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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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[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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[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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[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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[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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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

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(PMID = 17617782.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antiviral Agents; P9G3CKZ4P5 / Ganciclovir

   

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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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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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[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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[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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[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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[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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[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

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[Copyright] Copyright 2009 Wiley-Liss, Inc.

(PMID = 19813250.001).

[ISSN] 1545-5017

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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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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[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

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(PMID = 17537996.001).

[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 / Arsenicals; 0 / BAD protein, human; 0 / Glucocorticoids; 0 / Oxides; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / bcl-Associated Death Protein; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide; VB0R961HZT / Prednisone; W36ZG6FT64 / Sirolimus

   

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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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[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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[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

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(PMID = 16039715.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Neoplasm Proteins

   

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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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[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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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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[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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[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

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(PMID = 19157546.001).

[ISSN] 1873-5835

[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 / Antineoplastic Agents; 9PHQ9Y1OLM / Prednisolone

   

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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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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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[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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[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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[Cites] Radiol Clin North Am. 1982 Sep;20(3):561-8 [7111707.001]

[Cites] AJR Am J Roentgenol. 1983 Oct;141(4):685-90 [6604418.001]

[Cites] AJR Am J Roentgenol. 1999 Feb;172(2):343-8 [9930779.001]

[Cites] Clin Pediatr (Phila). 1999 Sep;38(9):545-6 [10500889.001]

[Cites] J Clin Ultrasound. 2002 Nov-Dec;30(9):552-6 [12404522.001]

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[Cites] Eur Radiol. 2000;10(6):1031 [10879725.001]

(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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[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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[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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[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

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(PMID = 20339086.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Validation Studies

[Publication-country] United States

[Chemical-registry-number] 0 / Anticoagulants; 0 / Enoxaparin; 0 / Steroids; EC 3.5.1.1 / Asparaginase

[Other-IDs] NLM/ PMC2890143

   

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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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[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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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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[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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[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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[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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[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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[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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[ErratumIn] Blood. 2008 May 1;111(9):4830

(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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[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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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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[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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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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[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

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[CommentIn] Blood. 2010 Apr 29;115(17):3420-1 [20430960.001]

(PMID = 20040760.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Multicenter Study

[Publication-country] United States

   

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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

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(PMID = 19167686.001).

[ISSN] 1523-6536

[Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation

[ISO-abbreviation] Biol. Blood Marrow Transplant.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / HLA Antigens; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / HLA-DR Antigens

   

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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