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[Title] Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.

The t(9;22) BCR/ABL fusion is associated with over 90% of chronic myelogenous and 25% of acute lymphocytic leukemia.

Chromosome 11q23 translocations in acute myeloid and lymphoid leukemia cells demonstrate myeloid lymphoid leukemia (MLL) fusions with over 40 gene partners, like AF9 and AF4 on chromosomes 9 and 4, respectively.

Therapy-related leukemia is associated with the above gene rearrangements following the treatment with topoisomerase II (topo II) inhibitors.

In this report, using cell lines and primary cells, chromatin structural elements were analyzed in BCR, ABL and AF4 and, for comparison, in MLL2, which is a homolog to MLL, but not associated with chromosome translocations.

Although MLL2 was expressed in all cell lines tested, except for the presence of one DNAse I site in the promoter, no other structural elements were found in MLL2.

A NHR model presented demonstrates the importance of chromatin structure in chromosome translocations involved with leukemia.

[MeSH-major] Chromatin / chemistry. Chromosome Breakage. Chromosomes, Human / genetics. Leukemia / genetics. Leukemia / metabolism. Translocation, Genetic

[MeSH-minor] Acute Disease. Cell Line, Tumor. Cells, Cultured. Chronic Disease. Humans. K562 Cells. Proto-Oncogene Proteins c-bcr / chemistry. Proto-Oncogene Proteins c-bcr / genetics. Recombination, Genetic

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(PMID = 16572268.001).

[ISSN] 0340-6717

[Journal-full-title] Human genetics

[ISO-abbreviation] Hum. Genet.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies

[Publication-country] Germany

[Chemical-registry-number] 0 / Chromatin; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr

   

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[Title] ZAP-70 methylation status is associated with ZAP-70 expression status in chronic lymphocytic leukemia.

BACKGROUND AND OBJECTIVES: ZAP-70 expression is a recognized prognostic marker in chronic lymphocytic leukemia (CLL).

DESIGN AND METHODS: Patients with CLL (n=87), acute lymphoblastic leukemia (n=13), mantle cell leukemia (n=13) and splenic marginal zone lymphoma (n=14) of known immunoglobulin gene mutation (IgVH) status were studied.

[MeSH-major] DNA Methylation. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. ZAP-70 Protein-Tyrosine Kinase / genetics

[MeSH-minor] 5' Untranslated Regions / genetics. Conserved Sequence. Dinucleoside Phosphates / genetics. Humans. Introns. Leukemia / genetics. Reference Values. Restriction Mapping

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[CommentIn] Haematologica. 2005 Aug;90(8):1012 [16079094.001]

(PMID = 16079107.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Italy

[Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / Dinucleoside Phosphates; 2382-65-2 / cytidylyl-3'-5'-guanosine; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase

   

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[Title] [Treatment results of acute leukemia in elderly patients: analysis of 61 consecutive patients in a single institution].

In order to investigate the clinical characteristics and management of elderly patients with acute leukemia, we retrospectively analyzed treatment results for 61 acute leukemia patients aged 65 years or more (median age 72) admitted to our department between October 1995 and September 2006.

There were 6 elderly patients with ALL (acute lymphocytic leukemia) and 55 patients with AML (acute myelogenous leukemia).

The intensive chemotherapy group and the de novo leukemia group showed a significantly higher CR rate and longer survival.

Intensive chemotherapy was effective for 65-74-year-old patients with de novo AML.

In future, we consider that the prognosis for elderly patients with acute leukemia will improve, if made-to-order treatment is given, depending on evidence-based stratification of patients with organs having low reserve capacity.

[MeSH-major] Leukemia, Lymphoid / drug therapy. Leukemia, Myeloid, Acute / drug therapy

[MeSH-minor] Acute Disease. Age Distribution. Aged. Aged, 80 and over. Female. Humans. Male. Retrospective Studies. Survival Rate

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(PMID = 18281758.001).

[ISSN] 0385-0684

[Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy

[ISO-abbreviation] Gan To Kagaku Ryoho

[Language] jpn

[Publication-type] English Abstract; Journal Article

[Publication-country] Japan

   

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[Title] T-cell receptor gamma and delta junctional gene rearrangements as diagnostic and prognostic biomarker for T-cell acute lymphoblastic leukemia.

[MeSH-major] Biomarkers, Tumor. Gene Rearrangement. Leukemia, T-Cell / diagnosis. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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(PMID = 16886283.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Letter

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Antigen, T-Cell, gamma-delta

   

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[Title] Heritable T-cell malignancy models established in a zebrafish phenotypic screen.

T-cell neoplasias are common in pediatric oncology, and include acute lymphoblastic leukemia (T-ALL) and lymphoblastic lymphoma (T-LBL).

These cancers have worse prognoses than their B-cell counterparts, and their treatments carry significant morbidity.

Although many pediatric malignancies have characteristic translocations, most T-lymphocyte-derived diseases lack cytogenetic hallmarks.

Although dysregulation of the NOTCH1 pathway occurs in a substantial fraction of cases, many other genetic lesions of T-cell malignancy have not yet been determined.

Using transgenic fish with T-lymphocyte-specific expression of enhanced green fluorescent protein (EGFP), we performed chemical mutagenesis, screened animals for GFP(+) tumors, and identified multiple lines with a heritable predisposition to T-cell malignancy.

T-cell receptor analyses confirmed their clonality.

Malignancies were transplantable and contained leukemia-initiating cells, like their human correlates.

In summary, we have identified multiple zebrafish mutants that recapitulate human T-cell neoplasia and show heritable transmission.

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(PMID = 19516274.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] ENG

[Grant] United States / NICHD NIH HHS / HD / K08 HD053350-03; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / K08-HD53350; United States / NICHD NIH HHS / HD / R21 HD060310; United States / NICHD NIH HHS / HD / R21 HD060310-01; United States / NIDDK NIH HHS / DK / T32-DK007115; United States / NIDDK NIH HHS / DK / T32 DK007115; United States / NICHD NIH HHS / HD / K08 HD053350; United States / NIAID NIH HHS / AI / R21-AI079784; United States / NICHD NIH HHS / HD / K12 HD001410; United States / NICHD NIH HHS / HD / K12-HD001410; United States / NICHD NIH HHS / HD / K08 HD053350-02; United States / NCI NIH HHS / CA / P30 CA042014

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / enhanced green fluorescent protein; 147336-22-9 / Green Fluorescent Proteins

[Other-IDs] NLM/ NIHMS112911; NLM/ PMC2761994

   

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[Title] Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.

In the T-cell lineage, calcineurin activation is important for pre-T-cell receptor (TCR) signaling, TCR-mediated positive selection of thymocytes into mature T cells, and many aspects of the immune response.

We observed sustained calcineurin activation in human B- and T-cell lymphomas and in all mouse models of lymphoid malignancies analyzed.

In intracellular NOTCH1 (ICN1)- and TEL-JAK2-induced T-cell lymphoblastic leukemia, two mouse models relevant to human malignancies, in vivo inhibition of calcineurin activity by CsA or FK506 induced apoptosis of leukemic cells and rapid tumor clearance, and substantially prolonged mouse survival.

In contrast, ectopic expression of a constitutively activated mutant of calcineurin favored leukemia progression.

Moreover, CsA treatment induced apoptosis in human lymphoma and leukemia cell lines.

[MeSH-major] Antineoplastic Agents / pharmacology. Calcineurin / metabolism. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / enzymology

[MeSH-minor] Animals. Calcineurin Inhibitors. Cell Line, Tumor. Cyclosporine / pharmacology. Disease Models, Animal. Enzyme Activation / drug effects. Humans. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Oncogene Proteins, Fusion / deficiency. Oncogene Proteins, Fusion / genetics. Receptor, Notch1 / physiology. Tacrolimus / pharmacology

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[CommentIn] Nat Med. 2007 Jun;13(6):669-71 [17554330.001]

(PMID = 17515895.001).

[ISSN] 1078-8956

[Journal-full-title] Nature medicine

[ISO-abbreviation] Nat. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Calcineurin Inhibitors; 0 / NOTCH1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; 0 / TEL-JAK2 fusion protein, mouse; 83HN0GTJ6D / Cyclosporine; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus

   

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[Title] Development of cell-based assays for cytokine receptor signaling, using an AlphaScreen SureFire assay format.

The signal transducers and activators of transcription (STAT) proteins are a small family of signaling proteins that are crucial for cytokine and growth factor receptor-mediated signaling in various blood cell types.

Despite their central role in immune and hematopoietic cellular regulation, there are relatively few options for monitoring receptor-mediated JAK/STAT signaling events in a cell-based format, without the need for cellular transfections or labor intensive methodology.

With three different cell lines (human acute monocytic leukemia THP-1 cells, human erythroleukemic TF-1 cells, and human T lymphocytic Jurkat cells), we have optimized a rapid and homogeneous methodology for monitoring endogenous, receptor-mediated signaling via STAT 1, STAT 3, or STAT 5 phosphorylation, in response to several agonists.

[MeSH-minor] Biochemistry / methods. Blotting, Western. Cell Line, Tumor. Humans. Jurkat Cells. Phosphorylation. STAT1 Transcription Factor / metabolism. STAT3 Transcription Factor / metabolism. STAT5 Transcription Factor / metabolism

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[Copyright] Copyright 2010 Elsevier Inc. All rights reserved.

(PMID = 20382104.001).

[ISSN] 1096-0309

[Journal-full-title] Analytical biochemistry

[ISO-abbreviation] Anal. Biochem.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Cytokine; 0 / STAT Transcription Factors; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / STAT5 Transcription Factor

   

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On three separate nights, they provided pre-activity, post-activity, and next-morning saliva samples and completed brief questionnaires at the last two timepoints.

Women's T was higher pre-intercourse than pre-control activity.

Women's T was also higher post-intercourse than post-control activity, though the percent change in T from pre- to post-activity was highest for cuddling, then intercourse, then exercise.

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(PMID = 17320881.001).

[ISSN] 0018-506X

[Journal-full-title] Hormones and behavior

[ISO-abbreviation] Horm Behav

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 3XMK78S47O / Testosterone

   

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Thus, expression of these critical regulators is dependent on continued expression of upstream regulators, which may include cell-extrinsic signals.

[MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cell Line. DNA / metabolism. Embryo, Nonmammalian / cytology. Embryo, Nonmammalian / embryology. Embryo, Nonmammalian / metabolism. Endothelial Cells / cytology. Endothelial Cells / metabolism. Erythroid Cells / cytology. Erythroid Cells / metabolism. Gene Expression Regulation, Developmental. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / metabolism. LIM Domain Proteins. Mice. Myeloid Cells / cytology. Myeloid Cells / metabolism. Phenotype. Protein Binding. Transcription Factors

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(PMID = 17090656.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / GM63904; United Kingdom / Medical Research Council / / MC/ U137981013; United States / NCI NIH HHS / CA / P01CA65493; United States / NIGMS NIH HHS / GM / R01 GM063904-01; United States / NIGMS NIH HHS / GM / R01 GM063904

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 0 / Zebrafish Proteins; 0 / lmo2 protein, zebrafish; 0 / tal1 protein, zebrafish; 9007-49-2 / DNA

   

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Nelarabine is indicated for the treatment of adult and pediatric patients with T-cell acute lymphoblastic leukemia or T-cell lymphoblastic lymphoma whose disease has not responded to, or has relapsed after treatment with, at least two chemotherapy regimens.

[MeSH-major] Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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(PMID = 16922610.001).

[ISSN] 1479-6694

[Journal-full-title] Future oncology (London, England)

[ISO-abbreviation] Future Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Arabinonucleosides; 60158CV180 / nelarabine

[Number-of-references] 22

   

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Analysis of null mutants showed that Gli3 is involved at the transitions from DN1 to CD44+ CD25+ DN (DN2) cell and from DN to CD4+ CD8+ double-positive (DP) cell.

Gli3 is required for differentiation from DN to DP thymocyte, after pre-T-cell receptor (TCR) signaling but is not necessary for pre-TCR-induced proliferation or survival.

The effect of Gli3 was dose dependent, suggesting its direct involvement in the transcriptional regulation of genes controlling T-cell differentiation during fetal development.

[MeSH-major] Antigens, CD / analysis. Cell Differentiation. DNA-Binding Proteins / physiology. Nerve Tissue Proteins / physiology. T-Lymphocytes / cytology. Thymus Gland / cytology. Transcription Factors / physiology

[MeSH-minor] Animals. Antigens, CD4. Antigens, CD8. Cell Lineage. Embryo, Mammalian / cytology. Embryo, Mammalian / immunology. Gene Expression Regulation, Developmental. Kruppel-Like Transcription Factors. Mice. Mice, Inbred C57BL. Mice, Mutant Strains

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(PMID = 15855276.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United Kingdom / Wellcome Trust / / 061000; United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / DNA-Binding Proteins; 0 / Gli3 protein, mouse; 0 / Kruppel-Like Transcription Factors; 0 / Nerve Tissue Proteins; 0 / Transcription Factors

[Other-IDs] NLM/ PMC1274277; NLM/ UKMS5313

   

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In this study, we covalently link the antitumor agent doxorubicin (Dox) to the DNA aptamer sgc8c, which was selected by the cell-SELEX method.

In doing so, we expected that this sgc8c-Dox conjugate would specifically kill the target CCRF-CEM (T-cell acute lymphoblastic leukemia, T-cell ALL) cells, but with minimal toxicity towards nontarget cells.

Cell viability tests demonstrate that the sgc8c-Dox conjugates not only possess potency similar to unconjugated Dox, but also have the required molecular specificity that is lacking in most current targeted drug delivery strategies.

Furthermore, we found that nonspecific uptake of membrane-permeable Dox to nontarget cell lines could also be inhibited by linking the drug with the aptamer; thus, the conjugates are selective for cells that express higher amounts of target proteins.

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(PMID = 19253922.001).

[ISSN] 1439-7633

[Journal-full-title] Chembiochem : a European journal of chemical biology

[ISO-abbreviation] Chembiochem

[Language] ENG

[Grant] United States / NIGMS NIH HHS / GM / R01 GM079359; United States / NIGMS NIH HHS / GM / R01 GM079359-01; None / None / / R01 GM079359-01; United States / NIGMS NIH HHS / GM / R01 GM079359-02; United States / NIGMS NIH HHS / GM / R01 GM079359-03; None / None / / R01 GM079359-02; None / None / / R01 GM079359-01S1; United States / NIGMS NIH HHS / GM / R01 GM079359-01S1

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aptamers, Nucleotide; 0 / Drug Carriers; 0 / Immunoconjugates; 80168379AG / Doxorubicin

[Other-IDs] NLM/ NIHMS149610; NLM/ PMC2992821

   

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In order to fully understand T cell-mediated immunity, the mechanisms that regulate clonal expansion and cytokine production by CD4(+) antigen-specific effector T cells in response to a wide range of antigenic stimulation needs clarification.

For this purpose, panels of antigen-specific CD4(+) T cell clones with different thresholds for antigen-induced proliferation were generated by repeated stimulation with high- or low-dose antigen.

There was no significant difference in antigen-dependent cytokine production by TG40 cells transfected with TCR obtained from either high- or low-dose-responding T cell clones, suggesting that the affinity of TCRs for their ligands is not primary determinant of T cell antigen reactivity.

The proliferative responses of all T cell clones to both peptide stimulation and to TCRbeta crosslinking revealed parallel dose-response curves.

Finally, the antigen responses of high- and low-peptide-responding T cell clones reveal that clonal expansion and cytokine production of effector T cells occur independently of antigen concentration.

[MeSH-minor] Animals. Cell Adhesion Molecules / metabolism. Clone Cells. Flow Cytometry. Mice. Mice, Inbred BALB C. Ovalbumin / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-Cell / metabolism

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(PMID = 19338745.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Cytokines; 0 / OVA 323-339; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell; 9006-59-1 / Ovalbumin

   

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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.

Control of apoptosis via death ligands plays a basic role for lymphocyte homeostasis and lymphoma development.

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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Genetic studies have demonstrated that the Bcl-2 family member Mcl-1 is an important anti-apoptotic protein in the development of multiple cell types including T lymphocytes.

In this study, we examined the expression pattern of Mcl-1 in different populations of T cells at the single-cell level and found that Mcl-1 protein is constitutively expressed in all T cell populations and up-regulated upon TCR stimulation.

We then investigated the role of Mcl-1 in the survival of these different populations by conditionally deleting Mcl-1 at various T cell stages.

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(PMID = 18566418.001).

[ISSN] 0022-1767

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / R01 AI074754; United States / NIAID NIH HHS / AI / AI054658-05; United States / NCI NIH HHS / CA / R01 CA092123; United States / NCI NIH HHS / CA / CA092123-05; United States / NIAID NIH HHS / AI / R01 AI054658-05; United States / NIAID NIH HHS / AI / AI54683; United States / NCI NIH HHS / CA / R01 CA092123-05; United States / NCI NIH HHS / CA / CA92123; United States / NIAID NIH HHS / AI / R01 AI054658

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein

[Other-IDs] NLM/ NIHMS66462; NLM/ PMC2561902

   

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Work in Dr. Look's laboratory focuses on the molecular pathogenesis of leukemia.

His group has been credited with the identification and functional analysis of several chimeric oncogenes activated by chromosomal translocations, including the E2A-HLF transcription factor, which was shown to act through an evolutionarily conserved genetic pathway to promote leukemia cell survival.

Their efforts in human T-cell acute lymphoblastic leukemia have revealed key multistep mutational pathways that drive the pathogenesis of this disease and demonstrated that NOTCH1 receptors are mutationally activated in a majority of these cases.

Look's laboratory developed the first transgenic model of leukemia in the zebrafish, opening the way for chemical and genome-wide genetic modifier screens in a vertebrate disease model.

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(PMID = 18248181.001).

[ISSN] 1557-8542

[Journal-full-title] Zebrafish

[ISO-abbreviation] Zebrafish

[Language] eng

[Publication-type] Interview

[Publication-country] United States

   

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[Title] Hemangioblastomas share protein expression with embryonal hemangioblast progenitor cell.

Hemangioblastomas are central nervous system (CNS) tumors of unknown histogenesis, which can occur sporadically or in von Hippel-Lindau disease.

Failure to specify the cytologic origin of the stromal cell has precluded the development of nonsurgical therapies and limits understanding of its basic biology.

We report that the stromal cells express proteins (Scl, brachyury, Csf-1R, Gata-1, Flk-1, and Tie-2) that characterize embryonic progenitor cells with hemangioblastic differentiation potential and conclude that embryonic progenitors with hemangioblast potential represent a possible cytologic equivalent of the stromal cell.

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(PMID = 16618738.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[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 / Angiopoietin-1; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Brachyury protein; 0 / Fetal Proteins; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Proto-Oncogene Proteins; 0 / T-Box Domain Proteins; 135471-20-4 / TAL1 protein, human; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, TIE-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2

   

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[Title] Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment.

Methotrexate (MTX) is a key drug in the chemotherapy for childhood acute lymphocytic leukemia (ALL).

[MeSH-major] Acute Kidney Injury / chemically induced. Antimetabolites, Antineoplastic / adverse effects. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

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(PMID = 18045317.001).

[ISSN] 1328-8067

[Journal-full-title] Pediatrics international : official journal of the Japan Pediatric Society

[ISO-abbreviation] Pediatr Int

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Australia

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate

   

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[Title] Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands.

OBJECTIVE: Enteropathy-associated T-cell lymphomas (EATLs) are T-cell non-Hodgkin lymphomas of the small bowel, which are specifically associated with coeliac disease (CD).

We included all T-cell lymphomas detected between January 2000 and December 2006 that initially presented in the small bowel.

Finally, the distribution of characteristics such as the localization, the Marsh classification and method of diagnosis are described.

Most EATLs were localized in the proximal small intestine and the diagnosis was made by surgical resection in the majority of cases.

CONCLUSIONS: EATL is a rare disease with an incidence of 0.10 per 100,000 inhabitants per year, occurring in older age, with a peak incidence in the 7th decade.

[MeSH-major] Celiac Disease / epidemiology. Lymphoma, T-Cell / epidemiology

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(PMID = 18618372.001).

[ISSN] 1502-7708

[Journal-full-title] Scandinavian journal of gastroenterology

[ISO-abbreviation] Scand. J. Gastroenterol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Norway

   

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[Title] How I treat acute and chronic leukemia in pregnancy.

The prevalence of pregnancy associated leukemia is approximately 1 case out of 10,000 pregnancies.

The treatment of a pregnant woman with leukemia may be associated with severe adverse fetal outcome including death and malformations, and therefore poses a difficult challenge for both the patient and the attending physician.

When acute leukemia is diagnosed during the 1st trimester, patients should be treated promptly similar to non-pregnant patients.

When the diagnosis is made later in pregnancy standard chemotherapy regimen should be considered and usually pregnancy termination is not mandatory.

Pregnancy associated chronic myelogenous leukemia (CML) can be treated with interferon throughout pregnancy with no apparent increase in adverse fetal outcome.

In the very rare case of chronic lymphocytic leukemia (CLL) during pregnancy treatment can usually be delayed until after delivery.

[MeSH-major] Antineoplastic Agents / adverse effects. Leukemia / drug therapy. Pregnancy Complications, Neoplastic / drug therapy. Prenatal Exposure Delayed Effects

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(PMID = 18472198.001).

[ISSN] 0268-960X

[Journal-full-title] Blood reviews

[ISO-abbreviation] Blood Rev.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Scotland

[Chemical-registry-number] 0 / Antineoplastic Agents

[Number-of-references] 111

   

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[Title] TCF1 and beta-catenin regulate T cell development and function.

T cell factor-1 (TCF1) critically regulates T cell development.

We have genetically manipulated the beta-catenin gene and generated mutant mice that have shown an essential role for beta-catenin and TCF1 during pre-T cell receptor (TCR) and TCR-dependent stages of T cell development.

[MeSH-major] Cell Differentiation. Gene Expression Regulation. T Cell Transcription Factor 1 / metabolism. T-Lymphocytes / cytology. T-Lymphocytes / immunology. beta Catenin / metabolism

[MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Humans. Mice. Receptors, Antigen, T-Cell / genetics. Receptors, Antigen, T-Cell / metabolism. Signal Transduction

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(PMID = 20082155.001).

[ISSN] 1559-0755

[Journal-full-title] Immunologic research

[ISO-abbreviation] Immunol. Res.

[Language] eng

[Grant] United States / Intramural NIH HHS / / Z01 AG000768-04

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; 0 / T Cell Transcription Factor 1; 0 / beta Catenin

[Other-IDs] NLM/ NIHMS172600; NLM/ PMC2891409

   

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BACKGROUND: Nkx2.5 is a homeodomain-containing nuclear transcription protein that has been associated with acute T-lymphoblastic leukemia.

In addition, the expression of Nkx2.5 was significantly increased in psoriasis and squamous cell carcinoma, but was barely detected in atopic dermatitis and basal cell carcinoma.

CONCLUSION: These results suggest that Nkx2.5 may play a role in the change from proliferation to differentiation of keratinocytes and in the pathogenesis of skin disease with aberrant keratinocyte differentiation.

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(PMID = 20523827.001).

[ISSN] 2005-3894

[Journal-full-title] Annals of dermatology

[ISO-abbreviation] Ann Dermatol

[Language] eng

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2861273

[Keywords] NOTNLM ; Keratinocyte differentiation / Nkx2.5 / Transcription factor

   

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[Title] Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.

Therapy-related acute lymphoblastic leukemia (t-ALL) is a rare secondary leukemia following chemotherapy and/or radiotherapy for primary malignancies.

Chromosomal 11q23 abnormality, frequently detected in therapy-related acute myeloid leukemia, is the most common cytogenetic alteration in t-ALL.

However, t-ALL cases without 11q23 abnormality have been rarely described.

In the 48 cases, an 11q23 abnormality involving the MLL gene locus was the predominant chromosomal aberration (32 [67%]), followed by t(9;22) (6 [13%]) and a normal karyotype (4 [8%]).

Compared with t-ALL cases with an 11q23 abnormality, cases without an 11q23 abnormality had a relatively longer latency period (median, 36 vs 19 months) and a different primary malignancy spectrum.

The t(8;14)(q11.2;q32), a rare, nonrandom, balanced chromosomal translocation differing from the more common translocation involving c-MYC on chromosome 8q24, was seen in 1 adult t-ALL case, which may suggest another possible pathogenesis of this disease.

[MeSH-major] Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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(PMID = 20023261.001).

[ISSN] 1943-7722

[Journal-full-title] American journal of clinical pathology

[ISO-abbreviation] Am. J. Clin. Pathol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 42

   

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[Title] An improved methodology to detect human T cell receptor beta variable family gene expression patterns.

Comprehensive gene expression analysis of the T cell receptor repertoire of an individual can be very useful in evaluating the immune response in a variety of conditions.

Antibody-based analysis methods can detect approximately 60% of the human T cell receptor beta variable (TCRBV) proteins, while gene expression analysis, primarily through employment of the polymerase chain reaction (PCR), has had somewhat greater success in the detection of additional TCRBV families.

We describe here a real-time reverse transcription polymerase chain reaction-based method, which allows efficient automation and integration of amplification, detection, and analysis with sequence-specific detection of all T cell receptor beta variable gene families, subfamilies, and alleles.

[MeSH-major] Gene Expression Profiling / methods. Multigene Family. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis. Receptors, Antigen, T-Cell, alpha-beta / genetics

[MeSH-minor] DNA Primers. Fluorometry / methods. Genetic Variation. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Polymerase Chain Reaction / methods. RNA, Messenger / biosynthesis

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(PMID = 16038929.001).

[ISSN] 0022-1759

[Journal-full-title] Journal of immunological methods

[ISO-abbreviation] J. Immunol. Methods

[Language] eng

[Grant] United States / NCRR NIH HHS / RR / 5 P20 RR16440-02

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] Netherlands

[Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell, alpha-beta

   

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Multiple tumor cell lines of varying histiotypes, including A549 (lung adenocarcinoma), 786-O (renal cell carcinoma), HeLa (cervical carcinoma), MDA-MB-231 (breast), K562 (chronic myelogenous leukemia), Jurkat (acute T-cell leukemia), MEC-2 (B-chronic lymphocytic leukemia), and U251 and D37 (glioma), as well as cells derived from primary human glioma tumors that are likely a more clinically relevant model were treated with sorafenib or bortezomib alone or in combination.

Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines.

These findings were accompanied by several biochemical changes, including decreased phosphorylation of vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and Akt and increased phosphorylation of stress-related c-Jun NH2-terminal kinase (JNK).

These findings show that sorafenib interacts synergistically with bortezomib to induce apoptosis in a broad spectrum of neoplastic cell lines and show an important role for the Akt and JNK pathways in mediating synergism.

[MeSH-minor] Antineoplastic Agents / pharmacology. Bortezomib. Cell Line, Tumor. Drug Synergism. Humans. Jurkat Cells. K562 Cells. MAP Kinase Signaling System / drug effects. Niacinamide / analogs & derivatives. Phenylurea Compounds. Proteasome Endopeptidase Complex / metabolism

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(PMID = 16985072.001).

[ISSN] 1535-7163

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Boronic Acids; 0 / Phenylurea Compounds; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 9ZOQ3TZI87 / sorafenib; EC 2.7.11.1 / Oncogene Protein v-akt; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex

   

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[Title] Does high-field MR imaging improve cortical lesion detection in multiple sclerosis?

OBJECTIVE: Cortical lesions in multiple sclerosis (MS) are notoriously difficult to visualize with standard MR imaging (MRI) techniques.

However, the use of higher field-strengths with intrinsically higher signal-to-noise, which can partly be used to increase spatial resolution, may improve cortical lesion detection.

Therefore, in this post mortem study, the sensitivity of high field-strength MRI (4.7 T) for cortical lesions was investigated, and compared to that of standard field-strength (1.5 T).

Proteolipid protein (PLP)-stained tissue sections (10 microm) of the same brain slices were matched to the corresponding MR images, and cortical lesions were scored on all three MR sequences (blinded to histology) and in tissue sections (blinded to MRI).

Sensitivity of the sequences for four cortical lesion types was calculated.

RESULTS: Sensitivity for purely intracortical lesions (histological lesion types II, III, and IV; n = 128) was below 10 % for both 1.5 T and 4.7 T MRI, while mixed gray matter-white matter (type I) lesions (n = 5) were detected in four out of five cases.

CONCLUSIONS: MRI sensitivity for post mortem detection of cortical lesions is low, even when a higher field-strength was used.

It varies, however, for different subtypes of cortical lesions.

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(PMID = 18231704.001).

[ISSN] 0340-5354

[Journal-full-title] Journal of neurology

[ISO-abbreviation] J. Neurol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Fixatives; 1HG84L3525 / Formaldehyde

   

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[Title] A novel diquinolonium displays preclinical anti-cancer activity and induces caspase-independent cell death.

Q(2 )induced cell death in leukemia, myeloma, and solid tumor cell lines with LD50s in the low to submicromolar range.

Moreover, Q(2) induced cell death in primary acute myeloid leukemia (AML) cells preferentially over normal hematopoietic cells.

In a mouse model of leukemia, Q(2) delayed tumor growth.

Mechanistically, Q(2) induced cell death through caspase independent mechanisms.

Potentially consistent with the induction of autophagic cell death, Q(2) treatment led to a punctate distribution of LC3 and increased MDC staining.

Thus, Q(2) is a novel quinolinium with preclinical activity in malignancies such as leukemia and myeloma and warrants further investigation.

[MeSH-major] Cell Death / drug effects. Quinolinium Compounds / pharmacology

[MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Animals. Autophagy / drug effects. Caspases / physiology. Cell Line, Tumor. Cell Survival / drug effects. HeLa Cells. Humans. Jurkat Cells. Lethal Dose 50. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Mice. Mice, Inbred DBA. Tumor Cells, Cultured. U937 Cells

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(PMID = 18415680.001).

[ISSN] 1573-675X

[Journal-full-title] Apoptosis : an international journal on programmed cell death

[ISO-abbreviation] Apoptosis

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / 1-methyl-2-(3-(1-methyl-1,2-dihydroquinolin-2-yliden)prop-1-enyl)quinolinium iodide; 0 / Amino Acid Chloromethyl Ketones; 0 / Quinolinium Compounds; 0 / benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone; EC 3.4.22.- / Caspases

   

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Consistent with this, the early pulse of SCL expression also expanded hematopoietic colony-forming cell numbers, while concomitantly repressing expression of paraxial and cardiac markers, and inhibited development of beating cardiomyocytes.

By mixing the inducible embryonic stem cells with fluorescently labeled wild-type cells in chimeric embryoid bodies, we show that these effects of SCL are cell autonomous.

[MeSH-minor] Animals. Antigens, Differentiation / biosynthesis. Antigens, Differentiation / genetics. Cell Line. Colony-Forming Units Assay. Endothelium, Vascular / cytology. Endothelium, Vascular / embryology. Mice. Myocytes, Cardiac / cytology. Myocytes, Cardiac / metabolism. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Time Factors. Transgenes / physiology. Vascular Endothelial Growth Factor Receptor-2 / genetics. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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(PMID = 18809240.001).

[ISSN] 0301-472X

[Journal-full-title] Experimental hematology

[ISO-abbreviation] Exp. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antigens, Differentiation; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2

   

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[Title] Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.

BCR-ABL plays an essential role in the pathogenesis of chronic myeloid leukemia (CML) and some cases of acute lymphocytic leukemia (ALL).

Although ABL kinase inhibitors have shown great promise in the treatment of CML, the persistence of residual disease and the occurrence of resistance have prompted investigations into the molecular effectors of BCR-ABL.

As several downstream mediators of BCR-ABL are regulated by the proteasome degradation pathway, we also show that inhibition of this pathway, using bortezomib, causes regression of CML-like disease.

Our data delineate the involvement of FoxO proteins in BCR-ABL-induced evasion of apoptosis and provide evidence that bortezomib is a candidate therapeutic in the treatment of BCR-ABL-induced leukemia.

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[ErratumIn] Cancer Res. 2009 Sep 1;69(17):7130. Rodin, Heather Yeckes [corrected to Yeckes-Rodin, Heather]

(PMID = 19654305.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / HL080192-05; United States / NHLBI NIH HHS / HL / HL080192; United States / NHLBI NIH HHS / HL / R01 HL080192; United States / NCI NIH HHS / CA / R01 CA131664; United States / NHLBI NIH HHS / HL / R01 HL080192-05; United States / NCI NIH HHS / CA / P30CA6516; United States / NCI NIH HHS / CA / R01 CA105306-05; United States / NCI NIH HHS / CA / R01 CA105306; United States / NCI NIH HHS / CA / CA105306; United States / NCI NIH HHS / CA / P30 CA006516; United States / NCI NIH HHS / CA / CA105306-05; United States / NCI NIH HHS / CA / CA131664

[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; 0 / Benzamides; 0 / Boronic Acids; 0 / Cysteine Proteinase Inhibitors; 0 / Forkhead Transcription Factors; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Pyrimidines; 0 / Tumor Suppressor Proteins; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

[Other-IDs] NLM/ NIHMS123965; NLM/ PMC2763358

   

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[Title] Effective lysis of lymphoma cells with a stabilised bispecific single-chain Fv antibody against CD19 and FcgammaRIII (CD16).

A recombinant bispecific single-chain fragment variable antibody (bsscFv), directed against the B-cell antigen CD19 and the low affinity Fc-receptor FcgammaRIII (CD16), was designed for use in the treatment of patients with leukaemias and lymphomas.

In antibody-dependent cellular cytotoxicity experiments, ds[CD19 x CD16] mediated specific lysis of both CD19-positive malignant human B-lymphoid cell lines and primary tumour cells from patients with B-cell chronic lymphocytic leukaemia or B-cell acute lymphoblastic leukaemia.

Natural killer cells, mononuclear cells (MNCs) from healthy donors and, in some instances, MNCs isolated from patients after allogeneic stem cell transplantation, were used as effectors.

[MeSH-major] Antibodies, Bispecific / immunology. Antibody-Dependent Cell Cytotoxicity / immunology. Antigens, CD19 / immunology. Lymphoma, B-Cell / immunology. Receptors, IgG / immunology

[MeSH-minor] Antibody Specificity. Antigens, Neoplasm / immunology. Burkitt Lymphoma / immunology. Burkitt Lymphoma / pathology. Child. Dose-Response Relationship, Immunologic. Humans. Immunoglobulin Variable Region / immunology. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Recombinant Fusion Proteins / immunology. Tumor Cells, Cultured

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(PMID = 16029450.001).

[ISSN] 0007-1048

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antigens, CD19; 0 / Antigens, Neoplasm; 0 / Immunoglobulin Variable Region; 0 / Receptors, IgG; 0 / Recombinant Fusion Proteins

   

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[Title] ABL1 rearrangements in T-cell acute lymphoblastic leukemia.

T-cell acute lymphoblastic leukemia (T-ALL) is the result of multiple oncogenic insults of thymocytes.

[MeSH-major] Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-abl / genetics

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(PMID = 20073070.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl

[Number-of-references] 60

   

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APO866 inhibits nicotinamide phosphoribosyltransferase (NMPRTase), a key enzyme involved in nicotinamide adenine dinucleotide (NAD) biosynthesis from the natural precursor nicotinamide.

Intracellular NAD is essential for cell survival, and NAD depletion resulting from APO866 treatment elicits tumor cell death.

Here, we determine the in vitro and in vivo sensitivities of hematologic cancer cells to APO866 using a panel of cell lines (n = 45) and primary cells (n = 32).

Most cancer cells (acute myeloid leukemia [AML], acute lymphoblastic leukemia [ALL], mantle cell lymphoma [MCL], chronic lymphocytic leukemia [CLL], and T-cell lymphoma), but not normal hematopoietic progenitor cells, were sensitive to low concentrations of APO866 as measured in cytotoxicity and clonogenic assays.

The NAD depletion led to cell death.

At 96 hours, APO866-mediated cell death occurred in a caspase-independent mode, and was associated with mitochondrial dysfunction and autophagy.

Further, in vivo administration of APO866 as a single agent prevented and abrogated tumor growth in animal models of human AML, lymphoblastic lymphoma, and leukemia without significant toxicity to the animals.

[MeSH-minor] Animals. Cell Death / drug effects. Dose-Response Relationship, Drug. HL-60 Cells. Humans. Jurkat Cells. K562 Cells. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Cells, Cultured. U937 Cells. Xenograft Model Antitumor Assays

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[CommentIn] Blood. 2009 Jun 4;113(23):6035-7; author reply 6037-8 [19498032.001]

(PMID = 19196867.001).

[ISSN] 1528-0020

[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 / Acrylamides; 0 / Antineoplastic Agents; 0 / Cytokines; 0 / N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide; 0 / Piperidines; 0U46U6E8UK / NAD; EC 2.4.2.12 / Nicotinamide Phosphoribosyltransferase; EC 2.4.2.12 / nicotinamide phosphoribosyltransferase, human

   

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[Title] Refractory chronic immune thrombocytopenic purpura in a child with acute lymphoblastic leukemia.

Immune thrombocytopenic purpura (ITP) has been associated with several hematologic malignancies such as Hodgkin and non-Hodgkin lymphomas and chronic lymphocytic leukemia, but it is rare in children with acute lymphoblastic leukemia (ALL).

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Purpura, Thrombocytopenic, Idiopathic / complications. Purpura, Thrombocytopenic, Idiopathic / surgery

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Chronic Disease. Female. Humans. Splenectomy. Treatment Outcome

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[Cites] Pediatr Blood Cancer. 2006 Mar;46(3):372-6 [15700256.001]

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(PMID = 19816666.001).

[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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[Title] Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.

Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance.

Here, we have analyzed the therapeutic potential of the novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable imidazoquinoline derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples.

NVP-BEZ235 was cytotoxic to a panel of T-ALL cell lines as determined by MTT assays.

NVP-BEZ235 treatment resulted in cell cycle arrest and apoptosis.

Remarkably, NVP-BEZ235 targeted the side population of both T-ALL cell lines and patient lymphoblasts, which might correspond to leukemia-initiating cells, and synergized with chemotherapeutic agents (cyclophosphamide, cytarabine, dexamethasone) currently used for treating T-ALL patients.

Taken together, our findings indicate that longitudinal inhibition at two nodes of the PI3K/Akt/mTOR network with NVP-BEZ235, either alone or in combination with chemotherapeutic drugs, may be an efficient treatment of those T-ALLs that have aberrant upregulation of this signaling pathway for their proliferation and survival.

[MeSH-major] Imidazoles / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quinolines / therapeutic use

[MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Autophagy / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Coculture Techniques. Flow Cytometry. Humans. Jurkat Cells / drug effects. Mice. Stromal Cells / drug effects

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[Copyright] ©2010 AACR.

(PMID = 20876803.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Imidazoles; 0 / Quinolines; RUJ6Z9Y0DT / dactolisib

   

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However, despite coregulation of Scl and Lyl1 by the same Ets and GATA factors, Scl expression was initiated prior to Lyl1 in embryonic stem (ES) cell differentiation assays.

[MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line. Conserved Sequence. Embryo, Mammalian / embryology. Embryo, Mammalian / metabolism. Endothelial Cells / metabolism. Gene Expression. Humans. Mice. Mice, Knockout. Molecular Sequence Data. Phenotype. Promoter Regions, Genetic / genetics. Sequence Alignment. Time Factors

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(PMID = 17053063.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / GATA2 Transcription Factor; 0 / Gata2 protein, mouse; 0 / Lyl1 protein, mouse; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Protein c-ets-1; 0 / Proto-Oncogene Proteins; 0 / Tal1 protein, mouse

   

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We show that NUP214-ABL1 displays attenuated transforming capacity as compared to BCR-ABL1 and that NUP214-ABL1 preferentially transforms T cells, which is in agreement with its unique occurrence in T cell acute lymphoblastic leukemia.

[MeSH-major] Cell Transformation, Neoplastic / metabolism. Nuclear Pore / enzymology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism

[MeSH-minor] Animals. Cell Line. Enzyme Activation. Humans. Mice. Nuclear Pore Complex Proteins / metabolism

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(PMID = 18614052.001).

[ISSN] 1097-4164

[Journal-full-title] Molecular cell

[ISO-abbreviation] Mol. Cell

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA8484

[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 / NUP214-ABL1 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases

   

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Observation of high frequencies of mutations in NOTCH1, NPM and JAK2 in T-cell acute lymphoblastic leukemia, acute myeloid leukemia with normal karyotype and myeloproliferative disorders (polycythemia vera, essential thrombocythemia and idiopathic myelofibrosis) have provided important suggestions for a better understanding of chromosomal translocations.

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(PMID = 16357566.001).

[ISSN] 1040-8746

[Journal-full-title] Current opinion in oncology

[ISO-abbreviation] Curr Opin Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases

[Number-of-references] 46

   

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[Title] Association of B-chronic lymphocytic leukemia and acute myeloid leukemia.

[MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasms, Multiple Primary / diagnosis

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(PMID = 17987806.001).

[ISSN] 0392-9078

[Journal-full-title] Journal of experimental & clinical cancer research : CR

[ISO-abbreviation] J. Exp. Clin. Cancer Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Italy

   

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[Title] Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism.

Glucocorticoids (GCs) are among the most important drugs for acute lymphoblastic leukaemia (ALL), yet despite their clinical importance, the exact mechanisms involved in GC cytotoxicity and the development of resistance remain uncertain.

We examined the baseline profile of a panel of T-ALL cell lines to determine factors that contribute to GC resistance without prior drug selection.

The data also provide the first evidence that altered expression of wild-type MLL may contribute to GC-resistant phenotypes.

[MeSH-major] Cell Proliferation / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Methylprednisolone / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction / drug effects

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(PMID = 19436302.001).

[ISSN] 1532-1827

[Journal-full-title] British journal of cancer

[ISO-abbreviation] Br. J. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Glucocorticoids; 7S5I7G3JQL / Dexamethasone; X4W7ZR7023 / Methylprednisolone

[Other-IDs] NLM/ PMC2714233

   

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[Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.

We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.

We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).

These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).

Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.

[MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics

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(PMID = 17483057.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1

   

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[Title] Pyridoxine treatment of vincristine-induced cranial polyneuropathy in an adult patient with acute lymphocytic leukemia: Case report and review of the literature.

[MeSH-major] Cranial Nerve Diseases / chemically induced. Cranial Nerve Diseases / drug therapy. Polyneuropathies / chemically induced. Polyneuropathies / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyridoxine / therapeutic use. Vincristine / adverse effects

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(PMID = 20167372.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 12001-76-2 / Vitamin B Complex; 5J49Q6B70F / Vincristine; KV2JZ1BI6Z / Pyridoxine

   

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It is now clear that the way a chemotherapeutic drug kills a tumour cell determines how that dying cell interacts with the immune system and whether the interaction leads to an immune response.

Furthermore, lymphodepletion triggers homeostatic T cell reconstitution, creating new populations of pre-T cells that need education in the thymic environment.

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(PMID = 17005292.001).

[ISSN] 0169-409X

[Journal-full-title] Advanced drug delivery reviews

[ISO-abbreviation] Adv. Drug Deliv. Rev.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines

[Number-of-references] 105

   

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The stem cell leukemia (SCL or tal-1) gene was initially identified as a translocation partner in a leukemia that possessed both lymphoid and myeloid differentiation potential.

Mice that lacked SCL expression showed a complete block in hematopoiesis; thus, SCL was associated with hematopoietic stem cell (HSC) function.

Using recently defined surface immunophenotypes, we fluorescence-activated cell-sorted (FACS) highly purified populations of primary human hematopoietic progenitors for reverse transcription-polymerase chain reaction (RT-PCR) analysis of SCL expression.

SCL expression was undetectable in immature cells of nonerythroid lineages, including pro-B cells, early thymic progenitors, and myeloid precursors expressing the M-CSF receptor.

[MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Basic Helix-Loop-Helix Transcription Factors. Bone Marrow Cells / cytology. Cell Differentiation. Cell Line. Cell Lineage. Cell Separation. Cells, Cultured. Down-Regulation. Flow Cytometry. Humans. Immunophenotyping. Mice. Models, Biological. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Stem Cells / cytology. Thymus Gland / metabolism. Time Factors

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(PMID = 15917481.001).

[ISSN] 1066-5099

[Journal-full-title] Stem cells (Dayton, Ohio)

[ISO-abbreviation] Stem Cells

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / K01 DK066163; United States / NCI NIH HHS / CA / P01CA59318; United States / NHLBI NIH HHS / HL / P50HL54850; United States / NHLBI NIH HHS / HL / R01HL77912

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human