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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. Fadilah SA, Goh KY: Breast and ovarian recurrence of acute lymphoblastic leukaemia after allogeneic peripheral blood haematopoietic stem cell transplantation. Singapore Med J; 2009 Dec;50(12):e407-9
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  • [Title] Breast and ovarian recurrence of acute lymphoblastic leukaemia after allogeneic peripheral blood haematopoietic stem cell transplantation.
  • Breast recurrence of acute lymphoblastic leukaemia (ALL) after stem cell transplant is uncommon, with less than 20 reported cases in the literature.
  • In the majority of cases, the lesions developed without simultaneous involvement of other sites or graft-versus-host disease (GvHD).
  • We describe the first case of simultaneous bilateral breast and ovarian relapses after allografting in ALL, occurring in an 18-year-old female Chinese patient while she was having oral and hepatic chronic GvHD, persistent haematological remission and donor haematopoiesis.
  • She received radiotherapy and chemotherapy, which resulted in resolution of the breast and ovarian lesions, and remained disease free ten months after the onset of the relapse.
  • [MeSH-major] Breast Neoplasms / secondary. Ovarian Neoplasms / secondary. Peripheral Blood Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Female. Graft vs Host Disease / complications. Humans. Tomography, X-Ray Computed

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  • (PMID = 20087541.001).
  • [ISSN] 0037-5675
  • [Journal-full-title] Singapore medical journal
  • [ISO-abbreviation] Singapore Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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3. 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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4. 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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  • [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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5. 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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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. Hulleman E, Kazemier KM, Holleman A, VanderWeele DJ, Rudin CM, Broekhuis MJ, Evans WE, Pieters R, Den Boer ML: Inhibition of glycolysis modulates prednisolone resistance in acute lymphoblastic leukemia cells. Blood; 2009 Feb 26;113(9):2014-21
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  • [Title] Inhibition of glycolysis modulates prednisolone resistance in acute lymphoblastic leukemia cells.
  • Treatment failure in pediatric acute lymphoblastic leukemia (ALL) is related to cellular resistance to glucocorticoids (eg, prednisolone).
  • Recently, we demonstrated that genes associated with glucose metabolism are differentially expressed between prednisolone-sensitive and prednisolone-resistant precursor B-lineage leukemic patients.
  • Here, we show that prednisolone resistance is associated with increased glucose consumption and that inhibition of glycolysis sensitizes prednisolone-resistant ALL cell lines to glucocorticoids.
  • Treatment of prednisolone-resistant Jurkat and Molt4 cells with 2-deoxy-D-glucose (2-DG), lonidamine (LND), or 3-bromopyruvate (3-BrPA) increased the in vitro sensitivity to glucocorticoids, while treatment of the prednisolone-sensitive cell lines Tom-1 and RS4; 11 did not influence drug cytotoxicity.
  • This sensitizing effect of the glycolysis inhibitors in glucocorticoid-resistant ALL cells was not found for other classes of antileukemic drugs (ie, vincristine and daunorubicin).
  • Moreover, down-regulation of the expression of GAPDH by RNA interference also sensitized to prednisolone, comparable with treatment with glycolytic inhibitors.
  • Importantly, the ability of 2-DG to reverse glucocorticoid resistance was not limited to cell lines, but was also observed in isolated primary ALL cells from patients.
  • [MeSH-major] Drug Resistance, Neoplasm. Glycolysis / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Prednisolone / therapeutic use
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Daunorubicin / administration & dosage. Deoxyglucose / administration & dosage. Deoxyglucose / pharmacokinetics. Drug Screening Assays, Antitumor. Drug Synergism. Gene Expression Profiling. Gene Expression Regulation, Leukemic / drug effects. Glucocorticoids / administration & dosage. Glucose / metabolism. Humans. Jurkat Cells. Oligonucleotide Array Sequence Analysis. Tumor Cells, Cultured. Vincristine / administration & dosage

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  • (PMID = 18978206.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 5J49Q6B70F / Vincristine; 9G2MP84A8W / Deoxyglucose; 9PHQ9Y1OLM / Prednisolone; IY9XDZ35W2 / Glucose; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ PMC4081395
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8. Talwar V, Sreedharan PS, Warrier NK, Guhan, Ramanan SG, Sagar TG: Acute lymphoblastic leukemia presenting as breast mass. J Assoc Physicians India; 2000 Dec;48(12):1212-3
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  • [Title] Acute lymphoblastic leukemia presenting as breast mass.
  • We present here a 34 years female who presented with bilateral breast lumps as the initial manifestation of acute lymphoblastic leukemia.
  • She was treated with consolidation chemotherapy and showed good response.
  • [MeSH-major] Breast Neoplasms / diagnosis. Lymphoma, Non-Hodgkin / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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  • [CommentIn] J Assoc Physicians India. 2001 Dec;49:1213-4 [11996453.001]
  • (PMID = 11280234.001).
  • [ISSN] 0004-5772
  • [Journal-full-title] The Journal of the Association of Physicians of India
  • [ISO-abbreviation] J Assoc Physicians India
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
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9. Latz D, Alfrink M, Nassar N, Beyerle C: Breast cancer in a male patient after treatment of acute lymphoblastic leukemia including total body irradiation and bone marrow transplantation. Onkologie; 2004 Oct;27(5):477-9
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  • [Title] Breast cancer in a male patient after treatment of acute lymphoblastic leukemia including total body irradiation and bone marrow transplantation.
  • BACKGROUND: With increasing numbers of patients subjected to total body irradiation and bone marrow transplantation for treatment of several systemic malignancies more and more patients with second malignancies were observed.
  • CASE REPORT: We report the case of a 29- year-old man who developed breast cancer 13 years after treatment for acute lymphoblastic leukemia.
  • Therapy for leukemia included total body irradiation (TBI) and bone marrow transplantation (BMT).
  • Breast cancer was treated with mastectomy and irradiation of the left chest wall.
  • 17 months later the patient developed malignant pleural effusion and died despite chemotherapy and hormonal therapy due to further tumor progression.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Breast Neoplasms, Male / diagnosis. Breast Neoplasms, Male / etiology. Neoplasms, Radiation-Induced / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Whole-Body Irradiation / adverse effects


10. McMillan A: Central nervous system-directed preventative therapy in adults with lymphoma. Br J Haematol; 2005 Oct;131(1):13-21
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  • [Title] Central nervous system-directed preventative therapy in adults with lymphoma.
  • All adult patients with Burkitt lymphoma or lymphoblastic lymphoma should receive central nervous system (CNS)-directed therapy with both intrathecal and high-dose systemic chemotherapy.
  • There is no evidence to support the routine use of prophylactic CNS-directed therapy in any specific subgroup of adult patients with 'low grade' lymphomas.
  • There are some anatomical sites where involvement by lymphoma is associated with a higher risk of CNS relapse.
  • These probably include testis, breast, paranasal sinuses and the epidural space.
  • There is evidence of good efficacy when intrathecal chemotherapy and high-dose systemic chemotherapy are used in combination.
  • It is not clear how the best balance between the 'sensitivity' and 'specificity' of the choice of patients to receive CNS-directed therapy can be achieved.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Central Nervous System Neoplasms / prevention & control. Lymphoma / prevention & control
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Burkitt Lymphoma / blood. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / prevention & control. Female. Humans. Injections, Spinal. L-Lactate Dehydrogenase / blood. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control. Prognosis. Recurrence. Risk Assessment

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  • (PMID = 16173958.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 1.1.1.27 / L-Lactate Dehydrogenase
  • [Number-of-references] 47
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11. 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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12. Swerts K, De Moerloose B, Dhooge C, Laureys G, Benoit Y, Philippé J: Prognostic significance of multidrug resistance-related proteins in childhood acute lymphoblastic leukaemia. Eur J Cancer; 2006 Feb;42(3):295-309
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  • [Title] Prognostic significance of multidrug resistance-related proteins in childhood acute lymphoblastic leukaemia.
  • An important problem in the treatment of children with acute lymphoblastic leukaemia (ALL) is pre-existent or acquired resistance to structurally and functionally unrelated chemotherapeutic compounds.
  • Best studied is the transmembrane protein-mediated efflux of cytotoxic compounds that leads to decreased cellular drug accumulation and toxicity.
  • Several MDR-related efflux pumps have been characterised, including P-glycoprotein (P-gp), multidrug resistance-associated protein 1 (MRP1), breast cancer resistance protein (BCRP) and lung resistance protein (LRP).
  • LRP might contribute to drug resistance in B-lineage ALL, but larger studies are needed to confirm these results.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Multidrug Resistance-Associated Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 16324833.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antineoplastic Agents; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; Y49M64GZ4Q / multidrug resistance-associated protein 1
  • [Number-of-references] 144
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13. 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 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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14. 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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15. 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


16. 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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17. 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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18. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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19. 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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20. Kaplan HG, Malmgren JA, Atwood M: Leukemia incidence following primary breast carcinoma treatment. Cancer; 2004 Oct 1;101(7):1529-36
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  • [Title] Leukemia incidence following primary breast carcinoma treatment.
  • BACKGROUND: The results of randomized clinical trials have suggested that after receiving radiotherapy and/or chemotherapy, patients with primary breast carcinoma have an increased risk of developing leukemia.
  • In the current study, the authors set out to assess the reported association between breast carcinoma treatment and leukemia risk.
  • METHODS: A registry of all patients with breast carcinoma who were treated at a community-based institution since 1989 (updated annually for recurrence and/or vital status) was linked to the National Cancer Institute Surveillance, Epidemiology, and End Results database to confirm complete ascertainment of leukemia cases occurring within this registry population.
  • Incidence rates were calculated for women who were treated for primary Stage 0-III breast carcinoma and had a follow-up duration of > or = 24 months (n = 2866).
  • Patients who did not undergo surgery (n = 5), patients for whom chemotherapy records were incomplete or who received nonstandard chemotherapy regimens (n = 69), patients who underwent stem cell transplantation (n = 83), and patients who were lost to follow-up or who had unknown disease status at follow-up (n = 81) were excluded from the analysis (total, n = 238).
  • RESULTS: Among patients diagnosed with breast carcinoma between 1992 and 1999, the crude overall leukemia incidence rate was 0.28%, and the acute myelogenous leukemia (AML)/myelodysplastic syndrome (MDS) incidence rate was 0.11%.
  • Eight incident cases of leukemia were documented (2 cases of AML, 1 case of acute lymphoblastic leukemia, 1 case of MDS/refractory anemia with excess blasts, 2 cases of chronic myelogenous leukemia, and 2 cases of chronic lymphocytic leukemia).
  • The incidence of leukemia by treatment category was as follows: no surgery/no chemotherapy/no radiotherapy, 2 of 154 patients (1.30%); surgery/no chemotherapy/radiotherapy, 4 of 1403 patients (0.29%); surgery/chemotherapy/no radiotherapy, 0 of 352 patients (0%); and surgery/chemotherapy/radiotherapy, 2 of 957 patients (0.21%).
  • CONCLUSIONS: In contrast to findings reported from previous randomized clinical trials, the authors did not find evidence of increased posttreatment leukemia incidence in association with the use of chemotherapy, including doxorubicin-based regimens.
  • [MeSH-major] Breast Neoplasms / therapy. Leukemia / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / epidemiology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / etiology. Leukemia, Myeloid, Acute / epidemiology. Leukemia, Myeloid, Acute / etiology. Middle Aged. Myelodysplastic Syndromes / epidemiology. Myelodysplastic Syndromes / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • [Copyright] (c) 2004 American Cancer Society.
  • [CommentIn] Cancer. 2004 Oct 1;101(7):1479-81 [15378475.001]
  • (PMID = 15378478.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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21. Baynes RD, Hamm C, Dansey R, Klein J, Cassells L, Karanes C, Abella E, Peters WP: Bone marrow and peripheral blood hematopoietic stem cell transplantation: focus on autografting. Clin Chem; 2000 Aug;46(8 Pt 2):1239-51
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  • [Title] Bone marrow and peripheral blood hematopoietic stem cell transplantation: focus on autografting.
  • This review focuses on certain of the principles involved in high-dose chemotherapy and radiation therapy along with autologous hematopoietic stem cell transplantation for the treatment of certain malignancies.
  • The malignancies highlighted include acute myeloid leukemia, acute lymphoblastic leukemia, non-Hodgkin lymphoma, Hodgkin disease, and breast cancer.
  • [MeSH-major] Bone Marrow Transplantation. Hematopoietic Stem Cell Transplantation. Neoplasms / therapy
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / radiotherapy. Breast Neoplasms / therapy. Combined Modality Therapy. Female. Hodgkin Disease / drug therapy. Hodgkin Disease / radiotherapy. Hodgkin Disease / therapy. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / radiotherapy. Leukemia, Myeloid / therapy. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / radiotherapy. Lymphoma, Non-Hodgkin / therapy. Multiple Myeloma / drug therapy. Multiple Myeloma / radiotherapy. Multiple Myeloma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Randomized Controlled Trials as Topic. Transplantation, Autologous

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  • (PMID = 10926918.001).
  • [ISSN] 0009-9147
  • [Journal-full-title] Clinical chemistry
  • [ISO-abbreviation] Clin. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Number-of-references] 82
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22. 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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23. Bhatia P, Das R, Ahluwalia J, Malhotra P, Varma N, Varma S, Sharma SC, Garewal G: Acute leukemia/myelodysplastic syndrome as a sequelae of carcinoma breast: a report of five cases from north India. Indian J Pathol Microbiol; 2009 Apr-Jun;52(2):167-70
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  • [Title] Acute leukemia/myelodysplastic syndrome as a sequelae of carcinoma breast: a report of five cases from north India.
  • Therapy-related myelodysplastic syndrome and acute leukemia are dreaded long-term complications of five cases of hematological malignancies following treatment for successful breast cancer therapy (therapeutic drugs or radiotherapy).
  • The patients presented 2-5 years after treatment of breast carcinoma.
  • One patient received chemotherapy after surgery.
  • One patient underwent only surgery and after 3 years presented with acute myeloid leukemia and bone marrow metastasis of carcinoma of the breast.
  • At the time of presentation, all the patients had either bicytopenia or pancytopenia.
  • A close follow-up with complete blood cell counts of the patients who previously had carcinoma of the breast is suggested for early detection of hematological abnormalities.
  • However, the poor prognosis, limited financial resources and poor health insurance coverage results in few patients and their family members opting for treatment.
  • [MeSH-major] Breast Neoplasms / complications. Breast Neoplasms / therapy. Leukemia, Myeloid, Acute / pathology. Myelodysplastic Syndromes / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Aged. Drug-Related Side Effects and Adverse Reactions. Female. Humans. India. Middle Aged. Pancytopenia / diagnosis. Radiotherapy / adverse effects


24. Pagano L, Pulsoni A, Mele L, Tosti ME, Cerri R, Visani G, Melillo L, Candoni A, Clavio M, Nosari A, Petti MC, Martino B, Mele A, Levis A, Allione B, Almici C, Equitani F, Leone G, Mandelli F, Gruppo Italiano Malattie Ematologiche dell'Adults: Acute myeloid leukemia in patients previously diagnosed with breast cancer: experience of the GIMEMA group. Ann Oncol; 2001 Feb;12(2):203-7
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  • [Title] Acute myeloid leukemia in patients previously diagnosed with breast cancer: experience of the GIMEMA group.
  • OBJECTIVE: To evaluate in a multicenter retrospective study, the clinical and laboratory characteristics and the outcome of patients with acute myeloid leukemia (sAML) previously diagnosed with breast cancer (BC) among an adult acute leukemia population.
  • Among sAML, 37 patients (29%) had a previous breast cancer.
  • Twenty-seven patients received chemo- and/or radiotherapy for breast cancer (7 only chemotherapy, 6 only radiotherapy, and 14 combined treatment).
  • All patients were surgically treated but in 10 patients surgical debridement was the sole therapy for breast cancer.
  • The drugs most frequently employed were alkylating agents (18 patients), topoisomerase II inhibitors (9 patients), antimetabolites (20 patients) (CMF, CEF and MMM combinations).
  • Thirty-four patients received chemotherapy for sAML, and twenty-five of them achieved a CR (74%), with a median duration of twenty-eight weeks (5-280+).
  • DISCUSSION: The high number of sAML we observed in patients with a previous breast cancer, may be due to the fact that this malignancy is the most frequent neoplasm in women and by the high probability of cure with a consequent long disease-free survival.
  • Our results suggest that the risk of sAML after recovery from breast cancer is increasing due to the rise in the number of patients cured from breast cancer, and in the future could be a relevant problem for haematologists.

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  • (PMID = 11300325.001).
  • [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] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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25. 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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26. Ke X, Yang Y, Zhao X, Wang L: Autologous peripheral blood stem cell transplantation in the patients with hematologic malignancies and solid tumors. Chin Med J (Engl); 2001 Feb;114(2):196-9
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  • [Title] Autologous peripheral blood stem cell transplantation in the patients with hematologic malignancies and solid tumors.
  • OBJECTIVE: To evaluate the long-term therapeutic effects of autologous peripheral blood stem cell transplantation (auto-PBSCT) on the treatment of hematological and solid tumors.
  • METHODS: Fifty-one patients were recruited in this auto-PBSCT study, in which several potentially important parameters were studied including the optimal time for stem cell collection, the dose of stem cell reinfusion, the time of hematopoietic reconstitution, the disease free survival (DFS) and overall survival (OS), complications related to transplantation, and maintenance chemotherapy after auto-PBSCT.
  • The mean time for patients' neutrophil to recover up to > 0.5 x 10(9)/L after APBSCT was 11.14 days in the group of the patients receiving G-CSF in contrast to 17.6 days in the group receiving no G-CSF.
  • CONCLUSION: Comparing with conventional chemotherapy, our study suggests that auto-PBSCT is a very important therapeutic option that can significantly improve the prognosis in the patients with hematological and solid tumors, especially in the patients with AML and NHL.
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation. Neoplasms / therapy
  • [MeSH-minor] Adolescent. Adult. Breast Neoplasms / mortality. Breast Neoplasms / pathology. Breast Neoplasms / therapy. Child. Female. Follow-Up Studies. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy. Lymphoma, Non-Hodgkin / mortality. Lymphoma, Non-Hodgkin / pathology. Lymphoma, Non-Hodgkin / therapy. Male. Middle Aged. Multiple Myeloma / mortality. Multiple Myeloma / pathology. Multiple Myeloma / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Survival Analysis. Survival Rate. Transplantation, Autologous. Treatment Outcome

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  • (PMID = 11780206.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
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27. Marie JP: Drug resistance in hematologic malignancies. Curr Opin Oncol; 2001 Nov;13(6):463-9
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  • [Title] Drug resistance in hematologic malignancies.
  • Drug resistance eventually occurs in most hematologic malignancies treated with chemotherapy.
  • The mechanisms responsible for drug resistance include expression of transporters of xenobiotics of the adenosine triphosphate-binding cassette protein superfamily (P-glycoprotein, multidrug resistance associated proteins, breast cancer resistance protein), modifications of enzymes like deoxycytidine kinase, and defects in chemotherapy-induced apoptosis.
  • The efforts to overcome this drug resistance have been focused, thus far, on modulation of P-glycoprotein.
  • The emergence of modulators with several adenosine triphosphate-binding cassette protein targets, like GG120918 (inhibiting P-glycoprotein and breast cancer resistance protein) and VX710 (inhibiting P-glycoprotein and multidrug resistance associated protein 1), are of clinical interest in malignancies often expressing several efflux pumps simultaneously.
  • Another approach is the use of "furtive" drugs like liposomal or nanoparticular anthracyclines.
  • [MeSH-major] ATP-Binding Cassette Transporters / pharmacology. ATP-Binding Cassette, Sub-Family B, Member 1 / pharmacology. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Leukemia, Myeloid, Acute / drug therapy. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 11673686.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 8L70Q75FXE / Adenosine Triphosphate
  • [Number-of-references] 57
  •  go-up   go-down


28. Bonneterre JM, French Adjuvant Study Group: Long-term efficacy and toxicity of the FEC100 regimen. Oncology (Williston Park); 2004 Dec;18(14 Suppl 14):56-8
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  • Adjuvant chemotherapy has been shown to be beneficial in patients with breast cancer, and anthracycline-containing regimens are more effective than non-anthracycline-containing ones.
  • The French Adjuvant Study Group (FASG) compared FEC100 and FEC50 (fluorouracil [5-FU]/epirubicin [Ellence]/cyclophosphamide [Cytoxan, Neosar]) in patients with node-positive breast cancer, with an endpoint of overall survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Cost-Benefit Analysis. Cyclophosphamide / administration & dosage. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Costs. Epirubicin / administration & dosage. Female. Fluorouracil / administration & dosage. Heart Diseases / chemically induced. Humans. Leukemia, Myelomonocytic, Acute / chemically induced. Lymph Nodes / pathology. Lymphatic Metastasis. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / chemically induced. Time Factors. Treatment Outcome

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  • (PMID = 15685837.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; FEC protocol
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29. Johnston K, Vowels M, Carroll S, Neville K, Cohn R: Failure to lactate: a possible late effect of cranial radiation. Pediatr Blood Cancer; 2008 Mar;50(3):721-2
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  • We conducted a retrospective review of the lactation experience of female survivors who received 24 Gy cranial radiotherapy as CNS prophylaxis for acute lymphoblastic leukemia in childhood prior to 1982 and who attend the Long-Term Follow-Up Clinic at Sydney Children's Hospital, Randwick, Australia.
  • Median time since diagnosis is 28 years (range 25-37 years).
  • Ten report minimal or no breast changes during pregnancy and failure to lactate postpartum.
  • These data suggest a high risk of failure of lactation in women treated during childhood with 24 Gy cranial irradiation.
  • [MeSH-major] Cranial Irradiation / adverse effects. Lactation Disorders / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Radiotherapy, High-Energy / adverse effects. Survivors
  • [MeSH-minor] Adult. Attitude of Health Personnel. Attitude to Health. Endocrine System Diseases / drug therapy. Endocrine System Diseases / etiology. Female. Follow-Up Studies. Hormone Replacement Therapy. Human Growth Hormone / deficiency. Humans. Infant, Newborn. Lactation / physiology. Lactation / psychology. Leukemia, Myeloid, Acute / radiotherapy. Pregnancy. Pregnancy Complications / drug therapy. Pregnancy Complications / etiology. Retrospective Studies

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17763465.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone
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30. 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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31. Firas AS, Demeckova E, Bojtarova E, Czako B, Hrubisko M, Mistrik M: Isolated extra-medullary relapse of acute leukemia following allogeneic bone marrow transplantation. Bratisl Lek Listy; 2008;109(8):358-61
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  • It is seen more commonly after BMT than after conventional chemotherapy (CHT) alone.
  • We describe the natural history and response to treatment in four patients with IEMR following allogeneic BMT.
  • The results indicate a stronger graft-versus-leukemia (GVL) effect in the marrow than in the peripheral tissues (Fig.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Leukemia, Myeloid, Acute / surgery. Leukemic Infiltration / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery
  • [MeSH-minor] Adult. Brain / pathology. Breast / pathology. Female. Graft vs Leukemia Effect. Humans. Middle Aged. Skin / pathology. Transplantation, Homologous / adverse effects

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  • (PMID = 18837244.001).
  • [ISSN] 0006-9248
  • [Journal-full-title] Bratislavské lekárske listy
  • [ISO-abbreviation] Bratisl Lek Listy
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Slovakia
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32. Uckun FM, D'Cruz OJ, Liu XP, Narla RK: Phenylarsonic acid compounds with broad-spectrum and potent cytotoxic activity against human cancer cells. Arzneimittelforschung; 2003;53(6):428-39
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  • The in vitro cytotoxic activity profile of nine novel phenylarsonic acid (CAS 98-05-5, PAA) compounds against 17 human cancer cell lines including (a) ovarian cancer cell lines ES-2, PA-1, CAOV-3, OVCAR-3, (b) testicular cancer cell lines Ntera-2, Tera-2, N2NICP, 833K, and 64CP, (c) multiple myeloma cell lines ARH77, HS-Sultan, RPMI-8226, and U266, and (d) acute lymphoblastic leukemia (ALL) cell lines NALM-6, MOLT-3, ALL-1, and RS4; 11, was determined by the MTT assay.
  • The lead compounds, 2-methylthio-4-[(4'-aminophenylazo)-phenylarsonic acid] pyrimidine (PHI-370) and 2-methylthio-4-(4'-phenylarsonic acid)-aminopyrimidine (PHI-380) caused apoptotic death in all 17 cancer cell lines at low micromolar concentrations, as documented by TUNEL assays and confocal laser scanning microscopy.
  • PHI-380 was also tested and found to be very active against primary tumor cells isolated from surgical biopsy specimens of 14 patients with therapy-refractory non-small cell lung cancer, breast cancer, colon cancer, lymphoma, hepatoblastoma, or Wilm's tumor as well.
  • Because of their broad-spectrum and potent anticancer activity and ability to induce apoptosis in primary tumor cells from therapy-refractory cancer patients, PAA compounds such as PHI-370 and PHI-380 may provide the basis for effective salvage regimens for patients with recurrent cancer.
  • [MeSH-minor] Apoptosis / drug effects. Cell Division / drug effects. Female. Flow Cytometry. Humans. In Situ Nick-End Labeling. Male. Microscopy, Confocal. Multiple Myeloma / prevention & control. Neoplasm Transplantation. Ovarian Neoplasms / prevention & control. Precursor Cell Lymphoblastic Leukemia-Lymphoma / prevention & control. Structure-Activity Relationship. Testicular Neoplasms / prevention & control. Tumor Cells, Cultured

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  • (PMID = 12872614.001).
  • [ISSN] 0004-4172
  • [Journal-full-title] Arzneimittel-Forschung
  • [ISO-abbreviation] Arzneimittelforschung
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals; 57F9KU116M / benzenearsonic acid
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33. 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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  • [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

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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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34. 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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35. 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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36. Armstrong GT, Sklar CA, Hudson MM, Robison LL: Long-term health status among survivors of childhood cancer: does sex matter? J Clin Oncol; 2007 Oct 1;25(28):4477-89
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  • Within this growing population of long-term survivors, considerable effort has been put forth to identify treatment-related risks for adverse health-related outcomes, such as exposure to alkylating agents, anthracyclines, radiotherapy, and surgery.
  • In this article, we review the literature, which generally supports associations between female sex and cognitive dysfunction after cranial irradiation, cardiovascular outcomes, obesity, radiation-associated differences in pubertal timing, development of primary hypothyroidism, breast cancer as a second malignant neoplasm and suggests an increased prevalence for the development of osteonecrosis among females.
  • Results of this review support future investigations to further define sex as a risk factor for other common treatment-specific exposures and outcomes.
  • Historically, evidence from both basic science and clinical research has been used to develop risk-stratified therapy, allowing reduction of toxic therapies to low-risk patients without compromising overall survival.
  • With greater knowledge of sex-specific risks, the potential application of sex-specific therapy designed to avoid poor long-term adverse outcomes may become a viable strategy.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Health Status. Neoplasms / complications. Neoplasms / therapy. Radiotherapy / adverse effects
  • [MeSH-minor] Adult. Child. Combined Modality Therapy / adverse effects. Female. Humans. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Risk Factors. Sex Factors. Survivors / statistics & numerical data

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  • (PMID = 17906209.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 164
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37. 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.
  • 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).
  • 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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38. Thomas X, Cannas G, Chelghoum Y: [Special issues related to the treatment of acute leukemias in women]. Bull Cancer; 2010 Aug;97(8):1011-22
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  • [Title] [Special issues related to the treatment of acute leukemias in women].
  • [Transliterated title] Problèmes spécifiques liés au traitement des leucémies aiguës chez la femme.
  • The treatment of acute leukemia is usually similar in women and men.
  • However, diagnosis in women poses additional challenges in clinical practice such as leukemia following breast or ovarian cancers, prevention of abnormal uterine bleeding in premenopausal females, treatment during pregnancy related-problems in long-term survivors.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / adverse effects. Breast Neoplasms / therapy. Female. Fertility / drug effects. Fertility / radiation effects. Humans. Ovarian Neoplasms / therapy. Ovary / drug effects. Pregnancy. Pregnancy Complications, Neoplastic / etiology. Pregnancy Complications, Neoplastic / therapy. Puberty, Delayed / chemically induced. Sex Factors. Uterine Neoplasms / therapy

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  • (PMID = 20435579.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 154
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39. Kantarjian HM, Gandhi V, Kozuch P, Faderl S, Giles F, Cortes J, O'Brien S, Ibrahim N, Khuri F, Du M, Rios MB, Jeha S, McLaughlin P, Plunkett W, Keating M: Phase I clinical and pharmacology study of clofarabine in patients with solid and hematologic cancers. J Clin Oncol; 2003 Mar 15;21(6):1167-73
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  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Arabinonucleosides / administration & dosage. Arabinonucleosides / adverse effects. Hematologic Neoplasms / drug therapy. Neoplasms / drug therapy
  • [MeSH-minor] Adenine Nucleotides. Adult. Aged. Bone Marrow / drug effects. Breast Neoplasms / drug therapy. Drug Administration Schedule. Female. Gastrointestinal Neoplasms / drug therapy. Humans. Infusions, Intravenous. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Liver / drug effects. Lung Neoplasms / drug therapy. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Treatment Outcome

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  • (PMID = 12637486.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA32839; United States / NCI NIH HHS / CA / CA57629; United States / NCI NIH HHS / CA / CA81534; United States / FDA HHS / FD / FD-R-001972
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; 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 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
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40. Sovalat H, Racadot E, Ojeda M, Lewandowski H, Chabouté V, Hénon P: CD34+ cells and CD34+CD38- subset from mobilized blood show different patterns of adhesion molecules compared to those from steady-state blood, bone marrow, and cord blood. J Hematother Stem Cell Res; 2003 Oct;12(5):473-89
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  • In our study the CAM-AgD was the lowest on CD34(+) cells in LKP which, on the contrary, contained the highest percentage of CD117(+), CD54(+), CD58(+) cell subsets.
  • The LKP-CD34(+) cell population contained a greater percentage of CD11a(+) cells when compared to mBM, but the lowest percentage of CD49d(+) and CD49e(+) cells when compared to all products.
  • [MeSH-major] ADP-ribosyl Cyclase / analysis. Antigens, CD / analysis. Antigens, CD34 / analysis. Bone Marrow Cells / chemistry. Cell Adhesion Molecules / analysis. Fetal Blood / chemistry. Leukocytes, Mononuclear / chemistry
  • [MeSH-minor] Adult. Antigens, CD38. Antigens, Surface / analysis. Breast Neoplasms / blood. Breast Neoplasms / therapy. Cell Count. Drug Therapy. Female. Flow Cytometry. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cell Mobilization. Hematopoietic Stem Cells / chemistry. Humans. Infant, Newborn. Leukapheresis. Leukemia, Myeloid / blood. Leukemia, Myeloid / therapy. Lymphoma, Non-Hodgkin / blood. Lymphoma, Non-Hodgkin / therapy. Membrane Glycoproteins. Middle Aged. Models, Biological. Multiple Myeloma / blood. Multiple Myeloma / therapy. Ovarian Neoplasms / blood. Ovarian Neoplasms / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 14594504.001).
  • [ISSN] 1525-8165
  • [Journal-full-title] Journal of hematotherapy & stem cell research
  • [ISO-abbreviation] J. Hematother. Stem Cell Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / Antigens, Surface; 0 / Cell Adhesion Molecules; 0 / Membrane Glycoproteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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41. Widemann BC, Balis FM, Shalabi A, Boron M, O'Brien M, Cole DE, Jayaprakash N, Ivy P, Castle V, Muraszko K, Moertel CL, Trueworthy R, Hermann RC, Moussa A, Hinton S, Reaman G, Poplack D, Adamson PC: Treatment of accidental intrathecal methotrexate overdose with intrathecal carboxypeptidase G2. J Natl Cancer Inst; 2004 Oct 20;96(20):1557-9
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of accidental intrathecal methotrexate overdose with intrathecal carboxypeptidase G2.
  • Antibodies to CPDG2 were not detected in plasma after treatment with intrathecal CPDG2.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Medication Errors. Methotrexate / adverse effects. Neoplasms / drug therapy. gamma-Glutamyl Hydrolase / therapeutic use
  • [MeSH-minor] Adult. Aged. Breast Neoplasms / drug therapy. Clinical Trials as Topic. Drainage. Drug Overdose. Female. Humans. Injections, Spinal. Lymphoma, Non-Hodgkin / drug therapy. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Recombinant Proteins / therapeutic use

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  • MedlinePlus Health Information. consumer health - Medication Errors.
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  • [CommentIn] J Natl Cancer Inst. 2005 Apr 20;97(8):609-10; author reply 610-1 [15840887.001]
  • (PMID = 15494606.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Recombinant Proteins; EC 3.4.19.9 / gamma-Glutamyl Hydrolase; YL5FZ2Y5U1 / Methotrexate
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42. Bienkowska JR, Dalgin GS, Batliwalla F, Allaire N, Roubenoff R, Gregersen PK, Carulli JP: Convergent Random Forest predictor: methodology for predicting drug response from genome-scale data applied to anti-TNF response. Genomics; 2009 Dec;94(6):423-32
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Convergent Random Forest predictor: methodology for predicting drug response from genome-scale data applied to anti-TNF response.
  • Biomarker development for prediction of patient response to therapy is one of the goals of molecular profiling of human tissues.
  • Furthermore, many genes may be responsible for drug response differences, but often only a few are sufficient for accurate prediction.
  • The aim is to select from genome-wide expression data a small number of non-redundant biomarkers that could be developed into a simple and robust diagnostic tool.
  • The first set contains transcript profiles of whole blood from rheumatoid arthritis patients, collected before anti-TNF treatment, and their subsequent response to the therapy.
  • In this set, CRF identified 8 transcripts predicting response to therapy with 89% accuracy.

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  • (PMID = 19699293.001).
  • [ISSN] 1089-8646
  • [Journal-full-title] Genomics
  • [ISO-abbreviation] Genomics
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / N01 AR012256; United States / NIAMS NIH HHS / AR / N01-AR-1-2256
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Biomarkers; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ NIHMS140198; NLM/ PMC4476397
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43. Relling MV, Altman RB, Goetz MP, Evans WE: Clinical implementation of pharmacogenomics: overcoming genetic exceptionalism. Lancet Oncol; 2010 Jun;11(6):507-9
Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 1183701930 for PMID:20413348 [PharmGKB] .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical implementation of pharmacogenomics: overcoming genetic exceptionalism.

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  • [ErratumIn] Lancet Oncol. 2010 Jun;11(6):516
  • (PMID = 20413348.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / U19 GM061388; United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / K12 CA090628; United States / NCI NIH HHS / CA / R37 CA036401; United States / NIGMS NIH HHS / GM / U01 GM061388; United States / NCI NIH HHS / CA / P50 CA116201; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061374; United States / NIGMS NIH HHS / GM / U01 GM092666
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.14.14.1 / Cytochrome P-450 CYP2D6; EC 2.1.1.- / Methyltransferases; EC 2.1.1.67 / thiopurine methyltransferase
  • [Other-IDs] NLM/ NIHMS727761; NLM/ PMC4633045
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