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1. Vakiani E, Savage DG, Pile-Spellman E, El-Tamer M, Singh IR, Murty VS, Alobeid B, Bhagat G: T-Cell lymphoblastic lymphoma presenting as bilateral multinodular breast masses: a case report and review of the literature. Am J Hematol; 2005 Nov;80(3):216-22
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  • [Title] T-Cell lymphoblastic lymphoma presenting as bilateral multinodular breast masses: a case report and review of the literature.
  • Non-Hodgkin lymphoma of T-cell lineage involving the breast is rare.
  • We report on a 41-year-old woman with T-cell lymphoblastic lymphoma who presented with multiple bilateral breast masses.
  • The patient was treated with intensive chemotherapy and mediastinal and whole-brain irradiation.
  • She remains in complete remission 24 months after diagnosis.
  • [MeSH-major] Breast Neoplasms / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Cranial Irradiation. Diagnosis, Differential. Female. Humans. Radiotherapy, Adjuvant. Remission Induction / methods

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  • (PMID = 16247747.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA149719
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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2. Zhu DM, Uckun FM: Calpain inhibitor II induces caspase-dependent apoptosis in human acute lymphoblastic leukemia and non-Hodgkin's lymphoma cells as well as some solid tumor cells. Clin Cancer Res; 2000 Jun;6(6):2456-63
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  • [Title] Calpain inhibitor II induces caspase-dependent apoptosis in human acute lymphoblastic leukemia and non-Hodgkin's lymphoma cells as well as some solid tumor cells.
  • Calpain is a calcium-dependent cysteine protease that is implicated in calcium-dependent cell death, and calpain inhibitors are generally considered as inhibitors of apoptosis.
  • To the contrary, in the present study, we found that calpain inhibitor II (CPI-2) triggers rapid apoptosis in acute lymphoblastic leukemia (ALL) and non-Hodgkin's lymphoma (NHL) cells.
  • All target cell lines were killed by CPI-2, including: ALL-1, a multidrug-resistant BCR-ABL fusion transcript-positive t(9;22) pro-B ALL cell line; RS4;11, a highly radiation-resistant MLL-AF4 fusion transcript-positive t(4;11) pre-pre B ALL cell line; RAMOS, a highly radiation-resistant and p53-deficient Burkitt's lymphoma cell line; DAUDI, a Burkitt's leukemia/lymphoma cell line; NALM-6, a pre-B ALL cell line; and JURKAT and MOLT-3, two T-lineage ALL/NHL cell lines.
  • CPI-2-induced apoptosis in LYN-deficient and BTK-deficient subclones of the DT-40 lymphoma B cell line as effectively as it did in wild-type DT-40 cells.
  • Unlike the high calpain-expressing ALL/NHL cell lines, myeloid leukemia cell lines HL-60/AML, K562/CML, and U937/AMML, or solid tumor cell lines BT-20/breast cancer, PC-3/prostate cancer, U373/glioblastoma, and HeLa/epitheloid cancer, were not susceptible to the cytotoxicity of CPI-2.
  • Taken together, our results identify calpain as a new molecular target for the treatment of ALL and NHL.
  • CPI-2 and its analogues represent a promising new class of antileukemia/lymphoma agents that deserves further development.
  • [MeSH-major] Apoptosis. Caspases / metabolism. Lymphoma, Non-Hodgkin / metabolism. Oligopeptides / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Cell Separation. DNA / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Flow Cytometry. Fluorescein-5-isothiocyanate / metabolism. HL-60 Cells. HeLa Cells. Humans. Immunoglobulin G / metabolism. In Situ Nick-End Labeling. Jurkat Cells. K562 Cells. Microscopy, Confocal. Protein-Tyrosine Kinases / metabolism. Time Factors. Tumor Cells, Cultured. U937 Cells. src-Family Kinases / metabolism

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  • (PMID = 10873099.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Oligopeptides; 110115-07-6 / N-acetylleucyl-leucyl-methioninal; 9007-49-2 / DNA; EC 2.7.10.1 / Agammaglobulinaemia tyrosine kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases; EC 3.4.22.- / Caspases; I223NX31W9 / Fluorescein-5-isothiocyanate
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3. Batova A, Cottam H, Yu J, Diccianni MB, Carrera CJ, Yu AL: EFA (9-beta-D-erythrofuranosyladenine) is an effective salvage agent for methylthioadenosine phosphorylase-selective therapy of T-cell acute lymphoblastic leukemia with L-alanosine. Blood; 2006 Feb 1;107(3):898-903
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  • [Title] EFA (9-beta-D-erythrofuranosyladenine) is an effective salvage agent for methylthioadenosine phosphorylase-selective therapy of T-cell acute lymphoblastic leukemia with L-alanosine.
  • The deficiency of methylthioadenosine phosphorylase (MTAP) in T-cell acute lymphoblastic leukemia (T-ALL) and other cancers, while constitutively expressed in normal cells, allows for selective therapy using L-alanosine, an inhibitor of de novo AMP synthesis.
  • We demonstrate that MTAP- T-ALL cells obtained at relapse are as sensitive to L-alanosine toxicity as diagnosis samples.
  • The therapeutic index of L-alanosine can be increased by the use of a MTAP substrate, which protects MTAP+ normal cells.

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  • (PMID = 16234352.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR00827
  • [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 / 9-beta-D-erythrofuranosyladenine; 0 / Antibiotics, Antineoplastic; 0 / Deoxyadenosines; 0 / Enzyme Inhibitors; 0 / Furans; 0 / Thionucleosides; 2CNI71214Y / alanosine; 634Z2VK3UQ / 5'-methylthioadenosine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase; EC 2.4.2.28 / 5'-methylthioadenosine phosphorylase; JAC85A2161 / Adenine; OF5P57N2ZX / Alanine
  • [Other-IDs] NLM/ PMC1895892
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4. Schult C, Dahlhaus M, Ruck S, Sawitzky M, Amoroso F, Lange S, Etro D, Glass A, Fuellen G, Boldt S, Wolkenhauer O, Neri LM, Freund M, Junghanss C: The multikinase inhibitor Sorafenib displays significant antiproliferative effects and induces apoptosis via caspase 3, 7 and PARP in B- and T-lymphoblastic cells. BMC Cancer; 2010;10:560
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  • [Title] The multikinase inhibitor Sorafenib displays significant antiproliferative effects and induces apoptosis via caspase 3, 7 and PARP in B- and T-lymphoblastic cells.
  • BACKGROUND: Targeted therapy approaches have been successfully introduced into the treatment of several cancers.
  • The multikinase inhibitor Sorafenib has antitumor activity in solid tumors and its effects on acute lymphoblastic leukemia (ALL) cells are still unclear.
  • METHODS: ALL cell lines (SEM, RS4;11 and Jurkat) were treated with Sorafenib alone or in combination with cytarabine, doxorubicin or RAD001.
  • Cell count, apoptosis and necrosis rates, cell cycle distribution, protein phosphorylation and metabolic activity were determined.
  • RESULTS: Sorafenib inhibited the proliferation of ALL cells by cell cycle arrest accompanied by down-regulation of CyclinD3 and CDK4.
  • Antiproliferative effects of Sorafenib were associated with a decreased phosphorylation of Akt (Ser473 and Thr308), FoxO3A (Thr32) and 4EBP-1 (Ser65 and Thr70) as early as 0.5 h after treatment.
  • Synergistic effects were seen when Sorafenib was combined with other cytotoxic drugs or a mTOR inhibitor emphasizing the Sorafenib effect.
  • CONCLUSION: Sorafenib displays significant antileukemic activity in vitro by inducing cell cycle arrest and apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. B-Lymphocytes / pathology. Benzenesulfonates / pharmacology. Caspase 3 / metabolism. Caspase 7 / metabolism. Poly(ADP-ribose) Polymerases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Pyridines / pharmacology. T-Lymphocytes / pathology
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Jurkat Cells. Niacinamide / analogs & derivatives. Phenylurea Compounds. Phosphorylation

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  • (PMID = 20950443.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 7
  • [Other-IDs] NLM/ PMC2972283
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5. Cho J, Hur M, Moon HW, Yun YM, Lee CH, Lee HG: A case of therapy-related ALL with MLL gene rearrangement following treatment of breast cancer. Korean J Lab Med; 2010 Jun;30(3):255-9
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  • [Title] A case of therapy-related ALL with MLL gene rearrangement following treatment of breast cancer.
  • ALL with MLL gene rearrangement secondary to chemotherapy has been rarely reported.
  • We report a case of therapy-related ALL (t-ALL) with MLL gene rearrangement in a patient who had undergone treatment for breast cancer.
  • A 60-yr-old woman with breast cancer underwent breast-conserving surgery followed by 6 cycles of adjuvant chemotherapy (cyclophosphamide, epirubicin, and fluorouracil) and radiation therapy (dose, 5,040 cGy to the left breast and a 1,000 cGy boost to the tumor bed).
  • A follow-up examination performed 14 months after the chemotherapy revealed no evidence of breast malignancy.
  • However, the patient's complete blood cell count indicated acute leukemia: white blood cell count, 174.1 x 10(9)/L with 88% blasts; Hb level, 12.5 g/dL; and platelet count, 103.0 x 10(9)/L.
  • The patient received induction chemotherapy with cyclophosphamide, vincristine, doxorubicin, and dexamethasone and achieved complete remission.
  • Following consolidation chemotherapy, she underwent allogenic peripheral blood stem cell transplantation and has been clinically stable.
  • To our knowledge, this is the first reported case of t-ALL with MLL gene rearrangement following treatment of breast cancer in Korea.
  • [MeSH-major] Breast Neoplasms / drug therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Translocation, Genetic
  • [MeSH-minor] Antibiotics, Antineoplastic / therapeutic use. Blood Cell Count. Bone Marrow / pathology. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Cytogenetic Analysis. Epirubicin / therapeutic use. Female. Fluorouracil / therapeutic use. Gene Rearrangement. Hematopoietic Stem Cell Transplantation. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence

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  • (PMID = 20603585.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; U3P01618RT / Fluorouracil
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6. Kahwash SB, Qualman SJ: Cutaneous lymphoblastic lymphoma in children: report of six cases with precursor B-cell lineage. Pediatr Dev Pathol; 2002 Jan-Feb;5(1):45-53
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  • [Title] Cutaneous lymphoblastic lymphoma in children: report of six cases with precursor B-cell lineage.
  • Precursor B lymphoblastic lymphomas (B-LBL) are generally rare, but appear to have a higher incidence in children than in adults.
  • Three occurred in the scalp, one in the skin of the thigh, one in the skin of the face and breast, and one in the subcutaneous tissue of the orbit.
  • None of the cases had bone marrow involvement, while two had bone involvement (maxilla, distal tibia, and distal humerus in one case, and distal tibia and orbital bone in another case); only one case had lymphadenopathy (retroperitoneal).
  • Cases in which cell marker studies by flow cytometry were performed showed positivity for CD10, CD19 with negative CD20, pan-T-cell, and myeloid markers.
  • The five patients who received multiagent chemotherapy are alive with follow-up intervals of 2 to 18 years.
  • Two patients had local recurrences and were given radiation therapy (one with repeating multiagent chemotherapy).
  • One patient (diagnosed in 1962) died of disseminated disease; she had been treated with radiation therapy and 6MP only.
  • Cutaneous B-LBL must be included in the differential diagnosis of small blue cell tumors, especially in children.
  • In contrast to its T-cell counterpart, B-LBL occurs more frequently in females, tends to present as skin or bone lesions, and is associated with a potential cure, even in cases that relapse.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / analysis. Child. Child, Preschool. Combined Modality Therapy. Fatal Outcome. Female. Flow Cytometry. Humans. Immunohistochemistry. Neoplasm Proteins / analysis. Neoplasm Recurrence, Local

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  • (PMID = 11815868.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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7. Lin P, Jones D, Dorfman DM, Medeiros LJ: Precursor B-cell lymphoblastic lymphoma: a predominantly extranodal tumor with low propensity for leukemic involvement. Am J Surg Pathol; 2000 Nov;24(11):1480-90
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Precursor B-cell lymphoblastic lymphoma: a predominantly extranodal tumor with low propensity for leukemic involvement.
  • Precursor B-cell lymphoblastic lymphoma (B-LBL) is uncommon and accounts for less than 10% of cases of lymphoblastic lymphoma.
  • Patients with concurrent precursor B-cell acute lymphoblastic leukemia (B-ALL) or a history thereof were excluded.
  • There was no evidence of bone marrow disease at the time of diagnosis in 23 patients; two patients had focal (<5%) involvement.
  • The treatment and survival data available for a subset of patients with B-LBL were compared with those from a series of patients with B-ALL at our institution.
  • The primary sites of disease were skin (nine cases), bones (five cases), soft tissue (four cases), lymph nodes, (three cases), breast (two cases), stomach and colon (one case), and mediastinum (one case).
  • All cases were positive for B-cell antigens and terminal deoxynucleotidyl transferase.
  • Of 14 patients with available survival data, all achieved complete clinical response after combination chemotherapy (13 patients) or surgical excision followed by local irradiation (one patient).
  • Five (35.7%) patients subsequently relapsed, including the patient who had received only irradiation, and four of these patients died after a median survival time of 60 months.
  • None of the patients had leukemia, although one patient developed extensive bone marrow involvement.
  • Unlike precursor T-cell lymphoblastic lymphoma, which commonly involves lymph nodes and the mediastinum, B-LBL usually involves extranodal sites, most often the skin, and rarely presents as a mediastinal mass.
  • With aggressive chemotherapy, patients with precursor B-LBL rarely develop leukemia and appear to have a better prognosis than do patients with B-ALL.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Precancerous Conditions / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 11075849.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / DNA, Neoplasm
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8. Fichtner I, Becker M, Baumgart J: Antileukaemic activity of treosulfan in xenografted human acute lymphoblastic leukaemias (ALL). Eur J Cancer; 2003 Apr;39(6):801-7
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  • [Title] Antileukaemic activity of treosulfan in xenografted human acute lymphoblastic leukaemias (ALL).
  • Treosulfan (L-threitol-1,4-bis-methanesulphonate; Ovastat(R)) is a bifunctional alkylating drug indicated for the treatment of advanced ovarian carcinoma.
  • Recent data revealed immunosuppressive characteristics and substantial haematopoietic stem cell toxicity after repeated dosing of mice.
  • Therefore, treosulfan is considered to be an alternative conditioning agent to busulfan (for example) administered prior to allogeneic/autologous stem cell transplantation of patients with haematological malignancies.
  • An antineoplastic activity for treosulfan has been previously shown in preclinical models of melanoma, breast, lung and renal-cell carcinomas.
  • Here, in vivo antileukaemic activity of treosulfan is compared with the activity of equitoxic doses of cyclophosphamide or busulfan for the first time using human acute lymphoblastic leukaemia (ALL)-models of paediatric origin xenotransplanted into non-obese diabetic (NOD)/severe combined immunodeficient (SCID) mice.
  • Treosulfan treatment achieved an optimum treated to control (T/C) value of 159% (survival time) against B-ALL-SCID 7 and a T/C value of 0% (tumour growth) against T-ALL-SCID 4 and proB-ALL-SCID 19, respectively.
  • Treosulfan can be considered a highly active antileukaemic drug whose corresponding clinical value is to be tested in appropriate protocols with leukaemic patients.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Busulfan / analogs & derivatives. Busulfan / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Animals. Body Weight. Cyclophosphamide / therapeutic use. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Female. Hematologic Diseases / chemically induced. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 12651206.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide; CO61ER3EPI / treosulfan; G1LN9045DK / Busulfan
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9. Lee SG, Choi JR, Kim JS, Park TS, Lee KA, Song J: Therapy-related acute lymphoblastic leukemia with t(9;22)(q34;q11.2):a case study and review of the literature. Cancer Genet Cytogenet; 2009 May;191(1):51-4
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  • [Title] Therapy-related acute lymphoblastic leukemia with t(9;22)(q34;q11.2):a case study and review of the literature.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) with t(9;22)(q34;q11.2) is rarely reported as a secondary malignant neoplasm.
  • We present a novel case of t-ALL with t(9;22) in a patient with primary breast cancer.
  • The interval between diagnosis of breast cancer and the appearance of ALL was 4 years.
  • The patient was treated with partial mastectomy and axillary lymph node dissection followed by six cycles of CMF (cyclophosphamide, methotrexate, 5-fluorouracil) chemotherapy and radiation therapy.
  • This case has the following unique features: BCR/ABL gene rearrangement in t-ALL, and two types of malignant cells (leukemic lymphoblasts and metastatic breast cancer cells) coexisted in the bone marrow.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Chromosomes, Human, Pair 9 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 19389510.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
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10. Andersen MK, Christiansen DH, Jensen BA, Ernst P, Hauge G, Pedersen-Bjergaard J: Therapy-related acute lymphoblastic leukaemia with MLL rearrangements following DNA topoisomerase II inhibitors, an increasing problem: report on two new cases and review of the literature since 1992. Br J Haematol; 2001 Sep;114(3):539-43
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  • [Title] Therapy-related acute lymphoblastic leukaemia with MLL rearrangements following DNA topoisomerase II inhibitors, an increasing problem: report on two new cases and review of the literature since 1992.
  • More recently, single cases of acute lymphoblastic leukaemia (ALL), often presenting balanced translocations involving chromosome band 11q23, have been observed.
  • We present two such cases with t(4;11)(q21;q23), one of whom had previously received only single-agent chemotherapy with 4-epi-doxorubicin.
  • A review of the literature since 1992 including these two patients reveals a total of 23 cases of ALL or lymphoblastic lymphoma after chemotherapy presenting balanced translocations to 11q23.
  • All 23 patients had previously received at least one topoisomerase II inhibitor, and in two patients 4-epi-doxorubicin had been administered as single-agent chemotherapy for breast cancer.
  • The latency period to development of t-ALL was 24 months or less in 20 out of 22 cases.
  • The MLL gene was found to be rearranged in 14 out of 14 cases, and in three out of six cases the breakpoint was at the telomeric part of the gene, as observed in most cases of AML following therapy with topoisomerase II inhibitors.
  • These results indicate that patients with ALL and balanced translocations to chromosome band 11q23 following chemotherapy with topoisomerase II inhibitors in the future should be included with cases of MDS or AML in calculations of risk of leukaemia.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Doxorubicin / adverse effects. Doxorubicin / analogs & derivatives. Leukemia, Prolymphocytic / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Proto-Oncogenes. Topoisomerase II Inhibitors. Transcription Factors
  • [MeSH-minor] Adult. Bone Neoplasms / secondary. Breast Neoplasms / drug therapy. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. DNA-Binding Proteins / genetics. Enzyme Inhibitors / adverse effects. Enzyme Inhibitors / therapeutic use. Female. Gene Rearrangement. Histone-Lysine N-Methyltransferase. Humans. Lymphatic Metastasis. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein. Seminoma / complications. Seminoma / drug therapy. Testicular Neoplasms / complications. Testicular Neoplasms / drug therapy. Translocation, Genetic

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  • (PMID = 11552977.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / MLL protein, human; 0 / Topoisomerase II Inhibitors; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 80168379AG / Doxorubicin; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  • [Number-of-references] 28
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11. Castagnola C, Lunghi M, Caberlon S, Bonfichi M, Pascutto C, Lazzarino M: Long-term outcome of ph-negative acute lymphoblastic leukaemia in adults: a single centre experience. Acta Haematol; 2005;113(4):234-40

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of ph-negative acute lymphoblastic leukaemia in adults: a single centre experience.
  • BACKGROUND AND OBJECTIVES: In adult acute lymphoblastic leukaemia (ALL), unlike in childhood ALL, the percentage of long-term remitters and survivors has not improved significantly over the last decades.
  • In the present analysis, we describe a series of adult ALL patients consecutively treated with the same regimen in order to analyse prognostic factors and treatment outcome as well as to define new risk-oriented strategies.
  • All patients received an induction phase treatment, consisting of a 4-week cycle with vincristine, daunorubicin, L-asparaginase and desametasone; the consolidation phase included cyclophosphamide, cytarabine, 6-mercaptopurine and central nervous system (CNS) prophylaxis, followed by three of months maintenance (methotrexate + 6-mercaptopurine), re-induction (4-week cycle with vincristine, adriamicin, desametasone), and 2-year maintenance with methotrexate + 6-mercaptopurine.
  • One patient had an ovarian and 2 had a breast relapse.
  • Eleven patients remained in first continuous CR after chemotherapy.
  • Initial white blood cell count </=30 x 10(9)/l, age <35 years, and time to complete remission </=40 days were the most significant prognostic factors for OS (p < 0.05).
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Immunophenotyping. Male. Middle Aged. Treatment Outcome

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel
  • (PMID = 15983429.001).
  • [ISSN] 0001-5792
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Switzerland
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12. Kourti M, Vavatsi N, Gombakis N, Sidi V, Tzimagiorgis G, Papageorgiou T, Koliouskas D, Athanassiadou F: Expression of multidrug resistance 1 (MDR1), multidrug resistance-related protein 1 (MRP1), lung resistance protein (LRP), and breast cancer resistance protein (BCRP) genes and clinical outcome in childhood acute lymphoblastic leukemia. Int J Hematol; 2007 Aug;86(2):166-73
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  • [Title] Expression of multidrug resistance 1 (MDR1), multidrug resistance-related protein 1 (MRP1), lung resistance protein (LRP), and breast cancer resistance protein (BCRP) genes and clinical outcome in childhood acute lymphoblastic leukemia.
  • The aim of this prospective study was to analyze the expression of messenger RNA of genes, such as MDR1, MRP1, BCRP, and LRP, implicated in the mechanism of multidrug resistance (MDR) in relation to the response to induction chemotherapy and relapse and these genes' correlation with each other and with pretreatment laboratory and clinical characteristics.
  • We prospectively studied 49 children (26 boys and 23 girls) with acute lymphoblastic leukemia (ALL) (median age, 5.5 years; range, 15 months to 12.5 years) who were treated with the BFM95 chemotherapy protocol.
  • Expression of each of the MDR genes was independent of the initial white blood cell count, immunophenotype, National Cancer Institute risk classification, and prednisone response.
  • Interestingly, MDR1 expression was significantly higher at relapse than at diagnosis for 4 sample pairs.
  • Evaluation of MDR1 expression at diagnosis of childhood ALL may contribute to the early identification of patients at risk of treatment failure.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Drug Resistance, Multiple / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Vault Ribonucleoprotein Particles / genetics
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette, Sub-Family B, Member 1 / genetics. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Case-Control Studies. Child. Child, Preschool. Female. Humans. Infant. Male. Multidrug Resistance-Associated Proteins / genetics. Neoplasm Proteins / genetics. Prognosis. Prospective Studies. RNA, Messenger / analysis. Survival Analysis. Treatment Outcome


13. Patriarca F, Sperotto A, Skert C, Damiani D, Prosdocimo S, Fanin R: Successful treatment of hematological and extramedullary relapse of MLL-positive acute lymphoblastic leukemia after bone marrow transplantation using donor leukocyte infusion. Ann Hematol; 2004 Oct;83(10):667-9
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  • [Title] Successful treatment of hematological and extramedullary relapse of MLL-positive acute lymphoblastic leukemia after bone marrow transplantation using donor leukocyte infusion.
  • Low response rates (range: 0-33%) were reported in acute lymphoblastic leukemia (ALL) patients who relapsed after bone marrow transplantation (BMT) and received donor leukocyte infusions (DLI).
  • We describe an ALL patient who presented with a relapse in blood, bone marrow, breast, and axillary nodes 3 months after BMT from an unrelated donor.
  • She achieved a second hematological complete remission (CR) after chemotherapy, with persistence of MLL-AF4 transcript in the bone marrow.
  • [MeSH-major] Bone Marrow Transplantation / methods. DNA-Binding Proteins / biosynthesis. Hematopoiesis, Extramedullary. Leukocyte Transfusion / methods. Neoplasm Recurrence, Local / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transcription Factors / biosynthesis

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  • (PMID = 15300405.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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14. Ishizawa S, Slovak ML, Popplewell L, Bedell V, Wrede JE, Carter NH, Snyder DS, Arber DA: High frequency of pro-B acute lymphoblastic leukemia in adults with secondary leukemia with 11q23 abnormalities. Leukemia; 2003 Jun;17(6):1091-5
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  • [Title] High frequency of pro-B acute lymphoblastic leukemia in adults with secondary leukemia with 11q23 abnormalities.
  • To evaluate the frequency and cytogenetic and immunophenotypic features of therapy-related, precursor B-cell acute lymphoblastic leukemia (ALL), 152 cases of immature B-cell ALL were reviewed.
  • These were compared to the frequency of therapy-related acute myeloid leukemia (t-AML) during the same time period.
  • Eight ALL cases with a prior diagnosis of malignancy were identified, including six (4.0%) with prior therapy considered to be therapy-related ALL (t-ALL).
  • The t-ALL cases followed treatment for breast carcinoma (two cases), lung carcinoma (two cases), lymphocyte predominance Hodgkin's disease and follicular lymphoma with a latency period of 13 months to 8 years.
  • During the same time period, 4.9% of all AML cases were considered t-AML.
  • Despite the similar frequency in therapy-related disease among ALL and AML cases, there were differences in the frequency of the diseases and t-ALL represented 12% of all therapy-related leukemias.
  • However, t-ALL represented 46% of all 11q23-positive therapy-related leukemias.
  • The immunogenetic features of t-ALL appear distinct and may aid in identifying more cases of this disease type in the future.
  • [MeSH-major] Burkitt Lymphoma / etiology. Chromosome Aberrations. Chromosomes, Human, Pair 11 / genetics. Leukemia, Myeloid / etiology. Neoplasms, Second Primary / etiology. Neoplasms, Second Primary / genetics
  • [MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / immunology. Antineoplastic Agents / therapeutic use. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Neoplasms / drug therapy. Neoplasms / radiotherapy. Translocation, Genetic

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  • (PMID = 12764373.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 30206; United States / NCI NIH HHS / CA / CA 33572
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antineoplastic Agents
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15. Advani AS, Gibson SE, Douglas E, Jin T, Zhao X, Kalaycio M, Copelan E, Sobecks R, Sekeres M, Sungren S, Hsi ED: Histone H4 acetylation by immunohistochemistry and prognosis in newly diagnosed adult acute lymphoblastic leukemia (ALL) patients. BMC Cancer; 2010;10:387
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  • [Title] Histone H4 acetylation by immunohistochemistry and prognosis in newly diagnosed adult acute lymphoblastic leukemia (ALL) patients.
  • BACKGROUND: Histone deacetylase (HDAC) inhibitors are a novel anti-tumor therapy.
  • To determine whether HDAC inhibitors may be useful in the treatment of adult acute lymphoblastic leukemia (ALL), we examined the acetylation of histone H4 by immunohistochemistry in newly diagnosed ALL patients and evaluated the impact of acetylation on complete remission (CR) rate, relapse-free survival (RFS), and overall survival (OS).
  • [MeSH-major] Histones / metabolism. Neoplasm Recurrence, Local / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Acetylation. Adolescent. Adult. Biopsy. Blotting, Western. Bone Marrow / drug effects. Bone Marrow / metabolism. Butyrates / pharmacology. Cells, Cultured. Humans. Immunoenzyme Techniques. Middle Aged. Prognosis. Remission Induction. Survival Rate. Young Adult

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  • (PMID = 20663136.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Butyrates; 0 / Histones
  • [Other-IDs] NLM/ PMC2921396
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16. Maniar TN, Braunstein I, Keefe S, Hussen S, Abrams T, De Michele A, El-Deiry WS: Childhood ALL and second neoplasms. Cancer Biol Ther; 2007 Oct;6(10):1525-31
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  • Second malignancies are a significant concern for survivors of childhood acute lymphoblastic leukemia (ALL), in particular patients who have been treated with cranial irradiation.
  • Breast cancer can occur in association with meningioma, but is not thought to be a consequence of treatment for childhood ALL.
  • We describe the molecular genetics and therapy of childhood ALL, the molecular genetics of meningioma, as well as the possible association between meningioma and breast cancer.
  • [MeSH-major] Breast Neoplasms / epidemiology. Meningeal Neoplasms / epidemiology. Meningioma / epidemiology. Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17952026.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 96
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17. Su Y, Lee SH, Sinko PJ: Inhibition of efflux transporter ABCG2/BCRP does not restore mitoxantrone sensitivity in irinotecan-selected human leukemia CPT-K5 cells: evidence for multifactorial multidrug resistance. Eur J Pharm Sci; 2006 Oct 01;29(2):102-10
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  • It has been shown that the human acute lymphoblastic leukemia (ALL) T cell line (RPMI 8402) selected with irinotecan (CPT-11) is transformed to a multidrug resistant (MDR) phenotype (CPT-K5) with cross-resistance to mitoxantrone (MX).
  • Since MX is a well-documented substrate for the efflux transporter breast cancer resistant protein (BCRP/ABCG2), we assessed the contribution of drug efflux to MX resistance in CPT-K5 cells.
  • These results suggest that up-regulation of BCRP plays a minimal role in conferring MX resistance to CPT-K5 cells, highlighting the existence of multiple, redundant mechanisms of drug resistance.
  • The current results support the concept of "multifactorial multidrug resistance", a recently-described phenomenon that ascribes multidrug resistance to many possible cellular mechanisms, not only by efflux drug transporters.
  • [MeSH-major] ATP-Binding Cassette Transporters / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Camptothecin / analogs & derivatives. Mitoxantrone / pharmacology. Neoplasm Proteins / antagonists & inhibitors. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Cell Line, Tumor. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Humans. RNA, Small Interfering / pharmacology

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  • (PMID = 16844360.001).
  • [ISSN] 0928-0987
  • [Journal-full-title] European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
  • [ISO-abbreviation] Eur J Pharm Sci
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI/DK-51214; United States / NIAID NIH HHS / AI / R01 AI42007
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 7673326042 / irinotecan; BZ114NVM5P / Mitoxantrone; XT3Z54Z28A / Camptothecin
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18. Lu Y, Hou SX, Chen T: [Advances in the study of vincristine: an anticancer ingredient from Catharanthus roseus]. Zhongguo Zhong Yao Za Zhi; 2003 Nov;28(11):1006-9
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  • It is effective to treat acute lymphocytic cell leukemia, Hodgkin disease and non-Hodgkin disease clinically.
  • But the severe side effects, such as neurotoxic and tissue damage, limit its application.
  • In this paper, we summarize physical, chemical, pharmacological and pharmacokinetical properties of VCR and advances in decreasing its side effects.
  • In clinic, association with other medication is adopted.
  • [MeSH-major] Antineoplastic Agents, Phytogenic. Catharanthus. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vincristine
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Humans. Liposomes. Liver Neoplasms / drug therapy. Plants, Medicinal / chemistry. Stomach Neoplasms / drug therapy

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  • (PMID = 15615402.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Liposomes; 5J49Q6B70F / Vincristine
  • [Number-of-references] 28
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19. Parker WB, Shaddix SC, Gilbert KS, Shepherd RV, Waud WR: Enhancement of the in vivo antitumor activity of clofarabine by 1-beta-D-[4-thio-arabinofuranosyl]-cytosine. Cancer Chemother Pharmacol; 2009 Jul;64(2):253-61
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  • PURPOSE: Clofarabine increases the activation of 1-beta-D-arabinofuranosyl cytosine (araC) in tumor cells, and combination of these two drugs has been shown to result in good clinical activity against various hematologic malignancies.
  • 1-beta-D-[4-thio-arabinofuranosyl] cytosine (T-araC) is a new cytosine analog that has exhibited excellent activity against a broad spectrum of human solid tumors and leukemia/lymphoma xenografts in mice and is currently being evaluated in patients as a new drug for the treatment of cancer.
  • Since T-araC has a vastly superior preclinical efficacy profile in comparison to araC, we have initiated studies to determine the potential value of clofarabine/T-araC combination therapy.
  • METHODS: In vitro studies have been conducted to determine the effect of clofarabine on the metabolism of T-araC, and in vivo studies have been conducted to determine the effect of the clofarabine/T-araC combination on five human tumor xenografts in mice.
  • RESULTS: Initial studies with various tumor cells in culture indicated that a 2-h incubation with clofarabine enhanced the metabolism of T-araC 24 h after its removal by threefold in three tumor cell types (HCT-116 colon, K562 leukemia, and RL lymphoma) and by 1.5-fold in two other tumor cell types (MDA-MB-435 breast (melanoma), and HL-60 leukemia).
  • Pretreatment with clofarabine resulted in a slight decrease in metabolism of T-araC in RPMI-8226 myeloma cells (65% of control) and inhibited metabolism of T-araC in CCRF-CEM leukemia cells by 90%.
  • Clofarabine and T-araC were administered on alternate days for five treatments each (q2dx5) with the administration of T-araC 24 h after each clofarabine treatment.
  • Combination treatment of HCT-116, K562, HL-60, or RL tumors with clofarabine and T-araC resulted in dramatically superior anti-tumor activity than treatment with either agent alone, whereas this combination resulted in antagonism in CCRF-CEM tumors.
  • CONCLUSIONS: These studies provide a rationale for clinical trials using this combination in the treatment of acute leukemias as well as solid tumors and suggest that this combination would exhibit greater antitumor activity than that of clofarabine plus araC.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Antineoplastic Agents / pharmacology. Arabinonucleosides / therapeutic use. Neoplasms, Experimental / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Animals. Drug Synergism. Drug Therapy, Combination. Humans. Mice. Mice, Nude. Mice, SCID. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 19002461.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA34200
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 4'-thio-arabinofuranosylcytosine; 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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20. Chopra R, Eaton JD, Grassi A, Potter M, Shaw B, Salat C, Neumeister P, Finazzi G, Iacobelli M, Bowyer K, Prentice HG, Barbui T: Defibrotide for the treatment of hepatic veno-occlusive disease: results of the European compassionate-use study. Br J Haematol; 2000 Dec;111(4):1122-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Defibrotide for the treatment of hepatic veno-occlusive disease: results of the European compassionate-use study.
  • Severe hepatic veno-occlusive disease (VOD) is a recognized complication of autologous and allogeneic stem cell transplantation (SCT) that is often fatal.
  • Preliminary studies have demonstrated activity for DF in the treatment of VOD, with minimal associated toxicity.
  • The median duration of therapy was 18 d (range, 2--71 d).
  • These results demonstrate that DF is an active treatment for VOD following SCT and a randomized trial is now underway in order to further evaluate its role.
  • [MeSH-major] Fibrinolytic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation. Hepatic Veno-Occlusive Disease / drug therapy. Polydeoxyribonucleotides / therapeutic use. Postoperative Complications / drug therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Bilirubin / analysis. Breast Neoplasms / drug therapy. Breast Neoplasms / surgery. Child. Child, Preschool. Female. Hodgkin Disease / drug therapy. Hodgkin Disease / surgery. Humans. Infant. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / surgery. Male. Middle Aged. Multiple Myeloma / drug therapy. Multiple Myeloma / surgery. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Treatment Outcome

  • MedlinePlus Health Information. consumer health - After Surgery.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
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  • (PMID = 11167751.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Fibrinolytic Agents; 0 / Polydeoxyribonucleotides; 438HCF2X0M / defibrotide; RFM9X3LJ49 / Bilirubin
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