plasma Cell / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Mitosis / drug effects. Mitotic Index. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transplantation, Heterologous. Up-Regulation

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  • (PMID = 18546271.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimitotic Agents; 0 / Arachidonic Acids; 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / RNA, Messenger; 0 / Receptor, Cannabinoid, CB1; 0 / Receptor, Cannabinoid, CB2; 150314-39-9 / methanandamide
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6. Keating M, O'Brien S: High-dose rituximab therapy in chronic lymphocytic leukemia. Semin Oncol; 2000 Dec;27(6 Suppl 12):86-90
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  • [Title] High-dose rituximab therapy in chronic lymphocytic leukemia.
  • Rituximab (Rituxan; Genentech, Inc, South San Francisco, CA and IDEC Pharmaceutical Corporation, San Diego, CA) is a chimeric monoclonal antibody that targets mature B cells in most lymphoid B-cell malignancies.
  • Rituximab is approved by the US Food and Drug Administration for therapy for recurrent B-cell lymphoma.
  • In initial clinical trials the activity in small lymphocytic lymphoma, the counterpart of chronic lymphocytic leukemia (CLL), was less than 20%.
  • In an attempt to increase the level of rituximab activity in CLL, we conducted a phase I dose-escalation study to overcome both the lower CD20 antigen density on CLL cells compared with lymphoma cells and the shorter half-life of rituximab in small lymphocytic lymphoma.
  • Severe toxicity (grades 3 and 4) noted following the first dose of therapy in variant forms of CLL, namely mantle cell lymphoma and prolymphocytic leukemia, was uncommon in typical CLL.
  • Further exploration of the dosing schedule of rituximab in CLL and development of combination therapies is necessary.
  • This agent shows promise for interaction in combined chemoimmunotherapy strategies for front-line and relapsed patients with CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphoid / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / physiology. Clinical Protocols. Dose-Response Relationship, Drug. Female. Humans. Male. Recurrence. Rituximab


7. Robak T: Monoclonal antibodies in the treatment of chronic lymphoid leukemias. Leuk Lymphoma; 2004 Feb;45(2):205-19
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  • [Title] Monoclonal antibodies in the treatment of chronic lymphoid leukemias.
  • In recent years preclinical and clinical studies have been undertaken with selected monoclonal antibodies (MoAbs) either alone or coniugated to toxins in patients with several lymphoid malignancies, including chronic lymphocytic leukemia (CLL), prolymphocytic leukemia (PLL) and hairy cell leukemia (HCL).
  • Two MoAbs, directed against CD20 antigen (Rituximab, RIT) and CD52 antigen (Campath-1H, alemtuzumab, ALT) demonstrate significant activity in CLL.
  • The most notable success to data has been achieved with ALT, both in previously treated and untreated patients with CLL.
  • ALT is a humanized rat IgG1 antibody that binds to the cell membrane of virtually all normal as well as malignant lymphocytes.
  • In the vast majority of CLL patients ALT causes constant reduction of abnormal blood lymphocytes, usually in less than 4 weeks, and disappearance of CD5/CD19 co-expression cells from blood.
  • ALT is also highly active in patients with CLL in progression, even refractory to fludarabine (FA).
  • RIT is also active in CLL in conventional doses.
  • The activity of ALT and RIT in CLL patients resistant to FA and their synergistic interactions with cytotoxic drugs suggests that a combination of these agents may lead to further progress in the treatment of this disease.
  • The T-cell variant of PLL has demonstrated impressive responses to ALT in several trials even if the patients were refractory to deoxycoformycin (DCF) and other agents.
  • Consequently, treatment with ALT may need to be associated with stem cell transplantation to consolidate and maintain long-term remissions.
  • The presented results indicate that these agents are highly active and well tolerated even if the patients were resistant to 2-CdA or DCF.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Cell Adhesion Molecules. Immunotherapy / methods. Leukemia, Lymphocytic, Chronic, B-Cell / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Animals. Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / pharmacology. Antigens, CD / biosynthesis. Antigens, CD19 / biosynthesis. Antigens, CD20 / biosynthesis. Antigens, CD5 / biosynthesis. Antigens, Differentiation, B-Lymphocyte / biosynthesis. Antigens, Neoplasm / biosynthesis. Antineoplastic Combined Chemotherapy Protocols. Cell Membrane / metabolism. Combined Modality Therapy. Glycoproteins / biosynthesis. Humans. Lectins / biosynthesis. Leukemia, B-Cell / therapy. Leukemia, Hairy Cell / therapy. Leukemia, Myeloid / therapy. Lymphatic Metastasis. Lymphocytes / metabolism. Middle Aged. Pentostatin / pharmacology. Rats. Rituximab. Sialic Acid Binding Ig-like Lectin 2. Simplexvirus / metabolism. Stem Cell Transplantation

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  • (PMID = 15101704.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, CD19; 0 / Antigens, CD20; 0 / Antigens, CD5; 0 / Antigens, Differentiation, B-Lymphocyte; 0 / Antigens, Neoplasm; 0 / CD22 protein, human; 0 / CD52 antigen; 0 / Cell Adhesion Molecules; 0 / Glycoproteins; 0 / Lectins; 0 / Sialic Acid Binding Ig-like Lectin 2; 395575MZO7 / Pentostatin; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 108
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8. McBride NC, Cavenagh JD, Ward MC, Grant I, Schey S, Gray A, Hughes A, Mills MJ, Cervi P, Newland AC, Kelsey SM: Liposomal daunorubicin (DaunoXome) in combination with cyclophosphamide, vincristine and prednisolone (COP-X) as salvage therapy in poor-prognosis non-Hodgkins lymphoma. Leuk Lymphoma; 2001 Jun;42(1-2):89-98
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  • We treated 33 patients with a variant of the standard 3 weekly CHOP regime, replacing doxorubicin with liposomal daunorubicin (DaunoXome, NeXstar Pharmaceuticals) 120 mg/m2 (COP-X).
  • Eighteen subjects had relapsed/refractory aggressive NHL and 15 had indolent NHL/CLL.
  • 88% of patients with aggressive NHL responded; three (18%) patients achieved complete remission (CR), 12 (70%) achieved partial remission (PR), 1 (6%) patient had stable disease (SD) and 1 (6%) patient progressed through treatment.
  • The response rate in indolent NHL/CLL was 73%.
  • Four (27%) patients achieved CR, 7 (46%) PR and 4 (27%) SD.
  • At two years post treatment, 55% of the patients with indolent NHL/CLL remain progression-free, although 4 patients have proceeded to consolidation therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Daunorubicin / administration & dosage. Lymphoma, Non-Hodgkin / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Aged. Cyclophosphamide / administration & dosage. Female. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Liposomes / administration & dosage. Male. Middle Aged. Prednisolone / administration & dosage. Prognosis. Remission Induction. Survival Analysis. Therapeutic Equivalency. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 11699226.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Liposomes; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin
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9. Lin K, Glenn MA, Harris RJ, Duckworth AD, Dennett S, Cawley JC, Zuzel M, Slupsky JR: c-Abl expression in chronic lymphocytic leukemia cells: clinical and therapeutic implications. Cancer Res; 2006 Aug 1;66(15):7801-9
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  • [Title] c-Abl expression in chronic lymphocytic leukemia cells: clinical and therapeutic implications.
  • c-Abl is important for normal B-cell development, but little is known about the function of this nonreceptor tyrosine kinase in chronic lymphocytic leukemia (CLL).
  • We show that the malignant cells of CLL predominantly express the type 1b splice variant of c-Abl and that the expression of c-Abl protein is higher in CLL cells than in normal peripheral blood B cells.
  • We also show that STI-571, an inhibitor of c-Abl kinase activity, induces apoptosis of CLL cells with high c-Abl expression levels through a mechanism involving inhibition of nuclear factor kappaB.
  • We conclude that overexpression of c-Abl is likely to play a pathogenetic role in CLL and that STI-571 may be of potential use in the treatment of this disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Piperazines / pharmacology. Proto-Oncogene Proteins c-abl / biosynthesis. Pyrimidines / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. B-Lymphocytes / metabolism. Benzamides. Genes, Immunoglobulin Heavy Chain. Humans. Imatinib Mesylate. Immunoglobulin Variable Region / genetics. Mutation. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Protein Isoforms. ZAP-70 Protein-Tyrosine Kinase / biosynthesis

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  • (PMID = 16885384.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Immunoglobulin Variable Region; 0 / NF-kappa B; 0 / Piperazines; 0 / Protein Isoforms; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase
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10. Hulkkonen J, Vilpo L, Hurme M, Vilpo J: Surface antigen expression in chronic lymphocytic leukemia: clustering analysis, interrelationships and effects of chromosomal abnormalities. Leukemia; 2002 Feb;16(2):178-85
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  • [Title] Surface antigen expression in chronic lymphocytic leukemia: clustering analysis, interrelationships and effects of chromosomal abnormalities.
  • Chronic lymphocytic leukemia (CLL) is a phenotypically distinguishable form of B-lymphoid leukemias.
  • The regularity of surface membrane antigen expression patterns, their interrelationships as well as the effects of the three frequent chromosomal aberrations, ie 11q deletion, 13q deletion and trisomy 12, were investigated in 35 classic CLL cases by flow cytometry.
  • Deletion of chromosome arm 11q attenuated expression of splicing variant CD45RA, but enhanced CD45RO expression.
  • The variable levels of signaling surface membrane antigens, their interactions and interference by genetic aberrations are likely to affect the clinical progression and drug response of CLL.
  • [MeSH-major] Antigens, CD / analysis. Antigens, Neoplasm / analysis. Antigens, Surface / analysis. B-Lymphocyte Subsets / immunology. Chromosome Aberrations. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Neoplastic Stem Cells / immunology. Receptors, Antigen, B-Cell / analysis

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  • (PMID = 11840283.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, B-Cell; EC 3.1.3.48 / Antigens, CD45; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; EC 3.2.2.5 / NAD+ Nucleosidase
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11. Johnson SA: Use of fludarabine in the treatment of mantle cell lymphoma, Waldenström's macroglobulinemia and other uncommon B- and T-cell lymphoid malignancies. Hematol J; 2004;5 Suppl 1:S50-61
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  • [Title] Use of fludarabine in the treatment of mantle cell lymphoma, Waldenström's macroglobulinemia and other uncommon B- and T-cell lymphoid malignancies.
  • After initial efforts using fludarabine as a single agent in the treatment of acute leukemia, its activity at lower and safer doses was demonstrated in chronic lymphocytic leukemia (CLL) patients who were refractory or had relapsed from traditional chemotherapies, representing a highly effective therapy for this condition.
  • Fludarabine was also rapidly shown to be beneficial as first-line therapy in CLL.
  • There is now considerable evidence that fludarabine is an effective agent in non-Hodgkin's lymphoma and in combination therapy for acute myeloid leukemia.
  • The actions of fludarabine are not restricted to these settings and its potential role in the treatment of a range of uncommon T- and B-cell lymphoid malignancies is slowly emerging.
  • This review will focus on the characteristics and treatment options for two B-cell disorders, mantle cell lymphoma and Waldenström's macroglobulinemia, with emphasis on the clinical activity of fludarabine.
  • These include B-cell neoplasms such as the CLL variant prolymphocytic leukemia, hairy cell leukemia and mucosa-associated lymphoid tissue-derived lymphomas; the T-cell disorders cutaneous T-cell lymphoma, angioimmunoblastic lymphadenopathy and other rarer T-cell diseases; and aggressive variants of non-Hodgkin's lymphoma including Richter's syndrome.

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  • (PMID = 15079153.001).
  • [ISSN] 1466-4860
  • [Journal-full-title] The hematology journal : the official journal of the European Haematology Association
  • [ISO-abbreviation] Hematol. J.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 108
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12. Fong D, Kaiser A, Spizzo G, Gastl G, Tzankov A: Hodgkin's disease variant of Richter's syndrome in chronic lymphocytic leukaemia patients previously treated with fludarabine. Br J Haematol; 2005 Apr;129(2):199-205
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  • [Title] Hodgkin's disease variant of Richter's syndrome in chronic lymphocytic leukaemia patients previously treated with fludarabine.
  • The transformation of chronic lymphocytic leukaemia (CLL) into large-cell lymphoma (Richter's syndrome, RS) is a well-documented phenomenon.
  • Only rarely does CLL transform into Hodgkin's lymphoma (HL).
  • To further analyse the clinico-pathological and genetic findings in the HL variant of RS, we performed a single-institution study in four patients, who developed HL within a mean of 107 months after diagnosis of CLL.
  • The sites involved by HL included supra- and infradiaphragmal lymph nodes and the tonsils; stage IV disease was also documented.
  • All patients presented with CLL treatment-resistant lymphadenopathies and B-symptoms.
  • In two of the MC cases, molecular analysis performed on CLL samples and microdissected Hodgkin and Reed-Sternberg cells (HRSC) suggested a clonal relationship, while in NS no indication of a clonal relationship was detected.
  • In summary, HL can occur in CLL patients at any site, up to 17 years after initial diagnosis, especially after treatment with fludarabine.
  • The majority present with B-symptoms and CLL treatment-resistant lymphadenopathy, are of the MC type, clonally related to CLL and might be triggered by an EBV infection.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hodgkin Disease / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use
  • [MeSH-minor] Cell Transformation, Viral. Clone Cells. Drug Resistance, Neoplasm. Epstein-Barr Virus Infections / immunology. Female. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Humans. Immunoglobulin Heavy Chains / genetics. Male. Micromanipulation. Middle Aged. Reed-Sternberg Cells / ultrastructure. Reed-Sternberg Cells / virology

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  • (PMID = 15813847.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunoglobulin Heavy Chains; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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