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1. Řezáčová M, Vávrová J, Vokurková D: Ionizing Radiation Sensitizes Leukemic MOLT-4 Cells to TRAIL-induced Apoptosis. Acta Medica (Hradec Kralove); 2008;51(2):101-105

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • However, leukemia cells studied to date have shown variable susceptibility to TRAIL.
  • Our study demonstrates that cells of acute T-lymphoblastic leukemia MOLT-4 are resistant to TRAIL and that ionizing radiation in the therapeutically achievable dose of 1 Gy sensitizes TRAIL-resistant cells MOLT-4 to the TRAIL-induced apoptosis by increase in death receptors for TRAIL DR5.
  • When TRAIL is applied after the irradiation in the time of increased DR5 positivity more efficient cell killing is achieved.

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  • (PMID = 28550838.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Czech Republic
  • [Keywords] NOTNLM ; Apoptosis / DR5 / Ionizing radiation / Leukemia / TRAIL
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2. Jeha S, Pei D, Raimondi SC, Onciu M, Campana D, Cheng C, Sandlund JT, Ribeiro RC, Rubnitz JE, Howard SC, Downing JR, Evans WE, Relling MV, Pui CH: Increased risk for CNS relapse in pre-B cell leukemia with the t(1;19)/TCF3-PBX1. Leukemia; 2009 Aug;23(8):1406-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increased risk for CNS relapse in pre-B cell leukemia with the t(1;19)/TCF3-PBX1.
  • To evaluate the impact of contemporary therapy on the clinical outcome of children with pre-B acute lymphoblastic leukemia (ALL) and the t(1;19)/TCF3/PBX1, we analyzed 735 patients with B-cell precursor ALL treated in four successive protocols at St Jude Children's Research Hospital.
  • The 41 patients with the t(1;19) had a comparable event-free survival to that of the 694 patients with other B-cell precursor ALL (P=0.63; 84.2+/-7.1% (s.e.) vs 84.0+/-1.8% at 5 years).
  • However, patients with the t(1;19) had a lower cumulative incidence of any hematological relapse (P=0.06; 0 vs 8.3+/-1.2% at 5 years) but a significantly higher incidence of central nervous system (CNS) relapse (P<0.001; 9.0+/-5.1% vs 1.0+/-0.4% at 5 years).
  • In a multivariate analysis, the t(1;19) was an independent risk factor for isolated CNS relapse.
  • [MeSH-major] Central Nervous System / pathology. Chromosomes, Human, Pair 1 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Leukemic Infiltration / epidemiology. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic / statistics & numerical data. Combined Modality Therapy. Cranial Irradiation. Disease-Free Survival. Female. Genotype. Humans. Incidence. Infant. Injections, Spinal. Male. Prognosis. Proportional Hazards Models. Risk. Risk Assessment. Treatment Outcome

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  • (PMID = 19282835.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-30; United States / NCI NIH HHS / CA / CA21765
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / TCF3-PBX1 fusion protein, human
  • [Other-IDs] NLM/ NIHMS110407; NLM/ PMC2731684
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3. Schlissel MS, Kuo TC: AID for innate immunity to retroviral transformation. Immunity; 2006 Jun;24(6):671-2
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this issue of Immunity, Gourzi et al. (2006) show that AID also plays a critical role in innate immunity to virally induced acute pro-B cell leukemia.
  • [MeSH-major] Abelson murine leukemia virus / immunology. Cytidine Deaminase / physiology. Leukemia, Experimental / enzymology. Retroviridae Infections / enzymology. Tumor Virus Infections / enzymology

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  • [CommentOn] Immunity. 2006 Jun;24(6):779-86 [16782033.001]
  • (PMID = 16782023.001).
  • [ISSN] 1074-7613
  • [Journal-full-title] Immunity
  • [ISO-abbreviation] Immunity
  • [Language] eng
  • [Publication-type] Comment; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
  • [Number-of-references] 10
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4. Nonomura C, Kikuchi J, Kiyokawa N, Ozaki H, Mitsunaga K, Ando H, Kanamori A, Kannagi R, Fujimoto J, Muroi K, Furukawa Y, Nakamura M: CD43, but not P-selectin glycoprotein ligand-1, functions as an E-selectin counter-receptor in human pre-B-cell leukemia NALL-1. Cancer Res; 2008 Feb 1;68(3):790-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD43, but not P-selectin glycoprotein ligand-1, functions as an E-selectin counter-receptor in human pre-B-cell leukemia NALL-1.
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL/B-precursor ALL) is characterized by a high rate of tissue infiltration.
  • The mechanism of BCP-ALL cell extravasation is not fully understood.
  • In the present study, we have investigated the major carrier of carbohydrate selectin ligands in the BCP-ALL cell line NALL-1 and its possible role in the extravascular infiltration of the leukemic cells.
  • B-precursor ALL cell lines and clinical samples from patients with BCP-ALL essentially exhibited positive flow cytometric reactivity with E-selectin, and the reactivity was significantly diminished by O-sialoglycoprotein endopeptidase treatment in NALL-1 cells.
  • B-precursor ALL cell lines adhered well to E-selectin but only very weakly to P-selectin with low-shear-force cell adhesion assay.
  • Although BCP-ALL cell lines did not express the well-known core protein P-selectin glycoprotein ligand-1 (PSGL-1), a major proportion of the carbohydrate selectin ligand was carried by a sialomucin, CD43, in NALL-1 cells.
  • Most clinical samples from patients with BCP-ALL exhibited a PSGL-1(neg/low)/CD43(high) phenotype.
  • NALL-1 cells rolled well on E-selectin, but knockdown of CD43 on NALL-1 cells resulted in reduced rolling activity on E-selectin.
  • [MeSH-major] Antigens, CD43 / metabolism. E-Selectin / metabolism. Membrane Glycoproteins / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Animals. CHO Cells. Cell Adhesion / physiology. Cell Line, Tumor. Cell Movement / physiology. Cricetinae. Cricetulus. Down-Regulation. HL-60 Cells. Humans. Mice. Mice, Inbred NOD. Mice, SCID. P-Selectin / metabolism. RNA, Small Interfering / genetics. Sialomucins / metabolism. Transfection

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  • (PMID = 18245480.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD43; 0 / E-Selectin; 0 / Membrane Glycoproteins; 0 / P-Selectin; 0 / P-selectin ligand protein; 0 / RNA, Small Interfering; 0 / Sialomucins; 0 / UN1 sialoglycoprotein, human
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5. Kolmannskog S, Flaegstad T, Helgestad J, Hellebostad M, Zeller B, Glomstein A: [Childhood acute lymphoblastic leukemia in Norway 1992-2000]. Tidsskr Nor Laegeforen; 2007 May 31;127(11):1493-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Childhood acute lymphoblastic leukemia in Norway 1992-2000].
  • [Transliterated title] Akutt lymfatisk leukemi hos barn i Norge 1992-2000.
  • BACKGROUND: Acute lymphoblastic leukemia is the most common malignancy in childhood.
  • RESULTS AND INTERPRETATION: The diagnosis was made in 301 children, 33 new cases per year (range 24 to 40) on average.
  • Four of 6 infants with acute lymphoblastic leukemia and all 4 with mature B-cell leukemia are alive.
  • The 10-year event-free survival (p-EFS) was 76%, and 244 of 289 (84%) were alive 4-13 years after the diagnosis was made.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Humans. Infant. Male. Neoplasm Recurrence, Local. Norway / epidemiology. Risk Factors. Stem Cell Transplantation. Treatment Outcome

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  • (PMID = 17551551.001).
  • [ISSN] 0807-7096
  • [Journal-full-title] Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række
  • [ISO-abbreviation] Tidsskr. Nor. Laegeforen.
  • [Language] nor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Norway
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11. Cobanoglu U, Sonmez M, Ozbas HM, Erkut N, Can G: The expression of LMO2 protein in acute B-cell and myeloid leukemia. Hematology; 2010 Jun;15(3):132-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of LMO2 protein in acute B-cell and myeloid leukemia.
  • LIM domain only-2 (LMO2) is an important regulator of hematopoietic stem cell development.
  • LMO2 is also expressed in blast cells of different types of acute leukemia.
  • Here, we analyzed the LMO2 protein expression in acute myeloid leukemia (AML) and B-cell acute lymphoblastic leukemia (B-ALL) and examined whether the LMO2 protein expression can predict outcomes of patients with acute leukemia.
  • Patients with acute B-ALL (22 cases) and AML (57 cases) were examined using immunohistochemistry for LMO2 on paraffin-embedded bone marrow biopsies.
  • We report that LMO2 protein is expressed in a significant proportion of B-ALL and AML and the staining of LMO2 protein does not predict survival in acute leukemia.
  • [MeSH-major] DNA-Binding Proteins / biosynthesis. Leukemia, B-Cell / metabolism. Leukemia, Myeloid, Acute / metabolism. Metalloproteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Adolescent. Adult. Aged. Cell Differentiation / physiology. Female. Gene Expression Regulation, Leukemic. Humans. LIM Domain Proteins. Male. Middle Aged. Young Adult

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  • (PMID = 20557670.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
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12. Giles FJ, O'Brien S, Rizzieri DA, Vey N, Krug U, Sekeres M, Jacobsen TF, Nilsson BI, Staudacher K: A phase II study with CP-4055 in patients with second salvage AML. J Clin Oncol; 2009 May 20;27(15_suppl):7047

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7047 Background: CP-4055 (cytarabine 5'-elaidic acid ester) is a novel derivative of cytarabine, independent of nucleoside transporters to enter the cell.
  • The aim of this study was to assess efficacy and safety of CP-4055 when given as second salvage therapy to patients (pts) with acute myeloid leukemia (AML).
  • METHODS: Adult pts who received two previous chemotherapy regimens and who had refractory/relapsed AML (CR after first salvage therapy lasting less than 6 months) were enrolled.
  • CP-4055 2,000 mg/m<sup>2</sup>/d was administered over 24 h (CIV) in a day (d) 1-5 q3w schedule.
  • Most frequently reported related AE ≥ grade 3 (CTCAE v3.0) were myelosuppression, abdominal pain, colitis, diarrhoea, nausea, fatigue, liver function test (LFT) elevation.
  • Clinical activity (IWG criteria for AML), 2 CR (1 with no CR1 or CR2), and 1 CRp (CR rate 15%), were reported.
  • Among all 40 patients 7 pts (18%) had LFT elevations of grade 3 or more and 4 pts (10%) had LFT elevations of grade 2.
  • CONCLUSIONS: CP-4055 given as second salvage therapy to AML pts show manageable toxicity when administered at 2,000 mg/m<sup>2</sup>/d, 24 h CIV, in a d1-5 q3w schedule.
  • Clinical activity (2 CR and 1 CRp) has been reported among the first 20 late stage AML pts.

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  • (PMID = 27961426.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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13. Yeh C, Ma W, Kantarjian H, Zhang ZJ, Cortes J, Albitar M: BCR-ABL truncation due to premature translation termination as a mechanism of resistance to kinase inhibitors. J Clin Oncol; 2009 May 20;27(15_suppl):7028

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 7028 Background: The major mechanism underlying imatinib resistance in patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with point mutations in the BCR-ABL tyrosine kinase.
  • We describe three novel ABL premature termination mutations leading to BCR-ABL truncation in leukemia patients with multidrug (imatinib/nilotinib/dasatinib) resistance.
  • Total nucleic acids were purified and subjected to two rounds of PCR analysis, with the first PCR designed to eliminate amplification of the wild-type, non-translocated ABL gene.
  • HL60 cells (a Ph-negative myeloid leukemia cell line) and peripheral blood of healthy subjects were used as negative controls; a human CML cell line (K562) was used as a positive control.
  • RESULTS: We identified an exon 7 deletion in three CML patients, a 4-nt insertion (908insCAGG) near the exon 5/6 junction in one CML case, and an exon 6 point mutation (997C>T) in one patient with acute lymphoblastic leukemia (ALL).

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  • (PMID = 27961401.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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14. Tsai DE, Wang W, Reshef R, Vogl D, Stadtmauer E, Andreadis C, Carlson A, Luger S: Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e20533

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of bexarotene on platelet counts in patients undergoing cancer treatment: An analysis of clinical trials in lung cancer and leukemia.
  • : e20533 Background: Bexarotene (Bex) is an oral retinoid X receptor agonist with activity against cutaneous T cell lymphoma and currently under investigation for other malignancies.
  • In patients receiving this agent for acute myeloid leukemia (AML), we noted increases in platelet counts.
  • METHODS: We analyzed platelet count data from 3 Bex clinical trials encompassing non-small cell lung cancer (NSCLC) and AML.
  • More patients on Bex than on placebo had an increase in platelet count of at least 50 K/uL (55% vs. 27% for CarP, p<0.0001; 81% vs. 66% for CisV, p<0.0001) over pre-treatment baseline.
  • The median increase in platelet count was higher on Bex than on placebo (69 vs 0 K/uL for CarP, p<0.0001; 168 vs. 95 K/uL for CisV, p<0.0001) and was maintained while on treatment.
  • Similar findings were seen in a phase I monotherapy trial in AML where 5/18 (28%) patients achieved platelet transfusion independence with peak platelet counts of 40-91 K/uL.
  • Its effect on megakaryopoiesis and its potential role as a supportive care measure should be further evaluated.

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  • (PMID = 27960979.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Iliopoulou EG, Kountourakis P, Karamouzis MV, Doufexis D, Ardavanis A, Baxevanis CN, Rigatos G, Papamichail M, Perez SA: A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC). J Clin Oncol; 2009 May 20;27(15_suppl):3001

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of adoptive transfer of allogeneic natural killer (NK) cells in patients (pts) with advanced non-small cell lung cancer (NSCLC).
  • : 3001 Background: HLA-mismatched NK cells have been found effective in acute myeloid leukemia pts.
  • CD56<sup>+</sup> cells were isolated from 150ml of donor peripheral blood and cultured for 20-23 days with 20ng/ml interleukin-15 and 10<sup>-5</sup>M hydrocortisone.
  • The number of NK cells to be injected was up to 2x10<sup>11</sup>/dose for up to 4 doses.
  • RESULTS: Between 11/2007 and 11/2008 16 pts (performance status 0-1) were enrolled; 1 pt had rapid disease progression before treatment.
  • Pts characteristics: M/F 12/4; histology: adenocarcinoma/squamous cell carcinoma 13/3; stage IIIb/IV 2/14; 1<sup>st</sup>/2<sup>nd</sup> line treatment 13/3; median age 64 years (range, 50-71).
  • The number of cells injected varied from 0.2-29x10<sup>6</sup>/Kg (mean 7.4x10<sup>6</sup>±7.7x10<sup>6</sup>).
  • With a median follow-up of 6 months (range, 1-14) 3 pts with partial response and 7 pts with disease stabilization were recorded.

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  • (PMID = 27962051.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Naik SG, Negrin R, Laport G, Miklos D, Shizuru J, Arai S, Blume K, Wong R, Lowsky R, Johnston L: Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):7033

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes of high-dose therapy using busulfan, etoposide, and cyclophosphamide followed by allogeneic hematopoietic cell transplantation for patients with high-risk or advanced stages of myeloid malignancies.
  • : 7033 Patients (pts) with high risk (HR) or advanced myeloid malignancies have limited effective treatment options.
  • These include high-dose therapy followed by allogeneic hematopoietic cell transplantation (HCT).
  • We report a single institution long-term follow-up of 96 pts, median age 50 (20-60) yrs, who received HLA matched related HCT between 1992 and 2007.
  • All pts were treated with a uniform preparatory regimen: busulfan 16.0 mg/kg (d-8 to-5), etoposide 60mg/kg (d-4), cyclophosphamide 60mg/kg (d-2), and graft-versus-host-disease (GVHD) prophylaxis of cyclosporine and prednisone.
  • Disease status at transplantation was induction failure (IF) acute myeloid leukemia (AML) (n = 10), HR AML in 1st complete remission (CR1) n = 11, in CR2 (n = 5), in CR3 (n = 2), relapsed refractory (RR) AML (n = 14), chronic myeloid leukemia (CML) in second chronic phase (n = 6), blast crisis (n = 2), myelofibrosis (n = 6), myeloproliferative disorders (n = 2), and MDS (n = 38).
  • With a median follow up of 5.6 yrs (1.6-14.6 yrs) actuarial 5-year overall survival (OS) was 32% (95% CI 22-42%) and 5-year probability for freedom from progression (FFP) was 64% (95% CI 52%-76%).
  • Cumulative incidence of acute (grade 3-4) and chronic GVHD was 28% (95% CI 19%-37%) and 38% (95% CI 24%-52%), respectively.
  • There was no statistically significant difference in OS; 31% versus 32% (p = 0.89) or FFP 71% versus 60% (p = 0.29) for recipients of BM versus PBMC with similar results in IF and RR AML.
  • These results confirm that pts with high-risk or advanced myeloid malignancies can achieve long-term survival following myeloablative allogeneic HCT with aggressive conditioning.
  • Relapse and acute GVHD remain significant causes of mortality.
  • Strategies to augment graft-versus-tumor reactions and reduce GVHD remain essential for improving long-term outcomes.

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  • (PMID = 27961395.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Ghavamzadeh A, Hashemi S, Alimoghaddam K, Nasri Moghaddam Z, Shadpour M, Jalili M: Phase II trial of old age acute myeloid leukemia treatment by arsenic trioxide and low-dose subcutaneous cytosin arabinoside. J Clin Oncol; 2009 May 20;27(15_suppl):7075

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II trial of old age acute myeloid leukemia treatment by arsenic trioxide and low-dose subcutaneous cytosin arabinoside.
  • : 7075 Background: AML is a disease of old age, but unfortunately due to several factors standard treatment can not be delivered to these patients.
  • Treatment consist of best supportive care plus administration of low dose ARA-C (20mg/day as SQ) for 10 days each months and arsenic trioxide 10 mg/day as 2 hour iv infusion each month.
  • Median WBC count Hb level and platelet count at presentation were 42,860μl, 8.3g/dl and 30,500/μl, respectively.
  • Complete remission observed in 6 and partial remission in one patient (RR = 63.6%), but remission was short live, after 6 months one patient was in CR and one in PR.
  • CONCLUSIONS: Although prognosis of old age AML remain poor, but with this type of treatment RR is acceptable.

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  • (PMID = 27961458.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Gupta N, Diderichsen PM, Steinberg J, Ricker JL, Humerickhouse R, Awni W, Pradhan R: Population pharmacokinetic (PK) analysis of ABT-869 in solid tumors and acute myelogenous leukemia (AML) patients. J Clin Oncol; 2009 May 20;27(15_suppl):3567

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Population pharmacokinetic (PK) analysis of ABT-869 in solid tumors and acute myelogenous leukemia (AML) patients.
  • The objectives of this analysis were to understand the population pharmacokinetics of ABT-869 and explore the effect of several demographic/disease state covariates influencing ABT-869 disposition.
  • METHODS: A population PK analysis of 181 patients (pts) enrolled in two phase 1 (multiple types of solid tumors and AML) and three phase 2 monotherapy studies (non-small cell lung cancer, hepatocellular carcinoma [HCC] and renal cell carcinoma) was conducted.
  • Potential covariates including body weight, body surface area (BSA), age, sex, creatinine clearance (CrCL) and disease state (HCC vs. non-HCC pts) were tested.
  • The ABT-869 plasma concentration time profile was well described by a one-compartment model with first order absorption and elimination process.
  • Oral clearance (CL/F) was not affected by body weight (range 35-177 kg); however, apparent volume of distribution (V/F) increased by 6L per 0.1 mg/m<sup>2</sup> increase in BSA.
  • CONCLUSIONS: Population PK analysis showed that ABT-869 PK can be well described by a one-compartment model with first order absorption and elimination.
  • HCC pts had lower CL/F value therefore a lower dose may be recommended in these patients.

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  • (PMID = 27961681.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Mayer F, Weidmann J, Federmann B, Schwarz S, Hartmann JT, Kanz L, Bethge W: Clinical impact and follow-up of taste disturbances following myeloablative or nonmyeloablative chemotherapy and stem cell transplantation. J Clin Oncol; 2009 May 20;27(15_suppl):e20609

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical impact and follow-up of taste disturbances following myeloablative or nonmyeloablative chemotherapy and stem cell transplantation.
  • : e20609 Background: Stem cell transplantation (SCT) after myeloablative (MA) or non-myeloablative (NMA) chemotherapy is a successful treatment option for a variety of diseases.
  • Indications for SCT included acute leukemia (n=38), myeloproliferative disease (n=20), lymphoma (n=13), and others (n=29).
  • 75% of pts reported moderate to severe changes in taste perception on a semiquantitative visual analogue scale during the acute phase of SCT with no differences between the three groups (73%, 79%, 75%).
  • This finding was more prevalent after allogeneic SCT (30% after MA conditioning, 28% after NMA) compared to pts with autologous grafts (10%).
  • The lower incidence of persiting changes in taste perception after autologous SCT might be attributed to the absence of graft versus host disease or the dispensability of immunosuppression.

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  • (PMID = 27961552.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Cadoo KA, Lowery MA, Cumiskey J, McCaffrey J, Carney DN: Long term follow-up of primary B and T cell non-Hodgkin's lymphoma (NHL) of the gastrointestinal (GI) tract. J Clin Oncol; 2009 May 20;27(15_suppl):e19516

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

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  • (PMID = 27960953.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Vey N, Bourhis J, Dombret H, Bordessoule D, Prebet T, Charbonnier A, Squiban P, Damholt B, Blaise D, Olive D: A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I study of the anti-natural killer inhibitory receptor (KIR) monoclonal antibody (1-7F9, IPH2101) in elderly patients with acute myeloid leukemia (AML).
  • We present the results of the first-in-human phase I trial of this agent in patients with AML in complete remission (CR).
  • METHODS: Patients aged 60-80 years with non promyelocytic AML in first CR following induction and 1-6 cycles of consolidation chemotherapy, normal renal, and hepatic functions, KIR-expression on patient NK-cells and who signed informed consent were eligible.Dose escalation (0.0003, 0.003, 0.015, 0.075, 0.3, 1, 3 mg/kg) was studied using a 3+3 scheme.
  • The first dose level resulted in a transient KIR occupancy ranging from 20 to 50%.
  • PK values were then in line with modelling data, resulting at 0.3 mg/kg in a Cmax= 6350 ± 504 ng/mL, >80% KIR saturation for one week, and desaturation in the following week.
  • As expected for an IgG4, NK cell numbers were unaffected by the treatment.
  • CONCLUSIONS: Anti-KIR treatment is safe and well tolerated to date.

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  • (PMID = 27962059.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Stuart RK, Stockerl-Goldstein K, Cooper M, Devetten M, Herzig R, Medeiros B, Schiller G, Wei A, Acton G, Rizzieri D: Randomized phase II trial of the nucleolin targeting aptamer AS1411 combined with high-dose cytarabine in relapsed/refractory acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7019

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized phase II trial of the nucleolin targeting aptamer AS1411 combined with high-dose cytarabine in relapsed/refractory acute myeloid leukemia (AML).
  • : 7019 Background: Aptamers are small synthetic oligonucleotides that form stable nuclease-resistant 3D structures and bind target proteins with specificity and affinity similar to antibodies.
  • AS1411 has synergistic effects in combination with cytarabine on AML cell lines in vitro and in vivo.
  • Patients in cohort I were randomized 2:1 to receive AS1411 10 mg/kg/day as continuous IVI on days 1-7 + HiDAC 1.5 g/m<sup>2</sup>/ twice daily on days 4-7 or HiDAC alone for 4 days.
  • Following safety assessment, a second cohort was randomized in a similar manner, with AS1411 escalated to 40 mg/kg/day.
  • Objectives were comparison of response rates (CR+CRp), safety and tolerability between treatment groups.
  • The main grade 3/4 toxicities were hematologic, notably febrile neutropenia, neutropenia, and thrombocytopenia; and infections.
  • Safety findings were similar across groups, except that grade 3 hypokalemia was more frequent with AS1411-40.
  • The combination of AS1411 at 10 or 40 mg/kg/day with HiDAC appears well tolerated and shows promising signs of activity in patients with relapsed/refractory AML.

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  • (PMID = 27961391.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Smith MA, Morton CL, Carol H, Gorlick RG, Kang MH, Keir ST, Kolb EA, Lock RB, Maris JM, Houghton PJ: Pediatric Preclinical Testing Program (PPTP) testing of the CENP-E inhibitor GSK923295A. J Clin Oncol; 2009 May 20;27(15_suppl):10015

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 10015 Background: GSK923295A is a small molecule inhibitor of centromere-associated protein E (CENP-E), a mitotic kinesin that is required for metaphase chromosome alignment and integration of mitotic spindle mechanics with mitotic checkpoint signaling.
  • METHODS: The PPTP includes a molecularly characterized in vitro panel of cell lines (n = 27) and in vivo panel of xenografts (n = 60) representing most of the common types of childhood solid tumors and childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: GSK923295A demonstrated potent in vitro activity against the PPTP cell line panel with a median IC50 of 27 nM (range 12 nM to > 10 μM).
  • Objective responses were noted in 13 of 35 xenografts, including 9 with maintained complete responses (MCR), 3 with complete response (CR), and 1 with partial response (PR).
  • Three of 5 Ewing sarcoma xenografts achieved MCR or CR, as did 2 of 3 rhabdoid tumor, and 2 of 5 rhabdomyosarcoma models.
  • For the neuroblastoma panel, the best response was progressive disease (PD) with growth delay compared to controls (PD2 response), which was observed in 5 of 6 xenografts.
  • The observed high level of preclinical activity for GSK923295A will need to be evaluated in the context of systemic exposures achieved in the xenograft models and those achievable in humans at tolerable doses. (Supported by NCI NO1CM42216) [Table: see text].

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  • (PMID = 27962529.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Pigazzi M, Manara E, Baron E, Beghin A, Basso G: The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e22045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The inducible cyclic adenosine 3',5'-monophosphate early repressor (ICER) enhances drug sensitivity in acute myeloid leukemia.
  • CREB was previously demonstrated to be overexpressed in acute leukemia, whereas ICER was found rapidly degradated being unable to control gene transcription.
  • ICER exogenous expression was demonstrated to repress CREB targets preventing leukemia progression.
  • We hypothesized that ICER restoration deserves a special consideration for playing a role in CREB oncogenic feature and in modeling leukemic cell phenotype.
  • We monitored transcription and translation of a series of genes involved in different pathways by quantitative gene expression and western blot analysis.
  • We investigate ICER's role in cell death after treatment with chemotherapic drugs.
  • RESULTS: We revealed that ICER was able to control gene expression in leukemia, principally of genes involved in cell death and survival.
  • Cell cycle analyses revealed a block in G2 phase, a lowered cell proliferation and clonogenic potential with respect to HL60 treated at the same conditions.
  • Other possible apoptotic pathways (AKT, ERK, JNK) were excluded because found severely disrupted.

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  • (PMID = 27963227.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Kim S, Lee J, Lee J, Kim D, Lim S, Lee Y, Kang Y, Seol M, Ryu S, Lee K: Pretransplant comorbidity as an outcome predictor in adult patients younger than 60 years of age receiving standard induction chemotherapy for de novo acute myeloid leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7055

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pretransplant comorbidity as an outcome predictor in adult patients younger than 60 years of age receiving standard induction chemotherapy for de novo acute myeloid leukemia.
  • : 7055 Background: Comorbidity has been evaluated as an outcome predictor in elderly patients receiving induction chemotherapy for acute myeloid leukemia (AML) as well as in patients undergoing allogeneic hematopoietic cell transplantation (HCT) for various hematologic disorders.
  • METHODS: A total of 276 patients, aged 14 to 59 years, who received standard induction chemotherapy consisting of cytarabine plus daunorubicin or idarubicin for de novo AML excluding M3 subtype between 2000 and 2007 were included.
  • Pre-treatment comorbidity score, assessed by the HCT specific comorbidity index (HCT-CI), was calculated using clinico- pathologic data, which were retrieved from Asan Medical Center Leukemia Registry Database.
  • RESULTS: In the univariate analyses, the HCT-CI score was not a significant prognostic factor for induction of complete remission (CR), whereas survival outcomes such as overall survival (OS), relapse-free survival (RFS) and event-free survival (EFS) were significantly different according to the HCT-CI scores (Table).
  • The multivariate models showed that the HCT-CI score was an independent prognostic factor for EFS (P=0.044), but not for OS (P=0.301) and RFS (P=0.119).
  • Other independent prognostic factors were age (P=0.001 for OS, P=0.002 for RFS, P=0.006 for EFS), initial leukocyte counts (P=0.006 for CR, P<0.001 for OS, P=0.039 for RFS), initial uric acid levels (P=0.004 for RFS, P=0.001 for EFS), and cytogenetic risk groups (P=0.012 for CR, P<0.001 for OS, P<0.001 for RFS, P=0.005 for EFS).
  • CONCLUSIONS: Pre-treatment comorbidity may provide additional prognostic information over established prognostic factors in patients younger than 60 years of age receiving standard induction chemotherapy for de novo AML.

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  • (PMID = 27961421.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Ruiz-Argüelles GJ, Gómez-Almaguer D, Vela-Ojeda J, Morales-Toquero A, David-Gómez-Rangel J, García-Ruiz-Esparza MA, López-Martínez B, Cantú-Rodríguez OG, Gutiérrez-Aguirre CH: Extramedullary Leukemic Relapses Following Hematopoietic Stem Cell Transplantation with Nonmyeloablative Conditioning. Int J Hematol; 2005 Oct;82(3):262

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extramedullary Leukemic Relapses Following Hematopoietic Stem Cell Transplantation with Nonmyeloablative Conditioning.
  • Of a group of 149 patients who underwent allogeneic stem cell transplantation using the "Mexican approach," a nonablative preparative regimen, 49 individuals developed bone marrow relapse, and 8 patients developed extramedullary relapse (EMR).
  • In contrast, bone marrow relapses presented in patients with myeloid or lymphoid malignancies.
  • When EMR was noted, acute graft-versus-host disease (GVHD) had presented in 4 patients, and limited forms of chronic GVHD were present in 3 patients.
  • The only individual alive 240 days after relapse shows no evidence of a full-blown hematologic relapse.
  • An EMR after allogeneic hematopoietic stem cell transplantation usually has a bad prognosis and presents mainly in individuals with high-risk malignancies.

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  • (PMID = 28401517.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Keywords] NOTNLM ; Allograft / Extramedullary / Leukemia / Nonmyeloablative / Relapse
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27. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

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

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  • (PMID = 27961357.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Fernandez HF, Sun Z, Litzow MR, Luger SM, Paietta EM, Dewald G, Ketterling RP, Rowe JM, Lazarus HM, Tallman MS: A randomized trial of anthracycline dose intensification during induction of younger patients with acute myeloid leukemia: Results of Eastern Cooperative Oncology Group study E1900. J Clin Oncol; 2009 May 20;27(15_suppl):7003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized trial of anthracycline dose intensification during induction of younger patients with acute myeloid leukemia: Results of Eastern Cooperative Oncology Group study E1900.
  • : 7003 Background: In younger adults with newly diagnosed acute myeloid leukemia (AML), anthracycline dose intensification during induction may improve complete remission (CR) rates; however, an improvement in overall survival (OS) in a randomized trial has not been demonstrated.
  • METHODS: Adult patients with previously untreated AML were randomized to receive either SDD (45 mg/m<sup>2</sup>/d) or HDD (90 mg/m<sup>2</sup>/d) each for 3days combined with standard-dose cytarabine (100 mg/m<sup>2</sup>/d) for 7 days by continuous intravenous infusion.
  • Those achieving a CR were allocated to allogeneic hematopoietic stem cell transplantation (HSCT) or high-dose cytarabine (with or without a single dose of gemtuzumab ozogamicin) prior to autologous HSCT.
  • The primary end point of this study was OS from the time of induction randomization.
  • There were no differences in patient demographics or disease characteristics between the two groups at presentation.
  • In an intention-to-treat analysis, HDD resulted in a significantly higher CR rate (63.3% vs. 47.7%, p = 0.0003) than SDD.
  • Median OS was superior for the HDD (23.7 months) over the SDD (15.1 months) group (p = 0.005).
  • In subgroup analysis, patients with favorable or intermediate-risk cytogenetics or age <55 years benefited from the HDD.
  • CONCLUSIONS: We demonstrate for the first time in a prospective randomized trial that intensifying induction therapy through a higher daily anthracycline dose, in the setting of identical intensive consolidation therapy, results in a higher CR rate as well as prolonged OS.
  • In younger AML patients a higher dose of anthracycline in induction should be considered the new standard of care.

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  • (PMID = 27961375.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Cheng PC, Crane J, Hunter T: Combination of bortezomib with a FLT3 inhibitor potentiates inhibition of proliferation and apoptosis of AML in vitro. J Clin Oncol; 2009 May 20;27(15_suppl):e14551

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14551 Background: FLT3 receptor tyrosine kinase activating mutations contribute to leukemogenesis and poor prognosis in approximately 30% of acute myeloid leukemia (AML).
  • METHODS: In the course of conducting a synthetic lethality screen with a FLT3 inhibitor on the Ba/F3 murine cell line stably expressing human FLT3 or FLT3-ITD, we identified bortezomib, a proteasome inhibitor, as having potent activity against FLT3-ITD cells.
  • The effects of drugs on proliferation, apoptosis, and phosphosignaling were quantified in Ba/F3 cells and in the HL60 (WT FLT3) and MV4-11 (FLT3-ITD) human cell lines, using an MTS- based colorimetric assay, caspase 3 and 7 activity assays, and immunoblotting, respectively.
  • When the FLT3 inhibitor and bortezomib were used at IC25 concentrations, a more pronounced inhibition of cell proliferation was observed when they were used in combination than with either alone.
  • CONCLUSIONS: Bortezomib preferentially kills FLT3- ITD cells, showing a four-fold more potent inhibition of cell proliferation, induces apoptosis, and abrogates activation of FLT3 and its downstream effector pathways.

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  • (PMID = 27963616.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Tong W, Stevenson W, Cortes J, Needham L, Brotherton D, Davidson A, Drummond A, Garcia-Manero G: In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e14579

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and in vivo anti-leukemia activity of CHR-2845, a cell-targeted HDAC inhibitor for use in monocytic leukemia.
  • : e14579 Background: Histone deacetylase inhibitors alter gene expression and induce apoptosis in a wide range of cancer cells including those derived from human leukemias.
  • METHODS: We studied the in vitro and in vivo anti-leukemia activity of CHR-2845 using cell proliferation assay, annexin V binding assay, cell cycle analysis, western blot and in vitro primary leukemia cell culture.
  • RESULTS: Both U937 and THP1 cells express high levels of hCE-1 whereas the myeloid cell line, HL60, does not.
  • In comparison to vorinostat, CHR-2845 showed increased anti-proliferative potency (IC<sub>50</sub>) against monocytic cell lines (THP1, 30 nM vs 700 nM and U937, 30 nM vs 475 nM), compared to a myeloid cell line (HL60, 700nM vs 470 nM).
  • In a broad panel of leukemic cell lines, the potency of CHR-2845 over vorinostat correlated completely with hCE-1 expression.
  • In monocytic cell lines, CHR-2845 induced more apoptosis than vorinostat (THP1: 45±5% vs 11±1% and U937: 23±14% vs 6±1%), as measured by flow cytometry using Annexin V.
  • Biochemical assessment of histone H3 and H4 protein acetylation by Western blot also indicateed that CHR-2845 is at least 10 times more potent than vorinostat in monocytic cell lines but not in HL-60 cells.
  • We also studied the anti-leukemia activity of CHR-2845 in primary leukemia cells from 8 patients with acute or chronic myelomonocytic leukemia.
  • CONCLUSIONS: These results indicated that CHR-2845 has potential to be efficacious in the treatment of patients with monocytic leukemia.

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  • (PMID = 27963654.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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31. Fauzdar A, Mahajan A, Jain D, Mishra M, Raina V: Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report. J Clin Oncol; 2009 May 20;27(15_suppl):e21000

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amplification of RUNX1 gene in two new cases of childhood B-cell precursor acute lymphoblastic leukemia: A case report.
  • : e21000 Background: Chromosome abnormalities of leukemia cells have important prognostic significance in childhood acute lymphoblastic leukemia (ALL).
  • B-cell precursor acute lymphoblastic leukemia (BCP-ALL) ETV6/RUNX1 (alias TEL/AML1) is most frequent i.e.
  • We report two new cases with Pre B- cell ALL without ETV6/RUNX1 rearrangement, showing amplification of AML1 gene detected by FISH analysis.
  • RESULTS: In first case a 3-year girl with four copies of AML (RUNX1) gene were observed in 95% of the cell with normal two copies of TEL (ETV6) gene in both interphase and metaphase FISH.

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  • (PMID = 27960689.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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32. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • OBJECTIVES: We reviewed all patients diagnosed with T-ALL to assess risk classification according to NCI criteria, type of therapy received, overall survival and causes of mortality.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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33. Ravandi Kashani F, Cortes J, Faderl S, Jones D, Byrd A, Brandt M, Garcia-Manero G, Levis M, Andreeff M, Kantarjian H: Phase I/II study of idarubicin (Ida), high-dose ara-C, and sorafenib (S) in patients (pts) younger than 65 years with acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7018

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of idarubicin (Ida), high-dose ara-C, and sorafenib (S) in patients (pts) younger than 65 years with acute myeloid leukemia (AML).
  • It selectively induces apoptosis in FLT3-mutant human AML cell lines at nM concentrations.
  • METHODS: Objectives of this study are to determine the tolerability and efficacy of combination of S with chemotherapy.
  • Ara-C 1.5 g/m<sup>2</sup> over 24 hrs daily x 4 (x 3 for pts over 60) and Ida 12 mg/m<sup>2</sup> daily x 3 are administered with S.
  • In the phase I part, pts with relapsed AML were treated with escalating doses of S (400 mg qod, 400 mg daily, 400 mg bid) for 7 days during induction, and 400 mg bid was established as safe.
  • Pts achieving CR receive up to 5 courses of consolidation with Ida 8 mg/m<sup>2</sup> daily x 2 and Ara-C 0.75 g/m<sup>2</sup> daily x 3 in addition to S 400 mg bid for up to 28 days per cycle repeated every 4 to 6 weeks.
  • 4 achieved CR; 6 failed.
  • Median presentation WBC was 4.9 x 10<sup>9</sup>/L (range 0.6 - 122.7 x 10<sup>9</sup>/L).
  • 40 pts are evaluable for response and 85% achieved CR (n = 30) or CRp (n = 4) (13 of 14 FLT3 mutated pts); 5 pts are too early (1 FLT3 mutated).
  • Most frequent grade 3 and higher related adverse events: hyperbilirubinemia (5), rash and hand-foot syndrome (3), raised transaminases (2), diarrhea (2), hypertension (2).
  • 5 pts have relapsed; median CR duration has not been reached, (range; 0.2+ - 10.6+ mo).
  • Among pts with FLT3 mutation, 4 have relapsed and 9 remain in CR.
  • Plasma inhibitory assay was performed using day 7 samples from 10 pts; mutant FLT3 was suppressed by all with 5-fold more potent suppression against mutant versus wild-type FLT3.
  • CONCLUSIONS: S can be safely combined with IA; it has a high CR rate in frontline therapy of younger pts with AML, in particular those with FLT3 mutations.
  • Correlative studies confirm potent activity of S against FLT3 signaling.

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  • (PMID = 27961390.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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34. Patel R, Kurian S, Sun C, Francisco L, Wong L, Sharp J, Armenian S, Forman S, Bhatia S: Challenges for retrospective cohort studies: A profile of patients who refuse participation or are lost to follow-up. J Clin Oncol; 2009 May 20;27(15_suppl):6615

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 6615 Background: As hematopoietic cell transplantation (HCT) has increasingly become a curative option for many diseases, studying long-term complications has assumed critical importance.
  • A major issue in conducting scientifically rigorous long-term follow up studies with large cohorts is the ability to track patients, and obtain informed consents.
  • Primary diagnoses included acute/chronic leukemia (43%), Hodgkin/non-Hodgkin lymphoma (36%), multiple myeloma (9%), and other miscellaneous diagnoses (12%).
  • CONCLUSIONS: This study demonstrates the critical need for maintaining up-to-date contact information on patients after HCT in order to obtain valid long-term follow-up data.
  • It also describes the characteristics of the sub-population that are more likely to refuse or be LTFU, information necessary for planning targeted interventions in long-term follow-up initiatives.

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  • (PMID = 27961771.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Barret J, Dumontet C, Annereau J, Brel V, Breillout F, Guminski Y, Imbert T, Guilbaud N, Bailly C: A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512. J Clin Oncol; 2009 May 20;27(15_suppl):11087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A functional procedure using fresh samples to select patients with acute myeloid leukemia prior to treatment with the novel targeted cytotoxic agent F14512.
  • This study was undertaken to investigate the potential of N-methyl-spermine-NBD, a proprietary fluorescent polyamine conjugate, designed to select patients with PTS-positive leukemic cells.
  • METHODS: The uptake of this probe was first measured by flow cytometry in a panel of human leukemia cell lines.
  • After the selection of the optimal CD gating, median value of fluorescence of our probe was measured by flow cytometry in lymphocytes and blastes of each patient.
  • RESULTS: Data showed that high level of fluorescence was detected in F14512 -sensitive cancer cell lines whereas leukemia cells responding poorly to F14512 generally exhibited very low levels of PTS.
  • We then demonstrated that human leukocytes incorporate N-methyl-spermine-NBD in a time, concentration and temperature dependent manner, confirming the active transport of polyamines in these cells.
  • The incorporation in lymphocytes was found low and with a weak inter-individual variation.
  • A panel of 50 fresh human acute myeloid leukemia samples showed a larger inter-individual variation and, interestingly, incorporation of the fluorescent probe was generally higher in leukemia blasts than in lymphocytes.

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  • (PMID = 27963178.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Epenetos AA, Kousparou C, Stylianou S: Inhibition of Notch and tumor regression. J Clin Oncol; 2009 May 20;27(15_suppl):e14623

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e14623 Background: Notch signaling is an evolutionary-conserved pathway in vertebrates and invertebrates which is involved many developmental processes, including cell fate decisions, apoptosis, proliferation, and stem-cell self renewal.
  • Increasing evidence suggests that the Notch signaling pathway is frequently up regulated in many forms of cancer including acute T-cell lymphoblastic leukemia, cervical, prostate, lung, breast and others.
  • METHODS: We have genetically engineered a fusion protein, consisting of the Drosophila transcription factor Antennapedia (ANTP) and with the truncated version of Mastermind-like (MAML) that behaves in a dominant negative (DN) fashion and inhibits Notch activation (ANTP/DN MAML, TR4).
  • RESULTS: Our data show that ANTP/DN MAML fusion protein, TR4 contains signals for proper cell targeting, internalization and nuclear transport.

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  • (PMID = 27964214.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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37. Beltran BE, Morales D, Quiñones P, Salas R, Castillo J: Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma.
  • : 8575 Background: Adult T-cell leukemia/lymphoma (ATLL) is associated with human T-cell lymphotropic virus type-I (HTLV-1) described in Southern Japan, Europe, Caribbean and South America.
  • Diagnosis was based on clinical history and histological findings consistent with ATLL and either positive HTLV-1 serology or evidence of HTLV-1 integration.
  • Clinical types were acute (n=45), lymphomatous (n=43), cutaneous (n=10), smoldering (n=3) and chronic (n=1).
  • Median OS for acute, lymphomatous, smoldering and cutaneous subtype were 2, 11, 17 and 39 months, respectively (log-rank 28.5, p<0.00001).
  • In the univariate analysis, presence of B symptoms, ECOG performance status 2, clinical stage II or higher, elevated LDH level and bone marrow (BM) involvement were independent factors for survival with p<0.05.
  • The IPI score was available in 92 patients; 13 (14%), 12 (13%), 29 (32%) and 38 (41%) patients were low, low-intermediate, high-intermediate and high-risk, respectively.
  • Median OS by IPI risk group was 40, 13, 6 and 2 months, respectively (p<0.005).
  • The prognostic index for T-cell lymphoma (PIT) score was determined in 80 patients; 20 (25%), 17 (21%), 33 (41%) and 10 (13%) patients had scores of 0-1, 2, 3 and 4, respectively.
  • Median OS by PIT risk group was 19, 5, 3 and 2 months, respectively (p<0.005).
  • CONCLUSIONS: This retrospective series represents the largest Latin-American experience on ATLL, which is a heterogeneous disease with distinct clinical features and outcomes.
  • The IPI ant PIT scores, used for risk-stratification of aggressive B-cell and peripheral T-cell lymphomas, respectively, appear as good prognostic indicators for ATLL as well.
  • Further research is needed to better risk-stratify this unique lymphoma.

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  • (PMID = 27962272.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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38. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

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

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  • (PMID = 27961262.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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39. Tsujimura H, Mimura N, Ise M, Sakai C, Shimada H, Nagata M, Kumagai K: Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e15663

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidence of therapy-related leukemia following chemoradiotherapy for esophageal cancer.
  • On the other hands, a sufficiently long survival time has increased treatment-related late toxicities.
  • However, the frequency and the pathogenesis of secondary malignancies that is the most serious late-onset complication are still unclear.
  • METHODS: From July 2000 to March 2008, 348 patients with esophageal squamous cell carcinoma underwent CRT.
  • All patients received chemotherapy consisting with nedaplatin (80 mg/m<sup>2</sup>, div day1) and fluorouracil (700 mg/m<sup>2</sup>, ci day 1-5) and concurrent long T field irradiation (2 Gy daily, up to 30 Gy).
  • RESULTS: Four patients, who achieved CR after CRT, developed leukemia.
  • Case1, 60-yo-male, developed overt acute myeloid leukemia (AML) from myelodysplastic syndrome 48 months after CRT.
  • Case3, 72-yo-male, developed Burkitt leukemia with t(8;14)(q24;q32) 19 months after CRT.
  • Case4, 65-yo-male, developed myeloid crisis of chronic myelogenous leukemia with complicated abnormalities including t(9;22)(q34;q11) 48 months after CRT.
  • Case 1 and 3 had localized disease and received single course of neoadjuvant CRT.
  • Case 2 and 4 had advance disease and received 2 courses of CRT.
  • All patients eventually died of leukemia.
  • CONCLUSIONS: Since platinum and fluorouracil have shown relatively low chance of secondary neoplasm, our data demonstrates that the concurrent radiotherapy which involves massive bone marrow tissue may increase the risk of leukomogenesis.
  • To this end, atypical cytogenetic abnormalities seen in the present cases give a new insight into the biology of therapy-related leukemia.
  • Notably, this is the first report presenting the incidence of secondary leukemia by nedaplatin.

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  • (PMID = 27962759.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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40. Mohty M, Balere M, Socie G, Milpied N, Ifrah N, Harousseau JL, Michallet M, Blaise D, Esperou H, Yakoub-Agha I, SFGM-TC: Effect of antithymocyte globulins (ATG) as part of the myeloablative conditioning (MAC) regimen on the risk of severe graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT) from matched-unrelated donors (MUD). J Clin Oncol; 2009 May 20;27(15_suppl):7025

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of antithymocyte globulins (ATG) as part of the myeloablative conditioning (MAC) regimen on the risk of severe graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT) from matched-unrelated donors (MUD).
  • : 7025 Here, we report the results of a multicenter retrospective study analyzing the effect of ATG, incorporated within the MAC regimen for MUD-transplants in leukemic patients.
  • The purpose of the study was to compare the incidence and severity of acute and chronic GVHD as well as overall outcome.
  • 171 adult patients with acute leukemia and MDS, for whom detailed allelic HLA typing (4 digits) was available, were included.
  • With a median follow-up of 30.3 (range, 2.6-68.1) months, grade 0-1 and 2-4 acute GVHD occurred in 74 (46%) and 88 patients (54%) respectively, with grade 3-4 acute GVHD being significantly lower in the ATG group (18% vs. 32%; p = 0.04).
  • Extensive chronic GVHD was significantly lower in the ATG group (5% vs. 33%; p = 0.001).
  • Patients from the ATG group had a higher incidence of limited chronic GVHD (33% vs. 18%; p = 0.06).
  • In multivariate analysis, an HLA allelic mismatch and the non-use of ATG were associated with an increased risk of grade 3-4 acute GVHD (RR = 2.80, 95% CI, 1.5-5.3, p = 0.001; and RR = 2.4, 95% CI, 1.1-5.0, p = 0.02 respectively).
  • Similarly, multivariate analysis showed that the absence of use of ATG was the unique parameter associated with an increased risk of extensive chronic GVHD (RR = 6.9; 95% CI, 1.7-29.0, p = 0.008).
  • Finally, LFS and OS at 2 years were not significantly different between the no-ATG and ATG group (48.8% vs. 41.3%, p = NS; and 53.6% vs. 54.3%, p = NS; respectively).
  • These results suggest a global long-term beneficial effect of ATG when used as part of the MAC regimen prior to allo-SCT from MUD (especially in the HLA mismatch setting).

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  • (PMID = 27961398.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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41. Iacobucci I, Storlazzi C, Lonetti A, Ferrari A, Messina M, Cilloni D, Papayannidis C, Baccarani M, Foà R, Martinelli G: IKZF1 (IKAROS) deletions as a prognostic marker in BCR-ABL1 positive acute lymphoblastic leukemia patients: A GIMEMA ALL WP Report. J Clin Oncol; 2009 May 20;27(15_suppl):11005

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IKZF1 (IKAROS) deletions as a prognostic marker in BCR-ABL1 positive acute lymphoblastic leukemia patients: A GIMEMA ALL WP Report.
  • : 11005 Expression of BCR-ABL1 in hematopoietic stem cells can alone induce a chronic myeloid leukemia (CML) but cooperating oncogenic lesions are required for the generation of a blastic leukemia.
  • To identify oncogenic sub-microscopic lesions that cooperate with BCR-ABL1 to induce ALL, by high resolution single nucleotide polymorphism (SNP) arrays (250K NspI and SNP 6.0, Affymetrix) we studied 106 patients (pts) with de novo adult BCR-ABL1-positive ALL.
  • The most frequent somatic copy number alteration was deletion on 7p12 of IKZF1 (68/106, 64%), which encodes the transcription factor Ikaros required for the earliest stages of lymphoid lineage commitment.
  • Gene expression profiling analysis of pts with IKZF1 deletion vs wild-type pts identified a unique signature characterized by a down-regulation of genes involved in pre-B-cell differentiation (e.g.
  • VPREB1, VPREB3, IGLL3, BLK), demonstrating that genomic IKZF1 alterations have a strong impact on trascriptoma and contribute to an impaired B-cell differentiation.
  • Univariate analysis showed that the IKZF1 deletion is a negative prognostic marker influencing the cumulative incidence of relapse (10.1 months for pts with deletion vs 56.1 months for wild-type pts, p=0.0103) and disease-free survival (DFS) (10.1 months vs 32.1 months, respectively, p=0.0229).

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  • (PMID = 27964054.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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42. Rao SR, Hassett M, Schwartz JH, Maloney B, Jacobson JO: Admissions for chemotherapy-related serious adverse effects (CR-SAEs) and rates of mortality among community cancer center patients. J Clin Oncol; 2009 May 20;27(15_suppl):6571

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Admissions for chemotherapy-related serious adverse effects (CR-SAEs) and rates of mortality among community cancer center patients.
  • : 6571 Background: Data regarding CR-SAE's come predominantly from clinical trials; little is known about the experiences of cancer patients treated in community settings.
  • Our goals were to describe admissions for CR-SAE's among cancer patients treated in a community setting and to identify rates and predictors of mortality for admitted patients.
  • METHODS: We conducted a prospective cohort study of adult cancer patients (excluding acute leukemia and stem cell transplant patients) admitted to a community hospital January 2003-December 2006.
  • We identified the type of SAE, outcome of each admission, time form chemotherapy to admission and from admission to discharge/death, and the disease and treatment characteristics of each patient.
  • RESULTS: 227 patients experienced 258 admissions for CR-SAE's (55.5% female; median age 68, range 17-89).
  • The most common cancers were colorectal (18.5%), lung (18.1%), lymphoma (16.3%), and breast (13.7%).
  • Approximately 7.4% of admissions led to fatalities, with a median of 9 days (range 1-35) from admission to death.
  • The average time from chemotherapy to admission was shorter for fatal vs. non-fatal admissions (3.6 vs. 7.7 days; p<.01).
  • CONCLUSIONS: Fatalities during admissions for CR-SAE's in a community cancer center are relatively uncommon and are not associated with age or type of SAE/cancer.
  • Chemotherapy-related mortality in the palliative care setting may be a valid quality indicator.

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  • (PMID = 27963798.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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43. Borthakur G, Faderl S, Ravandi F, Padmanabhan S, Stock W, Wu K, Li J, Curt G, Tallman M, Minden M: Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):3580

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical, pharmacokinetic (PK), and pharmacodynamic findings from a phase I trial of an Eg5 inhibitor (AZD4877) in patients with refractory acute myeloid leukemia (AML).
  • Eg5 inhibition is thus specific for dividing cells, resulting in monoastral mitotic spindles (monoasters) and apoptotic cell death.
  • Preclinically, hematologic tumor cell lines were generally more sensitive to AZD4877 than those derived from solid tumors.
  • The T<sub>1/2</sub> of AZD4877 ranged from 26 to 42 hr; PK were linear and drug levels non-cumulative.

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  • (PMID = 27961757.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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44. Arellano ML, Winton E, Pan L, Souza L, Sunay S, Lima L, McLemore M, Heffner LT, Langston A, Khoury HJ: Prognostic significance of leukopenia at the time of diagnosis in acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7070

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of leukopenia at the time of diagnosis in acute myeloid leukemia (AML).
  • : 7070 Background: In contrast to the poor prognosis associated with hyperleukocytosis, the prognostic significance of leukopenia at the time of diagnosis of AML is unknown.
  • METHODS: Single institution retrospective analysis of 225 consecutive, newly diagnosed AML patients (pts), homogeneously treated between July 1996 and February 2005; and divided into 2 groups based on presenting WBC: < 2,000/uL (30) and > 2,000/uL (195).
  • Simultaneously obtained peripheral blood and marrow blasts were analyzed for cell surface expression of CD34, cKit, CXCR4, PCAM, VLA-2, VLA-3, VLA-4, VLA-5, and FLT3 using flow cytometry.
  • RESULTS: Patients' characteristics (gender, secondary vs. de novo, and cytogenetic [CTG] risk) were comparable between the 2 groups.
  • Leukopenic AML pts were older (median 56 vs. 53 years, p = 0.02), and had lower induction complete remission [CR] rates: 63% vs. 81% (p = 0.03) by univariate analysis.
  • Event-free (EFS), disease-free (DFS), and overall survivals (OS) were lower in the leukopenic group: 12 vs. 14; 14 vs. 17; and 17 vs. 19 mos, respectively; but did not reach statistical significance.
  • By multivariate analysis, age (p < 0.0001) and CTG risk group (p < 0.0001) were independent predictors of OS, while CTG risk group predicted RFS (p < 0.0001).
  • The level of expression of cell surface adhesion molecules on blood and marrow blasts was comparable for the 2 groups.
  • Leukopenic AML did not have over-expression of cell surface adhesion molecules.

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  • (PMID = 27961453.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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45. Lonetti A, Iacobucci I, Ferrari A, Messina M, Cilloni D, Soverini S, Papayannidis C, Baccarani M, Foà R, Martinelli G: Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients. J Clin Oncol; 2009 May 20;27(15_suppl):7049

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of different isoforms of the B-cell mutator activation-induced cytidine deaminase (AID) in BCR-ABL1-positive acute lymphoblastic leukemia (ALL) patients.
  • : 7049 Since the activation-induced cytidine deaminase (AID) enzyme can target non-immunoglobulin (Ig) genes and may even act as a genome-wide mutator, we investigated AID expression in BCR-ABL1-positive ALL and in chronic myeloid leukemia (CML) at the time of progression to blast crisis.
  • On the 61 de novo adult BCR-ABL1-positive ALL patients (pts), AID mRNA and protein were detected in 36 (59%); their expression correlated with BCR-ABL1 transcript levels and disappeared after treatment with tyrosine kinase inhibitors at the time of remission.
  • AID expression was also found in lymphoid blast crisis CML (50%), but not in myeloid lineage or in chronic phase CML.
  • Different isoforms of AID were identified: 13/61 (21%) pts expressed the full-length isoform; 19/61 (31%) co-expressed the wild-type and different AID splice variants with deaminase activity (AIDΔE4a, with a 30 bp deletion of exon 4; AIDΔE4, with the exon 4 deletion; AIDins3, with the retention of intron 3-4); 4/61 (7%) expressed the AIDΔE3-E4 isoform without deaminase activity (deletion of exons 2 and 3).
  • Patients who expressed wild-type AID had a higher number of alterations compared to AID-negative (median copy number alteration of 14 versus 4. respectively, p < 0.03).
  • Our findings show that BCR-ABL1-positive ALL cells aberrantly express different isoforms of AID that can act as mutator outside the Ig gene loci in promoting genetic instability in leukemia cells.

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  • (PMID = 27961429.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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46. Ikawa Y, Sugimoto N, Koizumi S, Yachie A, Saikawa Y: Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene. J Clin Oncol; 2009 May 20;27(15_suppl):10045

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter DNA methylation of CD10 in infant acute lymphoblastic leukemia with MLL/AF4 fusion gene.
  • While CD10 negativity reflects an earlier stage of B-cell development, complete IgH gene rearrangements (VDJ<sub>H</sub>) show more mature IgH status.
  • METHODS: CD10-negative infant ALL with MLL/AF4, CD10-positive infant ALL with germ-line MLL, CD10-positive pre-B ALL cell line, infant AML (M5) with MLL/AF9 and pediatric AML (M2) with AML1/ETO were analyzed for VDJ<sub>H</sub> status and methylation of CD10 gene promoters.
  • RESULTS: Three of 4 cases with infant ALL revealed complete rearrangements of VDJ<sub>H</sub> gene with productive joints.
  • Bisulfite sequencing of CD 10 type 1 and 2 promoters identified more than 84% of methylated CpG dinucleotides in all three CD10-negative infant ALL cases with MLL/AF4.

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  • (PMID = 27962471.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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47. Zuo Z, Jones DM, Thomas DA, O'Brien S, Ravandi F, Kantarjian HM, Medeiros LJ, Luthra R, Chen SS: A nine-gene predictor of therapy response in adult Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL). J Clin Oncol; 2009 May 20;27(15_suppl):7014

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A nine-gene predictor of therapy response in adult Philadelphia-chromosome positive acute lymphoblastic leukemia (Ph+ ALL).
  • Expression of the selected genes was assessed using Applied Biosystems low density reverse transcription quantitative PCR (RT-qPCR) arrays in bone marrow (BM) samples from 27 adult Ph+ ALL patients treated with standard chemotherapy plus a tyrosine kinase inhibitor.
  • Therapy responses were defined at the molecular level by monitoring BCR/ABL1 levels, and categorized into 3 groups: optimal, persistent and relapse.
  • Median disease-free survival among the optimal and relapse groups were 12 and 5 months respectively (p = 0.002).
  • There was no statistical difference in age, initial peripheral blood white cell and BM blast counts, and initial normalized BCR/ABL1 levels between groups.
  • RESULTS: Data mining and pathway analysis of the published data identified 46 genes in 7 pathways potentially associated with therapy response (p < 0.001).

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  • (PMID = 27961387.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

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

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  • (PMID = 27963169.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Forester CM, Braunreiter CL, Yaish H, Hedlund GL, Afify Z: Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia. Pediatr Radiol; 2009 Nov;39(11):1230-3
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  • [Title] Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia.
  • In children, leukemia is the most common malignancy, and approximately 75% of leukemias are acute lymphoblastic leukemia (ALL).
  • Central nervous system leukemia is found at diagnosis in fewer than 5% of children with ALL.
  • Leukemic intracranial masses have been described with acute myeloid leukemia, but ALL presenting as a mass lesion is rare.
  • We describe a unique case of an intracranial confirmed precursor B cell (pre-B) ALL mass in a 13-year-old girl that was diagnosed by brain CT, MRI and cerebral angiography, and confirmed by biopsy.
  • [MeSH-major] Brain Neoplasms / diagnosis. Cerebral Angiography / methods. Magnetic Resonance Imaging / methods. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Tomography, X-Ray Computed / methods


50. Breakey VR, Abdelhaleem M, Weitzman S, Abla O: Hemophagocytic lymphohistiocytosis onset during induction therapy for precursor B-cell acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2008 Dec;30(12):956-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hemophagocytic lymphohistiocytosis onset during induction therapy for precursor B-cell acute lymphoblastic leukemia.
  • We report the clinical course of a child with precursor B-cell acute lymphoblastic leukemia who developed fever, hepatosplenomegaly, and refractory thrombocytopenia after initiation of chemotherapy.
  • Bone marrow aspiration on Day 8 of induction showed new onset of hemophagocytosis and he met clinical, laboratory, and histopathologic criteria for hemophagocytic lymphohistiocytosis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Lymphohistiocytosis, Hemophagocytic / chemically induced. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 19131791.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / pegaspargase; 30IQX730WE / Polyethylene Glycols; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.5.1.1 / Asparaginase
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51. Ju X, Li D, Shi Q, Hou H, Sun N, Shen B: Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2009 Jan;26(1):1-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential microRNA expression in childhood B-cell precursor acute lymphoblastic leukemia.
  • The analysis of differential microRNA expression profiles may be a powerful tool to allow us insight on the mechanisms of childhood B-cell precursor acute lymphoblastic leukemia (pre-B-ALL).
  • The results of this study offer a comprehensive and quantitative profile of miRNA expression in pre-B-ALL and their healthy counterpart, suggesting that miRNAs could play a primary role in the disease itself.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Child. Child, Preschool. Computational Biology. Gene Expression Profiling. Hematopoiesis / genetics. Humans. Infant. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19206004.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MIRN222 microRNA, human; 0 / MIRN373 microRNA, human; 0 / MIRN451 microRNA, human; 0 / MicroRNAs
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52. de Souza Thiago L, da Costa ES, Lopes DV, Borojevic R: Racemic Etodolac is cytotoxic and cytostatic for B-cell precursor acute lymphoblastic leukemia cells. Biomed Pharmacother; 2009 Aug;63(7):548-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Racemic Etodolac is cytotoxic and cytostatic for B-cell precursor acute lymphoblastic leukemia cells.
  • Several epidemiological studies have provided evidence that administration of nonsteroidal anti-inflammatory drugs (NSAIDs) could have a prophylactic effect against some cancers such as sporadic colorectal cancer and leukemia.
  • We evaluated the effect of racemic Etodolac on proliferation and cell survival in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells.
  • Etodolac decreased survival of Nalm-16 and Nalm-6 BCP-ALL cell lines and also decreased cell proliferation in Nalm-16 cell line.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antimetabolites, Antineoplastic / pharmacology. Cell Proliferation / drug effects. Cytostatic Agents / pharmacology. Etodolac / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Humans. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma. Stereoisomerism

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  • (PMID = 18993025.001).
  • [ISSN] 1950-6007
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antimetabolites, Antineoplastic; 0 / Cytostatic Agents; 2M36281008 / Etodolac
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53. Stachel D, Albert M, Meilbeck R, Paulides M, Schmid I: Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia. Oncol Rep; 2007 Jan;17(1):147-52
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of angiogenic factors in childhood B-cell precursor acute lymphoblastic leukemia.
  • Pathological angiogenesis is increasingly recognized to be an important feature of pathogenesis in solid tumors and also in leukemias.
  • Vascular endothelial growth factor (VEGF) seems to play a central role in tumor angiogenesis and is associated with a poor prognosis in both solid tumors and adult leukemias.
  • In pediatric acute lymphocytic leukemia however, the expression of angiogenic molecules and its relation to prognosis and relapse are unknown.
  • Therefore, we prospectively analyzed 46 pediatric patients with precursor B cell acute lymphocytic leukemia by semi-quantitative RT-PCR for expression of the angiogenic molecules VEGF, VEGF-C, iNOS and TGF-beta and correlated relapse and survival data with the expression of these factors.
  • Angiogenic factors are expressed in the bone marrow of patients with pediatric B cell precursor ALL and VEGF is a potential candidate for therapeutic intervention as it is significantly higher expressed in children with late relapses.
  • The mRNA expression of iNOS in the surviving children possibly reflects an increased activity of the immune system against the leukemia which leads to a superior survival.
  • [MeSH-major] Angiogenic Proteins / biosynthesis. Burkitt Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Bone Marrow Cells / metabolism. Child. Child, Preschool. Female. Fibroblast Growth Factor 2 / biosynthesis. Fibroblast Growth Factor 2 / genetics. Humans. Infant. Male. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Nitric Oxide Synthase Type II / biosynthesis. Nitric Oxide Synthase Type II / genetics. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Transforming Growth Factor beta / biosynthesis. Transforming Growth Factor beta / genetics. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics. Vascular Endothelial Growth Factor C / biosynthesis. Vascular Endothelial Growth Factor C / genetics

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  • (PMID = 17143492.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenic Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factor C; 103107-01-3 / Fibroblast Growth Factor 2; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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54. Bhatia S, Kaul D, Varma N: Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia. Mol Cell Biochem; 2010 Jul;340(1-2):97-106
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential tumor suppressive function of miR-196b in B-cell lineage acute lymphoblastic leukemia.
  • Keeping in view the fact that genes coding microRNAs (miRNAs) have been found to be localized in chromosomal regions susceptible to genetic translocations, this study was addressed to identify and characterize the miRNAs that are present near/within the regions involved in genetic translocations characteristic of B-cell acute lymphoblastic leukemia (B-cell ALL).
  • Out of six such identified miRNAs miR-196b was not only found to be significantly down-regulated in both EB-3 cell line as well as B-cell ALL patients as compared to that found in the corresponding controls, but also had the inherent capacity to down-regulate the highly expressed c-myc gene, a consequence of genetic translocation characteristic of EB-3 cells at both transcriptional and translational level.
  • This phenomenon was in conformity with the observed reciprocal relationship between the expressed genes coding for miR-196b and c-myc in B-cells derived from ALL patients as well as c-myc gene was found to be a putative target of miR-196b as predicted by bioinformatic algorithms.
  • Also down-regulation of c-myc gene was accompanied by decreased expressions of c-myc effector genes coding for hTERT, Bcl-2, and AATF.
  • Based upon these results, we propose for the first time that miR-196b has the inherent capacity to down-regulate the overamplified c-myc gene recognized as a common pathognomonic feature leading to cancer in general and B-cell ALL in particular.
  • Hence miR-196b can be assigned with the tumor suppressor function and can be of therapeutic importance in paving the way toward the treatment of B-cell ALL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. MicroRNAs / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Algorithms. Apoptosis / genetics. Apoptosis Regulatory Proteins / genetics. Case-Control Studies. Cell Line, Tumor. Cell Proliferation. Computational Biology. Down-Regulation. Humans. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics. Repressor Proteins / genetics. Telomerase / genetics. Transcription, Genetic. Transfection

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  • (PMID = 20549547.001).
  • [ISSN] 1573-4919
  • [Journal-full-title] Molecular and cellular biochemistry
  • [ISO-abbreviation] Mol. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / AATF protein, human; 0 / Apoptosis Regulatory Proteins; 0 / MIRN196 microRNA, human; 0 / MYC protein, human; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; 0 / Repressor Proteins; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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55. Morrissette JJ, Halligan GE, Punnett HH, McKenzie AS, Guerrero F, de Chadarévian JP: Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Aug;169(1):58-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Down syndrome with low hypodiploidy in precursor B-cell acute lymphoblastic leukemia.
  • We describe the rare finding of a 33-month-old child neonatally diagnosed with Down syndrome, who presented with pre-B acute lymphoblastic leukemia (ALL) with a pretreatment bone marrow karyotype in which a low hypodiploid cell line (38 chromosomes) was identified in 17/19 cells studied.
  • The abnormal cell line retained the extra constitutional chromosome 21.
  • Low hypodiploidy, associated with a high risk of relapse, is rare in pediatric ALL cases in the general population, and, to our knowledge, is previously unreported in patients with trisomy 21.
  • [MeSH-major] Burkitt Lymphoma / genetics. Diploidy. Down Syndrome / genetics

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  • (PMID = 16875938.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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56. Peterson MR, Noskoviak KJ, Newbury R: CD5-positive B-cell acute lymphoblastic leukemia. Pediatr Dev Pathol; 2007 Jan-Feb;10(1):41-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD5-positive B-cell acute lymphoblastic leukemia.
  • CD5-positive B-cell acute lymphoblastic leukemia (ALL) is an exceedingly rare entity, with only a single case report in the literature.
  • We report 2 additional cases of CD5-positive B-cell ALL in a 16-year-old male and a 15-year-old female.
  • Cytogenetic analysis of the 2nd case revealed trisomy 22, the 1st time this finding has been reported in ALL.
  • We conclude that CD5-positive B-cell ALL is a rare, aggressive malignancy with a poor prognosis that presents in adolescence.
  • Pathologists and clinicians should be aware of this entity to avoid confusion with other small blue-cell tumors.
  • [MeSH-major] Antigens, CD5 / metabolism. Biomarkers, Tumor / analysis. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology
  • [MeSH-minor] Adolescent. Antigens, CD / metabolism. Biopsy. Bone Marrow / pathology. Bone Marrow / surgery. Diagnosis, Differential. Diagnostic Errors. Female. Flow Cytometry. Humans. Immunohistochemistry. Leukemia / pathology. Lymphoma / pathology. Male. Prognosis. Sarcoma / pathology

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  • (PMID = 17378623.001).
  • [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 / Antigens, CD; 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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57. Wehrli LA, Braun J, Buetti LN, Hagleitner N, Hengartner H, Kühne T, Lüer S, Ozsahin H, Popovic MB, Niggli FK, Betts DR, Bourquin JP: Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2009 Feb;189(1):29-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-classical karyotypic features in relapsed childhood B-cell precursor acute lymphoblastic leukemia.
  • Karyotype analysis of acute lymphoblastic leukemia (ALL) at diagnosis has provided valuable prognostic markers for treatment stratification.
  • However, reports of cytogenetic studies of relapsed ALL samples are limited.
  • We compared the karyotypes from 436 nonselected B-cell precursor ALL patients at initial diagnosis and of 76 patients at first relapse.
  • We noticed a relative increase of karyotypes that did not fall into the classic ALL cytogenetic subgroups (high hyperdiploidy, t(12;21), t(9;22), 11q23, t(1;19), <45 chromosomes) in a group of 29 patients at relapse (38%) compared to 130 patients at presentation (30%).
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Child. Child, Preschool. Chromosome Aberrations. Female. Humans. Infant. Karyotyping. Male. Recurrence. Translocation, Genetic. Treatment Outcome


58. Yoda A, Yoda Y, Chiaretti S, Bar-Natan M, Mani K, Rodig SJ, West N, Xiao Y, Brown JR, Mitsiades C, Sattler M, Kutok JL, DeAngelo DJ, Wadleigh M, Piciocchi A, Dal Cin P, Bradner JE, Griffin JD, Anderson KC, Stone RM, Ritz J, Foà R, Aster JC, Frank DA, Weinstock DM: Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Jan 5;107(1):252-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional screening identifies CRLF2 in precursor B-cell acute lymphoblastic leukemia.
  • The prognosis for adults with precursor B-cell acute lymphoblastic leukemia (B-ALL) remains poor, in part from a lack of therapeutic targets.
  • We identified the type I cytokine receptor subunit CRLF2 in a functional screen for B-ALL-derived mRNA transcripts that can substitute for IL3 signaling.
  • We demonstrate that CRLF2 is overexpressed in approximately 15% of adult and high-risk pediatric B-ALL that lack MLL, TCF3, TEL, and BCR/ABL rearrangements, but not in B-ALL with these rearrangements or other lymphoid malignancies.
  • In a subset of cases, CRLF2 harbors a Phe232Cys gain-of-function mutation that promotes constitutive dimerization and cytokine independent growth.
  • Finally, cells dependent on CRLF2 signaling are sensitive to small molecule inhibitors of either JAKs or protein kinase C family kinases.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Cytokine / genetics. Signal Transduction / physiology


59. Troeger A, Siepermann M, Escherich G, Meisel R, Willers R, Gudowius S, Moritz T, Laws HJ, Hanenberg H, Goebel U, Janka-Schaub GE, Mahotka C, Dilloo D: Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia. Haematologica; 2007 Aug;92(8):1043-50
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  • [Title] Survivin and its prognostic significance in pediatric acute B-cell precursor lymphoblastic leukemia.
  • BACKGROUND AND OBJECTIVES: Impaired apoptosis, mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin, is thought to contribute to leukemic cell survival.
  • In contrast to low expression of survivin in normal differentiated adult tissues, very high levels of survivin have been described in a number of different tumors.
  • Overexpression of survivin was found to correlate with poor prognosis in a variety of cancers including hematologic malignancies.
  • To date, however, there is no information available on the prognostic role of survivin in pediatric precursor B-cell acute lymphocytic leukemia (BCP-ALL), the most frequent malignancy in childhood.
  • DESIGN AND METHODS: In a retrospective study including 66 pediatric patients we analyzed the impact of survivin protein levels on outcome in BCP-ALL.
  • RESULTS: Survivin overexpression, with an up to ten-fold increase of the normal level, was detected in 65% of the leukemic samples in contrast to negligible expression in non-malignant hematopoietic cells.
  • However, patients suffering relapse of disease or death had significantly higher survivin expression than those with a favorable outcome.
  • Overexpression of survivin is a significant prognostic marker for 3 year relapse free, event-free and overall survival, again independent of the established prognostic factors in ALL, such as age and leukocyte count at diagnosis as assessed in multivariate analysis.
  • Upon confirmation in a prospective analysis, survivin expression may, in the future, serve to further refine treatment stratification with intensification of therapy in those patients prone to relapse.
  • [MeSH-major] Inhibitor of Apoptosis Proteins / analysis. Microtubule-Associated Proteins / analysis. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism
  • [MeSH-minor] Adolescent. Apoptosis. Bone Marrow / pathology. Child. Child, Preschool. Cohort Studies. Disease-Free Survival. Female. Gene Expression Regulation, Leukemic. Humans. Infant. Kaplan-Meier Estimate. Male. Neoplastic Stem Cells / pathology. Prognosis. Retrospective Studies. Statistics, Nonparametric. Survival Analysis. Treatment Outcome

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  • (PMID = 17640858.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins
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60. Imataki O, Ohnishi H, Yamaoka G, Arai T, Kitanaka A, Kubota Y, Kushida Y, Ishida T, Tanaka T: Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse. Int J Clin Oncol; 2010 Feb;15(1):112-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lineage switch from precursor B cell acute lymphoblastic leukemia to acute monocytic leukemia at relapse.
  • A lineage switch in leukemia, in which the leukemic cell lineage at onset converts to another lineage at a later time, is an uncommon type of hybrid (mixed) leukemia regarded as a variation of bilineage leukemia.
  • We present a case of a 60-year-old female diagnosed with precursor B cell acute lymphoblastic leukemia (ALL), whose markers in flow cytometry shifted from their original status of CD19+, 22+, 79a+, 13+, HLA-DR+, and TdT+.
  • Although her bone marrow achieved remission after induction therapy, there was a small residual population of leukemic cells in the liver.
  • Residual disease was proved by biopsy and pathologically shown to have an immature phenotype of CD5+, CD10-, CD20-, CD79a- and myeloperoxidase negativity.
  • Two weeks after liver biopsy, blast cells progressively appeared in the peripheral blood; these cells had a monocytoid morphology and phenotype (CD13, 14) but were accompanied by myeloid (CD33) and lymphoid (CD2, 4, 20) cells.
  • This phenotypical conversion from B-ALL to hybrid leukemia featuring monocytoid characteristics is known as a lineage switch.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / pathology. Leukemia, Monocytic, Acute / pathology. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Biomarkers, Tumor / blood. Bone Marrow / pathology. Cell Lineage. Female. Humans. Immunophenotyping. Middle Aged. Recurrence

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  • (PMID = 20066454.001).
  • [ISSN] 1437-7772
  • [Journal-full-title] International journal of clinical oncology
  • [ISO-abbreviation] Int. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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61. Signer RA, Montecino-Rodriguez E, Witte ON, Dorshkind K: Immature B-cell progenitors survive oncogenic stress and efficiently initiate Ph+ B-acute lymphoblastic leukemia. Blood; 2010 Oct 7;116(14):2522-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immature B-cell progenitors survive oncogenic stress and efficiently initiate Ph+ B-acute lymphoblastic leukemia.
  • Philadelphia chromosome-positive (Ph(+)) B-acute lymphoblastic leukemia (B-ALL) can initiate in committed B-cell progenitors.
  • However, the stages of B-cell differentiation in which disease can initiate and the efficiency with which this occurs are unclear.
  • We now demonstrate that B-cell progenitors, up to and including the pro-B cell, efficiently initiate Ph(+) B-ALL.
  • However, cells at the pre-B-cell stage of development did not initiate disease.
  • We show that this difference in leukemia initiating potential is due to the level at which the Arf tumor suppressor gene is induced in specific stages of B lymphopoiesis.
  • Whereas immature B-cell progenitors survive the relatively low levels of Arf that are induced after oncogene expression, pre-B cells express the tumor suppressor gene at high levels and undergo massive apoptosis.
  • These data demonstrate that the molecular events that control Ph(+) B-ALL initiation and tumor suppression in the B-cell lineage are developmentally regulated.

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  • (PMID = 20562326.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-16042; United States / NIA NIH HHS / AG / R01 AG021450; United States / NIAID NIH HHS / AI / AI-28697; United States / NCI NIH HHS / CA / P30 CA016042; United States / NIAID NIH HHS / AI / R01 AI021256; United States / NIAID NIH HHS / AI / P30 AI028697; United States / Howard Hughes Medical Institute / / ; United States / NIA NIH HHS / AG / AG021450; United States / NIAID NIH HHS / AI / AI21256; United States / NIAID NIH HHS / AI / R37 AI021256
  • [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 / Cdkn2a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p16
  • [Other-IDs] NLM/ PMC2953887
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62. Gobbi G, Mirandola P, Malinverno C, Sponzilli I, Carubbi C, Ricci F, Binazzi R, Basso G, Giuliani-Piccari G, Ramazzotti G, Pasquantonio G, Cocco L, Vitale M: Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin. Int J Oncol; 2008 Aug;33(2):371-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant expression of B203.13 antigen in acute lymphoid leukemia of B-cell origin.
  • The B203.13 monoclonal antibody was developed by immunizing mice with the B/monocyte biphenotypic cell line B1b.
  • During normal hematopoiesis B203.13 is expressed on a fraction of CD34+ cells, while on mature cells it is only present on B-lymphocytes.
  • We tested this antibody as a marker of childhood B-acute lymphoblastic leukemia (B-ALL).
  • The CD10(+)/B203.13(+) phenotype was specific to B-ALL, since CD10(+)/CD20(+) cells from common acute lymphoblastic leukemia (c-ALL) did not express B203.13.
  • We concluded that the use of B203.13 in association with CD10 and CD20 provides meaningful information for distinguishing normal residual B-cells from leukemic B-lymphoblasts and that recurrence of a CD10(+)/B203.13(+) phenotype after transplantation may be a very early relapse indicator of early B-acute lymphoblastic leukemia.
  • [MeSH-major] Antigens, Neoplasm / biosynthesis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

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  • (PMID = 18636158.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Antigens, Neoplasm; EC 3.4.24.11 / Neprilysin
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63. Vanura K, Vrsalovic MM, Le T, Marculescu R, Kusec R, Jäger U, Nadel B: V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2009 Aug;48(8):725-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.
  • Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

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  • (PMID = 19455608.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases
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64. Novoa V, Nuñez N, Cervellini M, Starosta A, Carballo OG: [Presence of B cell clones in acute myelomonocytic leukemia]. Medicina (B Aires); 2010;70(2):163-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Presence of B cell clones in acute myelomonocytic leukemia].
  • [Transliterated title] Hallazgo de células clonales B en leucemia mielomonocítica aguda.
  • The coexistence of acute myeloid leukemia and chronic lymphocytic leukemia in the same patient is rare.
  • The majority of the cases correspond to patients that developed acute leukemia during the evolutionary course of a chronic lymphatic leukemia following treatment with chemotherapy drugs.
  • We report a case of acute myelomonocytic leukemia concurrent with untreated B-cell chronic lymphocytic leukemia in which the use of flow cytometry analysis with a large panel of monoclonal antibodies, allowed the demonstration of different pathological populations and determine immunophenotyping patterns.
  • Published cases of simultaneous chronic lymphocytic leukemia and acute leukemia are reviewed.
  • The use of multiparametric flow cytometry to differentiate the populations demonstrates the utility of this technology in the diagnosis of these hematological malignancies.
  • [MeSH-major] Antibodies, Monoclonal / analysis. B-Lymphocytes / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemia, Myelomonocytic, Acute / pathology. Neoplasms, Multiple Primary / pathology

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  • (PMID = 20447900.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
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65. Healy J, Richer C, Bourgey M, Kritikou EA, Sinnett D: Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia. Haematologica; 2010 Sep;95(9):1608-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Replication analysis confirms the association of ARID5B with childhood B-cell acute lymphoblastic leukemia.
  • Although childhood acute lymphoblastic leukemia is the most common pediatric cancer, its etiology remains poorly understood.
  • In an attempt to replicate the findings of 2 recent genome-wide association studies in a French-Canadian cohort, we confirmed the association of 5 SNPs [rs7073837 (P=4.2 x 10(-4)), rs10994982 (P=3.8 x 10(-4)), rs10740055 (P=1.6 x 10(-5)), rs10821936 (P=1.7 x 10(-7)) and rs7089424 (P=3.6 x 10(-7))] in the ARID5B gene with childhood acute lymphoblastic leukemia.
  • We also confirmed a selective effect for B-cell acute lymphoblastic leukemia with hyperdiploidy and report a putative gender-specific effect of ARID5B SNPs on acute lymphoblastic leukemia risk in males.
  • This study provides a strong rationale for more detailed analysis to identify the causal variants at this locus and to better understand the overall functional contribution of ARID5B to childhood acute lymphoblastic leukemia susceptibility.

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  • (PMID = 20460642.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ARID5B protein, human; 0 / DNA-Binding Proteins; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2930966
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66. Senadhi V, Emuron D, Gupta R: Acute hepatitis A induction of precursor B-cell acute lymphoblastic leukemia: a causal relationship? Case Rep Oncol; 2010 Sep;3(3):505-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute hepatitis A induction of precursor B-cell acute lymphoblastic leukemia: a causal relationship?
  • BACKGROUND: Precursor B-cell acute lymphoblastic leukemia accounts for 2% of all lymphoid neoplasms in the United States and occurs most frequently in childhood, but can also occur in adults with a median age of 39 years.
  • CASE REPORT: We present a case of a 51-year-old Caucasian female with the development of precursor B-cell acute lymphoblastic leukemia after suffering acute hepatitis A 4 weeks prior to her diagnosis.
  • CONCLUSION: Nonspecific viral transformation of bone marrow has been discussed in the literature, but we specifically describe hepatitis A-induced adult-onset precursor B-cell acute lymphoblastic leukemia, which is the first reported case in the literature.

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  • (PMID = 21611106.001).
  • [ISSN] 1662-6575
  • [Journal-full-title] Case reports in oncology
  • [ISO-abbreviation] Case Rep Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Other-IDs] NLM/ PMC3100275
  • [Keywords] NOTNLM ; Acute hepatitis A / Adult-onset ALL / Epstein-Barr virus / Hepatitis A-induced aplastic anemia / Precursor B-cell acute lymphoblastic leukemia
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67. Chatterton Z, Morenos L, Saffery R, Craig JM, Ashley D, Wong NC: DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia. Epigenomics; 2010 Oct;2(5):697-708
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation and miRNA expression profiling in childhood B-cell acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is the most common cancer in children in the modern world.
  • Recent efforts in characterizing the genetic contribution to this disease through uncovering gene mutations, deletions and structural variation by genome-scale methods have only accounted for a modest proportion of children with ALL.
  • [MeSH-major] DNA Methylation / physiology. Epigenesis, Genetic / physiology. High-Throughput Screening Assays / methods. MicroRNAs / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

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  • (PMID = 22122053.001).
  • [ISSN] 1750-192X
  • [Journal-full-title] Epigenomics
  • [ISO-abbreviation] Epigenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs
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68. Nowak NJ, Sait SN, Zeidan A, Deeb G, Gaile D, Liu S, Ford L, Wallace PK, Wang ES, Wetzler M: Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2010 May;199(1):15-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recurrent deletion of 9q34 in adult normal karyotype precursor B-cell acute lymphoblastic leukemia.
  • The prognosis of adult normal karyotype (NK) precursor B-cell acute lymphoblastic leukemia (B-ALL) has not improved over the last decade, mainly because separation into distinct molecular subsets has been lacking and no targeted treatments are available.

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20417863.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016056; None / None / / P30 CA016056-33; United States / NCI NIH HHS / CA / CA16056; United States / NCI NIH HHS / CA / P30 CA016056-33
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Homeodomain Proteins; 157907-48-7 / HoxA protein
  • [Other-IDs] NLM/ NIHMS173834; NLM/ PMC2862995
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69. Diffner E, Gauffin F, Anagnostaki L, Nordgren A, Gustafsson B, Sander B, Gustafsson B, Persson JL: Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry. J Pediatr Hematol Oncol; 2009 Sep;31(9):696-701
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of VEGF and VEGF receptors in childhood precursor B-cell acute lymphoblastic leukemia evaluated by immunohistochemistry.
  • We investigated the expression and clinical importance of VEGF and two of its receptors, VEGFR-1 and VEGFR-2, in childhood precursor B-cell acute lymphoblastic leukemia (pre-B ALL) by using immunohistochemistry.
  • [MeSH-major] Immunoenzyme Techniques. Neoplasm Proteins / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Vascular Endothelial Growth Factor A / analysis. Vascular Endothelial Growth Factor Receptor-1 / analysis. Vascular Endothelial Growth Factor Receptor-2 / analysis

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  • (PMID = 19707156.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
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70. Wandroo F, Bell A, Darbyshire P, Pratt G, Stankovic T, Gordon J, Lawson S, Moss P: ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia. Int J Lab Hematol; 2008 Apr;30(2):149-57
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ZAP-70 is highly expressed in most cases of childhood pre-B cell acute lymphoblastic leukemia.
  • The tyrosine kinase ZAP-70 plays a critical role in signal transduction in T cells and NK cells but has limited expression in primary human B cells.
  • ZAP-70 is, however, expressed in adult B cell chronic lymphocytic leukemia where it correlates with a poor prognosis.
  • We wished to determine if ZAP-70 is also expressed in pediatric B cell malignancy.
  • A quantitative PCR assay for ZAP-70 expression was established and ZAP-70 expression in a range of human B cell lines was compared with expression in the Jurkat T cell line.
  • ZAP-70 expression was then determined in bone marrow lymphoblasts obtained from 12 patients with pre-B cell acute lymphoblastic leukemia (ALL).
  • ZAP-70 expression was not detected in mature B cell lines but was detected in pre-B cell lines at a level comparable to that seen in T cells.
  • ZAP-70 expression was strongly expressed in nine of the 12 cases of primary pre-B cell lymphoblastic leukemia.
  • The T cell-associated protein kinase ZAP-70 is highly expressed in pre-B lineage cells and most cases of pre-B acute lymphoblastic leukemia.
  • ZAP-70 expression may hold prognostic value for pre-B ALL and raises the prospect of a novel therapeutic target.
  • [MeSH-major] B-Lymphocytes / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cells, B-Lymphoid / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism
  • [MeSH-minor] Adolescent. Blotting, Western. Bone Marrow Cells / metabolism. Cell Line, Transformed. Cell Line, Tumor. Child. Child, Preschool. Female. Flow Cytometry. Gene Expression. Humans. Jurkat Cells. Male. Polymerase Chain Reaction

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  • (PMID = 18333847.001).
  • [ISSN] 1751-5521
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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71. Jeha S, Behm F, Pei D, Sandlund JT, Ribeiro RC, Razzouk BI, Rubnitz JE, Hijiya N, Howard SC, Cheng C, Pui CH: Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia. Blood; 2006 Nov 15;108(10):3302-4
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of CD20 expression in childhood B-cell precursor acute lymphoblastic leukemia.
  • CD20 expression is associated with inferior survival in adults with acute lymphoblastic leukemia (ALL).
  • We analyzed the prognostic impact of CD20 expression in 353 children with B-cell precursor ALL treated in 3 consecutive St Jude Total Therapy studies.
  • There was no association between CD20 expression and E2A-PBX, TEL-AML1, ploidy, white blood cell count at diagnosis, or sex.

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  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
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  • (PMID = 16896151.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765
  • [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 / Antigens, CD20
  • [Other-IDs] NLM/ PMC1895438
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72. Gruber TA, Chang MS, Sposto R, Müschen M: Activation-induced cytidine deaminase accelerates clonal evolution in BCR-ABL1-driven B-cell lineage acute lymphoblastic leukemia. Cancer Res; 2010 Oct 1;70(19):7411-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activation-induced cytidine deaminase accelerates clonal evolution in BCR-ABL1-driven B-cell lineage acute lymphoblastic leukemia.
  • Occasionally, AID can target non-Ig genes and thereby promote GC B-cell lymphomagenesis.
  • We recently showed that the oncogenic BCR-ABL1 kinase induces aberrant expression of AID in pre-B acute lymphoblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis.
  • To elucidate the biological significance of aberrant AID expression, we studied loss of AID function in a murine model of BCR-ABL1 ALL.
  • Mice transplanted with BCR-ABL1-transduced AID(-/-) bone marrow had prolonged survival compared with mice transplanted with leukemia cells generated from AID(+/+) bone marrow.
  • Consistent with a causative role of AID in genetic instability, AID(-/-) leukemia had a lower frequency of amplifications and deletions and a lower frequency of mutations in non-Ig genes, including Pax5 and Rhoh compared with AID(+/+) leukemias.

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  • [Copyright] © 2010 AACR.
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  • (PMID = 20876806.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32CA09659; United States / NCI NIH HHS / CA / T32 CA009659; United States / NCI NIH HHS / CA / R21 CA152497; United States / NCI NIH HHS / CA / R21CA152497; United States / NCI NIH HHS / CA / R01CA137060; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / src-Family Kinases; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
  • [Other-IDs] NLM/ NIHMS228027; NLM/ PMC2948648
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73. Tchinda J, Volpert S, Berdel WE, Büchner T, Horst J: Novel three-break rearrangement and cryptic translocations leading to colocalization of MYC and IGH signals in B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2006 Mar;165(2):180-4
Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel three-break rearrangement and cryptic translocations leading to colocalization of MYC and IGH signals in B-cell acute lymphoblastic leukemia.
  • Reciprocal translocations involving the MYC locus and immunoglobulin heavy chain (IGH) and light chain (IgK and IgL) loci are characteristic for non-Hodgkin lymphomas, especially Burkitt lymphoma, and have been described in B-cell acute lymphoblastic leukemia (B-ALL).
  • We report on a case of B-ALL of L3 morphology with MYC-IGH translocation.
  • Additionally to other chromosome changes, a three-break rearrangement involving 6p21, 8q24, and 14q32, as well as cryptic translocations of IGH locus to MYC locus were detected.
  • To our knowledge, this is the first case with colocalizations of MYC and IGH in a three-break rearrangement involving 6p21 and on an additional derivative chromosome as results of cryptic translocations.
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Rearrangement. Genes, myc. Immunoglobulin Heavy Chains / genetics. Translocation, Genetic

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  • (PMID = 16527615.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains
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74. Maury S, Huguet F, Leguay T, Lacombe F, Maynadié M, Girard S, de Labarthe A, Kuhlein E, Raffoux E, Thomas X, Chevallier P, Buzyn A, Delannoy A, Chalandon Y, Vernant JP, Rousselot P, Macintyre E, Ifrah N, Dombret H, Béné MC, Group for Research on Adult Acute Lymphoblastic Leukemia: Adverse prognostic significance of CD20 expression in adults with Philadelphia chromosome-negative B-cell precursor acute lymphoblastic leukemia. Haematologica; 2010 Feb;95(2):324-8
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adverse prognostic significance of CD20 expression in adults with Philadelphia chromosome-negative B-cell precursor acute lymphoblastic leukemia.
  • The prognostic significance of CD20 expression in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) has been mostly studied in children and yielded conflicting results.
  • Notably, the negative impact of CD20 expression on CIR was only observed in patients with a white blood cell count (WBC) over 30x10(9)/L (P=0.006), while not in those with a lower WBC.
  • ClinicalTrials.gov ID, NCT00222027.
  • [MeSH-major] Antigens, CD20 / genetics. Gene Expression. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Clinical Trials as Topic. Humans. Leukocyte Count. Middle Aged. Philadelphia Chromosome. Prognosis. Recurrence. Young Adult

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  • (PMID = 19773266.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00222027
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD20
  • [Other-IDs] NLM/ PMC2817037
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75. Gaipa G, Basso G, Aliprandi S, Migliavacca M, Vallinoto C, Maglia O, Faini A, Veltroni M, Husak D, Schumich A, Ratei R, Biondi A, Dworzak MN, I-BFM-ALL-FCM-MRD-Study Group: Prednisone induces immunophenotypic modulation of CD10 and CD34 in nonapoptotic B-cell precursor acute lymphoblastic leukemia cells. Cytometry B Clin Cytom; 2008 May;74(3):150-5
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prednisone induces immunophenotypic modulation of CD10 and CD34 in nonapoptotic B-cell precursor acute lymphoblastic leukemia cells.
  • BACKGROUND: Immunophenotypic modulation is induced by steroids in pediatric B-cell precursor acute lymphoblastic leukemia (BCP-ALL) patients during remission induction therapy.
  • RESULTS: Leukemia samples that sustained the treatment in vitro with prednisone, showed significative reduction of CD10 and CD34 expression compared with control, and it was comparable with that observed in residual leukemic cells of the same patients in BM at day 15 of treatment.
  • [MeSH-major] Antigens, CD34 / metabolism. Neprilysin / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / drug effects. Precursor Cells, B-Lymphoid / immunology. Prednisone / pharmacology
  • [MeSH-minor] Adolescent. Cell Culture Techniques. Child. Child, Preschool. Female. Flow Cytometry. Humans. Immunophenotyping. Infant. Male. Remission Induction

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  • [Copyright] (c) 2008 Clinical Cytometry Society
  • (PMID = 18271020.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; EC 3.4.24.11 / Neprilysin; VB0R961HZT / Prednisone
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76. Prabhu S, Gottlieb DJ, Varikatt W, St Heaps L, Diaz S, Smith A: Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones. Cancer Genet Cytogenet; 2010 Aug;201(1):24-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult B-cell acute lymphoblastic leukemia with two unrelated abnormal cytogenetic clones.
  • The presence of two different abnormal cell lines at diagnosis in hematologic malignancies is rare and raises the question of etiology and pathogenesis--two separate malignant lineages occurring together or a common stem cell malignancy?
  • We present a 64-year-old woman who was evaluated for low platelet count and peripheral blasts.
  • On the basis of the morphology, flow cytometry, and lack of myeloid-associated markers, a diagnosis of precursor B-cell acute lymphoblastic leukemia (B-ALL) was made.
  • The dic(7;9) is a rare but recurrent abnormality in B-ALL, while trisomy 8 as a sole abnormality is most commonly associated with myeloid malignancies.
  • After standard treatment for B-ALL, BM cytogenetic analysis showed disappearance of the dic(7;9) cell line but persistence of cells with trisomy 8.
  • [MeSH-major] Leukemia, B-Cell / genetics

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  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20633764.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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77. Jakab K, Gopcsa L, Adam E, Domjan G, Sarkadi B, Paloczi K: Application of flow cytometry immunophenotyping and multidrug resistance assay in B-cell acute lymphoid leukemia and multiple myeloma. Neoplasma; 2005;52(1):36-42
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  • [Title] Application of flow cytometry immunophenotyping and multidrug resistance assay in B-cell acute lymphoid leukemia and multiple myeloma.
  • In this study we aimed to evaluate and compare the drug resistance in B-cell acute lymphoid leukemia (B-ALL) and multiple myeloma (MM) in association with their immunophenotypes and genotypes.
  • Markers CD19, CD20 and HLA-DR proved to be useful in identifying cells of B-lymphoid lineage.
  • CD34 progenitor cell antigen was present in high proportion of ALL blasts.
  • However, the mean MRP-1 values in MM were significantly lower than MAF-MDR-1 (1.85+/-3.8 versus 5.92+/-7.45, p=0.05), but we have found lower values in refractory conditions as expected from previous studies of acute myeloid leukemia.
  • The low activity of MDR- 1 and MRP-1 in MM need further clarification, indicating the involvement of different transport in the resistance mechanism.
  • [MeSH-major] Biomarkers, Tumor / analysis. Burkitt Lymphoma / drug therapy. Burkitt Lymphoma / genetics. Drug Resistance, Multiple. Multiple Myeloma / drug therapy. Multiple Myeloma / genetics

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  • (PMID = 15739024.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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78. Bernaldez-Rios R, Ortega-Alvarez MC, Perez-Saldivar ML, Alatoma-Medina NE, Del Campo-Martinez Mde L, Rodriguez-Zepeda Mdel C, Montero-Ponce I, Franco-Ornelas S, Fernandez-Castillo G, Nuñez-Villegas NN, Taboada-Flores MA, Flores-Lujano J, Argüelles-Sanchez ME, Juarez-Ocaña S, Fajardo-Gutierrez A, Mejia-Arangure JM: The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City. J Pediatr Hematol Oncol; 2008 Mar;30(3):199-203
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The age incidence of childhood B-cell precursor acute lymphoblastic leukemia in Mexico City.
  • The objective of this population-based survey was to assess the peak age of incidence of B-cell precursor acute lymphoblastic leukemia (ALL) in children in Mexico City (MC).
  • All patients were classified according to their immunophenotype, and only B-cell precursor and T-lineage were analyzed.
  • The frequency of B-cell precursor ALL was 76.1%, whereas T lineage ALL showed a frequency of 23.6%.
  • B-cell precursor ALL was the major contributor to peak age; T lineage ALL showed a peak among 1 and 3 years of age.
  • We conclude that the age peak for children with ALL in MC is within the ranges reported for developed countries and that B-cell precursor ALL is the main contributor to these peak.
  • [MeSH-major] Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / epidemiology

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  • (PMID = 18376281.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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79. DiGiuseppe JA, Fuller SG, Borowitz MJ: Overexpression of CD49f in precursor B-cell acute lymphoblastic leukemia: potential usefulness in minimal residual disease detection. Cytometry B Clin Cytom; 2009 Mar;76(2):150-5
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  • [Title] Overexpression of CD49f in precursor B-cell acute lymphoblastic leukemia: potential usefulness in minimal residual disease detection.
  • BACKGROUND: The persistence of minimal residual disease (MRD) following therapy is an established prognostic factor in precursor B-cell acute lymphoblastic leukemia (pB-ALL).
  • Detection of MRD in pB-ALL by flow cytometric immunophenotyping requires demonstration of abnormal antigen expression in leukemic B-cell precursors relative to that of normal B-cell precursors.
  • The gene encoding CD49f (integrin alpha-6) is one of several whose overexpression in pB-ALL at diagnosis has been associated with the subsequent detection of MRD.
  • METHODS: We evaluated CD49f expression by 4-color flow cytometry in normal B-cell precursors, and in a series of cases of pB-ALL, both at diagnosis and at intervals following the initiation of therapy.
  • RESULTS: In 10 control marrow samples, CD49f was undetectable or extremely dim in all but a minor subset of normal CD19+ B-lineage cells, whereas in 11 of 15 cases (73%) of pB-ALL, CD49f was moderate or bright at diagnosis, and persisted or became brighter after initiation of therapy.
  • Of the four pB-ALL cases in which CD49f was undetectable or dim at diagnosis, MRD was detected in two; in one of these, CD49f expression was substantially increased in the leukemic cells that persisted following initiation of therapy.
  • [MeSH-major] Flow Cytometry / methods. Integrin alpha6 / analysis. Integrin alpha6 / blood. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cells, B-Lymphoid / immunology
  • [MeSH-minor] Adolescent. Age Factors. B-Lymphocytes / immunology. B-Lymphocytes / metabolism. Biomarkers / analysis. Biomarkers / blood. Child. Child, Preschool. Female. Humans. Immunophenotyping / methods. Infant. Male. Neoplasm Recurrence, Local / blood. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / immunology. Neoplasm, Residual. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Predictive Value of Tests. Prognosis. Young Adult

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  • [Copyright] 2008 Clinical Cytometry Society.
  • (PMID = 18831072.001).
  • [ISSN] 1552-4957
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Integrin alpha6
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80. Tie LJ, Gu LJ, Chen J, Jiang LM, Dong L, Pan C, Ye H, Song DL, Xue HL, Tang JY, Wang YP, Chen J: [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia]. Zhonghua Xue Ye Xue Za Zhi; 2006 Feb;27(2):120-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Prognostic value of minimal residual disease in childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To assess the prognostic value of minimal residual disease (MRD) in childhood B-cell acute lymphoblastic leukemia (ALL) after induction chemotherapy.
  • MRD after induction therapy, before high-dose methotrexate and early intensification as well as at 1 year and 2 year maintenance therapy was detected by multiparameter-flow-cytometry (MP-FCM). RESULTS:.
  • (1) The probability of 39-month event-free survival (EFS) for patients with a level of MRD < 10(-4), was significantly higher than for those with a higher MRD [(83.00 +/- 9.90)% vs 0.00%, P < 0.01]. (2) Univariate analysis indicated that the MRD level at achieving complete remission (CR) had no relationship with the biologic features at presentation (gender, age, white blood cells and cytogenetic abnormalities), but did with Philadelphia chromosome, the time reaching CR, ALL-XH-99 risk group and lymphoblasts in bone marrow on day 19 after induction therapy (P < 0.05). (3) Multivariate analysis suggested that MRD level after the first induction course was an independent prognostic factor (hazard ratio, 5.381; 95% CI 0.004 to 0.624; P < 0.05).
  • CONCLUSION: The MRD level at achieving CR is one of important prognostic factor in the treatment of childhood B-cell ALL, and might be used to assess the early treatment response.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, B-Cell / drug therapy. Neoplasm, Residual

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  • (PMID = 16732969.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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81. Ye QD, Gu LJ, Tang JY, Xue HL, Chen J, Pan C, Chen J, Dong L, Zhou M, Jiang LM: [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Jun;10(3):333-6
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  • [Title] [Clinical importance of minimal residual disease testing in the therapy of childhood B-cell acute lymphoblastic leukemia].
  • OBJECTIVE: To study the role of minimal residual disease (MRD) in the evaluation of therapeutic effectiveness of childhood B-cell acute lymphoblastic leukemia (ALL).
  • METHODS: MRD testing was performed in 124 children with B-cell ALL, who were newly diagnosed and enrolled in the ALL-XH-99 treatment protocol from September 2001 to April 2005MRD was determined by 4-color flow cytometry in the different time points during the treatment period.
  • RESULTS: After induction therapy, 103, 13 and 8 patients showed MRD <0.01%, 0.01%-0.1% and >0.1%, respectively.
  • The 5-year relapse-free survival (RFS) in the patients with MRD <0.01%, 0.01%-0.1% and >0.1% was 88.9+/-3.9%, 70.0+/-14.5% and 0%, respectively and the 5-year event-free survival (EFS) was 82.4+/-4.4%, 21.2+/-18.0% and 0%, respectively.
  • There were significant differences in the RFS and EFS among the patients with different MRD levels (P<0.01).
  • Within half a year after induction remission, the 5-year RFS in patients with MRD negative (<0.01%) and positive was 87.7+/-4.1% and 58.3+/-14.2%, respectively (P<0.01) and the 5-year RFS was 80.7+/-4.6% and 25.6+/-13.8%, respectively (P<0.01).
  • After half a year with induction remission, the patients with MRD negative and positive also showed statistical differences in the 5-year RFS (92.0+/-3.6% vs 48.5+/-15.5%; P<0.01) and EFS (85.6+/-4.5% vs 21.4+/-11.0%; P<0.01).
  • Multivariate analysis confirmed that the MRD level after induction chemotherapy together with the reaction to prednisone, the bone marrow features on the 19th day of induction, and the fusion gene with BCR-ABL or MLL-AF4 had prognostic significance in childhood B-cell ALL.
  • CONCLUSIONS: The MRD level in the whole course of therapy is an important outcome indicator in childhood B cell ALL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Burkitt Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18554462.001).
  • [ISSN] 1008-8830
  • [Journal-full-title] Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
  • [ISO-abbreviation] Zhongguo Dang Dai Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
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82. Steere J, Perl A, Tomczak E, Bagg A: Large B-cell lymphoma masquerading as acute leukemia. J Clin Oncol; 2006 Apr 20;24(12):1950-1
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Large B-cell lymphoma masquerading as acute leukemia.
  • [MeSH-major] Leukemia / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Fatal Outcome. Flow Cytometry. Humans. Immunohistochemistry. Male

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  • (PMID = 16622271.001).
  • [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] Case Reports; Journal Article
  • [Publication-country] United States
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83. Kato I, Manabe A, Aoyama C, Kamiya T, Morimoto T, Matsufuji H, Suzuki K, Kitagawa Y, Hori T, Tsurusawa M, Kiyokawa N, Junichiro F, Hosoya R: Development of diffuse large B cell lymphoma during the maintenance therapy for B-lineage acute lymphoblastic leukemia. Pediatr Blood Cancer; 2007 Feb;48(2):230-2
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  • [Title] Development of diffuse large B cell lymphoma during the maintenance therapy for B-lineage acute lymphoblastic leukemia.
  • Non-Hodgkin lymphoma (NHL) is a very rare complication of acute lymphoblastic leukemia (ALL).
  • While he was receiving maintenance treatment 2 years and 9 months after the diagnosis of ALL, diffuse large B cell lymphoma (DLBL) was diagnosed from a biopsy of an abdominal mass.
  • [MeSH-major] Lymphoma, B-Cell / etiology. Lymphoma, Large B-Cell, Diffuse / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications


84. De Braekeleer E, Basinko A, Douet-Guilbert N, Morel F, Le Bris MJ, Berthou C, Morice P, Férec C, De Braekeleer M: Cytogenetics in pre-B and B-cell acute lymphoblastic leukemia: a study of 208 patients diagnosed between 1981 and 2008. Cancer Genet Cytogenet; 2010 Jul 1;200(1):8-15
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  • [Title] Cytogenetics in pre-B and B-cell acute lymphoblastic leukemia: a study of 208 patients diagnosed between 1981 and 2008.
  • The detection of chromosome abnormalities by conventional cytogenetics, now combined with analyses using fluorescence in situ hybridization (FISH), is an important component in assessing the risk stratification of acute lymphoblastic leukemia (ALL).
  • Identification of specific chromosome abnormalities led to the recognition of genetic subgroups based on modal chromosomal number, reciprocal translocations in B-cell ALL, or both.
  • We report here the cytogenetic analysis of 208 patients with pre-B and B-cell ALL referred to a single laboratory between 1981 and 2008.
  • Chromosome abnormalities were observed in 82.9% of L1/L2 ALL patients and in 83.3% of L3 patients with successful analysis at diagnosis.
  • Almost 17% of the patients studied at diagnosis had further cytogenetic analyses at relapse, the majority showing clonal evolution toward a more complex karyotype.
  • [MeSH-major] Chromosome Aberrations. Leukemia, B-Cell / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Histone-Lysine N-Methyltransferase. Humans. Middle Aged. Myeloid-Lymphoid Leukemia Protein / genetics. Recurrence. Time Factors. Translocation, Genetic

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  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20513528.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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85. Aleskog A, Larsson R, Höglund M, Kristensen J, Nygren P, Lindhagen E: In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia. Anticancer Drugs; 2005 Mar;16(3):277-83
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  • [Title] In vitro drug resistance in B cell chronic lymphocytic leukemia: a comparison with acute myelocytic and acute lymphocytic leukemia.
  • The aim of the study was to evaluate cellular drug resistance in B cell chronic lymphocytic leukemia (B-CLL) in vitro, and compare it with that in acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL).
  • In vitro drug resistance was analyzed by the fluorometric microculture cytotoxicity assay (FMCA) in all samples from patients with leukemia sent to our laboratory between 1992 and 2001.
  • Up to 14 standard drugs were evaluated in samples from 66 patients with B-CLL, 212 patients with AML and 80 patients with ALL.
  • B-CLL cells were found to be more sensitive than cells from both AML and ALL to cytarabine, cladribine, fludarabine, doxorubicin, idarubicin, vincristine and cyclophosphamide (p<0.05).
  • No difference in cellular drug resistance was found between B-CLL and ALL cells for prednisolone, whereas AML cells were more resistant (p<0.0001).
  • In B-CLL, cells from patients who had received previous chemotherapy were more resistant to almost all tested drugs as compared to cells from treatment-naive patients.
  • For all drugs, there was a good agreement between the activity in vitro and the known clinical disease-specific activity.
  • The study also demonstrated an acquired cellular drug resistance in B-CLL, but not in the acute leukemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy


86. Laille E, Ward R, Nasser A, Stoltz M, Cogle C, Gore S, Skikne BS, Garcia-Manero G: The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7087

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pharmacokinetics of azacitidine following subcutaneous treatment in patients with myelodysplastic syndromes (MDS) or acute myelogenous leukemia (AML).
  • : 7087 Background: 5-azacitidine (AZA), through its effects on DNA metabolism, gene expression, and cell differentiation, has proven beneficial in treatment of MDS and AML and AZA therapy significantly increases survival in higher-risk MDS and AML compared to conventional care.
  • Plasma PK of AZA are herein reported in patients receiving SC doses of 75 mg/m<sup>2</sup>.
  • METHODS: Adult patients with MDS or AML and ECOG status 0-2 were treated with 7 consecutive daily SC doses of 75 mg/m<sup>2</sup> AZA during their first treatment cycle.
  • The AUC<sub>inf</sub> after SC doses was 1170 hr*ng/mL.
  • The AZA concs declined in a pseudo bi-phasic manner with an elimination half-life of 1.25 hours.
  • AZA recovery in urine was very small relative to dose (<2%).
  • AZA was well tolerated and no unexpected toxicities were observed.
  • CONCLUSIONS: The AZA AUC<sub>inf</sub> after SC doses is similar to the published AUC value (1044 hr*ng/mL) after 75 mg/m<sup>2</sup> IV doses indicating approximating 100% systemic bioavailability.

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  • (PMID = 27961481.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Trageser D, Iacobucci I, Nahar R, Duy C, von Levetzow G, Klemm L, Park E, Schuh W, Gruber T, Herzog S, Kim YM, Hofmann WK, Li A, Storlazzi CT, Jäck HM, Groffen J, Martinelli G, Heisterkamp N, Jumaa H, Müschen M: Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function. J Exp Med; 2009 Aug 3;206(8):1739-53
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  • [Title] Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.
  • B cell lineage acute lymphoblastic leukemia (ALL) arises in virtually all cases from B cell precursors that are arrested at pre-B cell receptor-dependent stages.
  • Here, we demonstrate that the pre-B cell receptor functions as a tumor suppressor upstream of IKAROS through induction of cell cycle arrest in Ph(+) ALL cells.
  • Pre-B cell receptor-mediated cell cycle arrest in Ph(+) ALL cells critically depends on IKAROS function, and is reversed by coexpression of the dominant-negative IKAROS splice variant IK6.
  • IKAROS also promotes tumor suppression through cooperation with downstream molecules of the pre-B cell receptor signaling pathway, even if expression of the pre-B cell receptor itself is compromised.
  • In this case, IKAROS redirects oncogenic BCR-ABL1 tyrosine kinase signaling from SRC kinase-activation to SLP65, which functions as a critical tumor suppressor downstream of the pre-B cell receptor.
  • These findings provide a rationale for the surprisingly high frequency of IKAROS deletions in Ph(+) ALL and identify IKAROS-mediated cell cycle exit as the endpoint of an emerging pathway of pre-B cell receptor-mediated tumor suppression.

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  • (PMID = 19620627.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009659-16; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / T32 CA009659; United States / NCI NIH HHS / CA / R01 CA090321; United States / NCI NIH HHS / CA / R01CA090321; United States / NCI NIH HHS / CA / R21 CA152497; None / None / / R01 CA137060-02; None / None / / R01 CA139032-01; United States / NCI NIH HHS / CA / R01CA137060; United States / NCI NIH HHS / CA / R01 CA139032-02; None / None / / R01 CA139032-02; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA137060-02; United States / NCI NIH HHS / CA / R01 CA137060-01A1; None / None / / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060
  • [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 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / IKZF1 protein, human; 0 / Pre-B Cell Receptors; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC2722172
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88. Nahar R, Müschen M: Pre-B cell receptor signaling in acute lymphoblastic leukemia. Cell Cycle; 2009 Dec;8(23):3874-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pre-B cell receptor signaling in acute lymphoblastic leukemia.
  • B cell lineage ALL represents by far the most frequent malignancy in children and is also common in adults.
  • In a recent study on 111 cases of pre-B cell-derived human ALL, we found that ALL cells carrying a BCR-ABL1-gene rearrangement lack expression of a functional pre-B cell receptor in virtually all cases.
  • In a proof-of-principle experiment, we studied pre-B cell receptor function during progressive leukemic transformation of pre-B cells in BCR-ABL1-transgenic mice: Interestingly, signaling from the pre-B cell receptor and the oncogenic BCR-ABL1 kinase are mutually exclusive and only "crippled" pre-B cells that fail to express a functional pre-B cell receptor are permissive to transformation by BCR-ABL1.

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  • (PMID = 19901533.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA137606; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / R21 CA152497; None / None / / R01 CA139032-01; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / R01 CA137060-01A1; United States / NCI NIH HHS / CA / R01 CA139032; United States / NCI NIH HHS / CA / R01CA139032; United States / NCI NIH HHS / CA / R01 CA137060
  • [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 / ABI1 protein, human; 0 / Abi1 protein, mouse; 0 / Adaptor Proteins, Signal Transducing; 0 / B cell linker protein; 0 / Cytoskeletal Proteins; 0 / Pre-B Cell Receptors; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
  • [Other-IDs] NLM/ NIHMS230959; NLM/ PMC4047560
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89. Tassano E, Acquila M, Tavella E, Micalizzi C, Panarello C, Morerio C: MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Aug;49(8):682-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA-125b-1 and BLID upregulation resulting from a novel IGH translocation in childhood B-Cell precursor acute lymphoblastic leukemia.
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus are common abnormalities in mature B-cell neoplasms.
  • Recent findings have also revealed their significant role in B-cell precursor acute lymphoblastic leukemia.
  • In this study, we describe a pediatric case of B-cell precursor acute lymphoblastic leukemia showing microRNA-125b-1 (MIR125B1) and BLID gene overexpression, resulting from a novel t(11;14)(q24.1;q32) translocation involving IGH.
  • This is the first report describing the upregulation of a microRNA due to its juxtaposition to protein-coding gene regulatory elements and the overexpression of two neighboring genes as a consequence of transcriptional enhancers localized in the vicinity of the IGH gene.
  • [MeSH-major] BRCA2 Protein / genetics. Immunoglobulin Heavy Chains / genetics. MicroRNAs / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Apoptosis Regulatory Proteins. Child. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Female. Humans. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation

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  • (PMID = 20544842.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BLID protein, human; 0 / BRCA2 Protein; 0 / BRCA2 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / MIRN125 microRNA, human; 0 / MicroRNAs; 0 / RNA, Messenger
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90. Jakovljević G, Nakić M, Rogosić S, Kardum-Skelin I, Mrsić-Davidović S, Zadro R, Kruslin B: Pre-B-cell acute lymphoblastic leukemia with bulk extramedullary disease and chromosome 22 (EWSR1) rearrangement masquerading as Ewing sarcoma. Pediatr Blood Cancer; 2010 Apr;54(4):606-9
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  • [Title] Pre-B-cell acute lymphoblastic leukemia with bulk extramedullary disease and chromosome 22 (EWSR1) rearrangement masquerading as Ewing sarcoma.
  • After finding lymphoblasts in peripheral blood, the diagnosis of acute lymphoblastic leukemia was established.
  • The tissue was positive for immature B-cell markers and an immunoglobulin heavy chain gene rearrangement, which confirmed the final diagnosis of common type acute lymphoblastic leukemia with bulk extramedullary disease.
  • The patient was treated with chemotherapy and was in remission 30 months after the diagnosis.
  • [MeSH-major] Chromosomes, Human, Pair 22 / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Sarcoma, Ewing / diagnosis. Soft Tissue Neoplasms / diagnosis. Transcription Factors / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child, Preschool. Diagnosis, Differential. Female. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Proto-Oncogene Protein c-fli-1. RNA-Binding Protein EWS. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20049929.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / EWS-FLI fusion protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Protein c-fli-1; 0 / RNA-Binding Protein EWS; 0 / Transcription Factors
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91. Tembhare PR, Subramanian PG, Sehgal K, Yajamanam B, Kumar A, Gujral S: Hypergranular precursor B-cell acute lymphoblastic leukemia in a 16-year-old boy. Indian J Pathol Microbiol; 2009 Jul-Sep;52(3):421-3
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  • [Title] Hypergranular precursor B-cell acute lymphoblastic leukemia in a 16-year-old boy.
  • Presence of cytoplasmic granules in the blasts is a well known feature of myeloid leukemia.
  • ALL presenting with the numerous cytoplasmic granules in blasts is a rarity and may be misdiagnosed as acute myeloid leukemia.
  • We describe a rare case of hypergranular precursor B-cell acute lymphoblastic leukemia (ALL) in an adolescent male expressing CD10, CD19, CytoCD22, CD34, as well as CD13 and CD117.
  • In centers where immunophenotypic panel is usually decided on the basis of morphology with limited antibodies may result in an erroneous typing of such rare diseases.
  • Hence it is important to be aware of this rare entity and to confirm the lineage of acute leukemia by using a comprehensive panel of antibodies for immunophenotypic analysis.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cells, B-Lymphoid / pathology

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  • (PMID = 19679981.001).
  • [ISSN] 0974-5130
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 0 / Antigens, CD; EC 1.11.1.7 / Peroxidase; EC 3.1.3.2 / Acid Phosphatase
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92. Claviez A, Eckert C, Seeger K, Schrauder A, Schrappe M, Henze G, von Stackelberg A: Rituximab plus chemotherapy in children with relapsed or refractory CD20-positive B-cell precursor acute lymphoblastic leukemia. Haematologica; 2006 Feb;91(2):272-3
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  • [Title] Rituximab plus chemotherapy in children with relapsed or refractory CD20-positive B-cell precursor acute lymphoblastic leukemia.
  • We treated three children with relapsed or refractory CD20 positive B-cell precursor acute lymphoblastic leukemia with rituximab in combination with chemotherapy, which produced a decreasing or persistent low positive minimal residual disease load.
  • Two children subsequently underwent allogeneic stem cell transplantation and remain in complete remission at days +399 and +332.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Salvage Therapy / methods
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, CD20. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Hematopoietic Stem Cell Transplantation. Humans. Male. Rituximab. Treatment Outcome

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  • (PMID = 16461321.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab
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93. Ambati S, Chamyan G, Restrepo R, Escalon E, Fort J, Pefkarou A, Khatib ZA, Dehner LP: Rosai-Dorfman disease following bone marrow transplantation for pre-B cell acute lymphoblastic leukemia. Pediatr Blood Cancer; 2008 Sep;51(3):433-5
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  • [Title] Rosai-Dorfman disease following bone marrow transplantation for pre-B cell acute lymphoblastic leukemia.
  • A child with acute pre-B cell lymphoblastic leukemia underwent haploidentical bone marrow transplantation (BMT) after first relapse.
  • A biopsy of the presenting lesion demonstrated a polymorphous infiltrate composed predominantly of S-100 protein and CD68 immunoreactive histiocytic cells.
  • Together with the presence of emperipolesis, the process was interpreted as Rosai-Dorfman (R-D) disease.
  • Only one previous example of acute lymphoblastic leukemia in childhood has been reported with R-D disease.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Graft vs Host Disease / etiology. Histiocytosis, Sinus / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18493991.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD68 antigen, human; 0 / S100 Proteins
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94. Meloni-Ehrig AM, Tirado CA, Chen K, Jahn J, Suchan S, Scheerle J, Crosby MG, Meany H, Seibel N, Leitenberg D, Heritage DW, Mowrey PN: Isolated del(14)(q21) in a case of precursor B-cell acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2005 Aug;161(1):82-5
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  • [Title] Isolated del(14)(q21) in a case of precursor B-cell acute lymphoblastic leukemia.
  • We present a case of del(14)(q21) as a sole abnormality in a 4-year-old boy diagnosed with precursor B-cell acute lymphoblastic leukemia (pre-B ALL).
  • Both samples showed a del(14)(q21) as the only abnormality.
  • [MeSH-major] Chromosomes, Human, Pair 4 / genetics. Gene Deletion. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 16080963.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Immunoglobulin Heavy Chains; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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95. Stanciu-Herrera C, Morgan C, Herrera L: Anti-CD19 and anti-CD22 monoclonal antibodies increase the effectiveness of chemotherapy in Pre-B acute lymphoblastic leukemia cell lines. Leuk Res; 2008 Apr;32(4):625-32
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  • [Title] Anti-CD19 and anti-CD22 monoclonal antibodies increase the effectiveness of chemotherapy in Pre-B acute lymphoblastic leukemia cell lines.
  • The monoclonal antibodies (MAbs) HD37 and RFB4 bind to receptors on precursor B acute lymphoblastic leukemia (ALL) cells.
  • HD37 and not RFB4 increased the in vitro cytotoxicity of daunorubicin (DNR) and vincristine (VCR) in three Pre-B ALL cell lines.

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  • (PMID = 17706771.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA101897-04; United States / NCI NIH HHS / CA / K01 CA101897-04
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antigens, CD19; 0 / Antineoplastic Agents, Phytogenic; 0 / Sialic Acid Binding Ig-like Lectin 2; 5J49Q6B70F / Vincristine; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS42262; NLM/ PMC2276361
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96. Nishida H, Yamazaki H, Yamada T, Iwata S, Dang NH, Inukai T, Sugita K, Ikeda Y, Morimoto C: CD9 correlates with cancer stem cell potentials in human B-acute lymphoblastic leukemia cells. Biochem Biophys Res Commun; 2009 Apr 24;382(1):57-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD9 correlates with cancer stem cell potentials in human B-acute lymphoblastic leukemia cells.
  • Cancer stem cell (CSC) theory suggests that only a small subpopulation of cells having stem cell-like potentials can initiate tumor development.
  • While recent data on acute lymphoblastic leukemia (ALL) are conflicting, some studies have demonstrated the existence of such cells following CD34-targeted isolation of primary samples.
  • Although CD34 is a useful marker for the isolation of CSCs in leukemias, the identification of other specific markers besides CD34 has been relatively unsuccessful.
  • To identify new markers, we first performed extensive analysis of surface markers on several B-ALL cell lines.
  • Our data demonstrated that every B-ALL cell line tested did not express CD34 but certain lines contained cell populations with marked heterogeneity in marker expression.
  • Moreover, the CD9(+) cell population possessed stem cell characteristics within the clone, as demonstrated by in vitro and transplantation experiments.
  • [MeSH-major] Antigens, CD / biosynthesis. Antigens, Neoplasm / biosynthesis. Biomarkers, Tumor / biosynthesis. Membrane Glycoproteins / biosynthesis. Neoplastic Stem Cells / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Animals. Antigens, CD9. Cell Line, Tumor. Humans. Mice. Transplantation, Heterologous

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  • (PMID = 19254692.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD9; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CD9 protein, human; 0 / Cd9 protein, mouse; 0 / Membrane Glycoproteins
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97. Amare Kadam PS, Raje GC, Pais AP, Banavali S: Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL. Cancer Genet Cytogenet; 2008 Apr 1;182(1):27-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL.
  • Out of 76 pediatric cases of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) positive for ETV6/RUNX1 (previously TEL/AML1) resulting from t(12;21), 7 cases revealed coexistence of ETV6/RUNX1 and MLL aberrations.
  • ETV6/RUNX1 and MLL aberration clone size in these cases was suggestive of ETV6/RUNX1 as an early primary event, originating in the embryonic or infant stage and developing into leukemia by later acquisition of MLL aberration, ETV6 loss, and ETV6/RUNX1 duplication as secondary events.
  • We conclude that the cases with coexisting ETV6/RUNX1 and MLL aberrations probably exist as a small, hidden group of ETV6/RUNX1-positive BCP-ALL, which invites further investigation, in large series from different populations, to confirm the findings and establish the biological mechanisms and prognostic significance.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18328947.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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98. Dyer MJ, Akasaka T, Capasso M, Dusanjh P, Lee YF, Karran EL, Nagel I, Vater I, Cario G, Siebert R: Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers? Blood; 2010 Feb 25;115(8):1490-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers?
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus define common subgroups of B-cell lymphoma but are rare in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Recent fluorescent in situ hybridization and molecular cloning studies have identified several novel IGH translocations involving genes that play important roles in normal hemopoiesis, including the cytokine receptor genes CRLF2 and EPOR, all members of the CCAAT enhancer-binding protein gene family, as well as genes not normally expressed in hemopoietic cells including inhibitor of DNA binding 4.
  • Despite their rarity, IGH chromosomal translocations in BCP-ALL therefore define not only new mechanisms of B-cell transformation but also clinically important subgroups of disease and suggest new targeted therapeutic approaches.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Transformation, Neoplastic / metabolism. Immunoglobulin Heavy Chains / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Quantitative Trait Loci. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Animals. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic / genetics. Hematopoiesis / genetics. Humans. Inhibitor of Differentiation Proteins / biosynthesis. Inhibitor of Differentiation Proteins / genetics. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Prognosis. Receptors, Cytokine / biosynthesis. Receptors, Cytokine / genetics. Receptors, Erythropoietin / biosynthesis. Receptors, Erythropoietin / genetics

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  • (PMID = 20042721.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRLF2 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / ID4 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Inhibitor of Differentiation Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Cytokine; 0 / Receptors, Erythropoietin; 0 / TEL-AML1 fusion protein
  • [Number-of-references] 87
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99. Bachmann PS, Gorman R, Mackenzie KL, Lutze-Mann L, Lock RB: Dexamethasone resistance in B-cell precursor childhood acute lymphoblastic leukemia occurs downstream of ligand-induced nuclear translocation of the glucocorticoid receptor. Blood; 2005 Mar 15;105(6):2519-26
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dexamethasone resistance in B-cell precursor childhood acute lymphoblastic leukemia occurs downstream of ligand-induced nuclear translocation of the glucocorticoid receptor.
  • Glucocorticoids are among the most effective agents used in the treatment of childhood acute lymphoblastic leukemia (ALL), and patient response to treatment is an important determinant of long-term outcome.
  • Despite its clinical significance, the molecular basis of glucocorticoid resistance in lymphoid malignancies is still poorly understood.
  • The in vivo and in vitro responses of a panel of these xenografts to the glucocorticoid, dexamethasone, reflected the outcome of the patients from whom they were derived.
  • In this report we show that glucocorticoid resistance in B-cell precursor (BCP) ALL xenografts was not due to down-regulation of the glucocorticoid receptor (GR) nor to defective ligand binding of the GR.
  • [MeSH-major] Antineoplastic Agents, Hormonal / administration & dosage. Burkitt Lymphoma / metabolism. Dexamethasone / administration & dosage. Drug Resistance, Neoplasm. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Signal Transduction
  • [MeSH-minor] Active Transport, Cell Nucleus. Adolescent. Animals. Apoptosis. Apoptosis Regulatory Proteins / metabolism. Cell Nucleus / metabolism. Child. Child, Preschool. Female. Gene Expression Regulation, Leukemic. Humans. Ligands. Male. Membrane Proteins / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Neoplasm Transplantation. Proto-Oncogene Proteins / metabolism. Receptors, Glucocorticoid / metabolism. Transplantation, Heterologous


100. Primo D, Tabernero MD, Perez JJ, Rasillo A, Sayagués JM, Espinosa AB, Lopez-Berges MC, García-Sanz R, Gutierrez NC, Hernandez JM, Romero M, Osuna CS, Giralt M, Barbon M, San Miguel JF, Orfao A: Genetic heterogeneity of BCR/ABL+ adult B-cell precursor acute lymphoblastic leukemia: impact on the clinical, biological and immunophenotypical disease characteristics. Leukemia; 2005 May;19(5):713-20
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic heterogeneity of BCR/ABL+ adult B-cell precursor acute lymphoblastic leukemia: impact on the clinical, biological and immunophenotypical disease characteristics.
  • Philadelphia-positive (Ph(+)) B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is a genetically heterogeneous disease with a very poor prognosis.
  • In this study, we analyzed the frequency of supernumerary Ph, trisomy 8, monosomy 7, and del(9p21) by FISH and its relationship with the characteristics of the disease, in 46 BCR/ABL(+) adult BCP-ALL patients.
  • [MeSH-major] Burkitt Lymphoma / genetics. Fusion Proteins, bcr-abl / genetics. Genetic Heterogeneity. Immunophenotyping
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. DNA / genetics. Disease-Free Survival. Female. Flow Cytometry / methods. Humans. In Situ Hybridization, Fluorescence / methods. Interphase. Karyotyping. Male. Middle Aged. Ploidies. Time Factors

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  • (PMID = 15789066.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 9007-49-2 / DNA; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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