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1. Burmeister T, Meyer C, Schwartz S, Hofmann J, Molkentin M, Kowarz E, Schneider B, Raff T, Reinhardt R, Gökbuget N, Hoelzer D, Thiel E, Marschalek R: The MLL recombinome of adult CD10-negative B-cell precursor acute lymphoblastic leukemia: results from the GMALL study group. Blood; 2009 Apr 23;113(17):4011-5
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  • [Title] The MLL recombinome of adult CD10-negative B-cell precursor acute lymphoblastic leukemia: results from the GMALL study group.
  • MLL translocations in adult B-cell precursor (BCP) acute lymphoblastic leukemia (ALL) are largely restricted to the immature CD10(-) immunophenotypes.
  • Characteristic features of MLL(+) patients were significantly lower CD10 expression, expression of the NG2 antigen, a higher white blood count at diagnosis, and female sex.
  • [MeSH-major] Myeloid-Lymphoid Leukemia Protein / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Recombinant Fusion Proteins / metabolism

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  • (PMID = 19144982.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00198991/ NCT00199056
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Recombinant Fusion Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.4.24.11 / Neprilysin
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2. Mori A, Toyoshima N, Saito M, Oka T, Irie T, Morioka M: [Hypercalcemia and multiple osteolytic lesions associated with proinflammatory cytokines in a patient with acute lymphoblastic leukemia]. Rinsho Ketsueki; 2007 Jul;48(7):559-64
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  • [Title] [Hypercalcemia and multiple osteolytic lesions associated with proinflammatory cytokines in a patient with acute lymphoblastic leukemia].
  • Bone marrow aspiration revealed increased lymphoblasts (48%), and the patient was diagnosed as having acute lymphoblastic leukemia (ALL, L2).
  • However, he died of acute pneumonia and gastrointestinal bleeding.
  • The postmortem findings showed leukemic cell involvement of the left tibia.
  • [MeSH-major] Cytokines / physiology. Hypercalcemia / etiology. Osteolysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology

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  • (PMID = 17695305.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-6; 0 / Parathyroid Hormone-Related Protein; 0 / Tumor Necrosis Factor-alpha
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3. Antillon F, de Maselli T, Garcia T, Rossi E, Sala A: Nutritional status of children during treatment for acute lymphoblastic leukemia in the Central American Pediatric Hematology Oncology Association (AHOPCA): preliminary data from Guatemala. Pediatr Blood Cancer; 2008 Feb;50(2 Suppl):502-5; discussion 517
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  • [Title] Nutritional status of children during treatment for acute lymphoblastic leukemia in the Central American Pediatric Hematology Oncology Association (AHOPCA): preliminary data from Guatemala.
  • Preliminary data reveal some degree of nutritional depletion in up to 54% of newly diagnosed children with acute lymphoblastic leukemia in Guatemala.
  • [MeSH-major] Nutritional Status. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18064654.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 15
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4. Koyama N, Koschmieder S, Tyagi S, Portero-Robles I, Chromic J, Myloch S, Nürnberger H, Rossmanith T, Hofmann WK, Hoelzer D, Ottmann OG: Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive leukemia cells to the ABL kinase inhibitor STI571. Clin Cancer Res; 2006 Apr 1;12(7 Pt 1):2025-31
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  • [Title] Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive leukemia cells to the ABL kinase inhibitor STI571.
  • To investigate whether PTP1B modulates the biological effects of the abl kinase inhibitor STI571 in BCR-ABL-positive cells, we transfected Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia cell-derived K562 cells with either wild-type PTP1B (K562/PTP1B), a substrate-trapping dominant-negative mutant PTP1B (K562/D181A), or empty vector (K562/mock).
  • In both K562/mock and K562/PTP1B cells, 0.25 to 1 mumol/L STI571 induced dose-dependent growth arrest and apoptosis, as measured by a decrease of cell proliferation and an increase of Annexin V-positive cells and/or of cells in the sub-G(1) apoptotic phase.
  • Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.
  • In conclusion, functional PTP1B is involved in STI571-induced growth and cell cycle arrest, apoptosis, and differentiation, and attenuation of PTP1B function may contribute to resistance towards STI571.
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Imatinib Mesylate. K562 Cells. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 1. Structure-Activity Relationship. Vanadates / pharmacology

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  • (PMID = 16609011.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 0 / bis(N,N-dimethylhydroxamido)hydroxooxovanadate; 3WHH0066W5 / Vanadates; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.48 / PTPN1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases
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5. Nagai K, Hashimoto H, Itoh K, Matsushita A, Shimoji S, Kimura T, Inoue D, Mori M, Nagai Y, Tabata S, Yanagida M, Takahashi T: [Graft-versus-leukemia effect by lymphocytes from the first donor after second cord blood transplantation in a patient with T-lymphoblastic lymphoma]. Rinsho Ketsueki; 2010 Jun;51(6):413-21
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  • [Title] [Graft-versus-leukemia effect by lymphocytes from the first donor after second cord blood transplantation in a patient with T-lymphoblastic lymphoma].
  • A 19-year-old girl with T-lymphoblastic lymphoma (T-LBL) was referred to our hospital because of refractory disease.
  • [MeSH-major] Cord Blood Stem Cell Transplantation. Graft vs Leukemia Effect / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. T-Lymphocytes. T-Lymphocytes, Cytotoxic / immunology. Tissue Donors
  • [MeSH-minor] Acute Disease. Asparaginase / therapeutic use. Bone Marrow Transplantation. Chronic Disease. Female. Graft vs Host Disease / immunology. Humans. Minor Histocompatibility Antigens. Transplantation Conditioning. Young Adult

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  • (PMID = 20622488.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Minor Histocompatibility Antigens; EC 3.5.1.1 / Asparaginase
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6. Intermesoli T, Mangili G, Salvi A, Biondi A, Bassan R: Abnormally expanded pro-B hematogones associated with congenital cytomegalovirus infection. Am J Hematol; 2007 Oct;82(10):934-6
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  • We present the case of a newborn with an atypical, marked expansion of hematogones similar to the pro-B cells of infant acute lymphoblastic leukemia, which demonstrated their nonleukemic nature through gene rearrangement analysis and were associated with a congenital cytomegalovirus infection.
  • [MeSH-major] Cytomegalovirus Infections / diagnosis. Infant, Premature, Diseases / diagnosis. Lymphocyte Subsets / pathology
  • [MeSH-minor] Adult. Antiviral Agents / therapeutic use. Bone Marrow / pathology. Diagnosis, Differential. Female. Ganciclovir / therapeutic use. Hepatitis, Viral, Human / congenital. Hepatitis, Viral, Human / surgery. Humans. Infant, Newborn. Infant, Premature. Infectious Disease Transmission, Vertical. Liver Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Pregnancy. Pregnancy Complications, Infectious / diagnosis


7. Sharma VM, Calvo JA, Draheim KM, Cunningham LA, Hermance N, Beverly L, Krishnamoorthy V, Bhasin M, Capobianco AJ, Kelliher MA: Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc. Mol Cell Biol; 2006 Nov;26(21):8022-31
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  • [Title] Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.
  • Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL).
  • To identify Notch1 target genes in leukemia, we developed mouse T-cell leukemic lines that express intracellular Notch1 in a doxycycline-dependent manner.
  • Using gene expression profiling and chromatin immunoprecipitation, we identified c-myc as a novel, direct, and critical Notch1 target gene in T-cell leukemia. c-myc mRNA levels are increased in primary mouse T-cell tumors that harbor Notch1 mutations, and Notch1 inhibition decreases c-myc mRNA levels and inhibits leukemic cell growth.
  • Consistent with these findings, retroviral insertional mutagenesis screening of our T-cell leukemia mouse model revealed common insertions in either notch1 or c-myc genes.

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  • (PMID = 16954387.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA-096889
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Myc protein, mouse; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC1636748
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8. Bram EE, Stark M, Raz S, Assaraf YG: Chemotherapeutic drug-induced ABCG2 promoter demethylation as a novel mechanism of acquired multidrug resistance. Neoplasia; 2009 Dec;11(12):1359-70
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  • Herein, we explored the impact of drug treatment on the methylation status of the ABCG2 promoter and consequent reactivation of ABCG2 gene expression in parental tumor cell lines and their MDR sublines.
  • We demonstrate that ABCG2 promoter methylation is common in T-cell acute lymphoblastic leukemia (T-ALL) lines, also present in primary T-ALL lymphoblast specimens.
  • Furthermore, drug selection with sulfasalazine and topotecan induced a complete demethylation of the ABCG2 promoter in the T-ALL and ovarian carcinoma model cell lines CCRF-CEM and IGROV1, respectively.
  • Remarkably, mimicking cytotoxic bolus drug treatment through 12- to 24-hour pulse exposure of ABCG2-silenced leukemia cells, to clinically relevant concentrations of the chemotherapeutic agents daunorubicin and mitoxantrone, resulted in a marked transcriptional up-regulation of ABCG2.
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Antineoplastic Agents / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Cytidine / analogs & derivatives. Cytidine / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Humans. Jurkat Cells. K562 Cells. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20019844.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 5CSZ8459RP / Cytidine; 776B62CQ27 / decitabine; 7A9Y5SX0GY / pyrimidin-2-one beta-ribofuranoside; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2794517
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9. Neudenberger J, Hotfilder M, Rosemann A, Langebrake C, Reinhardt D, Pieters R, Schrauder A, Schrappe M, Röttgers S, Harbott J, Vormoor J: Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11). Br J Haematol; 2006 May;133(3):337-44
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  • [Title] Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11).
  • Therefore, these leukaemic stem cells should be the target cells for therapy and for minimal residual disease (MRD) detection.
  • Six acute myeloid leukaemia (AML)/abn(11q23) and three acute lymphoblastic leukaemia (ALL)/t(4;11) samples were analysed by four-colour flow cytometry for NG2 expression on primitive cell populations.
  • Candidate leukaemic cell populations were defined by the antigen profiles CD34+CD38- in AML and CD34+CD19-CD117+ in ALL.
  • Surprisingly, in all patients these candidate stem cell populations were shown to lack expression of NG2.
  • Instead, a correlation between the expression of the myeloid differentiation marker CD33 and increasing levels of NG2 on maturing cells could be demonstrated.
  • Thus, NG2 appears to be upregulated with differentiation and not to be expressed on primitive disease-maintaining cells.
  • [MeSH-major] Antigens / metabolism. Biomarkers, Tumor / metabolism. Leukemia, Myeloid / metabolism. Neoplastic Stem Cells / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proteoglycans / metabolism
  • [MeSH-minor] Acute Disease. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Flow Cytometry / methods. Humans. Neoplasm Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Sialic Acid Binding Ig-like Lectin 3. Translocation, Genetic

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  • (PMID = 16643437.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Neoplasm Proteins; 0 / Proteoglycans; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / chondroitin sulfate proteoglycan 4
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10. Heuser M, Beutel G, Krauter J, Döhner K, von Neuhoff N, Schlegelberger B, Ganser A: High meningioma 1 (MN1) expression as a predictor for poor outcome in acute myeloid leukemia with normal cytogenetics. Blood; 2006 Dec 1;108(12):3898-905
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  • [Title] High meningioma 1 (MN1) expression as a predictor for poor outcome in acute myeloid leukemia with normal cytogenetics.
  • The translocation t(12;22) involves MN1 and TEL and is rarely found in acute myeloid leukemia (AML).
  • MN1 was highly expressed in some patients with acute lymphoblastic but not chronic lymphocytic or myeloid leukemia.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Tumor Suppressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Animals. Cytogenetic Analysis / methods. Disease-Free Survival. Female. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / mortality. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / mortality. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Male. Mice. Middle Aged. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Transcription Factors / biosynthesis. Transcription Factors / genetics

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  • (PMID = 16912223.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0 / MN1 protein, human; 0 / MN1-TEL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / homeobox protein HOXA9
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11. De Keersmaecker K, Lahortiga I, Mentens N, Folens C, Van Neste L, Bekaert S, Vandenberghe P, Odero MD, Marynen P, Cools J: In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia. Haematologica; 2008 Apr;93(4):533-42
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  • [Title] In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia.
  • BACKGROUND: Activating NOTCH1 mutations are common in T-cell acute lymphoblastic leukemia.
  • Inhibition of NOTCH1 signaling with gamma-secretase inhibitors causes cell cycle block, but only after treatment for several days.
  • We further documented the effects of gamma-secretase inhibitor treatment on T-cell acute lymphoblastic leukemia cell lines and tested whether combining gamma-secretase inhibitors with other anti-cancer drugs offers a therapeutic advantage.
  • DESIGN AND METHODS: The effect of gamma-secretase inhibitor treatment and combinations of gamma-secretase inhibitors with chemotherapy or glucocorticoids was assessed on T-cell acute lymphoblastic leukemia cell lines.
  • We sequenced NOTCH1 in T-cell acute lymphoblastic leukemia cases with ABL1 fusions and tested combinations of gamma-secretase inhibitors and the ABL1 inhibitor imatinib in a T-cell acute lymphoblastic leukemia cell line.
  • RESULTS: gamma-secretase inhibitor treatment for 5-7 days reversibly inhibited cell proliferation, caused cell cycle block in sensitive T-cell acute lymphoblastic leukemia cell lines, and caused differentiation of some T-cell acute lymphoblastic leukemia cell lines.
  • The cytotoxic effects of the chemotherapeutic agent vincristine were not significantly enhanced by addition of gamma-secretase inhibitors to T-cell acute lymphoblastic leukemia cell lines, but gamma-secretase inhibitor treatment sensitized cells to the effect of dexamethasone.
  • NOTCH1 mutations were identified in all T-cell acute lymphoblastic leukemia patients with ABL1 fusions and in a T-cell acute lymphoblastic leukemia cell line expressing NUP214-ABL1.
  • In this cell line, the anti-proliferative effect of imatinib was increased by pre-treatment with gamma-secretase inhibitors.
  • CONCLUSIONS: Short-term treatment of T-cell acute lymphoblastic leukemia cell lines with gamma-secretase inhibitors had limited effects on cell proliferation and survival.
  • Combinations of gamma-secretase inhibitors with other drugs may be required to obtain efficient therapeutic effects in T-cell acute lymphoblastic leukemia, and not all combinations may be useful.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Benzodiazepinones / pharmacology. Carbamates / pharmacology. Dipeptides / pharmacology. Enzyme Inhibitors / pharmacology. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Apoptosis / drug effects. Benzamides. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / enzymology. DNA, Neoplasm / genetics. Daunorubicin / administration & dosage. Daunorubicin / pharmacology. Dexamethasone / administration & dosage. Dexamethasone / pharmacology. Drug Screening Assays, Antitumor. Drug Synergism. Humans. Imatinib Mesylate. In Vitro Techniques. Mutation. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / genetics. Piperazines / administration & dosage. Piperazines / pharmacology. Pyrimidines / administration & dosage. Pyrimidines / pharmacology. Sequence Analysis, DNA. Vincristine / administration & dosage. Vincristine / pharmacology

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  • [CommentIn] Haematologica. 2008 Apr;93(4):493-7 [18379008.001]
  • (PMID = 18322257.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzodiazepinones; 0 / Carbamates; 0 / DNA, Neoplasm; 0 / Dipeptides; 0 / Enzyme Inhibitors; 0 / L 685458; 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8A1O1M485B / Imatinib Mesylate; EC 3.4.- / Amyloid Precursor Protein Secretases; ZS7284E0ZP / Daunorubicin
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12. Muzzafar T, Medeiros LJ, Wang SA, Brahmandam A, Thomas DA, Jorgensen JL: Aberrant underexpression of CD81 in precursor B-cell acute lymphoblastic leukemia: utility in detection of minimal residual disease by flow cytometry. Am J Clin Pathol; 2009 Nov;132(5):692-8
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  • [Title] Aberrant underexpression of CD81 in precursor B-cell acute lymphoblastic leukemia: utility in detection of minimal residual disease by flow cytometry.
  • We studied CD81 expression by flow cytometry (FC) on benign precursor B cells (hematogones) and leukemic blasts in precursor B-cell acute lymphoblastic leukemia (pre-B-ALL) and established its usefulness in minimal residual disease (MRD) assays.
  • In 98 pre-B-ALLs at diagnosis or overt relapse, 80 (82%) showed aberrantly decreased CD81 intensity.
  • [MeSH-major] Antigens, CD / biosynthesis. Biomarkers, Tumor / analysis. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 19846809.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD81; 0 / Biomarkers, Tumor; 0 / CD81 protein, human
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13. Suzuki N, Yumura-Yagi K, Yoshida M, Hara J, Nishimura S, Kudoh T, Tawa A, Usami I, Tanizawa A, Hori H, Ito Y, Miyaji R, Oda M, Kato K, Hamamoto K, Osugi Y, Hashii Y, Nakahata T, Horibe K, Japan Association of Childhood Leukemia Study (JACLS): Outcome of childhood acute lymphoblastic leukemia with induction failure treated by the Japan Association of Childhood Leukemia study (JACLS) ALL F-protocol. Pediatr Blood Cancer; 2010 Jan;54(1):71-8
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  • [Title] Outcome of childhood acute lymphoblastic leukemia with induction failure treated by the Japan Association of Childhood Leukemia study (JACLS) ALL F-protocol.
  • BACKGROUND: Children with acute lymphoblastic leukemia (ALL) who fail to achieve complete remission (CR) after induction therapy (induction failure: IF) have a poor prognosis; however, there have been few prospective studies in patients with IF.
  • Twenty-three of these patients entered the F-protocol study, which mainly consisted of acute-myeloid-leukemia-oriented chemotherapy followed by scheduled hematopoietic cell transplantation (HCT).
  • RESULTS: Seventeen (73.9%) of the 23 patients responded to re-induction chemotherapy with CR.
  • The 5-year OS rate of the 17 patients who obtained CR by re-induction therapy and the 6 who did not were 47.1 +/- 12.1% and 0%, respectively (P < 0.001).
  • CONCLUSION: Acute-myeloid-leukemia-oriented chemotherapy followed by scheduled HCT is a promising treatment strategy for non-Ph(+) ALL patients with IF.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy


14. Cho J, Hur M, Moon HW, Yun YM, Lee CH, Lee HG: A case of therapy-related ALL with MLL gene rearrangement following treatment of breast cancer. Korean J Lab Med; 2010 Jun;30(3):255-9
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  • However, the patient's complete blood cell count indicated acute leukemia: white blood cell count, 174.1 x 10(9)/L with 88% blasts; Hb level, 12.5 g/dL; and platelet count, 103.0 x 10(9)/L.
  • Following consolidation chemotherapy, she underwent allogenic peripheral blood stem cell transplantation and has been clinically stable.
  • [MeSH-major] Breast Neoplasms / drug therapy. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology. Translocation, Genetic
  • [MeSH-minor] Antibiotics, Antineoplastic / therapeutic use. Blood Cell Count. Bone Marrow / pathology. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Cytogenetic Analysis. Epirubicin / therapeutic use. Female. Fluorouracil / therapeutic use. Gene Rearrangement. Hematopoietic Stem Cell Transplantation. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence

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  • (PMID = 20603585.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; U3P01618RT / Fluorouracil
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15. Bornhauser BC, Bonapace L, Lindholm D, Martinez R, Cario G, Schrappe M, Niggli FK, Schäfer BW, Bourquin JP: Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway. Blood; 2007 Sep 15;110(6):2084-91
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  • [Title] Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway.
  • Incorporation of apoptosis-inducing agents into current therapeutic regimens is an attractive strategy to improve treatment for drug-resistant leukemia.
  • We tested the potential of arsenic trioxide (ATO) to restore the response to dexamethasone in glucocorticoid (GC)-resistant acute lymphoblastic leukemia (ALL).
  • Low-dose ATO markedly increased in vitro GC sensitivity of ALL cells from T-cell and precursor B-cell ALL patients with poor in vivo response to prednisone.
  • In GC-resistant cell lines, this effect was mediated, at least in part, by inhibition of Akt and affecting downstream Akt targets such as Bad, a proapoptotic Bcl-2 family member, and the X-linked inhibitor of apoptosis protein (XIAP).
  • [MeSH-major] Antineoplastic Agents / pharmacology. Arsenicals / administration & dosage. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Glucocorticoids / pharmacology. Oxides / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
  • [MeSH-minor] Apoptosis / drug effects. Blotting, Western. Caspases. Cell Line, Tumor / drug effects. Cell Survival / drug effects. Drug Synergism. Humans. Neoplasm, Residual / diagnosis. Phosphorylation / drug effects. Prednisone / pharmacology. RNA, Small Interfering / pharmacology. Reactive Oxygen Species / metabolism. Remission Induction. Sirolimus / pharmacology. Transfection. X-Linked Inhibitor of Apoptosis Protein / metabolism. bcl-Associated Death Protein / metabolism


16. Vilimas T, Mascarenhas J, Palomero T, Mandal M, Buonamici S, Meng F, Thompson B, Spaulding C, Macaroun S, Alegre ML, Kee BL, Ferrando A, Miele L, Aifantis I: Targeting the NF-kappaB signaling pathway in Notch1-induced T-cell leukemia. Nat Med; 2007 Jan;13(1):70-7
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  • [Title] Targeting the NF-kappaB signaling pathway in Notch1-induced T-cell leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL), unlike other ALL types, is only infrequently associated with chromosomal aberrations, but it was recently shown that most individuals with T-ALL carry activating mutations in the NOTCH1 gene.
  • [MeSH-major] Leukemia, T-Cell / pathology. NF-kappa B / metabolism. Receptor, Notch1 / metabolism
  • [MeSH-minor] Animals. Antigens, CD4 / analysis. Antigens, CD8 / analysis. Boronic Acids / pharmacology. Bortezomib. COS Cells. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Cercopithecus aethiops. DNA-Binding Proteins / genetics. Gene Expression Profiling. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Interleukin Receptor Common gamma Subunit / genetics. Leukemia, Experimental / genetics. Leukemia, Experimental / metabolism. Leukemia, Experimental / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Microscopy, Confocal. Mutation. Pyrazines / pharmacology. Signal Transduction / genetics. Signal Transduction / physiology. Survival Analysis

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  • (PMID = 17173050.001).
  • [ISSN] 1078-8956
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / P01AG025531; United States / NCI NIH HHS / CA / R01CA105129; United States / NCI NIH HHS / CA / R01CA84065
  • [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, CD4; 0 / Antigens, CD8; 0 / Boronic Acids; 0 / DNA-Binding Proteins; 0 / Il2rg protein, mouse; 0 / Interleukin Receptor Common gamma Subunit; 0 / NF-kappa B; 0 / NOTCH1 protein, human; 0 / Pyrazines; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 147336-22-9 / Green Fluorescent Proteins; 69G8BD63PP / Bortezomib
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17. Betts DR, Stanchescu R, Niggli FK, Cohen N, Rechavi G, Amariglio N, Trakhtenbrot L: SKY reveals a high frequency of unbalanced translocations involving chromosome 6 in t(12;21)-positive acute lymphoblastic leukemia. Leuk Res; 2008 Jan;32(1):39-43
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  • [Title] SKY reveals a high frequency of unbalanced translocations involving chromosome 6 in t(12;21)-positive acute lymphoblastic leukemia.
  • The G-band cryptic t(12;21)(p13;q22) is the most common chromosomal rearrangement in childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 6. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Spectral Karyotyping. Translocation, Genetic

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  • [CommentIn] Leuk Res. 2007 Dec;31(12):1761-2 [17560648.001]
  • (PMID = 17418891.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Validation Studies
  • [Publication-country] England
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18. Yang Y, Takeuchi S, Hofmann WK, Ikezoe T, van Dongen JJ, Szczepański T, Bartram CR, Yoshino N, Taguchi H, Koeffler HP: Aberrant methylation in promoter-associated CpG islands of multiple genes in acute lymphoblastic leukemia. Leuk Res; 2006 Jan;30(1):98-102
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  • [Title] Aberrant methylation in promoter-associated CpG islands of multiple genes in acute lymphoblastic leukemia.
  • Methylation profile was analyzed in 10 childhood acute lymphoblastic leukemia (ALL) and nine adult ALL cases.
  • [MeSH-major] CpG Islands. DNA Methylation. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism


19. Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL): Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases. Eur J Haematol; 2010 Oct;85(4):300-8
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  • [Title] Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
  • OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes) acute lymphoblastic leukemia (NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
  • METHODS: The members of the European Group for Immunophenotyping of Leukemias (EGIL) searched retrospectively their databases for NT-ALL patients.
  • Ten children were diagnosed as T-cell ALL (T-ALL) EGIL categories (T-I n=2, T-II n=2, T-III n=3, T-IV n=3) and four displayed various structural chromosomal abnormalities.
  • B-cell precursor (BCP) ALL was diagnosed in 26 children.
  • One girl with hypodiploid and NT metaphases and ETV6-RUNX1-negative BCP-ALL and one of two boys with NT-BCP-ALL not examined for ETV6-RUNX1 died of infection after stem cell transplantation in 2nd/3rd CR.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20561032.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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20. Infante-Rivard C, Vermunt JK, Weinberg CR: Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia. Am J Epidemiol; 2007 Jun 1;165(11):1248-54
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  • [Title] Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia.
  • Topoisomerase II is a DNA-processing enzyme, and secondary acute myeloid leukemia has been associated with exposure to drugs that inhibit its action.
  • Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood leukemia.
  • To assess its role in the etiology of childhood acute lymphoblastic leukemia, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000).
  • [MeSH-major] Family Health. Inheritance Patterns. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17332311.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES045005-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; J64922108F / Benzene
  • [Other-IDs] NLM/ NIHMS33454; NLM/ PMC2080583
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21. O'Brien S, Ravandi F, Riehl T, Wierda W, Huang X, Tarrand J, O'Neal B, Kantarjian H, Keating M: Valganciclovir prevents cytomegalovirus reactivation in patients receiving alemtuzumab-based therapy. Blood; 2008 Feb 15;111(4):1816-9
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  • Alemtuzumab is an immunosuppressive antibody that depletes normal T cells and B cells.
  • Diagnoses included chronic lymphocytic leukemia (29), T-cell prolymphocytic leukemia (3), hairy cell leukemia (1), adult T-cell leukemia/lymphoma (ATLL) (1), marginal zone leukemia (1), large granular lymphocyte leukemia (2), acute lymphoblastic leukemia (1), and T-cell lymphoma (2).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Cytomegalovirus / physiology. Cytomegalovirus Infections / prevention & control. Ganciclovir / analogs & derivatives. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Virus Activation / physiology

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  • [CommentIn] Blood. 2008 Sep 1;112(5):2167 [18725576.001]
  • (PMID = 18039954.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00562770
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / valganciclovir; 3A189DH42V / alemtuzumab; P9G3CKZ4P5 / Ganciclovir
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22. Benketira A, Tichit R, Tenenbaum J, Margueritte G, Bernard F: [BK virus infection in a child after an hematopoietic stem cell transplantation]. Arch Pediatr; 2005 Apr;12 Suppl 1:S64-6
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  • [Title] [BK virus infection in a child after an hematopoietic stem cell transplantation].
  • [Transliterated title] Infection à BK Virus après allogreffe de cellules hématopoïétiques. A propos d'un cas.
  • A 10-year old boy with poor-prognosis acute T lymphoblastic leukaemia underwent cord blood allogeneic stem cell transplantation while in his first relapse.
  • Macroscopic haematuria and low back pain occurred by day 95, in the context of acute graft versus host disease and pulmonary aspergillosis.
  • Histopathologic examination showed a cytopathogenetic effect consistent with the diagnosis of BKV infection.
  • The current understanding, diagnosis, and treatment of BKV-associated infection is discussed.
  • [MeSH-major] BK Virus / pathogenicity. Cytosine / analogs & derivatives. Hematopoietic Stem Cell Transplantation / adverse effects. Polyomavirus Infections / etiology
  • [MeSH-minor] Antiviral Agents / therapeutic use. Child. Humans. Leukemia-Lymphoma, Adult T-Cell / therapy. Male. Organophosphonates / therapeutic use. Prognosis

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  • (PMID = 15893243.001).
  • [ISSN] 0929-693X
  • [Journal-full-title] Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
  • [ISO-abbreviation] Arch Pediatr
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Organophosphonates; 8J337D1HZY / Cytosine; JIL713Q00N / cidofovir
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23. Goto H, Naruto T, Tanoshima R, Kato H, Yokosuka T, Yanagimachi M, Fujii H, Yokota S, Komine H: Chemo-sensitivity in a panel of B-cell precursor acute lymphoblastic leukemia cell lines, YCUB series, derived from children. Leuk Res; 2009 Oct;33(10):1386-91
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  • [Title] Chemo-sensitivity in a panel of B-cell precursor acute lymphoblastic leukemia cell lines, YCUB series, derived from children.
  • Sensitivity to 10 anticancer drugs was evaluated in 6 childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cell lines.
  • Authenticity of newly established cell lines was confirmed by genomic fingerprinting.
  • The line YCUB-5R established at relapse was more resistant to 4-hydroperoxy-cyclophosphamide, cytarabine, L-asparaginase, topotecan, fludarabine, and etoposide than YCUB-5 from the same patient at diagnosis.
  • This cell line panel offers an in vitro model for the development of new therapies for childhood BCP-ALL.
  • [MeSH-major] B-Lymphocytes / pathology. DNA Fingerprinting / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Division / drug effects. Cell Line, Tumor / drug effects. Cell Survival / drug effects. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Leukocyte Count. Male. Prednisolone / pharmacology


24. Yoshimi A, Ito M, Kojima S: Leukemic cell death induced by antithymocyte globulin. Leuk Res; 2005 Jul;29(7):821-7
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  • [Title] Leukemic cell death induced by antithymocyte globulin.
  • We studied the cytotoxic effects of antithymocyte globulin (ATG) in leukemic cells obtained from five patients with acute T lymphoblastic leukemia or precursor T lymphoblastic leukemia.
  • We also examined apoptotic cell death using Annexin-V.
  • Cell incubation with ATG increased Annexin-V binding significantly compared with horse IgG (50.3+/-7.6% versus 95.7+/-1.8%, p = or < 0.0001).
  • However, ATG did not induce apparent DNA fragmentation in a human T-ALL cell line.
  • These results suggest that ATG induces leukemic cell death in a Fas/Fas-ligand- and caspase-independent manner.
  • [MeSH-major] Antilymphocyte Serum / pharmacology. Cell Death / drug effects. Immunosuppressive Agents / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Horses. Humans. Immunoglobulin G / pharmacology

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  • (PMID = 15893374.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antilymphocyte Serum; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents
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25. Bosch FJ, Badenhorst L, Le Roux JA, Louw VJ: Successful treatment of Chromobacterium violaceum sepsis in South Africa. J Med Microbiol; 2008 Oct;57(Pt 10):1293-5
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  • As far as could be ascertained, this infection has never been reported in a patient with leukaemia.
  • We describe what we believe to be the first such case of C. violaceum sepsis, in a 16-year-old female patient with acute biphenotypic leukaemia, which developed during the neutropenic phase after intensive chemotherapy.
  • [MeSH-minor] Adolescent. Antifungal Agents / pharmacology. Candidiasis / complications. Candidiasis / drug therapy. Female. Humans. Leukemia / complications. Neutropenia / complications. South Africa / epidemiology. Treatment Outcome

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  • (PMID = 18809561.001).
  • [ISSN] 0022-2615
  • [Journal-full-title] Journal of medical microbiology
  • [ISO-abbreviation] J. Med. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antifungal Agents
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26. van Brussel M, Takken T, Lucia A, van der Net J, Helders PJ: Is physical fitness decreased in survivors of childhood leukemia? A systematic review. Leukemia; 2005 Jan;19(1):13-7
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  • [Title] Is physical fitness decreased in survivors of childhood leukemia? A systematic review.
  • The aim of this review is to determine whether physical fitness, assessed by peak oxygen uptake (VO(2peak)) measurement, is reduced in survivors of acute lymphoblastic leukemia (ALL) compared to healthy children.
  • [MeSH-major] Physical Fitness. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Survivors

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  • (PMID = 15526028.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 38
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27. Bayrak IK, Yalin T, Ozmen Z, Aksoz T, Doughanji R: Acute lymphoblastic leukemia presented as multiple breast masses. Korean J Radiol; 2009 Sep-Oct;10(5):508-10
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  • [Title] Acute lymphoblastic leukemia presented as multiple breast masses.
  • Breast metastases in cases leukemia are very rare and occur primarily in patients with acute myeloid leukemia.
  • We report the involvement of breast metastases in a 30-year-old woman with acute T cell lymphoblastic leukemia.
  • [MeSH-major] Breast Neoplasms / secondary. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Mammography. Ultrasonography, Mammary

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  • (PMID = 19721836.001).
  • [ISSN] 2005-8330
  • [Journal-full-title] Korean journal of radiology
  • [ISO-abbreviation] Korean J Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Number-of-references] 10
  • [Other-IDs] NLM/ PMC2731869
  • [Keywords] NOTNLM ; Acute lymphoblastic leukemia / Breast metastasis / Mammography / Ultrasonography
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28. Cohen MH, Johnson JR, Justice R, Pazdur R: FDA drug approval summary: nelarabine (Arranon) for the treatment of T-cell lymphoblastic leukemia/lymphoma. Oncologist; 2008 Jun;13(6):709-14
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  • [Title] FDA drug approval summary: nelarabine (Arranon) for the treatment of T-cell lymphoblastic leukemia/lymphoma.
  • Food and Drug Administration (FDA) approval of nelarabine (Arranon), a new purine analogue, for the treatment of patients with T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL) whose disease has not responded to or has relapsed following treatment with at least two chemotherapy regimens.
  • [MeSH-major] Arabinonucleosides / therapeutic use. Drug Approval / legislation & jurisprudence. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 18586926.001).
  • [ISSN] 1083-7159
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arabinonucleosides; 60158CV180 / nelarabine
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29. Ausserlechner MJ, Obexer P, Geley S, Kofler R: G1 arrest by p16INK4A uncouples growth from cell cycle progression in leukemia cells with deregulated cyclin E and c-Myc expression. Leukemia; 2005 Jun;19(6):1051-7
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  • [Title] G1 arrest by p16INK4A uncouples growth from cell cycle progression in leukemia cells with deregulated cyclin E and c-Myc expression.
  • The cell cycle inhibitor p16(INK4A) is frequently inactivated in acute lymphoblastic T-cell leukemia (T-ALL).
  • CCRF-CEM cells with tetracycline-regulated p16(INK4A) expression underwent stable G1-phase cell cycle arrest for 72 h followed by massive apoptosis. p16(INK4A) expression caused pRB hypophosphorylation and repression of certain E2F target genes.
  • Thus, p16(INK4A), although unable to repress the expression of deregulated cyclin E and c-Myc, functionally inactivated these potential oncogenes. p16(INK4A)-arrested cells showed morphologic changes, induction of T-cell-specific surface markers and repression of telomerase activity, suggesting differentiation.
  • Taken together, p16(INK4A) reconstitution in p16(INK4A)-deficient T-ALL cells induced cell cycle arrest in the presence of cyclin E and c-Myc expression, uncoupled growth from cell cycle progression and caused a sequential process of growth, differentiation and apoptosis.
  • [MeSH-major] Cyclin E / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Genes, myc / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology
  • [MeSH-minor] Apoptosis / physiology. Biomarkers, Tumor. Cell Differentiation / physiology. Cell Division / physiology. Child. G1 Phase / physiology. Gene Expression Regulation, Leukemic. Humans. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phosphorylation. Retinoblastoma-Like Protein p107. T-Lymphocytes / pathology. T-Lymphocytes / physiology. Telomerase / metabolism. Transcriptional Activation / physiology

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  • (PMID = 15800668.001).
  • [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] 0 / Biomarkers, Tumor; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / RBL1 protein, human; 0 / Retinoblastoma-Like Protein p107; EC 2.7.7.49 / Telomerase
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30. Mitchell L, Lambers M, Flege S, Kenet G, Li-Thiao-Te V, Holzhauer S, Bidlingmaier C, Frühwald MC, Heller C, Schmidt W, Pautard B, Nowak-Göttl U: Validation of a predictive model for identifying an increased risk for thromboembolism in children with acute lymphoblastic leukemia: results of a multicenter cohort study. Blood; 2010 Jun 17;115(24):4999-5004
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  • [Title] Validation of a predictive model for identifying an increased risk for thromboembolism in children with acute lymphoblastic leukemia: results of a multicenter cohort study.
  • Among risk factors for developing thromboembolism (VTE) in children with acute lymphoblastic leukemia were Escherichia coli asparaginase, concomitant steroid use, presence of central venous lines, and thrombophilic abnormalities.
  • In multivariate analysis adjusted for age, duration of asparaginase administration, enoxaparin prophylaxis, and T-immunophenotype, the HRG was significantly associated with VTE compared with the LRG (hazard/95% confidence interval [CI], 8.22/1.85-36.53).
  • On the basis of the high specificity, the model may identify children with leukemia at risk of VTE.
  • [MeSH-major] Models, Statistical. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Thromboembolism / diagnosis. Thromboembolism / epidemiology


31. Inukai T, Zhang X, Kameyama T, Suzuki Y, Yoshikawa K, Kuroda I, Nemoto A, Akahane K, Sato H, Goi K, Nakamoto K, Hamada J, Tada M, Moriuchi T, Sugita K: A specific linkage between the incidence of TP53 mutations and type of chromosomal translocations in B-precursor acute lymphoblastic leukemia cell lines. Am J Hematol; 2010 Jul;85(7):535-7
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  • [Title] A specific linkage between the incidence of TP53 mutations and type of chromosomal translocations in B-precursor acute lymphoblastic leukemia cell lines.
  • [MeSH-major] Mutation. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Cell Line, Tumor. Humans. Oncogene Proteins, Fusion

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  • (PMID = 20575032.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Protein p53
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32. Wu S, Gessner R, Taube T, von Stackelberg A, Henze G, Seeger K: Expression of interleukin-10 splicing variants is a positive prognostic feature in relapsed childhood acute lymphoblastic leukemia. J Clin Oncol; 2005 May 1;23(13):3038-42
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  • [Title] Expression of interleukin-10 splicing variants is a positive prognostic feature in relapsed childhood acute lymphoblastic leukemia.
  • This study aimed to determine the expression of a splicing-derived variant of interleukin (IL) -10 in leukemic cells and its clinical relevance in children with acute lymphoblastic leukemia (ALL) at first relapse.
  • PATIENTS AND METHODS: Between January 1997 and December 2001, bone marrow (BM) samples were collected from 98 children with first relapse of ALL at diagnosis.
  • CONCLUSION: These results indicate that splicing-derived IL-10 isoforms may modulate IL-10-mediated biologic effects and therapeutic efficacy in lymphatic disease, and expression of IL-10delta3 is a positive prognostic feature in relapsed childhood ALL.
  • [MeSH-major] Gene Expression Profiling. Genetic Variation. Interleukin-10 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology

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  • (PMID = 15860861.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 130068-27-8 / Interleukin-10
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33. Zweier-Renn LA, Hawley TS, Burkett S, Ramezani A, Riz I, Adler RL, Hickstein DD, Hawley RG: Hematopoietic immortalizing function of the NKL-subclass homeobox gene TLX1. Genes Chromosomes Cancer; 2010 Feb;49(2):119-31
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  • Translocations resulting in ectopic expression of the TLX1 homeobox gene (previously known as HOX11) are recurrent events in human T-cell acute lymphoblastic leukemia (T-ALL).
  • Transduction of primary murine hematopoietic stem/progenitor cells with retroviral vectors expressing TLX1 readily yields immortalized hematopoietic progenitor cell lines.
  • Additionally, the generation of murine hematopoietic progenitor cell lines due to retroviral integrations into Evi1 or Prdm16 has also been recently reported.
  • Here, we determined by linker-mediated nested polymerase chain reaction the integration sites in eight TLX1-immortalized hematopoietic cell lines.
  • Notably, no common integration site was observed among the cell lines.
  • However, neither Lmo2 nor any of the other genes examined surrounding the integration sites showed differential vector-influenced expression compared to the cell lines lacking such insertions.

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  • (PMID = 19862821.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01 HL065519-08; United States / NHLBI NIH HHS / HL / R01 HL066305-05; United States / NHLBI NIH HHS / HL / HL065519-08; United States / NHLBI NIH HHS / HL / R01 HL065519; United States / Intramural NIH HHS / / ; United States / NHLBI NIH HHS / HL / R01 HL066305; United States / NHLBI NIH HHS / HL / HL066305-05; United States / NHLBI NIH HHS / HL / R01HL66305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ NIHMS155591; NLM/ PMC2795049
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34. Trentin L, Giordan M, Dingermann T, Basso G, Te Kronnie G, Marschalek R: Two independent gene signatures in pediatric t(4;11) acute lymphoblastic leukemia patients. Eur J Haematol; 2009 Nov;83(5):406-19
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  • [Title] Two independent gene signatures in pediatric t(4;11) acute lymphoblastic leukemia patients.
  • METHOD: In our study we sought to overcome these limitations and for proof of principle, we analyzed the rare t(4;11) leukemia disease entity.
  • First, gene expression data of each t(4;11) leukemia patient were normalized by pairwise subtraction against normal bone marrow (n = 3) to identify significantly deregulated gene sets for each patient.
  • RESULT: A 'core signature' of 186 commonly deregulated genes present in each investigated t(4;11) leukemia patient was defined.
  • Linking the obtained gene sets to four biological discriminators (HOXA gene expression, age at diagnosis, fusion gene transcripts and chromosomal breakpoints) divided patients into two distinct subgroups: the first one comprised infant patients with low HOXA genes expression and the MLL breakpoints within introns 11/12.
  • CONCLUSION: A yet homogeneous leukemia entity was further subdivided, based on distinct genetic properties.
  • This approach provided a simplified way to obtain robust and disease-specific gene signatures even in smaller cohorts.
  • [MeSH-major] Chromosomes, Human, Pair 11 / metabolism. Chromosomes, Human, Pair 4 / metabolism. Gene Expression Regulation, Leukemic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Translocation, Genetic
  • [MeSH-minor] Female. Gene Expression Profiling / methods. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics. Humans. Male. Myeloid-Lymphoid Leukemia Protein / biosynthesis. Myeloid-Lymphoid Leukemia Protein / genetics. Oligonucleotide Array Sequence Analysis / methods. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics

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  • (PMID = 19558506.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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35. Wang Z, Hu T, Cao LZ, Kang R, Zhao MY, Yu Y, Xu WQ: [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin]. Zhongguo Dang Dai Er Ke Za Zhi; 2008 Oct;10(5):620-4
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  • [Title] [Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin].
  • OBJECTIVE: To investigate whether WASP/Verprolin homologous protein 1 (WAVE1) plays a role in the pathogenesis of childhood acute lymphoblastic leukemia (ALL).
  • The cell proliferation was detected with MTT.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Doxorubicin / pharmacology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Wiskott-Aldrich Syndrome Protein Family / physiology
  • [MeSH-minor] Adolescent. Blotting, Western. Cell Proliferation / drug effects. Child. Child, Preschool. Female. Humans. Infant. Jurkat Cells. Male. RNA, Messenger / analysis

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  • (PMID = 18947485.001).
  • [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
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / RNA, Messenger; 0 / WASF1 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family; 80168379AG / Doxorubicin
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36. Jelinek J, Oki Y, Gharibyan V, Bueso-Ramos C, Prchal JT, Verstovsek S, Beran M, Estey E, Kantarjian HM, Issa JP: JAK2 mutation 1849G&gt;T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia. Blood; 2005 Nov 15;106(10):3370-3
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  • [Title] JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.
  • The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in acute myeloid leukemia (AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).
  • JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic myelogenous leukemia (CML), 2 (18%) of 11 patients with megakaryocytic AML, 7 (13%) of 52 patients with chronic myelomonocytic leukemia, and 1 (1%) of 68 patients with myelodysplastic syndromes.
  • No mutation was found in Ph(+)CML (99 patients), AML M0-M6 (28 patients), or acute lymphoblastic leukemia (20 patients).
  • We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but not critical for transformation to the acute phase of these diseases and that it is generally rare in aggressive leukemias.

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  • (PMID = 16037387.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50CA100632
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
  • [Other-IDs] NLM/ PMC1895065
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37. Rezvani K, Yong AS, Savani BN, Mielke S, Keyvanfar K, Gostick E, Price DA, Douek DC, Barrett AJ: Graft-versus-leukemia effects associated with detectable Wilms tumor-1 specific T lymphocytes after allogeneic stem-cell transplantation for acute lymphoblastic leukemia. Blood; 2007 Sep 15;110(6):1924-32
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  • [Title] Graft-versus-leukemia effects associated with detectable Wilms tumor-1 specific T lymphocytes after allogeneic stem-cell transplantation for acute lymphoblastic leukemia.
  • To determine whether the leukemia-associated Wilms tumor antigen (WT1) contributes to a graft-versus-leukemia (GVL) effect after allogeneic stem-cell transplantation (SCT) for acute lymphoblastic leukemia (ALL), we studied CD8(+) T-cell responses to WT1 in 10 human lymphocyte antigen (HLA)-A*0201-positive ALL patients during the early phase of immune recovery after SCT (days 30-120).
  • Using WT1/HLA-A*0201 tetramers and intracellular interferon-gamma (IFN-gamma) staining, WT1(+) CD8(+) T-cell responses after SCT were found only in patients with detectable WT1 expression before SCT (5 of 7 vs. 0 of 3; P < .05).
  • To monitor the kinetics of WT1(+) CD8(+) T-cell responses and disease regression after SCT, absolute WT1(+) CD8(+) T-cell numbers and WT1 expression were studied for each time point.
  • Loss of WT1(+) CD8(+) T-cell responses was associated with reappearance of WT1 transcripts, consistent with a molecular relapse (P < .001).
  • [MeSH-major] Burkitt Lymphoma / therapy. Graft vs Leukemia Effect. Immunologic Memory. Stem Cell Transplantation. T-Lymphocytes / metabolism. WT1 Proteins / metabolism
  • [MeSH-minor] Adolescent. Adult. CD8-Positive T-Lymphocytes. Child. Cytomegalovirus / pathogenicity. Cytomegalovirus Infections / immunology. Cytomegalovirus Infections / therapy. Cytomegalovirus Infections / virology. Female. Graft vs Host Disease. HLA-A Antigens / metabolism. HLA-A2 Antigen. Humans. Male. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Donors. Transplantation, Homologous

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  • (PMID = 17505014.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501963
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC1976363
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38. Winter SS, Jiang Z, Khawaja HM, Griffin T, Devidas M, Asselin BL, Larson RS, Children's Oncology Group: Identification of genomic classifiers that distinguish induction failure in T-lineage acute lymphoblastic leukemia: a report from the Children's Oncology Group. Blood; 2007 Sep 1;110(5):1429-38
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  • [Title] Identification of genomic classifiers that distinguish induction failure in T-lineage acute lymphoblastic leukemia: a report from the Children's Oncology Group.
  • The clinical and cytogenetic features associated with T-cell acute lymphoblastic leukemia (T-ALL) are not predictive of early treatment failure.
  • Seven genes were similarly upregulated in both the genomic classifier for IF patients and T-ALL cell lines having acquired resistance to neoplastic agents, identifying potential target genes for further study in drug resistance.

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  • (PMID = 17495134.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA29139; United States / NCI NIH HHS / CA / R21 CA098251; United States / NCI NIH HHS / CA / U10 CA98543-03-14305; United States / NCI NIH HHS / CA / R01 CA114589; United States / NCI NIH HHS / CA / U10 CA029139; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA114589-01; United States / NCI NIH HHS / CA / R21 CA098251-01
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1975833
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39. Pottier N, Yang W, Assem M, Panetta JC, Pei D, Paugh SW, Cheng C, Den Boer ML, Relling MV, Pieters R, Evans WE, Cheok MH: The SWI/SNF chromatin-remodeling complex and glucocorticoid resistance in acute lymphoblastic leukemia. J Natl Cancer Inst; 2008 Dec 17;100(24):1792-803
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  • [Title] The SWI/SNF chromatin-remodeling complex and glucocorticoid resistance in acute lymphoblastic leukemia.
  • BACKGROUND: Glucocorticoids are used in the curative treatment of acute lymphoblastic leukemia (ALL).
  • Prednisolone resistance was higher in SMARCA4 shRNA-transfected Jurkat cells (drug concentration lethal to 50% of the leukemia cells [LC(50)] = 277 microM) than in control shRNA-transfected cells (LC(50) = 174 microM, difference = 103 microM, 95% confidence interval of the difference = 100 to 106 microM; P < .001, t test).

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  • (PMID = 19066270.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA78224; United States / NCI NIH HHS / CA / R37 CA36401; United States / NIGMS NIH HHS / GM / U01 GM61393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Chromosomal Proteins, Non-Histone; 0 / Glucocorticoids; 0 / Nuclear Proteins; 0 / SWI-SNF-B chromatin-remodeling complex; 0 / Transcription Factors; 9PHQ9Y1OLM / Prednisolone; EC 3.6.1.- / SMARCA4 protein, human; EC 3.6.4.- / DNA Helicases
  • [Other-IDs] NLM/ PMC2639326
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40. Pluta A, Nyman U, Joseph B, Robak T, Zhivotovsky B, Smolewski P: The role of p73 in hematological malignancies. Leukemia; 2006 May;20(5):757-66
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  • Thus, p73 is involved in the regulation of cell cycle, cell death and development.
  • Overexpression of p73 protein and aberrant expression of its particular isoforms, with very low frequency of P73 hypermethylation or mutations, were found in malignant myeloproliferations, including acute myeloblastic leukemia.
  • In contrast, hypermethylation and subsequent inactivation of the P73 gene are the most common findings in malignant lymphoproliferative disorders, especially acute lymphoblastic leukemia (ALL) and non-Hodgkin's lymphomas.

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  • (PMID = 16541141.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
  • [Number-of-references] 99
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41. Damnjanovic T, Milicevic R, Novkovic T, Jovicic O, Bunjevacki V, Jekic B, Lukovic L, Novakovic I, Redzic D, Milasin J: Association between the methylenetetrahydrofolate reductase polymorphisms and risk of acute lymphoblastic leukemia in Serbian children. J Pediatr Hematol Oncol; 2010 May;32(4):e148-50
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  • [Title] Association between the methylenetetrahydrofolate reductase polymorphisms and risk of acute lymphoblastic leukemia in Serbian children.
  • We investigated a possible association of MTHFR polymorphisms (677C>T and 1298A>C) and increased risk for acute lymphoblastic leukemia in 78 affected children.
  • A significant association between CT/TT individuals and reduced risk of acute lymphoblastic leukemia was found.
  • [MeSH-major] Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Case-Control Studies. Child. Child, Preschool. Female. Genetic Predisposition to Disease. Genotype. Humans. Infant. Male. Prognosis. Risk Factors. Serbia

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  • (PMID = 20445408.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
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42. Li X, Gounari F, Protopopov A, Khazaie K, von Boehmer H: Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1. J Exp Med; 2008 Nov 24;205(12):2851-61
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  • Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human T cell acute lymphoblastic leukemia (T-ALL).
  • Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+) T cell receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification.

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  • (PMID = 18981238.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE12948
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / T32 CA070083; United States / NCI NIH HHS / CA / T32-CA70083; United States / NIAID NIH HHS / AI / R01 AI45846; United States / NCI NIH HHS / CA / CA109901
  • [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 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2585834
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43. Klingebiel T, Cornish J, Labopin M, Locatelli F, Darbyshire P, Handgretinger R, Balduzzi A, Owoc-Lempach J, Fagioli F, Or R, Peters C, Aversa F, Polge E, Dini G, Rocha V, Pediatric Diseases and Acute Leukemia Working Parties of the European Group for Blood and Marrow Transplantation (EBMT): Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group. Blood; 2010 Apr 29;115(17):3437-46
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  • [Title] Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group.
  • T cell-depleted haploidentical hematopoietic stem cell transplantation (haploHSCT) is an option to treat children with very high-risk acute lymphoblastic leukemia (ALL) lacking an HLA-identical donor.
  • The 5-year leukemia-free survival (LFS) was 30%, 34%, 22%, and 0%, respectively.
  • In a multivariate analysis, haploHSCT performed in larger centers (performing > or = 231 allotransplantations in the studied period) was associated with improved LFS rate and decreased RI (adjusted P = .01 and P = .04, respectively), adjusting for different patient-, disease-, and transplant-related factors such as number of previous autotransplantations, cytomegalovirus serology status, type of T-cell depletion, and use of total body irradiation and antithymocyte globulin.
  • In conclusion, higher CD34(+) cell dose and better patient selection may improve outcomes of children with ALL who undergo a haploHSCT.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Hospitals, Pediatric. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Europe. Female. Humans. Infant. Male. Remission Induction. Risk Factors. Survival Rate. Transplantation, Homologous


44. Huang XJ, Liu DH, Liu KY, Xu LP, Chen H, Han W, Chen YH, Zhang XH, Lu DP: Treatment of acute leukemia with unmanipulated HLA-mismatched/haploidentical blood and bone marrow transplantation. Biol Blood Marrow Transplant; 2009 Feb;15(2):257-65
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  • [Title] Treatment of acute leukemia with unmanipulated HLA-mismatched/haploidentical blood and bone marrow transplantation.
  • Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains one of the best therapeutic options to cure acute leukemia (AL).
  • Recently, we developed a new method for HLA-mismatched/haploidentical transplantation without in vitro T cell depletion (TCD).
  • The incidence of grade 2-4 acute graft-versus-host disease (aGVHD) was 45.8%, and that of grades 3 and 4 was 13.4%, which was not associated with the extent of HLA disparity.
  • One hundred forty-one of the 250 patients survived free of disease recurrence at a median of 1092 days (range: 442-2437 days) of follow-up.
  • Seventeen patients received DLI as a treatment for relapse after transplantation and 7 patients achieved leukemia-free survival (LFS).
  • The 3-year probability of LFS for acute myelogenous leukemia (AML) was 70.7% and 55.9%, and for acute lymphoblastic leukemia (ALL) it was 59.7% and 24.8% in standard-risk and high-risk groups, respectively.
  • Lower LFS were associated with diagnosis of acute leukemia in the high-risk group (P= .001, relative risk [RR], 95% confidence interval [CI]: 2.94[1.535-5.631]) and the occurrence of aGVHD of grades 3 and 4 (P= .004).
  • [MeSH-major] Bone Marrow Transplantation / methods. HLA Antigens / immunology. Haplotypes / immunology. Histocompatibility / immunology. Leukemia / therapy. Peripheral Blood Stem Cell Transplantation / methods
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Child. Child, Preschool. Disease-Free Survival. Female. Graft vs Host Disease / immunology. HLA-A Antigens. HLA-B Antigens. HLA-DR Antigens. Humans. Leukemia, Myeloid, Acute / mortality. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Transplantation, Homologous / immunology. Treatment Outcome. Young Adult


45. Fischer G S, Neira L L, Ferreiro M M, Torres C MT, Giadrosich R V, Milinarsky T A, Arriagada M M, Arinoviche S R: [Bone mineral density in leukemic children after completing one month of chemotherapy]. Rev Med Chil; 2005 Jan;133(1):71-6
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  • [Transliterated title] Densitometría ósea en niños leucémicos al completar el primer mes de quimioterapia.
  • BACKGROUND: An important loss of bone mineral density, associated to pain and fractures, has been reported in children with acute lymphoblastic leukemia (ALL).
  • AIM: To measure bone mineral density among children with acute lymphoblastic leukemia (ALL) that completed the remission induction phase with chemotherapy, that lasts 30 days.
  • [MeSH-major] Bone Density. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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  • (PMID = 15768152.001).
  • [ISSN] 0034-9887
  • [Journal-full-title] Revista médica de Chile
  • [ISO-abbreviation] Rev Med Chil
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Chile
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46. Ozbek U, Kandilci A, van Baal S, Bonten J, Boyd K, Franken P, Fodde R, Grosveld GC: SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice. Am J Pathol; 2007 Aug;171(2):654-66
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  • [Title] SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice.
  • Leukemia-specific chromosome translocations involving the nucleoporin CAN/NUP214 lead to expression of different fusion genes including DEK-CAN, CAN-ABL, and SET-CAN.
  • DEK-CAN and CAN-ABL1 are associated with acute myeloid leukemia and T-cell acute lymphoblastic leukemia, respectively, whereas SET-CAN was identified in a patient with acute undifferentiated leukemia.
  • Although SET-CAN mice showed expansion of an early progenitor cell pool and partial depletion of lymphocytes, the animals were not leukemia-prone and did not show shortening of disease latency after retroviral tagging.
  • This suggests that SET-CAN expression in acute undifferentiated leukemia might determine the primitive phenotype of the disease, whereas secondary genetic lesions are necessary for disease development.

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  • (PMID = 17569777.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-76480
  • [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 / Chromosomal Proteins, Non-Histone; 0 / Ki-67 Antigen; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion
  • [Other-IDs] NLM/ PMC1934515
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47. Xu T, Gu J, Zhou Y, Du L: Improving detection of differentially expressed gene sets by applying cluster enrichment analysis to Gene Ontology. BMC Bioinformatics; 2009;10:240
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  • When used with two acute leukemia (ALL and ALL/AML) microarray expression datasets, CeaGO correctly identified specifically enriched GO groups that were overlooked by other individual test methods.
  • CeaGO is currently available at http://chgc.sh.cn/en/software/CeaGO/.
  • [MeSH-minor] Cell Cycle. Cluster Analysis. Leukemia, Myeloid, Acute / genetics. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 19653916.001).
  • [ISSN] 1471-2105
  • [Journal-full-title] BMC bioinformatics
  • [ISO-abbreviation] BMC Bioinformatics
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2731756
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48. Cauwelier B, Cavé H, Gervais C, Lessard M, Barin C, Perot C, Van den Akker J, Mugneret F, Charrin C, Pagès MP, Grégoire MJ, Jonveaux P, Lafage-Pochitaloff M, Mozzicconacci MJ, Terré C, Luquet I, Cornillet-Lefebvre P, Laurence B, Plessis G, Lefebvre C, Leroux D, Antoine-Poirel H, Graux C, Mauvieux L, Heimann P, Chalas C, Clappier E, Verhasselt B, Benoit Y, Moerloose BD, Poppe B, Van Roy N, Keersmaecker KD, Cools J, Sigaux F, Soulier J, Hagemeijer A, Paepe AD, Dastugue N, Berger R, Speleman F: Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2007 Jan;21(1):121-8
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  • [Title] Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34) and t(7;7)(p15;q34) involving the T-cell receptor beta (TCRbeta) (7q34) and the HOXA gene locus (7p15) in 5% of T-cell acute lymphoblastic leukemia (T-ALL) patients leading to transcriptional activation of especially HOXA10.
  • [MeSH-major] Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • (PMID = 17039236.001).
  • [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] 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 140441-81-2 / HOXA10 protein, human
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49. Mandal C, Srinivasan GV, Chowdhury S, Chandra S, Mandal C, Schauer R, Mandal C: High level of sialate-O-acetyltransferase activity in lymphoblasts of childhood acute lymphoblastic leukaemia (ALL): enzyme characterization and correlation with disease status. Glycoconj J; 2009 Jan;26(1):57-73
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  • [Title] High level of sialate-O-acetyltransferase activity in lymphoblasts of childhood acute lymphoblastic leukaemia (ALL): enzyme characterization and correlation with disease status.
  • Previous studies had established an over-expression of 9-O-acetylated sialoglycoproteins (Neu5,9Ac(2)-GPs) on lymphoblasts of childhood acute lymphoblastic leukaemia (ALL).
  • Here, we report the discovery and characterization of sialate-O-acetyltransferase enzyme in ALL-cell lines and lymphoblasts from bone marrow of children diagnosed with B- and T-ALL.
  • Sialate-O-acetyltransferase activity in cell lysates or microsomal fractions of lymphoblasts of patients was always higher than that in healthy donors reaching up to 22-fold in microsomes.
  • Sialate-O-acetyltransferase activity increased at the diagnosis of leukaemia, decreased with clinical remission and sharply increased again in relapsed patients as determined by radiometric-assay.
  • [MeSH-major] Acetyltransferases / metabolism. Bone Marrow / enzymology. Microsomes / enzymology. Neoplasm Proteins / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / enzymology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / enzymology
  • [MeSH-minor] Acetyl Coenzyme A / metabolism. Adolescent. Cell Line, Tumor. Child. Child, Preschool. Cytidine Monophosphate / metabolism. Humans. Infant. Male. N-Acetylneuraminic Acid / metabolism

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  • (PMID = 18677580.001).
  • [ISSN] 1573-4986
  • [Journal-full-title] Glycoconjugate journal
  • [ISO-abbreviation] Glycoconj. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 72-89-9 / Acetyl Coenzyme A; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.- / N-acylneuraminate-9(7)-O-acetyltransferase; F469818O25 / Cytidine Monophosphate; GZP2782OP0 / N-Acetylneuraminic Acid
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50. Nakazawa H, Ito T, Makishima H, Misawa N, Okiyama W, Uehara T, Hidaka E, Kiyosawa K, Ishida F: Adenovirus fulminant hepatic failure: disseminated adenovirus disease after unrelated allogeneic stem cell transplantation for acute lymphoblastic leukemia. Intern Med; 2006;45(16):975-80
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  • [Title] Adenovirus fulminant hepatic failure: disseminated adenovirus disease after unrelated allogeneic stem cell transplantation for acute lymphoblastic leukemia.
  • Adenovirus is one of the major causes of non-relapse morbidity and mortality after allogeneic hematopoietic stem cell transplantation for hematological malignancy.
  • Extremely high mortality and aggressiveness of the clinical course have been posing clinical challenges for the diagnosis as well as for the treatment.
  • Here, we report a case with disseminated adenovirus disease presenting with fulminant hepatic failure after bone marrow transplantation for acute lymphoblastic leukemia.
  • [MeSH-major] Adenoviridae Infections / complications. Adenoviridae Infections / etiology. Hematopoietic Stem Cell Transplantation / adverse effects. Liver Failure, Acute / virology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / surgery. Stem Cell Transplantation / adverse effects

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  • (PMID = 16974062.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 47
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51. Szczepanek J, Pogorzala M, Konatkowska B, Juraszewska E, Badowska W, Olejnik I, Kuzmicz M, Stanczak E, Malinowska I, Stefaniak J, Sobol G, Szczepanski T, Czyzewski K, Wysocki M, Styczynski J: Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia. Anticancer Res; 2010 Jun;30(6):2119-24
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  • [Title] Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia.
  • The objective of this study was the analysis of the ex vivo activity of bortezomib in paediatric acute lymphoblastic leukaemia (ALL), in comparison to paediatric acute myeloid leukaemia (AML).
  • A total of 159 patients entered the study, including 106 ALL (including 86 precursor-B-cell ALL, and 20 T-cell ALL) and 53 AML children.
  • With respect to immunophenotype, ex vivo drug resistance in T-cell ALL (T-ALL) was higher for most of the drugs.
  • No differences in drug resistance between T-ALL and common/pre-B-cell-ALL were found for daunorubicin, mitoxantrone and 6-thioguanine.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrazines / therapeutic use

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  • (PMID = 20651360.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib
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52. Tirado CA, Meloni-Ehrig AM, Edwards T, Scheerle J, Burks K, Repetti C, Christacos NC, Kelly JC, Greenberg J, Murphy C, Croft CD, Heritage D, Mowrey PN: Cryptic ins(4;11)(q21;q23q23) detected by fluorescence in situ hybridization: a variant of t(4;11)(q21;q23) in an infant with a precursor B-cell acute lymphoblastic leukemia report of a second case. Cancer Genet Cytogenet; 2007 Apr 15;174(2):166-9
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  • [Title] Cryptic ins(4;11)(q21;q23q23) detected by fluorescence in situ hybridization: a variant of t(4;11)(q21;q23) in an infant with a precursor B-cell acute lymphoblastic leukemia report of a second case.
  • We report the chromosomal findings in a 4-year-old female with precursor B-cell acute lymphoblastic leukemia (ALL).
  • Our case exemplifies the importance of FISH in the further characterization of precursor B-cell ALL cases without any apparent prognostically significant chromosomal abnormalities.
  • [MeSH-major] Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Child, Preschool. Chromosome Banding. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Mutagenesis, Insertional. Myeloid-Lymphoid Leukemia Protein / genetics

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  • (PMID = 17452260.001).
  • [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 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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53. Panagopoulos I, Lilljebjörn H, Strömbeck B, Hjorth L, Olofsson T, Johansson B: MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia. Haematologica; 2006 Sep;91(9):1287-8
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  • [Title] MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia.
  • MLL/GAS7, resulting from t(11;17)(q23;p13), has been reported in one case of treatment-related acute myeloid leukemia (AML).
  • We present a de novo case of t(11;17)-positive pediatric acute lymphoblastic leukemia.
  • [MeSH-major] Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Female. Humans. Infant. Myeloid-Lymphoid Leukemia Protein / genetics. Nerve Tissue Proteins / genetics

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  • (PMID = 16956839.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / GAS7 protein, human; 0 / MLL-GAS7 fusion protein; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
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54. Fujiwara S, Yamashita Y, Choi YL, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Ozawa K, Mano H: Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening. Leuk Lymphoma; 2007 May;48(5):978-86
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  • Biphenotypic acute leukemia (BAL) is a relatively rare subtype of acute leukemia characterized by the presence of both myeloid and lymphoid cell surface antigens.
  • Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in leukemia patients, especially in those with refractory disease.
  • Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of acute leukemia.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia / genetics. Leukemia / metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism
  • [MeSH-minor] 3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism. Cell Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic

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  • (PMID = 17487742.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y
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55. Tragiannidis A, Athanassiadou F, Papageorgiou T, Petsatodis G: Severe skeletal complications in a child with acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2006 Sep;23(6):523-5; author reply 527-8
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  • [Title] Severe skeletal complications in a child with acute lymphoblastic leukemia.
  • [MeSH-major] Osteoporosis / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [CommentOn] Pediatr Hematol Oncol. 2005 Oct-Nov;22(7):543-50 [16166046.001]
  • (PMID = 16849284.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] X1J18R4W8P / Alendronate
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56. Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY: [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL]. Nan Fang Yi Ke Da Xue Xue Bao; 2009 Mar;29(3):512-5
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  • [Title] [Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].
  • OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive acute lymphoblastic leukemia (BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.
  • METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the diagnosis of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.
  • The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem cell transplantation (allo-HSCT) (16 cases).
  • In patients with peripheral white blood cell (WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).
  • According to the FAB classification, 56 cases were divided into L1, L2 and biphenotypic acute leukemia (BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).
  • In terms of immunophenotype grouping by EGIL, the patients with ALL, myeloid antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).
  • In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22) abnormality, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem Cell Transplantation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 19304540.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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57. Papaemmanuil E, Hosking FJ, Vijayakrishnan J, Price A, Olver B, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Tomlinson IP, Taylor M, Greaves M, Houlston RS: Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia. Nat Genet; 2009 Sep;41(9):1006-10
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  • [Title] Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia.
  • To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls.
  • The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-cell precursor ALL with hyperdiploidy.
  • These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into disease causation of this specific hematological cancer.
  • Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-cell progenitors.
  • [MeSH-major] Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 7. Genetic Predisposition to Disease. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology


58. Dong X, Xiong L, Jiang X, Wang Y: Quantitative proteomic analysis reveals the perturbation of multiple cellular pathways in jurkat-T cells induced by doxorubicin. J Proteome Res; 2010 Nov 5;9(11):5943-51
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  • Doxorubicin remains an important part of chemotherapy regimens in the clinic and is considered an effective agent in the treatment of acute lymphoblastic leukemia (ALL).
  • Here we utilized mass spectrometry, together with stable isotope labeling by amino acids in cell culture (SILAC), to analyze comparatively the protein expression in Jurkat-T cells before and after treatment with a clinically relevant concentration of doxorubicin.

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  • (PMID = 20822187.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA116522; United States / NCI NIH HHS / CA / R01 CA 116522
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 80168379AG / Doxorubicin; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ NIHMS235911; NLM/ PMC2974774
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59. Bacher U, Schnittger S, Haferlach C, Haferlach T: Molecular diagnostics in acute leukemias. Clin Chem Lab Med; 2009;47(11):1333-41
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  • [Title] Molecular diagnostics in acute leukemias.
  • Acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) both represent highly heterogeneous entities on the basis of diverse cyto- and molecular genetic alterations with considerable influence on prognosis and therapeutic decisions.
  • Thus, molecular analysis based on various techniques, such as polymerase chain reaction (PCR) has become an essential part of the diagnostic panel for acute leukemia.
  • In addition, cytomorphology, cytogenetics, fluorescence in situ hybridization (FISH), and immunophenotyping with multiparameter flow cytometry (MFC) need to be applied for diagnosis.
  • During the course of disease, the residual leukemic cell load can be monitored by highly sensitive quantitative PCR techniques ("real-time PCR").
  • This demonstrates that molecular diagnostics for acute leukemias are in continuous development.
  • This review summarizes the most important recurrent molecular markers seen in acute leukemias, their role in prognosis and therapy and provides an overview on the relevant PCR techniques.

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  • (PMID = 19817644.001).
  • [ISSN] 1437-4331
  • [Journal-full-title] Clinical chemistry and laboratory medicine
  • [ISO-abbreviation] Clin. Chem. Lab. Med.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 78
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60. Baldazzi C, Iacobucci I, Luatti S, Ottaviani E, Marzocchi G, Paolini S, Stacchini M, Papayannidis C, Gamberini C, Martinelli G, Baccarani M, Testoni N: B-cell acute lymphoblastic leukemia as evolution of a 8p11 myeloproliferative syndrome with t(8;22)(p11;q11) and BCR-FGFR1 fusion gene. Leuk Res; 2010 Oct;34(10):e282-5
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  • [Title] B-cell acute lymphoblastic leukemia as evolution of a 8p11 myeloproliferative syndrome with t(8;22)(p11;q11) and BCR-FGFR1 fusion gene.
  • [MeSH-major] Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 8. Gene Fusion. Myeloproliferative Disorders / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-bcr / genetics. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Translocation, Genetic

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  • (PMID = 20594995.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
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61. Braun FK, Fecker LF, Schwarz C, Walden P, Assaf C, Dürkop H, Sterry W, Eberle J: Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells. J Invest Dermatol; 2007 Oct;127(10):2425-37
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  • [Title] Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells.
  • In this study, cutaneous T-cell lymphoma (CTCL) cell lines revealed pronounced resistance to death ligands as compared to cell lines of T-cell acute lymphoblastic leukemia (T-ALL).
  • The proapoptotic activity of tumor necrosis factor (TNF)-alpha was blocked, sensitivity to TNF-related apoptosis-inducing ligand was significantly reduced, and 1/4 CTCL cell lines was resistant to CD95 activation.
  • No indication for a responsibility of typical downstream regulators of apoptosis was obtained, but loss of CD95 was found in 1/4, loss of TNF-R1 in 3/4, loss of caspase-10 in 2/4, loss of Bid in 1/4, and overexpression of cellular flice inhibitory protein was found in 4/4 CTCL cell lines.
  • [MeSH-major] Apoptosis / physiology. Lymphoma, T-Cell, Cutaneous / pathology. Receptors, Death Domain / antagonists & inhibitors. Signal Transduction / physiology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD95 / physiology. BH3 Interacting Domain Death Agonist Protein / physiology. CASP8 and FADD-Like Apoptosis Regulating Protein / physiology. Caspase 10 / physiology. Cell Line, Tumor. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17495957.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Receptors, Death Domain; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 10
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62. Huang X, Chen S, Shen Q, Yang L, Li B, Zhong L, Geng S, Du X, Li Y: Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia. J Hematol Oncol; 2010;3(1):44
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  • [Title] Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia.
  • BACKGROUND: In a human T-cell acute lymphoblastic leukemia (T-ALL) cell line (Molt-4), siRNA-mediated suppression of BCL11B expression was shown to inhibit proliferation and induce apoptosis, functions which may be related to genes involved in apoptosis (such as TNFSF10 and BCL2L1) and TGF-β pathways (such as SPP1and CREBBP).
  • [MeSH-major] CREB-Binding Protein / biosynthesis. Gene Expression Regulation, Neoplastic / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Repressor Proteins / biosynthesis. Tumor Suppressor Proteins / biosynthesis. bcl-X Protein / biosynthesis

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  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
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  • (PMID = 21080944.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL11B protein, human; 0 / BCL2L1 protein, human; 0 / CREBBP protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / bcl-X Protein; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC2992472
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63. Gumy-Pause F, Wacker P, Maillet P, Betts DR, Sappino AP: ATM variants and predisposition to childhood T-lineage acute lymphoblastic leukaemia. Leukemia; 2006 Mar;20(3):526-7; author reply 527
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  • [Title] ATM variants and predisposition to childhood T-lineage acute lymphoblastic leukaemia.
  • [MeSH-major] Cell Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Genetic Predisposition to Disease. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics

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  • [CommentOn] Leukemia. 2005 Nov;19(11):1887-95 [16167060.001]
  • (PMID = 16408093.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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64. Slavov SN, Gimenes Teixeira HL, Rego EM: The role of micro-ribonucleic acids in normal hematopoiesis and leukemic T-lymphogenesis. Braz J Med Biol Res; 2010 Jul;43(7):619-26
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  • Although many data are available about the role of microRNAs in various lymphoproliferative disorders, their impact on the development of acute lymphoblastic leukemia of T-cell progenitors is largely unknown.

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  • (PMID = 20549139.001).
  • [ISSN] 1414-431X
  • [Journal-full-title] Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • [ISO-abbreviation] Braz. J. Med. Biol. Res.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / MicroRNAs; 0 / RNA, Neoplasm
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65. Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S: Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia. J Clin Exp Hematop; 2010;50(1):51-8
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  • [Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
  • We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
  • The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.
  • Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).
  • [MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

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  • (PMID = 20505276.001).
  • [ISSN] 1880-9952
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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66. Tie LJ, Gu LJ, Jiang LM, Zhao JC, Chen J, Pan C, Dong L, Chen J, Xue HL, Tang JY, Wang YP: [Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia]. Zhongguo Dang Dai Er Ke Za Zhi; 2009 Apr;11(4):246-50
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  • [Title] [Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia].
  • OBJECTIVE: Minimal residual disease (MRD) is one of the most important prognostic factors in childhood acute lymphoblastic leukemia (ALL).
  • Using sets of combined antibodies, immunophenotypic expression of leukemia cells was observed in 95 of 106 B-lineage ALL cases (89.6%).
  • Only one aberrant immunophenotype was observed in 11 cases (11.6%) and most patients with B-lineage ALL (88.4%) expressed at least two suitable targets.
  • 2. Using PCR technique, T-cell receptor (TCR) or immunoglobulin gene rearrangements were identified in 26 of 27 patients (96.3%).
  • The majority (70%) of T-lineage ALL cases contained TCRVgammaI-Jgamma1.3/2.3.
  • Cross-lineage TCR rearrangements were found in 57.1% of cases with B-lineage ALL.
  • Cross-lineage TCR rearrangements and bi-allelic gene rearrangements were observed in many patients.
  • [MeSH-major] Flow Cytometry / methods. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19374803.001).
  • [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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67. Osugi Y, Yamada H, Hosoi G, Noma H, Ikemiya M, Ishii T, Sako M: Treatment with candesartan combined with angiotensin-converting enzyme inhibitor for immunosuppressive treatment-resistant nephrotic syndrome after allogeneic stem cell transplantation. Int J Hematol; 2006 Jun;83(5):454-8
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  • [Title] Treatment with candesartan combined with angiotensin-converting enzyme inhibitor for immunosuppressive treatment-resistant nephrotic syndrome after allogeneic stem cell transplantation.
  • Most cases of nephrotic syndrome following stem cell transplantation (SCT) occur 6 months after SCT.
  • A 15-year-old boy with acute lymphoblastic leukemia underwent allogeneic peripheral blood SCT from a completely HLA-matched sibling after completion of a conditioning regimen composed of 12-Gy doses of total-body irradiation, 600 mg/m2 thiotepa, and 140 mg/m2 melphalan.
  • [MeSH-major] Angiotensin-Converting Enzyme Inhibitors / administration & dosage. Antihypertensive Agents / administration & dosage. Benzimidazoles / administration & dosage. Nephrotic Syndrome / drug therapy. Stem Cell Transplantation. Tetrazoles / administration & dosage
  • [MeSH-minor] Adolescent. Drug Resistance / drug effects. Humans. Immunosuppressive Agents / administration & dosage. Male. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Proteinuria / drug therapy. Proteinuria / etiology. Proteinuria / pathology. Time Factors. Transplantation, Homologous

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  • (PMID = 16787879.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antihypertensive Agents; 0 / Benzimidazoles; 0 / Immunosuppressive Agents; 0 / Tetrazoles; S8Q36MD2XX / candesartan
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68. Kolenova A, Hikkel I, Ilencikova D, Hikkelova M, Sejnova D, Kaiserova E, Cizmar A, Puskacova J, Bubanska E, Oravkinova I, Gencik M: Minimal residual disease detection using real-time quantitative PCR analysis of immunoglobulin and T-cell receptor gene rearrangements in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: Slovak experience. Neoplasma; 2010;57(6):552-61
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  • [Title] Minimal residual disease detection using real-time quantitative PCR analysis of immunoglobulin and T-cell receptor gene rearrangements in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: Slovak experience.
  • Acute lymphoblastic leukemia is the most common form of cancer in children.
  • An intense effort has been made to develop methods to determine the degree of minimal residual leukemia cells present in patients considered to be in morphological remission.
  • Because of the strong correlation between minimal residual disease (MRD) levels and risk of relapse, monitoring of MRD provides unique information regarding treatment response.
  • The MRD monitoring based on real-time quantitative PCR detection of patient-specific immunoglobulin and T-cell receptor (Ig/TCR) gene rearrangements is currently considered to be the most reliable tool for MRD-based diagnosis in ALL.
  • A total of 40 patients with BCP-ALL ( B cell precursor ALL) and 4 patients with T ALL were analyzed for Ig/TCR rearrangement.
  • [MeSH-major] Gene Rearrangement. Gene Rearrangement, T-Lymphocyte. Genes, Immunoglobulin. Polymerase Chain Reaction / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Immunophenotyping. Infant. Leukocyte Count. Male. Neoplasm, Residual / diagnosis

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  • (PMID = 20845994.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
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69. Ercan TE, Soycan LY, Apak H, Celkan T, Ozkan A, Akdenizli E, Kasapçopur O, Yildiz I: Antibody titers and immune response to diphtheria-tetanus-pertussis and measles-mumps-rubella vaccination in children treated for acute lymphoblastic leukemia. J Pediatr Hematol Oncol; 2005 May;27(5):273-7
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  • [Title] Antibody titers and immune response to diphtheria-tetanus-pertussis and measles-mumps-rubella vaccination in children treated for acute lymphoblastic leukemia.
  • The objective of this study was to investigate the diphtheria-tetanus-pertussis and/or measles-mumps antibody titers before and after vaccination at various time points of acute lymphoblastic leukemia (ALL) therapy and to suggest an appropriate vaccination approach for ALL patients.
  • [MeSH-major] Antibody Formation. Diphtheria-Tetanus-Pertussis Vaccine / therapeutic use. Measles Vaccine / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Rubella Vaccine / therapeutic use


70. Ek T, Mellander L, Andersson B, Abrahamsson J: Immune reconstitution after childhood acute lymphoblastic leukemia is most severely affected in the high risk group. Pediatr Blood Cancer; 2005 May;44(5):461-8
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  • [Title] Immune reconstitution after childhood acute lymphoblastic leukemia is most severely affected in the high risk group.
  • OBJECTIVE: The aim was to examine the immune reconstitution after current chemotherapy for childhood ALL, with a special focus on finding immunologic variables that predict a poor immune response to vaccinations.
  • PROCEDURE: In a cross-sectional study of 31 children after treatment with the NOPHO ALL-1992 protocol peripheral blood lymphocyte subsets, T- and B-cell function in vitro and serum immunoglobulins (Ig) were measured.
  • Naive T-cell subsets were more reduced than memory subsets.
  • Total B-cell number was low at 1 month, but normal at 6 months.
  • Antigen-independent T- and B-cell function in vitro were affected at 1 month, but virtually normalized at 6 months.
  • The most intensively treated patients still have persistent abnormalities in T-, B-, and NK-cell subsets at 6 months post therapy and show a poor response to immunization with T-cell dependent antigens.
  • In the HR group, routine re-immunizations before this time point are of limited benefit, and the effect of repeated vaccinations should be evaluated.
  • [MeSH-major] Immune System / physiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Regeneration. Vaccination


71. Giebel S, Krawczyk-Kuliś M, Adamczyk-Cioch M, Czyz A, Lech-Marańda E, Piatkowska-Jakubas B, Paluszewska M, Pałynyczko G, Piszcz J, Hołowiecki J, Polish Adult Leukemia Group: Prophylaxis and therapy of central nervous system involvement in adult acute lymphoblastic leukemia: recommendations of the Polish Adult Leukemia Group. Pol Arch Med Wewn; 2008 Jun;118(6):356-61
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  • [Title] Prophylaxis and therapy of central nervous system involvement in adult acute lymphoblastic leukemia: recommendations of the Polish Adult Leukemia Group.
  • The central nervous system (CNS) is one of the most frequent extramedullary locations of adult acute lymphoblastic leukemia (ALL), affecting approximately 5% of patients at diagnosis.
  • T-lineage ALL, high initial leukocyte counts and mediastinal involvement are the predisposing factors.
  • As the prognosis of patients with isolated or mixed CNS relapse is particularly poor, adequate prophylaxis seems critical.
  • [MeSH-major] Central Nervous System Neoplasms / prevention & control. Central Nervous System Neoplasms / therapy. Neoplasm Recurrence, Local. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quality of Life

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  • (PMID = 18619191.001).
  • [Journal-full-title] Polskie Archiwum Medycyny Wewnetrznej
  • [ISO-abbreviation] Pol. Arch. Med. Wewn.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 28
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72. Yoshida K, Hasegawa D, Takusagawa A, Kato I, Ogawa C, Echizen N, Ohkoshi K, Yamaguchi T, Hosoya R, Manabe A: Bullous exudative retinal detachment due to infiltration of leukemic cells in a child with acute lymphoblastic leukemia. Int J Hematol; 2010 Oct;92(3):535-7
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  • [Title] Bullous exudative retinal detachment due to infiltration of leukemic cells in a child with acute lymphoblastic leukemia.
  • Acute lymphoblastic leukemia (ALL) is known to cause several ocular involvements, but exudative retinal detachment is a rare complication.
  • We describe a case report of a 4-year-old boy with T cell ALL who developed bilateral exudative retinal detachment caused by leukemic infiltration in the retinas after achieving hematological remission.
  • Intravenous steroid pulse therapy and local irradiation reversed the condition, but it recurred concurrently with disease progression after a second relapse in the bone marrow.
  • It is suggested that ophthalmic examination is crucial for ALL patients, especially for those whose white blood cell count is very high at onset.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Retinal Detachment / etiology. Retinal Detachment / pathology

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  • (PMID = 20838956.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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73. Gao YJ, Zhu XH, Yang Y, Wu Y, Lu FJ, Zhai XW, Wang HS: Prevalence of ETV6-RUNX1 fusion gene in children with acute lymphoblastic leukemia in China. Cancer Genet Cytogenet; 2007 Oct 1;178(1):57-60
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  • [Title] Prevalence of ETV6-RUNX1 fusion gene in children with acute lymphoblastic leukemia in China.
  • A series of 92 Chinese children newly diagnosed with acute lymphoblastic leukemia (ALL) were examined for the ETV6-RUNX1 (previously TEL-AML1) fusion gene by using a nested reverse transcriptase-polymerase chain reaction.
  • ETV6-RUNX1 fusion transcripts were detected in 21 of 92 patients (22.8%): 16 with common ALL, 4 with precursor B-cell ALL, and 1 with T-ALL.
  • The prevalence of ETV6-RUNX1 positivity was 24.7% (20/81) in childhood B-lineage ALL.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / biosynthesis. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / biosynthesis. Repressor Proteins / genetics

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  • (PMID = 17889709.001).
  • [ISSN] 0165-4608
  • [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 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
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74. Lazić J, Dokmanović L, Krstovski N, Predojević J, Tosić N, Pavlović S, Janić D: [Immunoglobulin genes and T-cell receptors as molecular markers in children with acute lymphoblastic leukaemia]. Srp Arh Celok Lek; 2009 Jul-Aug;137(7-8):384-90
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  • [Title] [Immunoglobulin genes and T-cell receptors as molecular markers in children with acute lymphoblastic leukaemia].
  • INTRODUCTION: Acute lymphoblastic leukaemia (ALL) is a malignant clonal disease, one of the most common malignancies in childhood.
  • The ability of molecular genetic methods help to establish submicroscopic classification and minimal residual disease (MRD) follow up, in major percent responsible for relapse.
  • METHODS: Forty-one children with ALL were enrolled in the study group, with initial diagnosis of IgH and TCR gene rearrangements by polimerase chain reaction (PCR).
  • RESULTS: In the study group IgH rearrangement was detected in 82.9% of children at the diagnosis, while TCR rearrangement was seen in 56.1%.
  • MRD stands out as a precise predictive factor for the relapse of disease.
  • [MeSH-major] Gene Rearrangement. Immunoglobulin Heavy Chains / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 19764592.001).
  • [ISSN] 0370-8179
  • [Journal-full-title] Srpski arhiv za celokupno lekarstvo
  • [ISO-abbreviation] Srp Arh Celok Lek
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell
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75. Matsuzaki A, Suminoe A, Koga Y, Kusuhara K, Hara T, Ogata R, Sata T, Hara T: Fatal visceral varicella-zoster virus infection without skin involvement in a child with acute lymphoblastic leukemia. Pediatr Hematol Oncol; 2008 Apr-May;25(3):237-42
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  • [Title] Fatal visceral varicella-zoster virus infection without skin involvement in a child with acute lymphoblastic leukemia.
  • A 5-year-old girl with acute lymphoblastic leukemia in remission suffered from fatal visceral varicella-zoster virus (VZV) infection after the oral administration of a high-dose dexamethasone.
  • [MeSH-major] Chickenpox / etiology. Herpesvirus 3, Human. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
  • [MeSH-minor] Antigens, Viral / blood. Antineoplastic Agents, Hormonal / administration & dosage. Child, Preschool. DNA, Viral / blood. Dexamethasone / administration & dosage. Disseminated Intravascular Coagulation / etiology. Fatal Outcome. Female. Humans. Liver Failure, Acute / etiology

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  • (PMID = 18432508.001).
  • [ISSN] 1521-0669
  • [Journal-full-title] Pediatric hematology and oncology
  • [ISO-abbreviation] Pediatr Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Antineoplastic Agents, Hormonal; 0 / DNA, Viral; 7S5I7G3JQL / Dexamethasone
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76. Chen LJ, Li JY, Wu YJ, Yang H, Qian SX, Wu HX, Lu H, Xu W, Sheng RL: [Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2007 Aug;15(4):692-5
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  • [Title] [Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia].
  • The objective of this study was to investigate the immunophenotypic characteristics of T-cell acute lymphoblastic leukemia (T-ALL).
  • The results showed that the T-lineage-associated antigen expressions were CD7 > CD2 > CD3 > CD5 successively.
  • Among 140 cases of T-ALL, 12 (8.57%) was accompanied by B-lineage associated antigen expression.
  • Myeloid antigen expression was identified in 31 out of 136 cases (22.79%).
  • The positive rate of myeloid antigen expression in CD34(+) T-ALL (36.58%) was significantly higher than that in CD34(-) T-ALL (15.38%) (p < 0.01).
  • It is concluded that immunophenotyping is an important tool for diagnosis of T-ALL.

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  • (PMID = 17708784.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
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77. Bacher U, Kohlmann A, Haferlach T: Perspectives of gene expression profiling for diagnosis and therapy in haematological malignancies. Brief Funct Genomic Proteomic; 2009 May;8(3):184-93
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  • [Title] Perspectives of gene expression profiling for diagnosis and therapy in haematological malignancies.
  • Considering the heterogeneity of leukaemias and the widening spectrum of therapeutic strategies, novel diagnostic methods are urgently needed for haematological malignancies.
  • For a decade, gene expression profiling (GEP) has been applied in leukaemia research.
  • Thus, various studies demonstrated worldwide that the majority of genetically defined leukaemia subtypes are accurately predictable by GEP, for example, with respect to reciprocal rearrangements in acute myeloid leukaemia (AML).
  • Considering the lymphatic malignancies, GEP studies defined novel clinically relevant subtypes in diffuse large B cell lymphoma (DLBCL), and improved the discrimination of Burkitt lymphoma and DLBCL cases, overcoming considerable overlaps of these entities that exist from morphological and genetic perspectives.
  • Treatment-specific sensitivity assays are being developed for targeted drugs such as farnesyl transferase inhibitors in AML or imatinib in BCR-ABL1 positive acute lymphoblastic leukaemia (ALL).
  • Large multicentre studies such as the MILE Study (Microarray Innovations in LEukemia) aim at translating this methodology into clinical routine workflows and to catalyze this process.
  • [MeSH-major] Gene Expression Profiling. Hematologic Neoplasms / diagnosis. Hematologic Neoplasms / therapy

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  • (PMID = 19474126.001).
  • [ISSN] 1477-4062
  • [Journal-full-title] Briefings in functional genomics & proteomics
  • [ISO-abbreviation] Brief Funct Genomic Proteomic
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 90
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78. Matsuno N, Hoshino K, Nanri T, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N: p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia. Leuk Res; 2005 May;29(5):557-64
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  • [Title] p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia.
  • Cyclin-dependent kinase inhibitor p15 is frequently inactivated by either methylation or deletion in patients with acute leukemia.
  • To examine pathologic and clinical significance of the p15 gene inactivation, we established a quantitative assay of p15 mRNA expression in the bone marrow cells by real-time quantitative reverse transcriptase-polymerase chain reaction. p15 mRNA expression in 14 patients with precursor B-cell acute lymphoblastic leukemia (PBC-ALL) well correlated with status of deletion and methylation in the p15 gene analyzed by Southern blotting.
  • Furthermore, two patients with PBC-ALL and 11 acute myeloblastic leukemia (AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
  • Among 108 AML patients, p15 mRNA expression was significantly lower in the myeloid lineage (M1, M2, M3) than the monocytic lineage (M4, M5) (P = 0.0019).
  • [MeSH-major] Burkitt Lymphoma / genetics. Cell Cycle Proteins / genetics. DNA Methylation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA, Messenger / metabolism. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Acute Disease. Adult. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology. Cell Lineage. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15. Humans. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Tumor Cells, Cultured

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  • (PMID = 15755508.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
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79. Porkka K, Koskenvesa P, Lundán T, Rimpiläinen J, Mustjoki S, Smykla R, Wild R, Luo R, Arnan M, Brethon B, Eccersley L, Hjorth-Hansen H, Höglund M, Klamova H, Knutsen H, Parikh S, Raffoux E, Gruber F, Brito-Babapulle F, Dombret H, Duarte RF, Elonen E, Paquette R, Zwaan CM, Lee FY: Dasatinib crosses the blood-brain barrier and is an efficient therapy for central nervous system Philadelphia chromosome-positive leukemia. Blood; 2008 Aug 15;112(4):1005-12
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  • [Title] Dasatinib crosses the blood-brain barrier and is an efficient therapy for central nervous system Philadelphia chromosome-positive leukemia.
  • Although imatinib, a BCR-ABL tyrosine kinase inhibitor, is used to treat acute Philadelphia chromosome-positive (Ph(+)) leukemia, it does not prevent central nervous system (CNS) relapses resulting from poor drug penetration through the blood-brain barrier.
  • Imatinib and dasa-tinib (a dual-specific SRC/BCR-ABL kinase inhibitor) were compared in a preclinical mouse model of intracranial Ph(+) leukemia.
  • Clinical dasatinib treatment in patients with CNS Ph(+) leukemia was assessed.
  • Stabilization and regression of CNS disease were achieved with continued dasa-tinib administration.
  • The drug also demonstrated substantial activity in 11 adult and pediatric patients with CNS Ph(+) leukemia.
  • Dasatinib has promising therapeutic potential in managing intracranial leukemic disease and substantial clinical activity in patients who experience CNS relapse while on imatinib therapy.
  • [MeSH-major] Blood-Brain Barrier / metabolism. Central Nervous System Neoplasms / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / administration & dosage. Pyrimidines / pharmacokinetics. Thiazoles / administration & dosage. Thiazoles / pharmacokinetics
  • [MeSH-minor] Adolescent. Adult. Aged. Animals. Child. Cytogenetic Analysis. Dasatinib. Disease Models, Animal. Drug Evaluation, Preclinical. Drug Monitoring. Female. Humans. Male. Mice. Middle Aged. Precursor Cell Lymphoblastic Leukemia-Lymphoma. Remission Induction. Spinal Puncture. Survival Rate. Treatment Outcome. Tumor Burden / drug effects

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  • (PMID = 18477770.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00108719/ NCT00110097
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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80. Baeumler J, Szuhai K, Falkenburg JH, van Schie ML, Ottmann OG, Nijmeijer BA: Establishment and cytogenetic characterization of a human acute lymphoblastic leukemia cell line (ALL-VG) with ETV6/ABL1 rearrangement. Cancer Genet Cytogenet; 2008 Aug;185(1):37-42
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  • [Title] Establishment and cytogenetic characterization of a human acute lymphoblastic leukemia cell line (ALL-VG) with ETV6/ABL1 rearrangement.
  • Here we present the generation of an ETV6/ABL1 positive human acute lymphoblastic leukemia (ALL) cell line, ALL-VG.
  • The cell line expressed ETV6/ABL1 fusion transcripts and displayed sensitivity to imatinib with an IC(50) of 0.1 microM.
  • The ALL-VG cell line may serve as a tool for the study of ETV6/ABL1.
  • [MeSH-major] Cell Line, Tumor. Chromosomes, Human, Pair 6. Genes, abl. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Benzamides. Cell Survival / drug effects. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 12. Cytogenetic Analysis. Dose-Response Relationship, Drug. Humans. Imatinib Mesylate. Inhibitory Concentration 50. Male. Piperazines / pharmacology. Protein-Tyrosine Kinases / pharmacology. Pyrimidines / pharmacology. Remission Induction. Sensitivity and Specificity

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  • (PMID = 18656692.001).
  • [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
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
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81. Novara F, Beri S, Bernardo ME, Bellazzi R, Malovini A, Ciccone R, Cometa AM, Locatelli F, Giorda R, Zuffardi O: Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood. Hum Genet; 2009 Oct;126(4):511-20
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  • [Title] Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood.
  • Deletion of chromosome 9p21 is a crucial event for the development of several cancers including acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Sequence Deletion / genetics

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  • (PMID = 19484265.001).
  • [ISSN] 1432-1203
  • [Journal-full-title] Human genetics
  • [ISO-abbreviation] Hum. Genet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers
  • [Other-IDs] NLM/ PMC2762534
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82. Huh J, Chung W: [A Case of Acute Lymphoblastic Leukemia with ider(9)(q10)t(9;22)(q34;q11.2).]. Korean J Lab Med; 2006 Jun;26(3):223-6
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  • [Title] [A Case of Acute Lymphoblastic Leukemia with ider(9)(q10)t(9;22)(q34;q11.2).].
  • It is known to be rarely observed in acute lymphoblastic leukemia (ALL) or lymphoblastic crisis transformed from chronic myelogenous leukemia.
  • We herein describe a 26-year-old female patient with precursor B-cell ALL, cytogenetically characterized by ider(9)(q10)t(9;22).
  • Although a t(9;22) and a deletion of the short arm of chromosome 9 are known to be associated with a poor prognostic factor in acute lymphoblastic leukemia, a larger study is needed to determine the prognosis of ider(9)(q10)t(9;22) cases.

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  • (PMID = 18156729.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Korea (South)
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83. Jeeninga RE, Jan B, van der Linden B, van den Berg H, Berkhout B: Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-cell lines: towards a new virotherapy approach. Cancer Res; 2005 Apr 15;65(8):3347-55
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  • [Title] Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-cell lines: towards a new virotherapy approach.
  • T-cell acute lymphoblastic leukemia is a high-risk type of blood-cell cancer.
  • We analyzed the possibility of developing virotherapy for T-cell acute lymphoblastic leukemia.
  • This mini-HIV virus has five deletions (vif, vpR, vpU, nef, and U3) and replicated in the SupT1 cell line, but did not replicate in normal peripheral blood mononuclear cells.
  • The stripped down mini-HIV variant was also able to efficiently remove leukemic cells from a mixed culture with untransformed control cells.
  • In contrast to wild-type HIV-1, we did not observe bystander killing in mixed culture experiments with the mini-HIV variant.
  • The mini-HIV variant that uses CD4 and CXCR4 for cell entry could potentially be used against CXCR4-expressing malignancies such as T-lymphoblastic leukemia/lymphoma, natural killer leukemia, and some myeloid leukemias.
  • [MeSH-major] HIV-1 / physiology. Leukemia-Lymphoma, Adult T-Cell / therapy. Leukemia-Lymphoma, Adult T-Cell / virology. T-Lymphocytes / virology
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Cell Line, Tumor. Female. Gene Deletion. Genes, nef / genetics. Genes, vif / genetics. Genes, vpr / genetics. Genes, vpu / genetics. HIV Long Terminal Repeat / genetics. Humans. Jurkat Cells. Receptors, CXCR4 / biosynthesis. Virus Replication

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  • (PMID = 15833868.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R21-AI47017-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Receptors, CXCR4
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84. Li HL, Xiang Z, Zhao T: [Expressions of surviving, MMP2, TIMP1, CD44 and nm23 of two tumors originating from different immunosurveillance in the same patient]. Nan Fang Yi Ke Da Xue Xue Bao; 2010 Jun;30(6):1291-4
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  • METHODS: The expressions of survivin, MMP2, TIMP1, CD44, and nm23 proteins were detected immunohistochemically in a patient with acute lymphoblastic leukemia and lymphoma after allogeneic blood stem cell transplantation.
  • RESULTS: Survivin, MMP2, TIMP1, CD44, and nm23 proteins were positive in acute lymphoblastic leukemia samples obtained before transplantation and negative in the lymphoma tissue occurring after the transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / adverse effects. Inhibitor of Apoptosis Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Neoplasms, Second Primary / metabolism. Tissue Inhibitor of Metalloproteinase-1 / metabolism
  • [MeSH-minor] Adult. Antigens, CD44 / metabolism. Female. Humans. Matrix Metalloproteinase 2 / metabolism. NM23 Nucleoside Diphosphate Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

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  • (PMID = 20584660.001).
  • [ISSN] 1673-4254
  • [Journal-full-title] Nan fang yi ke da xue xue bao = Journal of Southern Medical University
  • [ISO-abbreviation] Nan Fang Yi Ke Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / BIRC5 protein, human; 0 / CD44 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / TIMP1 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-1; EC 2.7.4.6 / NME1 protein, human; EC 3.4.24.24 / MMP2 protein, human; EC 3.4.24.24 / Matrix Metalloproteinase 2
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85. Matsunaga T, Kamiya T, Sumi D, Kumagai Y, Kalyanaraman B, Hara A: L-Xylulose reductase is involved in 9,10-phenanthrenequinone-induced apoptosis in human T lymphoma cells. Free Radic Biol Med; 2008 Mar 15;44(6):1191-202
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  • 9,10-Phenanthrenequinone (9,10-PQ), a major component in diesel exhaust particles, is suggested to generate reactive oxygen species (ROS) through its redox cycling, leading to cell toxicity. l-Xylulose reductase (XR), a NADPH-dependent enzyme in the uronate pathway, strongly reduces alpha-dicarbonyl compounds and was thought to act as a detoxification enzyme against reactive carbonyl compounds.
  • Here, we have investigated the role of intracellular ROS generation in apoptotic signaling in human acute T-lymphoblastic leukemia MOLT-4 cells treated with 9,10-PQ and the role of XR in the generation of ROS.
  • Surprisingly, the ROS generation and cytotoxicity by 9,10-PQ were augmented in an XR-transformed cell line.
  • [MeSH-minor] Blotting, Western. Caspases / drug effects. Caspases / metabolism. Cell Line, Tumor. Flow Cytometry. Humans. Membrane Potential, Mitochondrial / drug effects. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes

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  • (PMID = 18206670.001).
  • [ISSN] 0891-5849
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants; 0 / Phenanthrenes; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; EC 1.- / Oxidoreductases; EC 3.4.22.- / Caspases
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86. Hubeek I, Peters GJ, Broekhuizen R, Zwaan CM, Kaaijk P, van Wering ES, Gibson BE, Creutzig U, Janka-Schaub GE, den Boer ML, Pieters R, Kaspers GJ: In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia. Haematologica; 2006 Jan;91(1):17-23
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  • [Title] In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia.
  • BACKGROUND AND OBJECTIVES: Cytarabine (ara-C) is a key drug in the treatment of acute leukemia.
  • DESIGN AND METHODS: Using the MTT assay, we determined in vitro sensitivity and cross-resistance to deoxynucleoside analogs in 362 acute leukemia samples from untreated children and 32 normal bone marrow mononuclear cell samples.
  • RESULTS: Normal bone marrow samples were significantly more resistant to ara-C, cladribine and fludarabine than were acute myeloid leukemia (AML) samples and significantly more resistant to ara-C and fludarabine than were acute lymphoblastic leukemia (ALL) samples.
  • T-ALL was significantly more resistant to cladribine than B-cell precursor ALL.
  • We observed cross-resistance between ara-C and other deoxynucleoside analogs, as well as between ara-C and drugs with different modes of action in childhood acute leukemia.
  • [MeSH-major] Drug Resistance, Multiple. Leukemia / drug therapy. Nucleosides / therapeutic use
  • [MeSH-minor] Acute Disease. Child. Cytarabine / therapeutic use. Drug Screening Assays, Antitumor. Humans

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  • (PMID = 16434366.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Nucleosides; 04079A1RDZ / Cytarabine
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87. Aventín A, Sánchez J, Nomdedéu JF, Estany C, Forcada P, La Starza R, Mecucci C: Novel IGHalpha translocations, t(2;14)(q14.3;q32) and t(14;17)(q32;q21), in B-cell precursor acute lymphoblastic leukemia. Cancer Genet Cytogenet; 2008 Aug;185(1):57-9
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  • [Title] Novel IGHalpha translocations, t(2;14)(q14.3;q32) and t(14;17)(q32;q21), in B-cell precursor acute lymphoblastic leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 2. Genes, Immunoglobulin Heavy Chain / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic

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  • (PMID = 18656697.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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88. Yamasaki N, Miyazaki K, Nagamachi A, Koller R, Oda H, Miyazaki M, Sasaki T, Honda ZI, Wolff L, Inaba T, Honda H: Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia. Oncogene; 2010 Apr 1;29(13):1963-75
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  • [Title] Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia.
  • E2A-hepatic leukemia factor (HLF) is a chimeric protein found in B-lineage acute lymphoblastic leukemia (ALL) with t(17;19).
  • To analyze the leukemogenic process and to create model mice for t(17;19)-positive leukemia, we generated inducible knock-in (iKI) mice for E2A-HLF.
  • Despite the induced expression of E2A-HLF in the hematopoietic tissues, no disease was developed during the long observation period, indicating that additional gene alterations are required to develop leukemia.
  • Virus infection induced acute leukemias in E2A-HLF iKI mice with higher morbidity and mortality than in control mice.
  • Interestingly, tumors with Zfp521 integration exclusively showed B-lineage ALL, which corresponds to the phenotype of human t(17;19)-positive leukemia.
  • In addition, ZNF521 (human counterpart of Zfp521) was found to be overexpressed in human leukemic cell lines harboring t(17;19).
  • Moreover, both iKI for E2A-HLF and transgenic for Zfp521 mice frequently developed B-lineage ALL.
  • These results indicate that a set of transcription factors promote leukemic transformation of E2A-HLF-expressing hematopoietic progenitors and suggest that aberrant expression of Zfp521/ZNF521 may be clinically relevant to t(17;19)-positive B-lineage ALL.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / genetics. DNA-Binding Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic. Humans. Mice. Mutation. Nuclear Proteins. Transcriptional Activation / genetics

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  • (PMID = 20062079.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / COPRS protein, human; 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, mouse; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / zinc finger protein 521, human
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89. Segal I, Rassekh SR, Bond MC, Senger C, Schreiber RA: Abnormal liver transaminases and conjugated hyperbilirubinemia at presentation of acute lymphoblastic leukemia. Pediatr Blood Cancer; 2010 Sep;55(3):434-9
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  • [Title] Abnormal liver transaminases and conjugated hyperbilirubinemia at presentation of acute lymphoblastic leukemia.
  • BACKGROUND: Acute lymphoblastic leukemia (ALL) is the most common malignancy in childhood.
  • While hepatitis is a well-known complication during the treatment phase of ALL, the association of abnormal liver biochemistries at initial presentation of leukemia is poorly described.
  • The aim of this study is to examine the prevalence and assess the clinical impact of hepatitis at diagnosis in children with ALL.
  • Risk factors for elevated transaminases included a high WBC count at diagnosis, older age, bulky disease, and T-cell leukemia.
  • [MeSH-major] Alanine Transaminase / blood. Aspartate Aminotransferases / blood. Hepatitis / complications. Hyperbilirubinemia / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [Copyright] 2010 Wiley-Liss, Inc.
  • (PMID = 20658613.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; RFM9X3LJ49 / Bilirubin
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90. Chen P, Chen YZ, Wu Y, Huang HF, Li NN: [Identification of the isoform in type II receptor of transforming growth factor-beta in patients with acute leukemia and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2006 Apr;14(2):221-4
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  • [Title] [Identification of the isoform in type II receptor of transforming growth factor-beta in patients with acute leukemia and its clinical significance].
  • To identify the mutation of TbetaR-II in patients with acute leukemia, the bone marrow samples from 6 patients with acute leukemia and 11 normal individuals as control were detected by long-range RT-PCR.
  • The results showed that there was existance of the isoform of TbetaR-II in 2 cases out of 6 patients with acute leukemia.
  • In conclusion, there was the isoform of TbetaR-II in partial patients with acute leukemia, and the isoform may be related with prognosis.

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  • (PMID = 16638184.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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91. Kanazawa T, Ogawa C, Taketani T, Taki T, Hayashi Y, Morikawa A: TLS/FUS-ERG fusion gene in acute lymphoblastic leukemia with t(16;21)(p11;q22) and monitoring of minimal residual disease. Leuk Lymphoma; 2005 Dec;46(12):1833-5
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  • [Title] TLS/FUS-ERG fusion gene in acute lymphoblastic leukemia with t(16;21)(p11;q22) and monitoring of minimal residual disease.
  • This study reports a 1-year-old boy with precursor B cell acute lymphoblastic leukemia (ALL) carrying t(16;21)(p11;q22).
  • Complete remission (CR) was achieved by chemotherapy oriented for acute myeloid leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Neoplasm, Residual / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic

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  • (PMID = 16263589.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin
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92. Riz I, Hawley TS, Luu TV, Lee NH, Hawley RG: TLX1 and NOTCH coregulate transcription in T cell acute lymphoblastic leukemia cells. Mol Cancer; 2010 Jul 09;9:181
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  • [Title] TLX1 and NOTCH coregulate transcription in T cell acute lymphoblastic leukemia cells.
  • BACKGROUND: The homeobox gene TLX1 (for T-cell leukemia homeobox 1, previously known as HOX11) is inappropriately expressed in a major subgroup of T cell acute lymphoblastic leukemia (T-ALL) where it is strongly associated with activating NOTCH1 mutations.
  • In addition, the TLX1/NOTCH/MYC transcriptional network coregulates genes involved in T cell development, such as CD1 and RAG family members, and therefore may prescribe the early cortical stage of differentiation arrest characteristic of the TLX1 subgroup of T-ALL.

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  • (PMID = 20618946.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA120316; United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01HL66305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 143275-75-6 / TLX1 protein, human
  • [Other-IDs] NLM/ PMC2913983
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93. Pfeifer H, Wassmann B, Pavlova A, Wunderle L, Oldenburg J, Binckebanck A, Lange T, Hochhaus A, Wystub S, Brück P, Hoelzer D, Ottmann OG: Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL). Blood; 2007 Jul 15;110(2):727-34
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  • [Title] Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL).
  • Acquired imatinib resistance in advanced Philadelphia-positive acute lymphoblastic leukemia (Ph(+) ALL) has been associated with mutations in the kinase domain (KD) of BCR-ABL.
  • Patients enrolled in the German Multicenter Study Group for Adult Acute Lymphoblastic Leukemia (GMALL) trial ADE10 for newly diagnosed elderly Ph(+) ALL were retrospectively examined for the presence of BCR-ABL KD mutations by denaturing high-performance liquid chromatography (D-HPLC), cDNA sequencing, and allele-specific polymerase chain reaction (PCR).
  • At relapse, the dominant cell clone harbored an identical mutation in 90% of cases, the overall prevalence of mutations at relapse was 80%.
  • BCR-ABL mutations conferring high-level imatinib resistance are present in a substantial proportion of patients with de novo Ph(+) ALL and eventually give rise to relapse.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Mutation. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Pyrimidines / therapeutic use

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  • (PMID = 17405907.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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94. Friedman AD, Cook JR, Scharpf J: Precursor T-cell acute lymphoblastic lymphoma presenting as a tongue mass. J Otolaryngol Head Neck Surg; 2009 Feb;38(1):E16-8
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  • [Title] Precursor T-cell acute lymphoblastic lymphoma presenting as a tongue mass.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Tongue Neoplasms / pathology

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  • (PMID = 19344598.001).
  • [ISSN] 1916-0216
  • [Journal-full-title] Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale
  • [ISO-abbreviation] J Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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95. Jiang XJ, Wang JS, Fang Q: [Gene expression of breast cancer resistance protein in adult acute lymphocytic leukemia and its clinical significance]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2008 Feb;16(1):31-4
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  • [Title] [Gene expression of breast cancer resistance protein in adult acute lymphocytic leukemia and its clinical significance].
  • The objective of this study was to investigate the relationship between the expressions of breast cancer resistance protein (BCRP) gene and drug resistance as well as prognosis in adult patients with acute lymphocytic leukemia (ALL).
  • Semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of BCRP gene in 97 adult patients with acute lymphocytic leukemia (ALL) and 30 normal subjects.
  • In immune types the BCRP gene expression of B-ALL was higher than that of T cell type, especially in mature B cell type with obviously statistical significance (p<0.01).
  • It is concluded that the high expression of BCRP gene may induce clinical drug resistance, and may be an unfavorable factor for prognosis in adult patients with acute lymphocytic leukemia.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Drug Resistance, Neoplasm / genetics. Neoplasm Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18315895.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Neoplasm Proteins
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96. Bryant J, Picot J, Levitt G, Sullivan I, Baxter L, Clegg A: Cardioprotection against the toxic effects of anthracyclines given to children with cancer: a systematic review. Health Technol Assess; 2007 Jul;11(27):iii, ix-x, 1-84
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  • RESULTS: Four randomised controlled trials (RCTs) met the inclusion criteria of the review, each considering a different cardioprotective intervention; all trials included children with acute lymphoblastic