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5. Asahi A, Okamoto S, Matsushita H, Hattori Y, Takayama N, Ikeda Y: [Follicular lymphoma in two brothers]. Rinsho Ketsueki; 2001 May;42(5):408-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Follicular lymphoma in two brothers].
  • Two brothers, whose parents had a history of exposure to atomic bomb radiation, developed non-Hodgkin's lymphoma.
  • The younger brother, a 48-year-old man, was diagnosed as having follicular small-cleaved cell lymphoma in October, 1996.
  • He had extranodal lymphoma involvement of the right kidney, bone marrow and skin, in addition to generalized lymphadenopathy.
  • He was treated with intermittent COP chemotherapy, and good control of the lymphoma was obtained.
  • The elder brother, aged 50 years, was diagnosed as having follicular mixed cell lymphoma in May, 1998.
  • He also had extranodal lymphoma involvement of the right parotid gland and bone marrow, as well as generalized lymphadenopathy.
  • After one course of CHOP chemotherapy, he developed paresis of the lower legs and was found to have a mass at the Th5-6 vertebrae by CT scan.
  • After four courses of CHOP chemotherapy followed by ESHAP chemotherapy and radiotherapy, he achieved complete remission, and has since been well.
  • Follicular lymphoma occurring among siblings is rare.
  • [MeSH-major] Lymphoma, Follicular / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Family Health. Humans. Male. Middle Aged. Nuclear Warfare. Prednisolone / administration & dosage. Prednisone / administration & dosage. Vincristine / administration & dosage

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  • (PMID = 11452461.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VB0R961HZT / Prednisone; COP protocol 2; VAP-cyclo protocol
  • [Number-of-references] 15
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6. Astrow AB, Tarabay G, Salerno VE, Cook WA, Lin R, Lascher S, Li Z, Mazumder A, Halperin I, Cho J, Jaffar Z, McLaughlin M, Blum RH, Kempin SJ: Long-term survival in patients with human immunodeficiency virus-associated small non-cleaved cell lymphoma: the role for short course intensive chemotherapy. Hematol Oncol; 2003 Sep;21(3):131-40
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  • [Title] Long-term survival in patients with human immunodeficiency virus-associated small non-cleaved cell lymphoma: the role for short course intensive chemotherapy.
  • While intensive chemotherapy is recommended for the treatment of non-HIV related adult small non-cleaved lymphoma (SNCL), including Burkitt's and Burkitt-like lymphoma, optimal treatment for patients with HIV-associated SNCL is not known.
  • Median follow-up, survival and survival at the median follow-up time were 4.5 months, 4 months and 49% respectively.
  • Of this cohort 39% were complete responders (CR) and 36% were long-term lymphoma-free survivors.
  • Short course intensive chemotherapy (McMaster) was administered to 23 patients; 17 received less intensive conventional combination chemotherapy; and four received single-agent chemotherapy or no treatment.
  • Conventional chemotherapy may be curative for early stage HIV-SNCL.
  • In advanced disease, McMaster chemotherapy was found to be associated with substantial early mortality but was curative in a significant number of patients.
  • [MeSH-major] Lymphoma, AIDS-Related / drug therapy. Lymphoma, AIDS-Related / mortality
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / virology. Cohort Studies. Female. Humans. Male. Middle Aged. Registries. Remission Induction. Time Factors. Treatment Outcome

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  • [Copyright] Copyright 2003 John Wiley & Sons, Ltd.
  • (PMID = 14579241.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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7. Kuruvilla J, Pond G, Tsang R, Gupta V, Lipton JH, Messner HA: Favorable overall survival with fully myeloablative allogeneic stem cell transplantation for follicular lymphoma. Biol Blood Marrow Transplant; 2008 Jul;14(7):775-82
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  • [Title] Favorable overall survival with fully myeloablative allogeneic stem cell transplantation for follicular lymphoma.
  • Allogeneic stem cell transplantation (Allo-SCT) remains an option for patients with follicular lymphoma (FL).
  • We performed a retrospective analysis to examine long-term disease control and treatment-related mortality (TRM) in a group of patients that underwent transplant for clinically high-risk disease.
  • Thirty-seven patients with indolent FL (follicular small cleaved [FSC], follicular mixed [FM] or FL grades 1 or 2 by WHO criteria) underwent allo-SCT.
  • Patients were in a chemosensitive remission at the time of SCT.
  • The median age at the time of transplant was 45 years (range: 24-58).
  • The median number of prior chemotherapy regimens was 3 (range: 1-6).
  • [MeSH-major] Graft vs Tumor Effect. Lymphoma, Follicular / therapy. Neoplasm Recurrence, Local / therapy. Stem Cell Transplantation / methods. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Age Factors. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Remission Induction. Retrospective Studies. Salvage Therapy / methods. Transplantation, Autologous

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  • (PMID = 18541196.001).
  • [ISSN] 1523-6536
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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8. Zhang C, Hazarika P, Ni X, Weidner DA, Duvic M: Induction of apoptosis by bexarotene in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action. Clin Cancer Res; 2002 May;8(5):1234-40
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  • [Title] Induction of apoptosis by bexarotene in cutaneous T-cell lymphoma cells: relevance to mechanism of therapeutic action.
  • PURPOSE: Bexarotene is the first synthetic rexinoid approved for the treatment of all stages of cutaneous T-cell lymphoma (CTCL) however the mechanism of bexarotene action is unknown.
  • We examined the effects of bexarotene on induction of apoptosis and expression of its cognate receptors in well-established CTCL cell lines (MJ, Hut78, and HH).
  • RESULTS: Bexarotene treatment at 1 and 10 microM for 96 h increased the number of cells with sub-G1 populations and annexin V binding in a dose-dependent manner compared with vehicle controls (DMSO) in all three cell lines, respectively.
  • Bexarotene treatment suppressed the expression of retinoid X receptor alpha and retinoic acid receptor alpha proteins in all three lines compared with untreated controls.
  • Bexarotene treatment decreased the protein levels of survivin, activated caspase-3, and cleaved poly(ADP-Ribose) polymerase, but had no obvious effect on expression of Fas/Fas ligand and bcl-2 proteins in all three CTCL lines.
  • CONCLUSIONS: Bexarotene treatment at clinically relevant concentrations causes apoptosis of CTCL cell lines in association with activation of caspase-3 and cleavage of poly(ADP-Ribose) polymerase, as well as down-regulation of retinoid X receptor alpha, retinoic acid receptor alpha, and survivin.
  • These findings support apoptosis as a mechanism for bexarotene therapy in CTCL.
  • [MeSH-major] Apoptosis / drug effects. Lymphoma, T-Cell, Cutaneous / drug therapy. Microtubule-Associated Proteins. Skin Neoplasms / drug therapy. Tetrahydronaphthalenes / pharmacology
  • [MeSH-minor] Annexin A5 / metabolism. Blotting, Western. Cell Cycle / drug effects. Cell Survival / drug effects. Chromosomal Proteins, Non-Histone / drug effects. Chromosomal Proteins, Non-Histone / metabolism. Dose-Response Relationship, Drug. Flow Cytometry. Humans. Inhibitor of Apoptosis Proteins. Neoplasm Proteins. Protein Binding / drug effects. Receptors, Retinoic Acid / drug effects. Receptors, Retinoic Acid / metabolism. Retinoid X Receptors. Time Factors. Transcription Factors / drug effects. Transcription Factors / metabolism. Tumor Cells, Cultured

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  • (PMID = 12006543.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / K24-CA 86815; United States / NCI NIH HHS / CA / R21-CA 74117
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / BIRC5 protein, human; 0 / Chromosomal Proteins, Non-Histone; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Tetrahydronaphthalenes; 0 / Transcription Factors; 0 / retinoic acid receptor alpha; A61RXM4375 / bexarotene
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9. Barişta I, Baltali E, Tekuzman G, Kars A, Ruacan S, Ozişik Y, Güler N, Güllü IH, Atahan IL, Firat D: Primary breast lymphomas--a retrospective analysis of twelve cases. Acta Oncol; 2000;39(2):135-9
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  • This study was undertaken to define the natural history and treatment results of patients with primary breast non-Hodgkin's lymphoma (NHL).
  • The most common histologic subtype was diffuse, small cleaved-cell lymphoma.
  • Chemotherapy regimens were employed in 9 patients.
  • An objective response was attained with surgery, chemotherapy, or radiotherapy alone in 2, 1, and 1 cases, respectively.
  • Combined modality treatment including either two or three modalities was successful in 7 cases.
  • The median progression-free and overall survival times were 49 and 56 months, respectively.
  • [MeSH-major] Breast Neoplasms / pathology. Breast Neoplasms / therapy. Lymphoma, Non-Hodgkin / pathology. Lymphoma, Non-Hodgkin / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Lymphatic Metastasis. Middle Aged. Prognosis. Radiotherapy, Adjuvant. Retrospective Studies

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  • (PMID = 10859001.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] NORWAY
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10. Lasota J, Nordling S, Miettinen M: Testicular diffuse large cell lymphoma with tubule preservation--molecular genetic evidence of transformation from previous follicular lymphoma. Virchows Arch; 2000 Mar;436(3):276-83
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  • [Title] Testicular diffuse large cell lymphoma with tubule preservation--molecular genetic evidence of transformation from previous follicular lymphoma.
  • Testicular lymphomas usually occur in older men and are mostly diffuse large B-cell lymphomas (DLBL).
  • They may be primary manifestation of lymphoma or represent a relapse of a previous non-Hodgkin's lymphoma.
  • This report details a testicular large cell lymphoma, which was proven to be large cell transformation of a low-grade follicular lymphoma biopsied 8 years earlier.
  • Initially, a 38-year old man was diagnosed with cervical lymphadenopathy, and biopsy was interpreted as reactive follicular hyperplasia; no treatment was given, and the lymphadenopathy resolved spontaneously.
  • The patient died 7 months later with evidence for intra-abdominal and central nervous system lymphoma after a brief but temporary response to M-BACOD chemotherapy.
  • Orchiectomy specimen and gastroscopic biopsy showed diffuse large B-cell lymphoma (CD20+), which infiltrated between well-preserved tubules in the testis.
  • Histological comparison with 20 testicular lymphomas without previous lymphoma showed tubule infiltration in all cases, suggesting that the tubule-preserving infiltration pattern could be a histological marker for secondary lymphoma involvement in testis.
  • On re-examination, the lymph node 8 years prior was verified as follicular, predominantly small, cleaved cell lymphoma with bcl2-positive follicles.
  • The earlier follicular lymphoma and the subsequent diffuse large cell lymphoma were analyzed using polymerase chain reaction and showed identical sequences of the t(14;18) translocation and immunoglobulin heavy chain gene rearrangement.
  • Analysis of the VH-gene sequences from the follicular lymphoma revealed sequence heterogeneity consistent with ongoing mutation.
  • However, the transformed diffuse large cell lymphoma had no intraclonal variation, with the sequence matching with one of the subclones from the low-grade follicular lymphoma.
  • These results confirm that the large cell transformation of follicular lymphoma occurs in a single follicular lymphoma cell.
  • This case also indicates that the selection of the transformed clone can be part of the natural history of disease and can occur without exposure to chemotherapy.
  • [MeSH-major] Cell Transformation, Neoplastic. Genes, Immunoglobulin. Lymphoma, Follicular / genetics. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Testicular Neoplasms / genetics. Testicular Neoplasms / pathology
  • [MeSH-minor] Base Sequence. Cell Differentiation. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 18. Gene Rearrangement, B-Lymphocyte. Humans. Immunoglobulin Heavy Chains / genetics. Male. Molecular Sequence Data. Polymerase Chain Reaction. Translocation, Genetic

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  • (PMID = 10782887.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
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11. Lichtman SM, Petroni G, Schilsky RL, Johnson JL, Perri RT, Niedzwiecki D, Sklar J, Barcos M, Peterson BA: High dose cyclophosphamide plus recombinant human granulocyte-colony stimulating factor (rhG-CSF) in the treatment of follicular, low grade non-Hodgkin's lymphoma: CALGB 9150. Leuk Lymphoma; 2001 Nov-Dec;42(6):1255-64
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  • [Title] High dose cyclophosphamide plus recombinant human granulocyte-colony stimulating factor (rhG-CSF) in the treatment of follicular, low grade non-Hodgkin's lymphoma: CALGB 9150.
  • The main objectives of this study were to determine the feasibility of administering high doses of cyclophosphamide plus recombinant human granulocyte-colony stimulating factor (rhG-CSF) every 14-21 days to patients with follicular small cleaved cell lymphoma.
  • For each patient, the treatment was not considered feasible if fewer than four cycles of cyclophosphamide chemotherapy could be administered on schedule (i.e. at least every 29 days) or (1) hospitalization of the patient for longer than three days was necessary for neutropenic fever (38 degrees C) or bacteriologically documented infection in > 50% of the cycles, or (2) grade > or = 2 hemorrhage in association with thrombocytopenia of grade > or = 3 severity occurred in > 50% of the cycles or (3) non-hematologic toxicity (excluding nausea/vomiting and alopecia) of grade > or = 3 occurred in > 50% of cycles.
  • The goal was to have a treatment program feasible in 75% or more of the treated patients.
  • The secondary objectives were to determine the toxicities, the complete and partial response rates, and the time to treatment failure (TTF).
  • The trial also attempted to assess the effectiveness of this treatment program in eradicating Bcl-2 rearrangements by PCR, and to assess complete remission duration in relationship to PCR results in patients who respond to this chemotherapy program.
  • Patients were required to have histologically documented non-Hodgkin's lymphoma of the subtypes follicular, predominantly small cleaved cell (IWF-B) or follicular mixed, (IWF-C).
  • The median follow-up time is 5.0 years, with a range of 2.5-6.7 years.
  • The 1-year estimated probability of freedom from treatment failure was 50% and of survival at 1 year was 92%.
  • Post-treatment specimens were submitted for seven of the 13 patients.
  • Four of the seven converted to Bcl-2 negative following treatment.
  • Eight of 13 Bcl-2 positive patients (62%) had a clinical response to treatment.
  • This study demonstrates that repetitive doses of cyclophosphamide at 4.5 g/m2 every two weeks with rhG-CSF support can be administered to selected younger patients with advanced follicular lymphoma with morphologic involvement of the bone marrow with acceptable non-hematologic toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Granulocyte Colony-Stimulating Factor / administration & dosage. Lymphoma, Follicular / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

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  • (PMID = 11911406.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 8N3DW7272P / Cyclophosphamide
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12. Ruskoné-Fourmestraux A, Audouin J: Primary gastrointestinal tract mantle cell lymphoma as multiple lymphomatous polyposis. Best Pract Res Clin Gastroenterol; 2010 Feb;24(1):35-42
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  • [Title] Primary gastrointestinal tract mantle cell lymphoma as multiple lymphomatous polyposis.
  • Primary gastrointestinal involvement of mantle cell lymphoma (MCL) is rare with a frequency reported between 4 and 9% of all gastrointestinal B-cell non-Hodgkin lymphomas.
  • The constant and typical phenotypic features of the small cleaved tumour cells, characterised as CD20+, CD5+ CD23- with a t(11;14) (q13;q32) and cyclin D1 overexpression on immunochemistry, allow MLP to be considered as the gastrointestinal counterpart of peripheral nodal MCL.
  • Response to intensive chemotherapy regimens usually results in regression of macroscopic and sometimes microscopic lesions but remissions are short and median survival from 3 to 4 years.
  • Prognosis has been significantly improved since in younger patients, intensive front-line immunochemotherapy with autologous stem cell transplantation has been proposed.
  • Earlier diagnosis with further studies integrating novel agents are still required to determine the optimal treatment with less toxicity.
  • [MeSH-major] Gastrointestinal Neoplasms. Intestinal Polyposis. Lymphoma, Mantle-Cell
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Stem Cell Transplantation. Transplantation, Autologous. Treatment Outcome

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  • [Copyright] 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20206107.001).
  • [ISSN] 1532-1916
  • [Journal-full-title] Best practice & research. Clinical gastroenterology
  • [ISO-abbreviation] Best Pract Res Clin Gastroenterol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 46
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13. Cohen Y, Amir G, Polliack A: Development and rapid dissemination of Merkel-cell carcinomatosis following therapy with fludarabine and rituximab for relapsing follicular lymphoma. Eur J Haematol; 2002 Feb;68(2):117-9
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  • [Title] Development and rapid dissemination of Merkel-cell carcinomatosis following therapy with fludarabine and rituximab for relapsing follicular lymphoma.
  • This report deals with an unusual case of a patient with follicular small cleaved lymphocytic lymphoma who developed Merkel-cell carcinoma soon after receiving chemoimmunotherapy with a fludarabine-containing regimen and rituximab.
  • The presentation of the Merkel-cell carcinoma in this patient was atypical because of the absence of dermal involvement and the very rapid clinical progression.
  • In the light of recent reports which suggest a possible link between the immunocompromised state and the development of Merkel-cell carcinoma, the atypical presentation seen in this patient may indeed imply a possible link between the therapy given and the development of Merkel-cell carcinoma.
  • To the best of our knowledge, this is the first documentation of Merkel-cell carcinoma appearing in a patient soon after treatment with fludarabine and/or rituximab.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antineoplastic Agents / adverse effects. Carcinoma, Merkel Cell / etiology. Lymphoma, Follicular / drug therapy. Vidarabine / adverse effects
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Humans. Male. Middle Aged. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / pathology. Recurrence. Rituximab. Salvage Therapy

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  • (PMID = 12061321.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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4. Shin HJ, Chung J, Park DY, Cho GJ: Prognostic significance of the cyclin D3 and the Ki-67 expression for predicting clinical outcome in diffuse large B-cell lymphoma. J Clin Oncol; 2004 Jul 15;22(14_suppl):6714

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  • [Title] Prognostic significance of the cyclin D3 and the Ki-67 expression for predicting clinical outcome in diffuse large B-cell lymphoma.
  • : 6714 Background: Cyclin D3 expression is associated with cell proliferation in lymphoid tissues, and high cyclin D3 expression in tumor cells of patients with diffuse large B-cell lymphoma (DLBCL) predicted poor response to chemotherapy and shorter overall survival in one study.
  • However, cyclin D3 expression may sensitize cells to apoptosis induced by caspase 2 overexpression by increasing the absolute amount of cleaved caspase 2.
  • Patients with high cyclin D3 expression had a more low Ki-67 expression associated with proliferation in tumor tissue (p=0.019).
  • CONCLUSIONS: This study shows that better response for chemotherapy may be related to the cell cycle regulatory protein cyclin D3 overexpression, which can be predictive and prognostic factor associated with longer overall survival and disease free survival in DLBCL.

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  • (PMID = 28014706.001).
  • [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. Meshref M, Sassolas F, Schell M, Chalabreysse L, Chassagne C, Mialou V, Marec Bérard P, Di Filippo S, Bergeron C: Primary cardiac Burkitt lymphoma in a child. Pediatr Blood Cancer; 2004 Apr;42(4):380-3
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  • [Title] Primary cardiac Burkitt lymphoma in a child.
  • Primary cardiac lymphoma (PCL) is a rare and usually fatal malignancy, seldom reported in children.
  • This report describes the case of a 10-year-old boy who presented with multiple intracardiac masses which, when biopsied, proved to be small non-cleaved cell (Burkitt's) lymphoma.
  • The first two cycles of chemotherapy according to the LMB 96 protocol were given under close cardiological supervision, with good response.
  • The treatment was then continued with full-dose chemotherapy, without any cardiological complication.
  • The patient who was treated by chemotherapy alone remains in complete remission 36 months after the end of treatment and can presently be considered as cured, without late cardiac effect.
  • [MeSH-major] Burkitt Lymphoma / drug therapy. Heart Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Disease-Free Survival. Echocardiography. Humans. Male. Remission Induction / methods

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 14966837.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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16. Fortney JE, Hall BM, Bartrug L, Gibson LF: Chemotherapy induces bcl-2 cleavage in lymphoid leukemic cell lines. Leuk Lymphoma; 2002 Nov;43(11):2171-8
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  • [Title] Chemotherapy induces bcl-2 cleavage in lymphoid leukemic cell lines.
  • Bcl-2 is the major anti-apoptotic protein evaluated in studies aimed at understanding programmed cell death.
  • Recent work suggests that the biological activity of Bcl-2 is modulated by proteolytic cleavage, with a 23 kDa cleaved Bcl-2 product having pro-apoptotic activity.
  • In the current study we evaluated the effect of chemotherapy on Bcl-2 cleavage in B lineage leukemic cell lines.
  • JM-1, SUP-B 15 and RS4 leukemic cell lines cleaved Bcl-2 to its 23 kDa form when exposed to the chemotherapeutic agents 1-beta-D-arabinofuranosyl-cytosine (Ara-C) or etoposide (VP-16).
  • Chemotherapy induced Bcl-2 cleavage was blunted by inhibition of caspase activity.
  • Co-culture of leukemic cells with bone marrow stromal cells during chemotherapy exposure resulted in reduced levels of 23 kDa Bcl-2 protein.
  • These observations suggest that the bone marrow microenvironment may contribute to maintenance of residual leukemic disease during treatment by reducing generation of pro-apoptotic 23 kDa Bcl-2.

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  • (PMID = 12533044.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL056888; United States / NHLBI NIH HHS / HL / HL56888
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; EC 3.4.- / Peptide Hydrolases
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17. Georgakis GV, Li Y, Rassidakis GZ, Medeiros LJ, Mills GB, Younes A: Inhibition of the phosphatidylinositol-3 kinase/Akt promotes G1 cell cycle arrest and apoptosis in Hodgkin lymphoma. Br J Haematol; 2006 Feb;132(4):503-11
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  • [Title] Inhibition of the phosphatidylinositol-3 kinase/Akt promotes G1 cell cycle arrest and apoptosis in Hodgkin lymphoma.
  • Activation of the phosphatidylinositol 3-kinase (PI(3)K) pathway has been linked with tumour cell growth, survival and resistance to therapy in several cancer types.
  • The active, phosphorylated form of Akt (pAkt) was found to be aberrantly expressed in Hodgkin lymphoma (HL)-derived cell lines and in Hodgkin-Reed-Sternberg (HRS) cells in 27 of 42 (64.3%) of primary lymph node sections of HL, indicative of PI(3)K activity.
  • Akt phosphorylation was not associated with loss of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) expression, but with its phosphorylation in HL-cell lines, suggesting that its biological function is impaired.
  • The PI(3)K inhibitor LY294002 demonstrated antiproliferative effects in a dose- and time-dependent manner, which was associated with Akt dephosphorylation on Thr308 and Ser473 sites and dephosphorylation of the downstream ribosomal protein S6.
  • LY209002 induced cell cycle arrest in the G0/G1 phase and apoptosis, which were associated with upregulation of MDM2, downregulation of cyclin D1, activation of caspase 9 and poly-ADP-ribose polymerase cleavage.
  • The Akt inhibitor QLT394 also demonstrated antiproliferative effects in a dose- and time-dependent manner, dephosphorylated ribosomal S6 and cleaved caspase 9.
  • [MeSH-minor] Antigens, CD / pharmacology. Apoptosis. CD30 Ligand. CD40 Ligand / pharmacology. Carrier Proteins / pharmacology. Caspase 9. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cells, Cultured. Chromones / pharmacology. Cyclin D1 / metabolism. Dose-Response Relationship, Drug. Flow Cytometry. G1 Phase. Humans. Membrane Glycoproteins / pharmacology. Morpholines / pharmacology. PTEN Phosphohydrolase / analysis. PTEN Phosphohydrolase / metabolism. Phosphorylation. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Tumor Necrosis Factors / pharmacology

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  • (PMID = 16412023.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CD30 Ligand; 0 / Carrier Proteins; 0 / Chromones; 0 / Membrane Glycoproteins; 0 / Morpholines; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / TNFRSF11A protein, human; 0 / TNFSF11 protein, human; 0 / TNFSF8 protein, human; 0 / Tumor Necrosis Factors; 136601-57-5 / Cyclin D1; 147205-72-9 / CD40 Ligand; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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18. Zhang C, Li B, Zhang X, Hazarika P, Aggarwal BB, Duvic M: Curcumin selectively induces apoptosis in cutaneous T-cell lymphoma cell lines and patients' PBMCs: potential role for STAT-3 and NF-kappaB signaling. J Invest Dermatol; 2010 Aug;130(8):2110-9
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  • [Title] Curcumin selectively induces apoptosis in cutaneous T-cell lymphoma cell lines and patients' PBMCs: potential role for STAT-3 and NF-kappaB signaling.
  • Curcumin inhibits cell growth and induces apoptosis in a number of tumor cell lines and animal models.
  • The purpose of this study was to address the antitumor effect of curcumin on cutaneous T-cell lymphoma (CTCL) cell lines and peripheral blood mononuclear cells (PBMCs) from patients with CTCL compared with healthy donors' controls.
  • Curcumin at 5-20 microM for 24 and 48 hours induced apoptosis in a time- and dose-dependent manner in three CTCL cell lines (namely MJ, Hut78, and HH).
  • Curcumin decreased protein and mRNA expression levels of signal transducer and activator of transcription (STAT)-3, bcl-2, and survivin in three cell lines and in patients' PBMCs.
  • Caspase-3 was activated and poly (ADP-Ribose) polymerase was cleaved after curcumin treatment.
  • Our findings provide a mechanistic rationale for the potential use of curcumin as a therapeutic agent for patients with CTCL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Curcumin / pharmacology. Lymphoma, T-Cell / drug therapy. NF-kappa B / metabolism. STAT3 Transcription Factor / metabolism. Skin Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Autophagy / drug effects. Autophagy / physiology. Caspase 3 / metabolism. Cell Division / drug effects. Cell Division / physiology. Cell Line, Tumor. Humans. I-kappa B Proteins / metabolism. Inhibitor of Apoptosis Proteins. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / metabolism. Leukocytes, Mononuclear / pathology. Microtubule-Associated Proteins / genetics. Microtubule-Associated Proteins / metabolism. Phosphorylation / drug effects. Phosphorylation / physiology. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / metabolism. Signal Transduction / drug effects. Signal Transduction / physiology

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  • (PMID = 20393484.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 16672; United States / NCI NIH HHS / CA / K24-CA 86815; United States / NCI NIH HHS / CA / R21-CA 74117
  • [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 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / I-kappa B Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 139874-52-5 / NF-kappaB inhibitor alpha; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
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19. Wei SH, Sheen JM, Huang CB, Hsiao CC: Primary spinal epidural non-Hodgkin's lymphoma in a child. Chang Gung Med J; 2001 Dec;24(12):820-5
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  • [Title] Primary spinal epidural non-Hodgkin's lymphoma in a child.
  • Non-Hodgkin's lymphoma usually involves the central nervous system by metastatic disease.
  • Primary spinal epidural non-Hodgkin's lymphoma (PSENL) is a relatively rare cause of spinal cord compression.
  • The proper treatment modalities are controversial in adults with PSENL.
  • Radiotherapy is the main strategy after surgery; the role of chemotherapy is uncertain.
  • Therapeutic experience in childhood PSENL is extremely limited.
  • Small non-cleaved cell non-Hodgkin's lymphoma of the epidural space was proven after subtotal tumor removal.
  • Other investigations including computed tomography of the chest and abdomen, bone scan, gallium scan, bone marrow aspiration, and cerebrospinal fluid study were all negative for occult disease.
  • The patient received combined therapy with irradiation and chemotherapy after surgery.
  • Esophageal stricture resulting from radiotherapy developed during treatment and colon interposition was performed.
  • [MeSH-major] Epidural Neoplasms / diagnosis. Lymphoma, Non-Hodgkin / diagnosis
  • [MeSH-minor] Child. Combined Modality Therapy. Humans. Male

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  • (PMID = 11858400.001).
  • [ISSN] 2072-0939
  • [Journal-full-title] Chang Gung medical journal
  • [ISO-abbreviation] Chang Gung Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China (Republic : 1949- )
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20. Xu RH, Jiang WQ, Li YH, Lin TY, Huang HQ, Xia ZJ, Sun XF, He YJ, Guan ZZ: [Curative effect on aggressive B cell non-Hodgkin's lymphoma and relevant influencing factors of its prognosis, a study of 203 cases]. Zhonghua Yi Xue Za Zhi; 2003 Feb 10;83(3):191-4
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  • [Title] [Curative effect on aggressive B cell non-Hodgkin's lymphoma and relevant influencing factors of its prognosis, a study of 203 cases].
  • OBJECTIVE: To analyze the curative effect of aggressive B cell non-Hodgkin's lymphoma and relevant influencing factors of its prognosis.
  • METHODS: The curative effects of aggressive non-Hodgkin's lymphoma which were diagnosed as diffuse small cleaved (E), diffuse mixed (F), diffuse large cell (G) or diffuse immunoblastic lymphoma (H) pathologically and certified as B cell lymphoma immunohistologically and treated with CHOP or other ADM-containing regimens for at least 4 cycles from 1993 to 1997 were analyzed.
  • CONCLUSION: The treatment with CHOP as its main component has a beneficial effect on aggressive B cell lymphoma in low risk group, but is less effective for the low-intermediate, high-intermediate, and high risk.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Cyclophosphamide / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Drug Administration Schedule. Follow-Up Studies. Humans. Infant. Middle Aged. Prednisone / administration & dosage. Prognosis. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 12812658.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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21. Bartlett NL, Petroni GR, Parker BA, Wagner ND, Gockerman JP, Omura GA, Canellos GP, Robert M, Johnson JL, Peterson BA: Dose-escalated cyclophosphamide, doxorubicin, vincristine, prednisone, and etoposide (CHOPE) chemotherapy for patients with diffuse lymphoma: Cancer and Leukemia Group B studies 8852 and 8854. Cancer; 2001 Jul 15;92(2):207-17
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  • [Title] Dose-escalated cyclophosphamide, doxorubicin, vincristine, prednisone, and etoposide (CHOPE) chemotherapy for patients with diffuse lymphoma: Cancer and Leukemia Group B studies 8852 and 8854.
  • BACKGROUND: To address the feasibility and outcome of moderate dose intensification with granulocyte-colony stimulating factor (G-CSF) for patients with aggressive non-Hodgkin lymphoma (NHL), the Cancer and Leukemia Group B (CALGB) conducted two studies evaluating dose-escalated cyclophosphamide and etoposide in the cyclophosphamide, doxorubicin, vincristine, prednisone, etoposide (CHOPE) regimen.
  • METHODS: Eligibility criteria included histologically documented, diffuse small cleaved, diffuse mixed, diffuse large cell, or immunoblastic lymphoma, Stage III--IV or bulky Stage II disease, and an ECOG performance status of 0--1.
  • The MTD in both studies was defined as the dose at which 50% of patients had 1) Grade 4 neutropenia or thrombocytopenia lasting 7 days or more, or 2) Grade 3--4 hemorrhage or nonhematologic toxicity (excluding alopecia, nausea, and emesis), or 3) were prevented from receiving 100% of drug on Day 22.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Granulocyte Colony-Stimulating Factor / administration & dosage. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large-Cell, Immunoblastic / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adult. Aged. Cyclophosphamide / administration & dosage. Disease-Free Survival. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Neutropenia / chemically induced. Neutropenia / prevention & control. Prednisone / administration & dosage. Treatment Outcome. Vincristine / administration & dosage

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  • [Copyright] Copyright 2001 American Cancer Society.
  • (PMID = 11466671.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / CA45418
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; EPOCH protocol
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22. Tulpule A, Rarick MU, Kolitz J, Bernstein J, Myers A, Buchanan LA, Espina BM, Traynor A, Letzer J, Justice GR, McDonald D, Roberts L, Boswell W, Nathwani B, Levine AM: Liposomal daunorubicin in the treatment of relapsed or refractory non-Hodgkin's lymphoma. Ann Oncol; 2001 Apr;12(4):457-62
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  • [Title] Liposomal daunorubicin in the treatment of relapsed or refractory non-Hodgkin's lymphoma.
  • PURPOSE: To assess the efficacy and toxicity of liposomal daunorubicin administered as a two-hour intravenous infusion to patients with relapsed or refractory non-Hodgkin's lymphoma (NHL).
  • PATIENTS AND METHODS: Eligible patients had relapsed or refractory NHL with measurable or evaluable disease, and low grade, select intermediate grade, or mantle cell pathologic types.
  • RESULTS: Thirty-three patients were accrued: twenty-three (70%) had low-grade histologies; six (18%) had intermediate-grade histologies (follicular large-cell and diffuse small cleaved); and four (12%) patients had mantle-cell lymphoma.
  • Six responders (50%) had received a prior anthracycline; one responder had mantle-cell histology.

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  • [CommentIn] Ann Oncol. 2001 Apr;12(4):433-4 [11398872.001]
  • (PMID = 11398876.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Liposomes; ZS7284E0ZP / Daunorubicin
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23. Foss FM: DAB(389)IL-2 (ONTAK): a novel fusion toxin therapy for lymphoma. Clin Lymphoma; 2000 Sep;1(2):110-6; discussion 117
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  • [Title] DAB(389)IL-2 (ONTAK): a novel fusion toxin therapy for lymphoma.
  • The ADP-ribosyltransferase activity of diphtheria toxin is cleaved in the endosome and is translocated into the cytosol where it inhibits protein synthesis, leading to apoptosis.
  • DAB(389)IL-2 and its predecessor, DAB(486)IL-2, have shown clinical activity in a variety of diseases, including B-cell non-Hodgkin's lymphoma, cutaneous T-cell lymphoma (CTCL), Hodgkin's disease, psoriasis, rheumatoid arthritis, and HIV infection.
  • The highest response rates were observed in CTCL, and this became the focus of clinical trials leading to its subsequent approval by the United States Food and Drug Administration for this disease.
  • [MeSH-major] Diphtheria Toxin / therapeutic use. Immunosuppressive Agents / therapeutic use. Immunotoxins / therapeutic use. Interleukin-2 / therapeutic use. Lymphoma / drug therapy. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 11707818.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / Immunosuppressive Agents; 0 / Immunotoxins; 0 / Interleukin-2; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 29
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24. Hsu CF, Ko SF, Hsiao CC, Shieh CS, Huang CC, Huang FC: Obstructive jaundice as the presenting manifestation of Burkitt's lymphoma in a 4-year-old boy. J Formos Med Assoc; 2003 Feb;102(2):105-8
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  • [Title] Obstructive jaundice as the presenting manifestation of Burkitt's lymphoma in a 4-year-old boy.
  • Obstructive jaundice often occurs as a late manifestation of non-Hodgkin's lymphoma (NHL), but has rarely been reported as a presenting manifestation, especially in children.
  • We report a case of a 4-year-old boy with Burkitt's lymphoma (small non-cleaved cell NHL) who presented with obstructive jaundice, resulting from encasement of the common bile duct by the tumor.
  • Combined chemotherapy was not given because of refusal by his family.
  • He received chemotherapy and the jaundice disappeared within 6 days.
  • Follow-up computed tomography 1 year later revealed total resolution of the tumor.
  • Second, relief of obstructive jaundice can be effectively accomplished by chemotherapy alone.
  • Third, chemotherapy should be given once NHL is diagnosed.

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  • (PMID = 12709739.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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25. Loong SL, Hwang JS, Lim ST, Yap SP, Tao M, Chong TW, Tan LH, Huynh H: An Epstein-Barr virus positive natural killer lymphoma xenograft derived for drug testing. Leuk Lymphoma; 2008 Jun;49(6):1161-7
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  • [Title] An Epstein-Barr virus positive natural killer lymphoma xenograft derived for drug testing.
  • Here we report an in vivo NK lymphoma xenograft (NK-S1) derived from the testicular metastasis of a patient with an extranodal NK lymphoma (nasal type).
  • Although doxorubicin, rapamycin, bevacizumab, rapamycin-doxorubicin, and bevacizumab-doxorubicin had no effects on the growth of subcutaneous NK-S1 xenografts, intraperitoneal (IP) delivery of cyclophosphamide caused complete tumor regression; this tumor regression was associated with apoptosis, upregulation of activated caspase-3, and cleaved Poly(ADP-ribose) polymerase (PARP).
  • In an IP model of NK lymphoma, cyclophosphamide also prolonged the survival of mice and potently inhibited tumor dissemination and ascites formation.
  • Our data suggest that the NK-S1 xenograft is a useful tool for screening preclinical drugs, and cyclophosphamide may be a useful drug for the treatment of this disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Epstein-Barr Virus Infections / drug therapy. Herpesvirus 4, Human / isolation & purification. Killer Cells, Natural / drug effects. Lymphoma, T-Cell, Peripheral / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Humanized. Apoptosis / drug effects. Bevacizumab. Blotting, Western. Caspase 3 / metabolism. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Enzyme Activation / drug effects. Humans. Injections, Intraperitoneal. Male. Mice. Mice, SCID. Middle Aged. Neoplasm Transplantation. Poly(ADP-ribose) Polymerases / metabolism. Sirolimus / administration & dosage. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 18452087.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 2S9ZZM9Q9V / Bevacizumab; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; W36ZG6FT64 / Sirolimus
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26. Taeda Y, Ariga N, Okamura K, Takei N, Komeno T, Ueki H, Ohtani H: Primary breast mucosa-associated lymphoid tissue (MALT) lymphoma with high-grade transformation evidenced by prominent lymphoepithelial lesions. Breast Cancer; 2006;13(3):322-7
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  • [Title] Primary breast mucosa-associated lymphoid tissue (MALT) lymphoma with high-grade transformation evidenced by prominent lymphoepithelial lesions.
  • Primary breast lymphoma, particularly primary mucosa-associated lymphoid tissue (MALT) lymphoma, is a rare disease.
  • We report here a case of a MALT lymphoma of the breast with high-grade transformation.
  • Pathologically the tumor tissue was composed of small to large lymphoid cells.
  • Among the small cells many small cleaved cells were present, which were more predominant in the peripheral areas.
  • MALT lymphoma with high-grade transformation was diagnosed.
  • Rituximab (anti-CD20 antibody) was prescribed as systemic treatment without chemotherapy or irradiation.
  • We emphasize the importance of lymphoepithelial lesions for the diagnosis of MALT lymphoma of the breast.
  • [MeSH-major] Breast Neoplasms / complications. Cell Transformation, Neoplastic. Epithelial Cells / pathology. Lymphoid Tissue / pathology. Lymphoma, B-Cell, Marginal Zone / complications
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / metabolism. Antineoplastic Agents / therapeutic use. Female. Humans. Lymphoma, B-Cell / pathology. Mastectomy. Rituximab

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  • (PMID = 16929129.001).
  • [ISSN] 1340-6868
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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27. Liu S, Breit S, Danckwardt S, Muckenthaler MU, Kulozik AE: Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines. Ann Hematol; 2009 Jul;88(7):613-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines.
  • Activation of Notch1 signaling plays an important role in the pathogenesis of precursor T-cell lymphoblastic leukemia (T-ALL).
  • The Notch1 receptor is cleaved and activated via the gamma-secretase complex.
  • Downregulation of Notch1 signaling by gamma-secretase inhibitors (GSIs) thus represents a potential novel therapeutic approach.
  • In this study, we analyzed the response of four T-ALL cell lines to compound E, a potent gamma-secretase inhibitor, and to the combination of compound E with vincristine, daunorubicin, L-asparaginase (L-ASP), and dexamethasone (DEX).
  • We identified two distinct types of responses: In type 1 cell lines, represented by TALL1 and HSB2, GSI-induced apoptosis followed cell cycle arrest and enhanced the induction of apoptosis caused by DEX and L-ASP.
  • In type 2 cell lines, represented by CEM and Jurkat J6, GSI caused neither cell cycle block nor cell death.
  • Notably, the combination of GSI with chemotherapy-induced resistance by decreasing apoptosis.
  • In type 2 cells, GSI induced the upregulation of Bcl-xl mRNA and protein, which was thus identified as a candidate mechanism for the inhibition of apoptosis.
  • In conclusion, the data presented here caution against clinical use of a combination treatment of GSI and chemotherapy in T-ALL.
  • [MeSH-major] Amyloid Precursor Protein Secretases / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Asparaginase / pharmacology. Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation. Humans. Signal Transduction. Vincristine / pharmacology

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  • (PMID = 19057901.001).
  • [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 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
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28. Ackler S, Xiao Y, Mitten MJ, Foster K, Oleksijew A, Refici M, Schlessinger S, Wang B, Chemburkar SR, Bauch J, Tse C, Frost DJ, Fesik SW, Rosenberg SH, Elmore SW, Shoemaker AR: ABT-263 and rapamycin act cooperatively to kill lymphoma cells in vitro and in vivo. Mol Cancer Ther; 2008 Oct;7(10):3265-74
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  • [Title] ABT-263 and rapamycin act cooperatively to kill lymphoma cells in vitro and in vivo.
  • Previous work has shown that this compound has low nanomolar cell-killing activity in a variety of lymphoma and leukemia cell lines, many of which overexpress Bcl-2 through a variety of mechanisms.
  • Rapamycin is a macrolide antibiotic that inhibits the mammalian target of rapamycin complex, leading to cell cycle arrest and inhibition of protein translation.
  • Rapamycin (and its analogues) has shown activity in a variety of tumor cell lines primarily through induction of cell cycle arrest.
  • Activity has also been shown clinically in mantle cell lymphoma and advanced renal cell carcinoma.
  • Here, we show that treatment of the follicular lymphoma lines DoHH-2 and SuDHL-4 with 100 nmol/L rapamycin induces substantial G(0)-G(1) arrest.
  • Apoptosis in these tumors was significantly enhanced by combination therapy as measured by staining with an antibody specific for cleaved caspase-3.
  • These data suggest that combination of ABT-263 and rapamycin or its analogues represents a promising therapeutic strategy for the treatment of lymphoma.
  • [MeSH-major] Aniline Compounds / pharmacology. Antineoplastic Agents / pharmacology. Lymphoma, Large B-Cell, Diffuse / pathology. Sirolimus / pharmacology. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. Drug Synergism. Humans. Immunohistochemistry. Mice. Mice, SCID. Remission Induction. Xenograft Model Antitumor Assays

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  • (PMID = 18852130.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / Antineoplastic Agents; 0 / Sulfonamides; W36ZG6FT64 / Sirolimus; XKJ5VVK2WD / navitoclax
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29. Ishida T, Kirchmeier MJ, Moase EH, Zalipsky S, Allen TM: Targeted delivery and triggered release of liposomal doxorubicin enhances cytotoxicity against human B lymphoma cells. Biochim Biophys Acta; 2001 Dec 1;1515(2):144-58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted delivery and triggered release of liposomal doxorubicin enhances cytotoxicity against human B lymphoma cells.
  • Liposomes stabilized with either a non-cleavable PEG (mPEG-DSPE) or mPEG-S-S-DSPE retained an encapsulated dye at pH 5.5, but treatment at pH 5.5 of liposomes stabilized with mPEG-S-S-DSPE with either dithiothreitol or cell-free extracts caused contents release due to cleavage of the PEG chains and concomitant destabilization of the DOPE liposomes.
  • While formulations loaded with doxorubicin (DXR) were stable in culture media, DXR was rapidly released in human plasma. pH-Sensitive liposomes, targeted to the CD19 epitope on B-lymphoma cells, showed enhanced DXR delivery into the nuclei of the target cells and increased cytotoxicity compared to non-pH-sensitive liposomes.
  • Pharmacokinetic studies suggested that mPEG-S-S-DSPE was rapidly cleaved in circulation.
  • In a murine model of B-cell lymphoma, the therapeutic efficacy of an anti-CD19-targeted pH-sensitive formulation was superior to that of a stable long-circulating formulation of targeted liposomes despite the more rapid drug release and clearance of the pH-sensitive formulation.
  • These results suggest that targeted pH-sensitive formulations of drugs may be able to increase the therapeutic efficacy of entrapped drugs.
  • [MeSH-major] Doxorubicin / administration & dosage. Drug Delivery Systems. Liposomes / chemistry
  • [MeSH-minor] Animals. Antigens, CD19 / chemistry. Cell Nucleus / metabolism. Chemistry, Pharmaceutical. Drug Carriers. Humans. Hydrogen-Ion Concentration. Lymphoma / drug therapy. Lymphoma / immunology. Mice. Mice, Inbred BALB C. Mice, SCID. Neoplasm Transplantation. Polyethylene Glycols. Tumor Cells, Cultured

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  • (PMID = 11718670.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / Drug Carriers; 0 / Liposomes; 30IQX730WE / Polyethylene Glycols; 80168379AG / Doxorubicin
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30. Hans CP, Weisenburger DD, Vose JM, Hock LM, Lynch JC, Aoun P, Greiner TC, Chan WC, Bociek RG, Bierman PJ, Armitage JO: A significant diffuse component predicts for inferior survival in grade 3 follicular lymphoma, but cytologic subtypes do not predict survival. Blood; 2003 Mar 15;101(6):2363-7
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  • [Title] A significant diffuse component predicts for inferior survival in grade 3 follicular lymphoma, but cytologic subtypes do not predict survival.
  • Grade 3 follicular lymphoma (FL3) is thought to have an aggressive clinical course.
  • On the basis of possible biologic differences, the new World Health Organization (WHO) classification of lymphoma suggests further subdivision of FL3 into grades 3a and 3b and states that the percentage of involvement by diffuse large B-cell lymphoma (DLBCL) should also be reported.
  • Therefore, we studied 190 newly diagnosed patients with lymph node-based FL3 who received anthracycline-containing combination chemotherapy.
  • The follicular component was subclassified as grade 3a (FL3a) or grade 3b (FL3b) according to the WHO criteria, or as follicular large cleaved cell type (FLC).
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Follicular / mortality. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bleomycin / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. Male. Middle Aged. Mitoxantrone / therapeutic use. Prednisolone / therapeutic use. Prednisone / therapeutic use. Procarbazine / therapeutic use. Prognosis. Survival Rate. Vincristine / therapeutic use

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  • (PMID = 12424193.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA36727
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 35S93Y190K / Procarbazine; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; BZ114NVM5P / Mitoxantrone; VB0R961HZT / Prednisone; CHOP protocol; COP-BLAM protocol; MCOP protocol
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34. Horning SJ, Negrin RS, Hoppe RT, Rosenberg SA, Chao NJ, Long GD, Brown BW, Blume KG: High-dose therapy and autologous bone marrow transplantation for follicular lymphoma in first complete or partial remission: results of a phase II clinical trial. Blood; 2001 Jan 15;97(2):404-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose therapy and autologous bone marrow transplantation for follicular lymphoma in first complete or partial remission: results of a phase II clinical trial.
  • Advanced stage follicular small cleaved and mixed cell lymphoma is characterized by relapse from remission and survival ranging from 6 to 12 years.
  • Because young patients have the greatest compromise in longevity, the efficacy and toxicity of high-dose radiochemotherapy and bone marrow transplantation after conventional chemotherapy was evaluated in a prospective phase II clinical trial.
  • Thirty-seven patients in a minimal disease state after conventional chemotherapy received fractionated total body irradiation and high-dose etoposide and cyclophosphamide, followed by purged autologous bone marrow.
  • There was a single lymphoma death yielding a 10-year disease-specific survival of 97%.
  • High tumor burden at diagnosis and incomplete response to chemotherapy adversely influenced survival in the reference but not in the transplanted patients.
  • The estimated risk of death of 14% and relapse of 30% at 10 years in our transplanted follicular lymphoma patients, the majority of whom had high tumor burdens, compares favorably with our observations in appropriately matched reference patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation / mortality. Lymphoma, Follicular / therapy
  • [MeSH-minor] Actuarial Analysis. Adult. Cohort Studies. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cyclophosphamide / standards. Cyclophosphamide / toxicity. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm, Residual. Prednisone / administration & dosage. Prednisone / standards. Prednisone / toxicity. Prospective Studies. Radiotherapy, Adjuvant. Recurrence. Remission Induction. Survival Rate. Transplantation, Autologous / mortality. Vincristine / administration & dosage. Vincristine / standards. Vincristine / toxicity

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  • (PMID = 11154216.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 34233; United States / NCI NIH HHS / CA / CA 49605
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; COP protocol 2
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35. Sposto R, Meadows AT, Chilcote RR, Steinherz PG, Kjeldsberg C, Kadin ME, Krailo MD, Termuhlen AM, Morse M, Siegel SE: Comparison of long-term outcome of children and adolescents with disseminated non-lymphoblastic non-Hodgkin lymphoma treated with COMP or daunomycin-COMP: A report from the Children's Cancer Group. Med Pediatr Oncol; 2001 Nov;37(5):432-41
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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 long-term outcome of children and adolescents with disseminated non-lymphoblastic non-Hodgkin lymphoma treated with COMP or daunomycin-COMP: A report from the Children's Cancer Group.
  • BACKGROUND: Early Children's Cancer Group (CCG) trials indicated that the cyclophosphamide, vincristine, methotrexate, and prednisone (COMP) regimen was superior to the LSA2L2 regimen for non-lymphoblastic (NLB) non-Hodgkin lymphoma (NHL).
  • Studies by other groups suggested that addition of anthracyclines to standard therapies could improve outcome.
  • Patients with CNS or marrow involvement (stage IV) were non-randomly treated with D-COMP (N = 120).
  • RESULTS: Ten-year event-free survival in COMP and D-COMP patients was similar: 55 +/- 4.3% (Estimate +/- SE) vs. 57 +/- 4.2% (not significant).
  • Stage I-III patients with large-cell (LC) NHL had worse 10-year event-free survival (EFS) (48 +/- 4.9%) than those with small non-cleaved cell (SNCC) NHL disease (61 +/- 3.5%, P < 0.05 in multivariate analysis), but equivalent survival (65 +/- 4.7% vs. 63 +/- 3.5%) due to significantly higher salvage rates in LC patients, especially those failing more than 12 months from diagnosis.
  • CONCLUSIONS: Addition of daunomycin to standard COMP therapy did not improve outcome in pediatric disseminated NLB NHL.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Daunorubicin / pharmacology. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cyclophosphamide / administration & dosage. Female. Follow-Up Studies. Heart Diseases / chemically induced. Humans. Infant. Infant, Newborn. Infusions, Intravenous. Male. Methotrexate / administration & dosage. Neutropenia / chemically induced. Prednisone / administration & dosage. Recurrence. Stomatitis / chemically induced. Survival Analysis. Thrombocytopenia / chemically induced. Treatment Outcome. Vincristine / administration & dosage

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11745871.001).
  • [ISSN] 0098-1532
  • [Journal-full-title] Medical and pediatric oncology
  • [ISO-abbreviation] Med. Pediatr. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 02649; United States / NCI NIH HHS / CA / CA 02971; United States / NCI NIH HHS / CA / CA 03526; United States / NCI NIH HHS / CA / CA 03750; United States / NCI NIH HHS / CA / CA 03888; United States / NCI NIH HHS / CA / CA 07306; United States / NCI NIH HHS / CA / CA 07431; United States / NCI NIH HHS / CA / CA 10382; United States / NCI NIH HHS / CA / CA 11796; United States / NCI NIH HHS / CA / CA 13539; United States / NCI NIH HHS / CA / CA 14560; United States / NCI NIH HHS / CA / CA 17829; United States / NCI NIH HHS / CA / CA 20320; United States / NCI NIH HHS / CA / CA 26044; United States / NCI NIH HHS / CA / CA 26126; United States / NCI NIH HHS / CA / CA 26270; United States / NCI NIH HHS / CA / CA 27678; United States / NCI NIH HHS / CA / CA 28851; United States / NCI NIH HHS / CA / CA 28882; United States / NCI NIH HHS / CA / CA 29013; United States / NCI NIH HHS / CA / CA 29314; United States / NCI NIH HHS / CA / CA 36004; United States / NCI NIH HHS / CA / CA 36015
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin; COMP protocol
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36. Lorusso V, Palmieri G, Bianco AR, Abate G, Catalano G, De Vita F, Dammacco F, Lauta VM, Lucarelli G, Polimeno G, Mantovani G, D'Aprile M, Marzullo F, De Lena M: CEOP-B/VIMB vs. promace-CytaBOM in the treatment of intermediate or high grade non-Hodgkin's lymphoma: A randomised multicenter study of Southern Italy Cooperative Group. Int J Oncol; 2000 Jan;16(1):149-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CEOP-B/VIMB vs. promace-CytaBOM in the treatment of intermediate or high grade non-Hodgkin's lymphoma: A randomised multicenter study of Southern Italy Cooperative Group.
  • From January 1992 to December 1995, 129 patients with previously untreated non-Hodgkin's lymphoma were randomised in a phase III multicenter trial to receive CEOP-B/VIMB or ProMACE-CytaBOM.
  • Eligibility criteria included intermediate or high grade lymphoma (follicular large cell, diffuse small cleaved-cell, diffuse mixed, diffuse large-cell and immunoblastic) with an Ann Arbor stage II bulky, III or IV.
  • At a median follow-up of 60 months there were no significant differences between the treatment response rates [82% (60%CR) for CEOP-B/VIMB vs. 81% (69% CR) for ProMACE-CytaBOM].
  • Conversely, with regard to disease-free survival, a significant difference was observed between the two treatment arms (42% for CEOP-B/VIMB vs. 24% for ProMACE-CytaBOM at 5 years; p=0.046).
  • Moreover, when response rates and outcome were analysed for different prognostic subgroups according to International Prognostic Index, no significant differences were observed between the treatment groups.
  • It is important to note that neither regimen was able to improve outcome of poor risk patients who fared badly with both treatments (median survival 9 and 8 months respectively).
  • Toxicity was also similar in both treatments with grade 3-4 leukopenia observed in 39% and 47% of cases and grade 3-4 thrombocytopenia in 24% and 27% of cases respectively.
  • In conclusion, in this study CEOP-B/VIMB was not superior to ProMACE-CytaBOM in aggressive lymphomas and the alternating strategy failed to improve outcome of poor risk patients in which newer more aggressive treatments are needed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Bleomycin / administration & dosage. Bleomycin / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Cytarabine / administration & dosage. Cytarabine / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Etoposide / administration & dosage. Etoposide / adverse effects. Female. Humans. Male. Methotrexate / administration & dosage. Methotrexate / adverse effects. Middle Aged. Neoplasm Staging. Prednisone / administration & dosage. Prednisone / adverse effects. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects

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  • (PMID = 10601560.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] GREECE
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 11056-06-7 / Bleomycin; 3Z8479ZZ5X / Epirubicin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; CEOP-B protocol; PROMACE-CytaBOM protocol
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37. Bobey NA, Stewart DA, Woodman RC: Successful treatment of posttransplant lymphoproliferative disorder in a renal transplant patient by autologous peripheral blood stem cell transplantation. Leuk Lymphoma; 2002 Dec;43(12):2421-3
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  • [Title] Successful treatment of posttransplant lymphoproliferative disorder in a renal transplant patient by autologous peripheral blood stem cell transplantation.
  • Posttransplant lymphoproliferative disorder (PTLD), a well recognized complication of organ transplantation, comprises a wide spectrum of heterogeneous lymphoid proliferations ranging from self-limiting mononucleosis through aggressive monoclonal non-Hodgkin's lymphoma (NHL).
  • There has been marginal success in treating PTLD using a number of treatment modalities, including combination chemotherapy.
  • There have been few reports of the use of high dose chemotherapy with stem cell rescue as a treatment for PTLD.
  • We report a renal allograft recipient who developed PTLD of the diffuse large cleaved B cell, NHL type.
  • Reduction of immunosuppression was initially effective, however the patient relapsed, and was treated successfully with CHOP chemotherapy.
  • Two years later he again relapsed and was treated with high dose melphalan followed by autologous peripheral blood stem cell transplantation (PSCT).
  • This case illustrates a potential role for high dose chemotherapy with stem cell transplantation for the treatment of PTLD.
  • [MeSH-major] Kidney Transplantation / adverse effects. Lymphoproliferative Disorders / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Disease-Free Survival. Humans. Immunosuppression / adverse effects. Lymphoma, B-Cell / etiology. Lymphoma, B-Cell / therapy. Lymphoma, Large B-Cell, Diffuse / etiology. Lymphoma, Large B-Cell, Diffuse / therapy. Male. Transplantation, Autologous

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  • (PMID = 12613536.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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38. Hjalmar V, Kimby E, Matutes E, Sundström C, Wallvik J, Hast R: Atypical lymphocytes in B-cell chronic lymphocytic leukemia and trisomy 12 studied by conventional staining combined with fluorescence in situ hybridization. Leuk Lymphoma; 2000 May;37(5-6):571-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical lymphocytes in B-cell chronic lymphocytic leukemia and trisomy 12 studied by conventional staining combined with fluorescence in situ hybridization.
  • Trisomy 12 is one of the most frequent chromosomal abnormalities in B-cell chronic lymphocytic leukemia (CLL), and is predominantly found in CLL with atypical morphology (aCLL).
  • In three patients, the proportion of atypical and typical lymphocytes with trisomy 12 was quite comparable, and so was the percentage of atypical cells with lymphoplasmacytoid morphology and those with cleaved nucleus showing trisomy 12.
  • However, this could be fully explained by the diluting effect of contaminating T-cells after chemotherapy.
  • This supports that both cell types have the same clonal origin and that different cell morphology cannot be explained alone by the acquisition of an additional chromosome 12.
  • [MeSH-major] B-Lymphocytes / pathology. Chromosomes, Human, Pair 12. In Situ Hybridization, Fluorescence. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Staining and Labeling / methods. Trisomy
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Nucleus / ultrastructure. Coloring Agents. Eosine Yellowish-(YS). Female. Humans. Immunophenotyping. Male. Methylene Blue. Middle Aged. Neoplastic Stem Cells / pathology

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  • (PMID = 11042517.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / May-Grunwald Giemsa; T42P99266K / Methylene Blue; TDQ283MPCW / Eosine Yellowish-(YS)
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39. Mahieux R, Pise-Masison C, Gessain A, Brady JN, Olivier R, Perret E, Misteli T, Nicot C: Arsenic trioxide induces apoptosis in human T-cell leukemia virus type 1- and type 2-infected cells by a caspase-3-dependent mechanism involving Bcl-2 cleavage. Blood; 2001 Dec 15;98(13):3762-9
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  • [Title] Arsenic trioxide induces apoptosis in human T-cell leukemia virus type 1- and type 2-infected cells by a caspase-3-dependent mechanism involving Bcl-2 cleavage.
  • Treatment of patients with adult T-cell leukemia-lymphoma (ATLL) using conventional chemotherapy has limited benefit because human T-cell leukemia virus type 1 (HTLV-1) cells are resistant to most apoptosis-inducing agents.
  • The recent report that arsenic trioxide induces apoptosis in HTLV-1-transformed cells prompted investigation of the mechanism of action of this drug in HTLV-1 and HTLV-2 interleukin-2-independent T cells and in HTLV-1-immortalized cells or in ex vivo ATLL samples.
  • Fluorescence-activated cell sorter analysis, fluorescence microscopy, and measures of mitochondrial membrane potential (Delta Psi m) demonstrated that arsenic trioxide alone was sufficient to induce programmed cell death in all HTLV-1 and -2 cells tested and in ATLL patient samples.
  • The antiapoptotic factor Bcl-2 was then cleaved, converting it to a Bax-like death effector.
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Caspases / metabolism. Human T-lymphotropic virus 1 / physiology. Human T-lymphotropic virus 2 / physiology. I-kappa B Proteins. Leukemia-Lymphoma, Adult T-Cell / pathology. Oxides / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Caspase 3. Cell Line, Transformed. Cell Nucleus / metabolism. Cytochrome c Group / metabolism. DNA-Binding Proteins / metabolism. Flow Cytometry. Humans. Interferon-alpha / pharmacology. Membrane Potentials. Microscopy, Fluorescence. Mitochondria / ultrastructure. NF-kappa B / metabolism. Phosphorylation. Proto-Oncogene Proteins / analysis. Tumor Suppressor Protein p53 / analysis. bcl-2-Associated X Protein. bcl-X Protein

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  • (PMID = 11739184.001).
  • [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 / Arsenicals; 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / Cytochrome c Group; 0 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / Interferon-alpha; 0 / NF-kappa B; 0 / Oxides; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 139874-52-5 / NF-kappaB inhibitor alpha; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide
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40. Mwinzi PN, Ganley-Leal L, Black CL, Secor WE, Karanja DM, Colley DG: Circulating CD23+ B cell subset correlates with the development of resistance to Schistosoma mansoni reinfection in occupationally exposed adults who have undergone multiple treatments. J Infect Dis; 2009 Jan 15;199(2):272-9
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  • [Title] Circulating CD23+ B cell subset correlates with the development of resistance to Schistosoma mansoni reinfection in occupationally exposed adults who have undergone multiple treatments.
  • However, Although B cells are the source of schistosome-specific IgE, little is known about B cell subsets or their functions in this infection.
  • We evaluated B cells and their expression of the low-affinity IgE receptor (CD23) in a unique cohort of men occupationally exposed to Schistosoma mansoni and longitudinally followed up through multiple treatments with praziquantel, cures, and reinfections.
  • The CD23(+) B cell subset was evaluated in whole blood by flow cytometry.
  • Higher levels of plasma sCD23, the cleaved form of mCD23, also correlated with resistance and other markers of resistance to reinfection, such as eosinophilia.
  • Understanding these complex host-parasite interactions may lead to insights into the development, mechanisms, and regulation of resistance to reinfection with S. mansoni.

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  • (PMID = 19072134.001).
  • [ISSN] 0022-1899
  • [Journal-full-title] The Journal of infectious diseases
  • [ISO-abbreviation] J. Infect. Dis.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI053695; United States / NIAID NIH HHS / AI / R21 AI074843-01A2; United Kingdom / Wellcome Trust / / 083607; United States / NIAID NIH HHS / AI / T32 AI060546; United States / FIC NIH HHS / TW / D43 TW007123; United States / NIAID NIH HHS / AI / R21 AI074843; United States / NIAID NIH HHS / AI / AI 053692; United States / PHS HHS / / D43 T007123W; United States / NIAID NIH HHS / AI / AI074843-01A2
  • [Publication-type] 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] United States
  • [Chemical-registry-number] 0 / Anthelmintics; 0 / Receptors, IgE; 6490C9U457 / Praziquantel
  • [Other-IDs] NLM/ NIHMS89681; NLM/ PMC2636678
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41. Hu XF, Li J, Yang E, Vandervalk S, Xing PX: Anti-Cripto Mab inhibit tumour growth and overcome MDR in a human leukaemia MDR cell line by inhibition of Akt and activation of JNK/SAPK and bad death pathways. Br J Cancer; 2007 Mar 26;96(6):918-27
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  • [Title] Anti-Cripto Mab inhibit tumour growth and overcome MDR in a human leukaemia MDR cell line by inhibition of Akt and activation of JNK/SAPK and bad death pathways.
  • Doxorubicin (DOX) selection of CCRF-CEM leukaemia cell line resulted in multidrug resistance (MDR) CEM/A7R cell line, which overexpresses MDR, 1 coded P-glycoprotein (Pgp).
  • Here, we report for the first time that oncoprotein Cripto, a founding member of epidermal growth factor-Cripto-FRL, 1-Criptic family is overexpressed in the CEM/A7R cells, and anti-Cripto monoclonal antibodies (Mab) inhibited CEM/A7R cell growth both in vitro and in an established xenograft tumour in severe combined immunodeficiency mice.
  • In particular, the combination of anti-Cripto Mab at less than 50% of inhibition concentrations with noncytotoxic concentrations of EPI or DAU inhibited more than 90% of CEM/A7R cell growth.
  • We demonstrated that anti-Cripto Mab-induced CEM/A7R cell apoptosis, which was associated with an enhanced activity of the c-Jun N-terminal kinase/stress-activated protein kinase and inhibition of Akt phosphorylation, resulting in an activation of mitochondrial apoptosis pathway as evidenced by dephosphorylation of Bad at Ser136, Bcl-2 at Ser70 and a cleaved caspase-9.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Intercellular Signaling Peptides and Proteins / immunology. Leukemia / therapy. MAP Kinase Kinase 4 / metabolism. Mitogen-Activated Protein Kinases / metabolism. Oncogene Protein v-akt / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspase 9 / metabolism. Cell Growth Processes / drug effects. Cell Line, Tumor. Cytarabine / pharmacokinetics. Cytarabine / pharmacology. Daunorubicin / pharmacokinetics. Daunorubicin / pharmacology. Drug Synergism. Enzyme Activation / drug effects. Epirubicin / pharmacokinetics. Epirubicin / pharmacology. Female. Humans. Mice. Mice, SCID. P-Glycoprotein / biosynthesis. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-Associated Death Protein / metabolism. bcl-X Protein / metabolism

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  • (PMID = 17342096.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / CFC1 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / P-Glycoprotein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-Associated Death Protein; 0 / bcl-X Protein; 04079A1RDZ / Cytarabine; 3Z8479ZZ5X / Epirubicin; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 3.4.22.- / Caspase 9; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ PMC2360102
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42. Horber DH, Cattaneo-Pangrazzi RM, von Ballmoos P, Schott H, Ludwig PS, Eriksson S, Fichtner I, Schwendener RA: Cytotoxicity, cell-cycle perturbations and apoptosis in human tumor cells by lipophilic N4-alkyl-1-beta-D-arabinofuranosylcytosine derivatives and the new heteronucleoside phosphate dimer arabinocytidylyl-(5'--&gt;5')-N4-octadecyl-1-beta-D-arabinofuranosylcytosi ne. J Cancer Res Clin Oncol; 2000 Jun;126(6):311-9
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  • [Title] Cytotoxicity, cell-cycle perturbations and apoptosis in human tumor cells by lipophilic N4-alkyl-1-beta-D-arabinofuranosylcytosine derivatives and the new heteronucleoside phosphate dimer arabinocytidylyl-(5'-->5')-N4-octadecyl-1-beta-D-arabinofuranosylcytosi ne.
  • The arabinofuranosylcytosine (AraC) derivative N4-octadecyl-1-beta-D-arabinofuranosylcytosine (NOAC) and its (5'-->5')-heterodinucleoside phosphate analog NOAC-AraC were compared with AraC for cytotoxicity, cell-cycle dependence, phosphorylation by deoxycytidine (dC) kinase and apoptosis induction in native, AraC- or NOAC-resistant HL-60 cells.
  • This suggests that NOAC-AraC may be cleaved intracellularly only at very slow rates to AraC and NOAC or to the 5'-monophosphates, whereas NOAC exerts different mechanisms of action from AraC.
  • In vitro the dimer was cleaved by phosphodiesterase or human serum to NOAC, AraC and AraC monophosphate.
  • Furthermore, treatment of the multidrug-resistant cell lines KB-ChR-8-5 and KB-V1 with the N4-hexadecyl-AraC derivative NHAC did not induce P-170 glycoprotein expression, suggesting that the N4-alkyl-AraC derivatives are able to circumvent MDR1 multidrug resistance.
  • [MeSH-major] Antimetabolites, Antineoplastic / pharmacology. Apoptosis / drug effects. Cytarabine / analogs & derivatives. Cytarabine / pharmacology. HL-60 Cells / drug effects. P-Glycoprotein / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Deoxycytidine Kinase / metabolism. Dimerization. Disease Models, Animal. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mice, Nude. Phosphates / metabolism. Phosphorylation. Prodrugs / pharmacology. Transplantation, Heterologous

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  • (PMID = 10870640.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / P-Glycoprotein; 0 / Phosphates; 0 / Prodrugs; 04079A1RDZ / Cytarabine; 130252-71-0 / N(4)-oleylcytosine arabinoside; EC 2.7.1.74 / Deoxycytidine Kinase
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43. Franco MI, Waisberg J, Lopes LS: Multiple lymphomatous polyposis of the gastrointestinal tract. Sao Paulo Med J; 2004 May 6;122(3):131-3

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  • CONTEXT: Gastrointestinal multiple lymphomatous polyposis is a rare type of malignant lymphoma that has aggressive biological behavior, early systemic dissemination and poor prognosis.
  • It is considered to be a manifestation of non-Hodgkin lymphoma and represents the gastrointestinal counterpart of mantle cell nodal lymphoma.
  • OBJECTIVE: A case of gastrointestinal multiple lymphomatous polyposis is presented and the anatomopathological, clinical, diagnostic and treatment aspects of this unusual neoplasia are discussed.
  • A rectal biopsy revealed infiltration of the mucosa and submucosa by diffuse lymphoma consisting of small cleaved cells.
  • After two cycles of chemotherapy there was a worsening of the general state, with an increase in the dimensions of the abdominal masses and sepsis, accompanied by progressive respiratory insufficiency, leading to death.
  • [MeSH-major] Gastrointestinal Neoplasms / pathology. Intestinal Polyposis / pathology. Lymphoma, Mantle-Cell / pathology

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  • (PMID = 15448813.001).
  • [ISSN] 1516-3180
  • [Journal-full-title] São Paulo medical journal = Revista paulista de medicina
  • [ISO-abbreviation] Sao Paulo Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Brazil
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44. Falà F, Blalock WL, Tazzari PL, Cappellini A, Chiarini F, Martinelli G, Tafuri A, McCubrey JA, Cocco L, Martelli AM: Proapoptotic activity and chemosensitizing effect of the novel Akt inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-cell acute lymphoblastic leukemia. Mol Pharmacol; 2008 Sep;74(3):884-95
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  • [Title] Proapoptotic activity and chemosensitizing effect of the novel Akt inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-cell acute lymphoblastic leukemia.
  • Constitutively activated AKT kinase is a common feature of T-cell acute lymphoblastic leukemia (T-ALL).
  • Here, we report that the novel AKT inhibitor (2S)-1-(1H-indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) leads to rapid cell death of T-ALL lines and patient samples.
  • Treatment of CEM, Jurkat, and MOLT-4 cells with nanomolar doses of the inhibitor led to AKT phosphorylation accompanied by dephosphorylation and activation of the downstream target, glycogen synthase kinase-3beta.
  • Effects were time- and dose-dependent, resulting in apoptotic cell death.
  • Treatment of Jurkat cells with A443654 resulted in activation of caspase-2, -3, -6, -8, and -9.
  • Apoptotic cell death was mostly dependent on caspase-2 activation, as demonstrated by preincubation with a selective pharmacological inhibitor.
  • It is remarkable that A443654 was highly effective against the drug-resistant cell line CEM-VBL100, which expresses 170-kDa P-glycoprotein.
  • Moreover, A443654 synergized with the DNA-damaging agent etoposide in both drug-sensitive and drug-resistant cell lines when coadministered [combination index (CI) = 0.39] or when pretreated with etoposide followed by A443654 (CI = 0.689).
  • The efficacy of A443654 was confirmed using blasts from six patients with T-ALL, all of whom displayed low levels of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and constitutive phosphorylation of Akt on Ser473.
  • At 1 microM, the inhibitor was able to induce apoptotic cell death of T-ALL blast cells, as indicated by flow cytometric analysis of samples immunostained for active (cleaved) caspase-3.
  • Because activated AKT is seen in a large percentage of patients with T-ALL, A443654, either alone or in combination with existing drugs, may be a useful therapy for primary and drug-resistant T-ALL.

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  • (PMID = 18577685.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098195-05; United States / NCI NIH HHS / CA / R01 CA098195-05; United States / NCI NIH HHS / CA / R01-CA091025
  • [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 / A 443654; 0 / Indazoles; 0 / Indoles; 1114-81-4 / Phosphothreonine; 17885-08-4 / Phosphoserine; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS79780; NLM/ PMC2659779
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45. Jiang JD, Denner L, Ling YH, Li JN, Davis A, Wang Y, Li Y, Roboz J, Wang LG, Perez-Soler R, Marcelli M, Bekesi G, Holland JF: Double blockade of cell cycle at g(1)-s transition and m phase by 3-iodoacetamido benzoyl ethyl ester, a new type of tubulin ligand. Cancer Res; 2002 Nov 1;62(21):6080-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Double blockade of cell cycle at g(1)-s transition and m phase by 3-iodoacetamido benzoyl ethyl ester, a new type of tubulin ligand.
  • In contrast to other known microtubule disrupters, 3-IAABE caused a double blockade in the cell cycle at G(1)-S transition and in M phase.
  • The blockade was determined by cell cycle analysis and chromosome distribution.
  • 3-IAABE treatment also increased p53 expression and dephosphorylated (or activated) retinoblastoma protein.
  • DNA fragmentation factor and poly(ADP-ribose) polymerase, the downstream substrates of caspase-3 and -6, were cleaved after 3 h of exposure to 3-IAABE, followed by DNA fragmentation.
  • 3-IAABE showed antitumor activities in the panel of 60 National Cancer Institute human tumor cell lines with total growth inhibition in the range of 0.22-4.3 micro M for solid tumor lines and 0.025-0.22 micro M for leukemia/lymphoma cell lines.
  • Besides being a novel lead for the design of new anticancer tubulin ligands, the activity of 3-IAABE in the cell cycle may also help us to understand the molecular pharmacology of microtubule-active drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Cycle / drug effects. Iodoacetamide / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / pathology. Drug Screening Assays, Antitumor. Humans. Ligands. Liver Neoplasms / drug therapy. Liver Neoplasms / pathology. Male. Mice. Mice, Nude. Microtubules / drug effects. Phosphorylation / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tubulin / metabolism. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / biosynthesis. U937 Cells / drug effects. Vincristine / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 12414632.001).
  • [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 / 3-iodoacetamido benzoyl ethyl ester; 0 / Antineoplastic Agents; 0 / Ligands; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tubulin; 0 / Tumor Suppressor Protein p53; 5J49Q6B70F / Vincristine; ZRH8M27S79 / Iodoacetamide
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46. Tulpule A, Sherrod A, Dharmapala D, Young LL, Espina BM, Sanchez MN, Gill PS, Levine AM: Multidrug resistance (MDR-1) expression in AIDS-related lymphomas. Leuk Res; 2002 Feb;26(2):121-7
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  • In non-Hodgkin's lymphoma, less than 20% of untreated de novo lymphomas express MDR-1 compared with approximately 50% after failure of chemotherapy.
  • We wished to study the expression of MDR-1 in AIDS-related non-Hodgkin's lymphoma (AIDS-NHL).
  • Tissue biopsies from 50 patients with newly diagnosed AIDS-NHL were studied by immunohistochemical analysis using C494, a monoclonal antibody specific for the MDR-1 isoform of P-gp.
  • MDR-1 expression was correlated with patient demographics, lymphoma characteristics, response to chemotherapy, and survival.
  • Thirty-two patients (63%) had received prior anti-HIV therapy, including a protease inhibitor in five (10%).
  • Pathologic types consisted of diffuse large cell in 13 (26%), immunoblastic in 13 (26%), small non-cleaved in 22 (44%), and high grade not otherwise specified in two (4%).
  • Pre-treatment lymphoma tissues from 33 patients (66%) stained positively for MDR-1.
  • Strategies to overcome MDR-1 expression may be important for initial treatment in patients with AIDS-NHL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / metabolism. Drug Resistance, Multiple / genetics. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Lymphoma, AIDS-Related / metabolism. Neoplasm Proteins / biosynthesis. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / mortality. Adult. Anti-HIV Agents / therapeutic use. Bleomycin / administration & dosage. Bleomycin / metabolism. Bleomycin / pharmacology. Cyclophosphamide / administration & dosage. Cyclophosphamide / metabolism. Cyclophosphamide / pharmacology. Dexamethasone / administration & dosage. Dexamethasone / metabolism. Dexamethasone / pharmacology. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / metabolism. Doxorubicin / pharmacology. Female. Humans. Leucovorin / administration & dosage. Leucovorin / metabolism. Leucovorin / pharmacology. Male. Methotrexate / administration & dosage. Methotrexate / metabolism. Methotrexate / pharmacology. Middle Aged. Prednisone / administration & dosage. Prednisone / metabolism. Prednisone / pharmacology. Remission Induction. Retrospective Studies. Survival Analysis. Vincristine / administration & dosage. Vincristine / metabolism. Vincristine / pharmacology

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  • (PMID = 11755462.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 11056-06-7 / Bleomycin; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; Q573I9DVLP / Leucovorin; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; CHOP protocol; M-BACOD protocol
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47. Hayakawa A, Kawamoto Y, Nakajima H, Sakai J, Takasawa R, Nakashima I, Magae J, Tanuma S: Bid truncation mediated by caspases-3 and -9 in vinorelbine-induced apoptosis. Apoptosis; 2008 Apr;13(4):523-30
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  • Vinorelbine is a chemotherapeutic vinca alkaloid clinically prescribed for non-small cell lung cancer and breast cancer.
  • Here we studied the mechanism for vinorelbine-induced apoptosis in a human T-cell lymphoma.
  • A downstream substrate for caspase-8, Bid, is also cleaved in vinorelbine-treated cells, but the Bid truncation is also observed in caspase-8-deficient Jurkat cells.
  • [MeSH-major] Apoptosis / drug effects. BH3 Interacting Domain Death Agonist Protein / metabolism. Caspase 3 / physiology. Caspase 9 / physiology. Lymphoma, T-Cell / drug therapy. Vinblastine / analogs & derivatives
  • [MeSH-minor] Caspase 8 / physiology. Cell Line, Tumor. Cytochromes c / metabolism. Humans. Jurkat Cells

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  • (PMID = 18297401.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 5V9KLZ54CY / Vinblastine; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9; Q6C979R91Y / vinorelbine
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48. Turturro F: Denileukin diftitox: a biotherapeutic paradigm shift in the treatment of lymphoid-derived disorders. Expert Rev Anticancer Ther; 2007 Jan;7(1):11-7
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  • [Title] Denileukin diftitox: a biotherapeutic paradigm shift in the treatment of lymphoid-derived disorders.
  • Denileukin diftitox is proteolytically cleaved within the endosome liberating the enzymatically active portion of the diphtheria toxin, the A fragment.
  • Diphtheria toxin fragment A is released into the cytosol inhibiting the protein synthesis through the ADP-ribosylation of the elongation factor-2, and leading to cell death.
  • This review focuses on the clinical trials that led to the FDA approval of the drug for cutaneous T cell lymphoma in the US, and investigational studies demonstrating drug-activity against B and T-cell non-Hodgkin's lymphoma, chronic lymphocytic lymphoma and acute graft versus disease within allogeneic hematopoietic stem cell transplant.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Hodgkin Disease / drug therapy. Interleukin-2 / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Hematopoietic Stem Cell Transplantation. Humans. Recombinant Fusion Proteins / pharmacokinetics. Recombinant Fusion Proteins / therapeutic use. Safety. United States. United States Food and Drug Administration

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  • (PMID = 17187516.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 30
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49. Liu J, Huang R, Lin D, Wu X, Peng J, Lin Q, Pan X, Zhang M, Hou M, Chen F: Apoptotic effect of oridonin on NB4 cells and its mechanism. Leuk Lymphoma; 2005 Apr;46(4):593-7

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  • Cell growth inhibition, apoptosis and related pathways were assessed by MTT assay as well as flow cytometry (FCM) and western blot analysis.
  • Marked changes of cell apoptosis were observed very clearly by using electron microscopy and DNA fragmentation analysis after the cells exposed to oridonin for 48 h; Western blotting showed cleavage of the caspase-3 zymogen protein (32-kDa) with the appearance of its 20-kDa subunit as well as a cleaved 89-kDa fragment of 116-kDa PARP when apoptosis occurred.
  • Furthermore, oridonin demonstrated apparent cell growth inhibition effects on fresh APL cells in vitro.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Diterpenes / pharmacology. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / metabolism
  • [MeSH-minor] Blotting, Western. Caspase 3. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Molecular Structure. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism

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  • (PMID = 16019488.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Proto-Oncogene Proteins c-bcl-2; 0APJ98UCLQ / oridonin; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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50. Hansen HP, Matthey B, Barth S, Kisseleva T, Mokros T, Davies SJ, Beckett RP, Foelster-Holst R, Lange HH, Engert A, Lemke H: Inhibition of metalloproteinases enhances the internalization of anti-CD30 antibody Ki-3 and the cytotoxic activity of Ki-3 immunotoxin. Int J Cancer; 2002 Mar 10;98(2):210-5
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  • However, CD30 is cleaved at the cell surface by tumor necrosis factor-alpha converting enzyme (TACE).
  • Such constitutive CD30 cleavage is enhanced after binding of most anti-CD30 antibodies, leading to a downregulation of CD30 and an increase of sCD30 in the cell environment.
  • Here, we demonstrate that CD30 shedding from the cell line Karpas 299 could effectively be blocked by the hydroxamic acid-based metalloproteinase inhibitors BB-3644 (IC50 = 180 nM), BB-2116 (IC50 = 230 nM), BB-94 (batimastat, IC50 = 230 nM) and BB-2516 (marimastat, IC50 = 1 microM).
  • This inhibition reduced the concentration of sCD30 in the cell environment to the background level, prolonged the persistence of the anti-CD30 antibody Ki-3 on Karpas 299 cells and favored its internalization.
  • Moreover, a nontoxic concentration of the inhibitor BB-3644 significantly increased the cytotoxic activity of the anti-CD30 ricin A-chain immunotoxin Ki-3.dgA towards the CD30(+) Hodgkin-derived cell line L540.
  • [MeSH-minor] Cell Survival. Dose-Response Relationship, Drug. Endocytosis. Humans. Kinetics. Lymphoma / metabolism. Lymphoma / therapy. Lymphoma, Large-Cell, Anaplastic / metabolism. Lymphoma, Large-Cell, Anaplastic / therapy. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 Wiley‐Liss, Inc.
  • (PMID = 11857410.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminopyridines; 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / BB 3644; 0 / Hydroxamic Acids; 0 / Immunotoxins; 0 / Protease Inhibitors; EC 3.4.24.- / Metalloendopeptidases
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51. Yang CP, Hung JJ, Jaing TH, Lin KH, Lin DT, Lu MY, Liang DC, Chen SH, Liu HC, Hsiao CC, Shu SG, Chen JS, Chang TT, Chiou SS, Hsieh YL, Lin MT, Lee MT, Peng CT, Cheng SN, Chen RL, Chen BW, Lin KS: Treatment results of the TPOG-NHL92 protocols for childhood non-Hodgkin's lymphomas in Taiwan: a report from the Taiwan Pediatric Oncology Group (TPOG). Acta Paediatr Taiwan; 2000 Jul-Aug;41(4):193-204

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  • [Title] Treatment results of the TPOG-NHL92 protocols for childhood non-Hodgkin's lymphomas in Taiwan: a report from the Taiwan Pediatric Oncology Group (TPOG)
  • A nation-wide chemotherapeutic trial for childhood non-Hodgkin's lymphoma (NHL) was conducted by the Taiwan Pediatric Oncology Group (TPOG).
  • Four TPOG-NHL92 protocols based on stage and histology were activated in 1992: TPOG-92LD (treatment duration: 8 months) was used for localized (stages I/II) NHL with any histology, 92LB (2 years), 92SNC (5 months), and 92LC (1 year) for advanced (stages III/IV) lymphoblastic (LB), small non-cleaved cell (SNC), and large cell (LC) lymphoma, respectively.
  • There were 54 (27.3%) patients with LB, 94 (47.5%) with SNC including B-cell acute lymphoblastic leukemia (B-ALL), and 50 (25.2%) with LC.
  • There were 176 patients eligible for evaluation of treatment results.
  • As of August 31, 1999, 26 patients relapsed, six died during remission, one patient developed secondary acute myelomonocytic leukemia, and 105 patients remained in continuous remission with a median remission duration of 49 months.
  • We concluded that following the strategy of stratification of therapy, only disease stages had prognostic significance in this study.
  • More efforts are needed to improve our treatment results.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy

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  • [CommentIn] Acta Paediatr Taiwan. 2000 Jul-Aug;41(4):175-6 [11021000.001]
  • (PMID = 11021005.001).
  • [ISSN] 1608-8115
  • [Journal-full-title] Acta paediatrica Taiwanica = Taiwan er ke yi xue hui za zhi
  • [ISO-abbreviation] Acta Paediatr Taiwan
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China (Republic : 1949- )
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52. Alhosin M, Abusnina A, Achour M, Sharif T, Muller C, Peluso J, Chataigneau T, Lugnier C, Schini-Kerth VB, Bronner C, Fuhrmann G: Induction of apoptosis by thymoquinone in lymphoblastic leukemia Jurkat cells is mediated by a p73-dependent pathway which targets the epigenetic integrator UHRF1. Biochem Pharmacol; 2010 May 1;79(9):1251-60
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  • We therefore attempted to identify the up- and down-stream events involved in the activation of the p73-dependent pro-apoptotic pathway, by focusing on the anti-apoptotic and epigenetic integrator UHRF1 which is essential for cell cycle progression.
  • For this purpose, we analyzed the effects of a known anti-neoplastic drug, thymoquinone (TQ), on the p53-deficient acute lymphoblastic leukemia (ALL) Jurkat cell line.
  • Our results showed that TQ inhibits the proliferation of Jurkat cells and induces G1 cell cycle arrest in a dose-dependent manner.
  • Moreover, TQ treatment triggers programmed cell death, production of reactive oxygen species (ROS) and alteration of the mitochondrial membrane potential (DeltaPsim).
  • TQ-induced apoptosis, confirmed by the presence of hypodiploid G0/G1 cells, is associated with a rapid and sharp re-expression of p73 and dose-dependent changes of the levels of caspase-3 cleaved subunits.
  • Knockdown of p73 expression restores UHRF1 expression, reactivates cell cycle progression and inhibits TQ-induced apoptosis.
  • Altogether our results showed that TQ mediates its growth inhibitory effects on ALL p53-mutated cells via the activation of a p73-dependent mitochondrial and cell cycle checkpoint signaling pathway which subsequently targets UHRF1.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Benzoquinones / pharmacology. CCAAT-Enhancer-Binding Proteins / metabolism. DNA-Binding Proteins / metabolism. Nuclear Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Cell Cycle. Gene Expression Regulation / drug effects. Humans. Jurkat Cells

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  • [Copyright] 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20026309.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoquinones; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / UHRF1 protein, human; 0 / tumor suppressor protein p73; 490-91-5 / thymoquinone
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53. Lee JS, Pei-Lin Ng P, Tao M, Lim WT: Paraneoplastic pemphigus resembling linear IgA bullous dermatosis. Int J Dermatol; 2006 Sep;45(9):1093-5
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  • He had stage IIIA follicular small cell cleaved non-Hodgkin's lymphoma diagnosed 5 years previously, and had received several lines of palliative chemotherapy, including two courses of chlorambucil, six cycles of cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP), and two four-cycle courses of rituximab, with disease stabilization at the time of presentation.
  • 4), satellite cell necrosis in the epidermis, and a superficial perivascular infiltrate of lymphocytes and eosinophils.
  • He declined rituximab therapy.

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  • (PMID = 16961519.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin A
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54. Kuznetsov G, Towle MJ, Cheng H, Kawamura T, TenDyke K, Liu D, Kishi Y, Yu MJ, Littlefield BA: Induction of morphological and biochemical apoptosis following prolonged mitotic blockage by halichondrin B macrocyclic ketone analog E7389. Cancer Res; 2004 Aug 15;64(16):5760-6
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  • Treatment of U937 human histiocytic lymphoma cells with E7389 led to time-dependent collection of cells in the G2-M phase of the cell cycle, beginning as early as 2 h and becoming maximal by 12 h.
  • The identity of hypodiploid events as apoptotic cells under these conditions was confirmed by two additional morphologic criteria: green to orange/yellow shifts on acridine orange/ethidium bromide staining, and cell surface annexin V binding as assessed by flow cytometry.
  • Several biochemical correlates of apoptosis also were seen following E7389 treatment, including phosphorylation of the antiapoptotic protein Bcl-2, cytochrome c release from mitochondria, proteolytic activation of caspase-3 and -9, and cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (PARP).
  • In LNCaP human prostate cancer cells, treatment with E7389 also led to generation of hypodiploid cells, activation of caspase-3 and -9, and appearance of cleaved PARP, indicating that E7389 can activate cellular apoptosis pathways under anchorage-independent and -dependent cell culture conditions.
  • These results show that prolonged mitotic blockage by E7389 can lead to apoptotic cell death of human cancer cells in vitro and can provide a mechanistic basis for the significant in vivo anticancer efficacy of E7389.
  • [MeSH-major] Apoptosis / drug effects. Ethers, Cyclic / pharmacology. Furans / pharmacology. Ketones / pharmacology. Mitosis / drug effects. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology
  • [MeSH-minor] Caspase 3. Caspase 9. Caspases / metabolism. Cell Line, Tumor. Cell Membrane / drug effects. Cell Membrane / physiology. Cell Polarity / drug effects. Cytochromes c / secretion. Diploidy. Enzyme Activation / drug effects. G2 Phase / drug effects. Humans. Male. Mitochondria / drug effects. Mitochondria / secretion. Phosphorylation / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. U937 Cells

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  • (PMID = 15313917.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ethers, Cyclic; 0 / Furans; 0 / Ketones; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / eribulin; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9; EC 3.4.22.- / Caspases
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55. Francisco JA, Cerveny CG, Meyer DL, Mixan BJ, Klussman K, Chace DF, Rejniak SX, Gordon KA, DeBlanc R, Toki BE, Law CL, Doronina SO, Siegall CB, Senter PD, Wahl AF: cAC10-vcMMAE, an anti-CD30-monomethyl auristatin E conjugate with potent and selective antitumor activity. Blood; 2003 Aug 15;102(4):1458-65
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  • The chimeric monoclonal antibody cAC10, directed against CD30, induces growth arrest of CD30+ cell lines in vitro and has pronounced antitumor activity in severe combined immunodeficiency (SCID) mouse xenograft models of Hodgkin disease.
  • We have significantly enhanced these activities by conjugating to cAC10 the cytotoxic agent monomethyl auristatin E (MMAE) to create the antibody-drug conjugate cAC10-vcMMAE.
  • The drug was stably attached to the antibody, showing only a 2% release of MMAE following 10-day incubation in human plasma, but it was readily cleaved by lysosomal proteases after receptor-mediated internalization.
  • Release of MMAE into the cytosol induced G2/M-phase growth arrest and cell death through the induction of apoptosis.
  • In SCID mouse xenograft models of anaplastic large cell lymphoma or Hodgkin disease, cAC10-vcMMAE was efficacious at doses as low as 1 mg/kg.
  • These data indicate that cAC10-vcMMAE may be a highly effective and selective therapy for the treatment of CD30+ neoplasias.
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Drug Stability. Hodgkin Disease / drug therapy. Hodgkin Disease / immunology. Hodgkin Disease / metabolism. Humans. Inhibitory Concentration 50. Mice. Mice, SCID. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12714494.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Antineoplastic Agents; 0 / Immunoconjugates; 0 / Immunotoxins; 0 / Oligopeptides; 0 / cAC10-vcMMAE
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56. Xue LY, Chiu SM, Oleinick NL: Differential responses of Mcl-1 in photosensitized epithelial vs lymphoid-derived human cancer cells. Oncogene; 2005 Oct 20;24(46):6987-92
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  • The antiapoptotic Bcl-2-family proteins, Bcl-2 and Bcl-xL, are recognized phototargets of photodynamic therapy (PDT) with the mitochondrion-targeting phthalocyanine photosensitizer Pc 4.
  • In the present study, we found that myeloid cell leukemia 1 (Mcl-1), another antiapoptotic member of the Bcl-2 family, was not photodamaged in Pc 4-PDT-treated human carcinoma cells MCF-7c3, MDA-MB468, DU145, and A431, although Mcl-1 turnover was observed after exposure of HeLa or MCF-7c3 cells to a supralethal dose of UVC.
  • In contrast, when human lymphoma U937 and Jurkat cells were treated with Pc 4-PDT, staurosporine (STS) or UVC, Mcl-1 was cleaved to generate a 28-kDa fragment over a 2-4 h period.
  • The 28-kDa cleaved fragment of Mcl-1, which has proapoptotic activity, was produced in PDT-treated lymphoid-derived cells, but not in cells of epithelial origin, suggesting that PDT-induced rapid and extensive apoptosis in lymphoma cells may result in part from the sensitivity of their Mcl-1 to caspase cleavage, removing an important negative control on apoptosis.
  • [MeSH-major] Epithelial Cells / drug effects. Indoles / pharmacology. Lymphoid Tissue / drug effects. Neoplasm Proteins / metabolism. Photosensitizing Agents / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Caspases / metabolism. Cell Line, Tumor. Cysteine Proteinase Inhibitors / pharmacology. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Staurosporine / pharmacology. Substrate Specificity. Ultraviolet Rays

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  • (PMID = 16007152.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA48735; United States / NCI NIH HHS / CA / P30 CA43703; United States / NCI NIH HHS / CA / R01 CA83917
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cysteine Proteinase Inhibitors; 0 / Indoles; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Photosensitizing Agents; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / phthalocyanine Pc 4; EC 3.4.22.- / Caspases; H88EPA0A3N / Staurosporine
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57. Soundararajan R, Sayat R, Robertson GS, Marignani PA: Triptolide: An inhibitor of a disintegrin and metalloproteinase 10 (ADAM10) in cancer cells. Cancer Biol Ther; 2009 Nov;8(21):2054-62
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  • The expression of ADAM10 is enhanced in several tumors including leukemia and is involved in malignant cell growth and cancer progression.
  • ADAM10 is a type 1 transmembrane glycoprotein that cleaves several plasma membrane proteins.
  • We show that triptolide, at concentrations in the nM range, resulted in a significant decrease in ADAM10 expression followed by the appearance of ADAM10 cleaved product.
  • Triptolide treatment of MCF-7 breast cancer cells expressing ectopic ADAM10 or dominant negative ADAM10 (DN ADAM10) resulted in a decreased expression of ADAM10 with a concomitant increase in ADAM10 cleaved products.
  • Interestingly, the combination of siRNA-mediated knockdown of ADAM10 mRNA expression and triptolide treatment lead to a further reduction in cell growth.
  • [MeSH-major] ADAM Proteins / antagonists & inhibitors. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents, Alkylating / pharmacology. Breast Neoplasms / drug therapy. Diterpenes / pharmacology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Membrane Proteins / antagonists & inhibitors. Phenanthrenes / pharmacology. Protease Inhibitors / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Chromatography, Affinity. Epoxy Compounds / pharmacology. Humans. U937 Cells

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  • [CommentIn] Cancer Biol Ther. 2009 Nov;8(21):2063-4 [19783897.001]
  • (PMID = 19783906.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / / MOP-67039
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Diterpenes; 0 / Epoxy Compounds; 0 / Membrane Proteins; 0 / Phenanthrenes; 0 / Protease Inhibitors; 19ALD1S53J / triptolide; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
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58. Crazzolara R, Cisterne A, Thien M, Hewson J, Baraz R, Bradstock KF, Bendall LJ: Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia. Blood; 2009 Apr 2;113(14):3297-306
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  • [Title] Potentiating effects of RAD001 (Everolimus) on vincristine therapy in childhood acute lymphoblastic leukemia.
  • Despite advances in the treatment of acute lymphoblastic leukemia (ALL), the majority of children who relapse still die of ALL.
  • Therefore, the development of more potent but less toxic drugs for the treatment of ALL is imperative.
  • We investigated the effects of the mammalian target of rapamycin inhibitor, RAD001 (Everolimus), in a nonobese diabetic/severe combined immunodeficiency model of human childhood B-cell progenitor ALL.
  • RAD001 treatment of established disease increased the median survival of mice from 21.3 days to 42.3 days (P < .02).
  • RAD001 together with vincristine significantly increased survival compared with either treatment alone (P < .02).
  • RAD001 induced a cell-cycle arrest in the G(0/1) phase with associated dephosphorylation of the retinoblastoma protein, and reduced levels of cyclin-dependent kinases 4 and 6.
  • In contrast, cleaved poly(ADP-ribose) polymerase suggested apoptosis in cells from animals treated with vincristine or the combination of RAD001 and vincristine, but not in those receiving RAD001 alone.
  • In conclusion, we have demonstrated activity of RAD001 in an in vivo leukemia model supporting further clinical development of target of rapamycin inhibitors for the treatment of patients with ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / analogs & derivatives. Vincristine / administration & dosage
  • [MeSH-minor] Adolescent. Animals. Child. Child, Preschool. Drug Synergism. Everolimus. Female. Humans. Male. Mice. Mice, Inbred NOD. Mice, SCID. Placebos. Survival Analysis. Xenograft Model Antitumor Assays


59. Ji J, Zhang L, Wu YY, Zhu XY, Lv SQ, Sun XZ: Induction of apoptosis by d-limonene is mediated by a caspase-dependent mitochondrial death pathway in human leukemia cells. Leuk Lymphoma; 2006 Dec;47(12):2617-24
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  • Using K562 and HL60 cell lines, we have investigated the anti-tumoral activity of d-limonene, a monocyclic monoterpene, in human leukemia cells.
  • Apoptosis was evaluated by Hoechst staining and by the annexin V/propidium iodide binding assay. d-Limonene induced apoptosis in a dose- and time-dependent manner in both cell lines.
  • Our findings and data, demonstrating an increase in Bax protein expression, the release of cytochrome c from mitochondria, and an increase in caspase-9 and cleaved caspase-3, but not caspase-8, after the treatment of d-limonene, all suggest that the mitochondrial death pathway is primarily involved in the development of d-limonene-induced apoptosis.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Apoptosis. Caspases / metabolism. Cyclohexenes / pharmacology. Leukemia / drug therapy. Leukemia / pathology. Mitochondria / metabolism. Terpenes / pharmacology
  • [MeSH-minor] Cell Differentiation. Cell Line, Tumor. Cell Survival. Cytochromes c / metabolism. DNA Fragmentation. HL-60 Cells. Humans. K562 Cells

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  • [RetractionIn] Leuk Lymphoma. 2016 May;57(5):1242 [27096893.001]
  • (PMID = 17169807.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Retracted Publication
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Cyclohexenes; 0 / Terpenes; 9007-43-6 / Cytochromes c; 9MC3I34447 / limonene; EC 3.4.22.- / Caspases
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60. Wu X, Shi J, Wu Y, Tao Y, Hou J, Meng X, Hu X, Han Y, Jiang W, Tang S, Zangari M, Tricot G, Zhan F: Arsenic trioxide-mediated growth inhibition of myeloma cells is associated with an extrinsic or intrinsic signaling pathway through activation of TRAIL or TRAIL receptor 2. Cancer Biol Ther; 2010 Dec 1;10(11):1201-14
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  • Arsenic trioxide (ATO) is a well-known inhibitor of cell proliferation.
  • In this study, the molecular mechanisms of ATO-induced myeloma apoptosis were explored on four myeloma cell lines of wild type or mutant p53 status and also on six primary myeloma cells.
  • ATO induced potent inhibition of myeloma cell growth and myeloma cell apoptosis compared with controls.
  • Further investigation showed that ATO down-regulated c-Myc and phosphorylated (p)-Rb while up-regulating p53, p21Cip1, and p27Kip1 proteins, resulting in G0/G1 or G2/M cell cycle arrest.
  • ATO treatment increased mRNA levels of interferon regulatory factor-1 and TRAIL, as well as protein levels of caspase 8 and cleaved caspase 3, indicating the involvement of the extrinsic apoptotic pathway in the mutated p53 myeloma cells.
  • ATO also activated caspases 3 and 9, indicating involvement of the intrinsic apoptotic pathway in the wild type p53 myeloma cells.
  • These observations may be employed as prognostic tools and lead to novel therapies in primary myelomas.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Arsenicals / pharmacology. Multiple Myeloma / drug therapy. Oxides / pharmacology. Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism. TNF-Related Apoptosis-Inducing Ligand / metabolism
  • [MeSH-minor] Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Survival / drug effects. Down-Regulation / drug effects. Humans. Interferon Regulatory Factor-1 / biosynthesis. Interferon Regulatory Factor-1 / genetics. Interferon Regulatory Factor-1 / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Recombinant Proteins / pharmacology. Signal Transduction / drug effects

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  • (PMID = 20953137.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA115399; United States / NCI NIH HHS / CA / R01 CA152105; United States / NCI NIH HHS / CA / R21 CA143887
  • [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 / Antineoplastic Agents; 0 / Arsenicals; 0 / IRF1 protein, human; 0 / Interferon Regulatory Factor-1; 0 / Oxides; 0 / RNA, Messenger; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFSF10 protein, human; S7V92P67HO / arsenic trioxide
  • [Other-IDs] NLM/ PMC3047108
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61. Park MJ, Kwon HY, Lee EO, Lee HJ, Ahn KS, Kim MO, Kim CH, Ahn KS, Kim SH: DMNQ-S17 inhibits constitutive NF-kappaB activation leading to induction of apoptosis through the activation of caspase-3 in human myeloid leukemia U937 cells. Life Sci; 2008 Sep 26;83(13-14):460-7
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  • In addition, DMNQ-S17 induced apoptotic features such as apoptotic bodies, cell shrinkage and chromatin condensation in U937 cells.
  • Furthermore, DMNQ-S17 effectively attenuated mitochondrial membrane potential, released cytochrome C, activated caspase-3 expression, and cleaved poly (ADP-ribose) polymerase (PARP).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Caspase 3 / biosynthesis. Leukemia, Myeloid / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. NF-kappa B / biosynthesis. Naphthoquinones / pharmacology
  • [MeSH-minor] Caspase Inhibitors. Cytochromes c / metabolism. Drug Screening Assays, Antitumor. Enzyme Inhibitors / pharmacology. Fluorescent Dyes. Humans. In Situ Nick-End Labeling. Indoles. Male. Membrane Potential, Mitochondrial / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. U937 Cells

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  • (PMID = 18718843.001).
  • [ISSN] 0024-3205
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 6-(1-oxobutyl)-5,8-dimethoxy-1,4-naphthoquinone; 0 / Antineoplastic Agents; 0 / Caspase Inhibitors; 0 / Enzyme Inhibitors; 0 / Fluorescent Dyes; 0 / Indoles; 0 / NF-kappa B; 0 / Naphthoquinones; 47165-04-8 / DAPI; 9007-43-6 / Cytochromes c; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
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62. Oyamada S, Osipov R, Bianchi C, Robich MP, Feng J, Liu Y, Burgess TA, Bell TM, Sheller MR, Sellke FW: Effect of dimerized thrombin fragment TP508 on acute myocardial ischemia reperfusion injury in hypercholesterolemic swine. J Pharmacol Exp Ther; 2010 Aug;334(2):449-59
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  • In addition, the expression of 27-kDa heat shock protein, alphaB-crystalline, and phosphorylated B-cell lymphoma 2 (Ser70) in the ischemic area at risk were higher in treated groups than in vehicle, whereas the expression of cleaved poly-ADP ribose polymerase was lower in treated groups.
  • This study suggests that TP508 dimer provides a myocardial-protective effect on acute ischemia reperfusion injury in hypercholesterolemic swine, similar to TP508 monomer, by up-regulating cell survival pathways or down-regulating apoptotic pathways.

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  • (PMID = 20460385.001).
  • [ISSN] 1521-0103
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01HL46716; United States / NHLBI NIH HHS / HL / R01 HL046716; United States / NHLBI NIH HHS / HL / R01 HL085647; United States / NHLBI NIH HHS / HL / R01 HL069024; United States / NHLBI NIH HHS / HL / T32 HL076130; United States / NHLBI NIH HHS / HL / R01HL85647; United States / NHLBI NIH HHS / HL / T32HL0074; United States / NHLBI NIH HHS / HL / T32HL076130; United States / NHLBI NIH HHS / HL / R01HL69024
  • [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 / Blood Glucose; 0 / Lipids; 0 / Peptide Fragments; 0 / Solutions; 0 / rusalatide acetate; EC 3.4.21.5 / Thrombin
  • [Other-IDs] NLM/ PMC2913770
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63. Osipov RM, Robich MP, Feng J, Liu Y, Clements RT, Glazer HP, Sodha NR, Szabo C, Bianchi C, Sellke FW: Effect of hydrogen sulfide in a porcine model of myocardial ischemia-reperfusion: comparison of different administration regimens and characterization of the cellular mechanisms of protection. J Cardiovasc Pharmacol; 2009 Oct;54(4):287-97
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The expression of B-cell lymphoma 2 (P = 0.059), heat shock protein 27 and alphaB-crystallin (P < 0.05) were lower in H2S-treated groups.
  • The expression of caspase 3 and cleaved caspase 3 were lower (P < 0.05), whereas the expression of phospho-Bad(Ser136) was higher in the bolus group versus control and infusion groups (P < 0.05).
  • The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cell count was lower in both H2S-treated groups compared with the control (P < 0.05).
  • [MeSH-major] Cardiotonic Agents / administration & dosage. Cardiotonic Agents / therapeutic use. Hydrogen Sulfide / administration & dosage. Hydrogen Sulfide / therapeutic use. Myocardial Infarction / prevention & control. Myocardial Reperfusion Injury / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Survival / drug effects. Coronary Circulation / drug effects. Disease Models, Animal. In Situ Nick-End Labeling. Infusions, Intravenous. Injections, Intravenous. Male. Microcirculation / drug effects. Myocardium / pathology. Swine. Troponin I / blood. Ventricular Function, Left / drug effects

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  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 19620880.001).
  • [ISSN] 1533-4023
  • [Journal-full-title] Journal of cardiovascular pharmacology
  • [ISO-abbreviation] J. Cardiovasc. Pharmacol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01HL46716; United States / NHLBI NIH HHS / HL / R01HL69024; United States / NHLBI NIH HHS / HL / R01HL85647; United States / NHLBI NIH HHS / HL / T32-HL076130
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 0 / Troponin I; YY9FVM7NSN / Hydrogen Sulfide
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