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1
acute t lymphocytic leukemia 2005:2010[pubdate] *count=100
1139 results
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acute t lymphocytic leukemia
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Items 1 to 100 of about 1139
1.
Ren SY, Xue F, Feng J, Skorski T:
Intrinsic regulation of the interactions between the SH3 domain of p85 subunit of phosphatidylinositol-3 kinase and the protein network of BCR/ABL oncogenic tyrosine kinase.
Exp Hematol
; 2005 Oct;33(10):1222-8
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OBJECTIVE: BCR/ABL fusion tyrosine kinase is responsible for the initiation and maintenance of the Philadelphia chromosome-positive chronic myelogenous
leukemia
(CML) and a cohort of
acute lymphocytic
leukemias
.
RESULTS: We show here that the SH3 domain of p85alpha (p85alpha-SH3) pulls down the p210BCR/ABL kinase from hematopoietic
cell
lysates.
[MeSH-minor]
Amino Acid Substitution. Animals.
Cell
Line, Tumor. Fusion Proteins, bcr-abl. Hematopoietic Stem Cells / metabolism. Humans. Immunoprecipitation / methods.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Mice. Mutagenesis, Site-Directed. Point Mutation / genetics. Protein Binding
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NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 16219545.001).
[ISSN]
0301-472X
[Journal-full-title]
Experimental hematology
[ISO-abbreviation]
Exp. Hematol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA83700
[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]
Netherlands
[Chemical-registry-number]
0 / Protein Subunits; 0 / Proto-Oncogene Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
2.
Cossu F:
Genetics of SCID.
Ital J Pediatr
; 2010;36:76
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Human SCID (Severe Combined Immunodeficiency) is a prenatal
disorder
of T lymphocyte development, that depends on the expression of numerous genes.
The knowledge of the genetic basis of SCID is essential for
diagnosis
(e.g., clinical phenotype, lymphocyte profile) and treatment (e.g., use and
type
of
pre
-hematopoietic stem
cell
transplant conditioning).Over the last years novel genetic defects causing SCID have been discovered, and the molecular and immunological mechanisms of SCID have been better characterized.
Distinct forms of SCID show both common and peculiar (e.g., absence or presence of nonimmunological features) aspects, and they are currently classified into six groups according to prevalent pathophysiological mechanisms: impaired cytokine-mediated signaling;
pre
-T
cell
receptor defects; increased lymphocyte apoptosis; defects in
thymus
embryogenesis; impaired calcium flux; other mechanisms.This review is the updated, extended and largely modified translation of the article "Cossu F: Le basi genetiche delle SCID", originally published in Italian language in the journal "Prospettive in Pediatria" 2009, 156:228-238.
[MeSH-minor]
Genetic Therapy. Genotype. Hematopoietic Stem
Cell
Transplantation. Humans. Infant, Newborn. Neonatal Screening. T-Lymphocytes / pathology
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(PMID = 21078154.001).
[ISSN]
1824-7288
[Journal-full-title]
Italian journal of pediatrics
[ISO-abbreviation]
Ital J Pediatr
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Other-IDs]
NLM/ PMC2999594
3.
Garbe AI, Krueger A, Gounari F, Zúñiga-Pflücker JC, von Boehmer H:
Differential synergy of Notch and T cell receptor signaling determines alphabeta versus gammadelta lineage fate.
J Exp Med
; 2006 Jun 12;203(6):1579-90
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[Title]
Differential synergy of Notch and T
cell
receptor signaling determines alphabeta versus gammadelta lineage fate.
Thymic precursors expressing the
pre
-T
cell
receptor (TCR), the gammadeltaTCR, or the alphabetaTCR can all enter the CD4+ 8+ alphabeta lineage, albeit with different efficacy.
In particular, in alphabeta lineage commitment, the
pre
-TCR synergizes more efficiently with Notch signals than the other two TCRs, whereas gammadeltaTCR-expressing cells can survive and expand in the absence of Notch signals, even though Notch signaling enhances their proliferation.
These observations suggest a new model of alphabeta versus gammadelta lineage choice in which lineage fate is determined by the extent of synergy between TCR and Notch signaling and in which the evolutionarily recent advent of the
cell
-autonomously signaling
pre
-TCR increased the efficacy of alphabeta T
cell
generation.
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(PMID = 16754723.001).
[ISSN]
0022-1007
[Journal-full-title]
The Journal of experimental medicine
[ISO-abbreviation]
J. Exp. Med.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA10990; United States / NIAID NIH HHS / AI / R01 AI47281; United States / NIAID NIH HHS / AI / R01 AI047281; United States / NIAID NIH HHS / AI / R01 AI45846
[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 / Homeodomain Proteins; 0 / Receptors, Antigen, T-Cell; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / Receptors, Notch; 128559-51-3 / RAG-1 protein
[Other-IDs]
NLM/ PMC2118312
Advertisement
4.
Derré L, Bruyninx M, Baumgaertner P, Ferber M, Schmid D, Leimgruber A, Zoete V, Romero P, Michielin O, Speiser DE, Rufer N:
Distinct sets of alphabeta TCRs confer similar recognition of tumor antigen NY-ESO-1157-165 by interacting with its central Met/Trp residues.
Proc Natl Acad Sci U S A
; 2008 Sep 30;105(39):15010-5
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Here, we studied T
cell
receptor (TCR) primary structure and function of 605 HLA-A*0201/NY-ESO-1(157-165)-specific CD8 T
cell
clones
derived
from five melanoma patients.
All remaining T
cell
clones belong to two additional sets expressing BV1 or BV13 TCRs, associated with alpha-chains with highly diverse VJ usage, CDR3 amino acid sequence, and length.
Yet, all T
cell
clonotypes recognize tumor antigen with similar functional avidity.
Two residues, Met-160 and Trp-161, located in the middle region of the NY-ESO-1(157-165) peptide, are critical for recognition by most of the T
cell
clonotypes.
[MeSH-major]
Neoplasm Proteins / immunology. Peptide Fragments / immunology. Receptors, Antigen, T-
Cell
, alpha-beta / immunology
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[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Neoplasm Proteins; 0 / Peptide Fragments; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / peptide NY-ESO-1 157-165; 2ZD004190S / Threonine; AE28F7PNPL / Methionine
[Other-IDs]
NLM/ PMC2567484
5.
Martínez-Delgado B, Cuadros M, Honrado E, Ruiz de la Parte A, Roncador G, Alves J, Castrillo JM, Rivas C, Benítez J:
Differential expression of NF-kappaB pathway genes among peripheral T-cell lymphomas.
Leukemia
; 2005 Dec;19(12):2254-63
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[Title]
Differential expression of NF-kappaB pathway genes among peripheral T-
cell
lymphomas.
Nuclear factor kappa B (NF-kappaB) is one important pathway in T-
cell
proliferation and survival.
In a previously reported microarray study, we found NF-kappaB pathway genes differentially expressed between peripheral (PTCL) and
lymphoblastic
lymphomas.
This distinction was found among all T-
cell lymphoma
categories analyzed (PTCL unspecified, angioimmunoblastic, cutaneous and natural killer/T lymphomas) with the exception of anaplastic lymphomas (ALCL), which were characterized by reduced NF-kappaB expression in anaplastic cells.
[MeSH-major]
Gene Expression Regulation, Neoplastic.
Lymphoma
, T-
Cell
, Peripheral / genetics. NF-kappa B / genetics
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(PMID = 16270046.001).
[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 / NF-kappa B
6.
Strick R, Zhang Y, Emmanuel N, Strissel PL:
Common chromatin structures at breakpoint cluster regions may lead to chromosomal translocations found in chronic and acute leukemias.
Hum Genet
; 2006 Jun;119(5):479-95
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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
7.
Corcoran M, Parker A, Orchard J, Davis Z, Wirtz M, Schmitz OJ, Oscier D:
ZAP-70 methylation status is associated with ZAP-70 expression status in chronic lymphocytic leukemia.
Haematologica
; 2005 Aug;90(8):1078-88
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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
8.
Sakai M, Takeyama H, Kojima Y, Shimokawa T:
[Treatment results of acute leukemia in elderly patients: analysis of 61 consecutive patients in a single institution].
Gan To Kagaku Ryoho
; 2008 Feb;35(2):239-44
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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
9.
Kode J, Dudhal N, Banavali S, Chiplunkar S:
T-cell receptor gamma and delta junctional gene rearrangements as diagnostic and prognostic biomarker for T-cell acute lymphoblastic leukemia.
Leuk Lymphoma
; 2006 Apr;47(4):769-70
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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
10.
Frazer JK, Meeker ND, Rudner L, Bradley DF, Smith AC, Demarest B, Joshi D, Locke EE, Hutchinson SA, Tripp S, Perkins SL, Trede NS:
Heritable T-cell malignancy models established in a zebrafish phenotypic screen.
Leukemia
; 2009 Oct;23(10):1825-35
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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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Curr Opin Hematol. 2001 Jul;8(4):189-91
[
11561153.001
]
(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
11.
Medyouf H, Alcalde H, Berthier C, Guillemin MC, dos Santos NR, Janin A, Decaudin D, de Thé H, Ghysdael J:
Targeting calcineurin activation as a therapeutic strategy for T-cell acute lymphoblastic leukemia.
Nat Med
; 2007 Jun;13(6):736-41
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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
12.
Osmond RI, Das S, Crouch MF:
Development of cell-based assays for cytokine receptor signaling, using an AlphaScreen SureFire assay format.
Anal Biochem
; 2010 Aug;403(1-2):94-101
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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
13.
Iversen PO, Sørensen DR, Tronstad KJ, Gudbrandsen OA, Rustan AC, Berge RK, Drevon CA:
A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of acute leukemia.
Clin Cancer Res
; 2006 Jun 1;12(11 Pt 1):3525-31
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[Title]
A bioactively modified fatty acid improves survival and impairs metastasis in preclinical models of
acute leukemia
.
PURPOSE: Polyunsaturated fatty acids (PUFA) and the sulfur-substituted fatty acid tetradecylthioacetic acid (TTA) inhibit proliferation and induce apoptosis in
lymphoma
and leukemic
cell
lines, but it is unknown if they can modify leukemogenesis in the intact organism.
EXPERIMENTAL DESIGN: We now examined the effects of PUFA and TTA in rats transplanted with either
acute
promyelocytic
leukemia
or
acute T
-
cell
leukemia
.
RESULTS: Whereas TTA prolonged survival (P < 0.05) in both types of rat
leukemia
, n-3 PUFA had no significant effect compared with controls.
CONCLUSIONS: Dietary intake of TTA, but not of n-3 PUFA, in rats with
acute leukemia
, prolonged their survival.
TTA intake was also associated with reduced leukemic
cell
burden as well as diminished extramedullar dissemination.
TTA represents a modified fatty acid that exerts unique effects on malignant hematopoietic cells, and the present study indicates that TTA may have a therapeutic potential in patients with
acute
leukemias
.
[MeSH-major]
Fatty Acids, Unsaturated / administration & dosage.
Leukemia
, Promyelocytic,
Acute
/ drug therapy.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ drug therapy. Sulfides / administration & dosage
[MeSH-minor]
Animals. Apoptosis / drug effects. Diet.
Disease
Models, Animal. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. Leukemic Infiltration /
diagnosis
. Matrix Metalloproteinases / drug effects. Neoplasm Metastasis. Rats. Structure-Activity Relationship. Survival Rate. Transplantation, Heterologous. Xenograft Model Antitumor Assays
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(PMID = 16740779.001).
[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 / Fatty Acids, Unsaturated; 0 / Sulfides; 2921-20-2 / 1-(carboxymethylthio)tetradecane; EC 3.4.24.- / Matrix Metalloproteinases
14.
van Anders SM, Hamilton LD, Schmidt N, Watson NV:
Associations between testosterone secretion and sexual activity in women.
Horm Behav
; 2007 Apr;51(4):477-82
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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
15.
Patterson LJ, Gering M, Eckfeldt CE, Green AR, Verfaillie CM, Ekker SC, Patient R:
The transcription factors Scl and Lmo2 act together during development of the hemangioblast in zebrafish.
Blood
; 2007 Mar 15;109(6):2389-98
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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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Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
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ZFIN.
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.
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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
16.
Roecker AM, Allison JC, Kisor DF:
Nelarabine: efficacy in the treatment of clinical malignancies.
Future Oncol
; 2006 Aug;2(4):441-8
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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
17.
Hager-Theodorides AL, Dessens JT, Outram SV, Crompton T:
The transcription factor Gli3 regulates differentiation of fetal CD4- CD8- double-negative thymocytes.
Blood
; 2005 Aug 15;106(4):1296-304
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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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.
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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
18.
Meijerink JP:
Genetic rearrangements in relation to immunophenotype and outcome in T-cell acute lymphoblastic leukaemia.
Best Pract Res Clin Haematol
; 2010 Sep;23(3):307-18
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[Title]
Genetic rearrangements in relation to immunophenotype and outcome in T-
cell
acute
lymphoblastic leukaemia
.
Mutually exclusive oncogenic rearrangements may delineate specific T-
cell
acute
lymphoblastic leukaemia
(T-ALL) subgroups, and so far at least 4 molecular-cytogenetic subgroups have been identified, i.e. the TAL/LMO, the TLX1/HOX11, the TLX3/HOX11L2 and the HOXA subgroups.
A fifth group with an immature immunophenotype that can be predicted by an early T-
cell precursor
signature has also been identified, and has been associated with poor outcome.
The association of these subgroups with the expression of specific immunophenotypic markers reflecting arrest at specific T-
cell
developmental stages will be reviewed.
[MeSH-major]
Gene Rearrangement.
Precursor
T-
Cell Lymphoblastic
Leukemia
-
Lymphoma
/ genetics. Signal Transduction
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[Copyright]
Copyright © 2010 Elsevier Ltd. All rights reserved.
(PMID = 21112032.001).
[ISSN]
1532-1924
[Journal-full-title]
Best practice & research. Clinical haematology
[ISO-abbreviation]
Best Pract Res Clin Haematol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptor, Notch1; 135471-20-4 / TAL1 protein, human
19.
DeAngelo DJ:
The treatment of adolescents and young adults with acute lymphoblastic leukemia.
Hematology Am Soc Hematol Educ Program
; 2005;:123-30
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[Title]
The treatment of adolescents and young adults with
acute
lymphoblastic
leukemia
.
Intensive chemotherapy regimens for children with
acute
lymphoblastic
leukemia
(ALL) have greatly improved, and the majority of children with
precursor
B-
cell ALL
are able to achieve a complete remission (CR), with an induction rate approaching 98% and a 5-year estimated event-free survival rate (EFS) of approximately 80%.
In addition, new insights into the molecular pathogenesis of T
cell ALL
have led to new therapeutic strategies.
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(PMID = 16304369.001).
[ISSN]
1520-4383
[Journal-full-title]
Hematology. American Society of Hematology. Education Program
[ISO-abbreviation]
Hematology Am Soc Hematol Educ Program
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
20.
Huang YF, Shangguan D, Liu H, Phillips JA, Zhang X, Chen Y, Tan W:
Molecular assembly of an aptamer-drug conjugate for targeted drug delivery to tumor cells.
Chembiochem
; 2009 Mar 23;10(5):862-8
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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
21.
Ohnuki K, Watanabe Y, Takahashi Y, Kobayashi S, Watanabe S, Ogawa S, Kotani M, Kozono H, Tanabe K, Abe R:
Antigen-specific CD4+ effector T cells: analysis of factors regulating clonal expansion and cytokine production: clonal expansion and cytokine production by CD4+ effector T cells.
Biochem Biophys Res Commun
; 2009 Mar 20;380(4):742-7
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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
22.
Braun FK, Fecker LF, Schwarz C, Walden P, Assaf C, Dürkop H, Sterry W, Eberle J:
Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells.
J Invest Dermatol
; 2007 Oct;127(10):2425-37
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[Title]
Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-
cell lymphoma
cells.
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
Genetic Alliance.
consumer health - Cutaneous T-Cell Lymphoma
.
MedlinePlus Health Information.
consumer health - Skin Cancer
.
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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
23.
Dzhagalov I, Dunkle A, He YW:
The anti-apoptotic Bcl-2 family member Mcl-1 promotes T lymphocyte survival at multiple stages.
J Immunol
; 2008 Jul 1;181(1):521-8
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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.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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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
24.
Look AT:
Investigator profile. An interview with A. Thomas Look, M.D. Interview by Vicki Glaser.
Zebrafish
; 2005;2(4):231-6
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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
25.
Gläsker S, Li J, Xia JB, Okamoto H, Zeng W, Lonser RR, Zhuang Z, Oldfield EH, Vortmeyer AO:
Hemangioblastomas share protein expression with embryonal hemangioblast progenitor cell.
Cancer Res
; 2006 Apr 15;66(8):4167-72
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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
.
MedlinePlus Health Information.
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.
COS Scholar Universe.
author profiles
.
The Lens.
Cited by Patents in
.
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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
26.
Isoda T, Ito S, Kajiwara M, Nagasawa M:
Successful high-dose methotrexate chemotherapy in a patient with acute lymphocytic leukemia who developed acute renal failure during the initial treatment.
Pediatr Int
; 2007 Dec;49(6):1018-9
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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
Hazardous Substances Data Bank.
METHOTREXATE
.
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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
27.
Verbeek WH, Van De Water JM, Al-Toma A, Oudejans JJ, Mulder CJ, Coupé VM:
Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands.
Scand J Gastroenterol
; 2008;43(11):1322-8
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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
Genetic Alliance.
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.
MedlinePlus Health Information.
consumer health - Celiac Disease
.
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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
28.
Shapira T, Pereg D, Lishner M:
How I treat acute and chronic leukemia in pregnancy.
Blood Rev
; 2008 Sep;22(5):247-59
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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
Genetic Alliance.
consumer health - Pregnancy
.
MedlinePlus Health Information.
consumer health - Childhood Leukemia
.
MedlinePlus Health Information.
consumer health - Leukemia
.
MedlinePlus Health Information.
consumer health - Tumors and Pregnancy
.
The Weizmann Institute of Science GeneCards and MalaCards databases.
gene/protein/disease-specific - MalaCards for chronic leukemia
.
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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
29.
Yu Q, Sharma A, Sen JM:
TCF1 and beta-catenin regulate T cell development and function.
Immunol Res
; 2010 Jul;47(1-3):45-55
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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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Curr Opin Immunol. 2009 Jun;21(3):274-80
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19524429.001
]
(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
30.
Hwang C, Jang S, Choi DK, Kim S, Lee JH, Lee Y, Kim CD, Lee JH:
The role of nkx2.5 in keratinocyte differentiation.
Ann Dermatol
; 2009 Nov;21(4):376-81
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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
31.
Chen W, Wang E, Lu Y, Gaal KK, Huang Q:
Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.
Am J Clin Pathol
; 2010 Jan;133(1):75-82
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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
32.
Brewer JL, Ericson SG:
An improved methodology to detect human T cell receptor beta variable family gene expression patterns.
J Immunol Methods
; 2005 Jul;302(1-2):54-67
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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
The Lens.
Cited by Patents in
.
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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
33.
Yu C, Friday BB, Lai JP, Yang L, Sarkaria J, Kay NE, Carter CA, Roberts LR, Kaufmann SH, Adjei AA:
Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways.
Mol Cancer Ther
; 2006 Sep;5(9):2378-87
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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
34.
Geurts JJ, Blezer EL, Vrenken H, van der Toorn A, Castelijns JA, Polman CH, Pouwels PJ, Bö L, Barkhof F:
Does high-field MR imaging improve cortical lesion detection in multiple sclerosis?
J Neurol
; 2008 Feb;255(2):183-91
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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
35.
Hurren R, Beheshti Zavareh R, Dalili S, Wood T, Rose D, Chang H, Jamal N, Messner H, Batey RA, Schimmer AD:
A novel diquinolonium displays preclinical anti-cancer activity and induces caspase-independent cell death.
Apoptosis
; 2008 Jun;13(6):748-55
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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
36.
Ismailoglu I, Yeamans G, Daley GQ, Perlingeiro RC, Kyba M:
Mesodermal patterning activity of SCL.
Exp Hematol
; 2008 Dec;36(12):1593-603
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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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consumer health - Stem Cells
.
COS Scholar Universe.
author profiles
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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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
37.
Ghinassi B, Verrucci M, Jelicic K, Di Noia A, Migliaccio G, Migliaccio AR:
Interleukin-3 and erythropoietin cooperate in the regulation of the expression of erythroid-specific transcription factors during erythroid differentiation.
Exp Hematol
; 2007 May;35(5):735-47
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OBJECTIVE: To characterize how interleukin-3 and erythropoietin regulate
cell
fate by modulating the expression of lineage-specific transcription factors.
METHODS: This study analyzed mRNA and protein levels, gene transcription rates, and mRNA and protein stabilities of erythroid-specific transcription factors in lineage-restricted cells
derived
from the 32D
cell
line cultured either in interleukin-3 or erythropoietin.
Switching the erythroid cells to erythropoietin induced
cell
maturation (within 48 hours) and reduced expression of Gata-2 and Idl (in 24 hours) but did not alter the expression of Gata-1.
[MeSH-minor]
Animals.
Cell
Differentiation / drug effects.
Cell
Differentiation / genetics.
Cell
Line. Gene Expression Profiling. Mice. Phenotype. RNA, Messenger / drug effects. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Structure-Activity Relationship. T-
Cell
Acute Lymphocytic Leukemia
Protein 1. Time Factors
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(PMID = 17577923.001).
[ISSN]
0301-472X
[Journal-full-title]
Experimental hematology
[ISO-abbreviation]
Exp. Hematol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01-CA108671-01A2
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Erythroid-Specific DNA-Binding Factors; 0 / Idb1 protein, mouse; 0 / Inhibitor of Differentiation Protein 1; 0 / Interleukin-3; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / T-Cell Acute Lymphocytic Leukemia Protein 1; 0 / Tal1 protein, mouse; 11096-26-7 / Erythropoietin
38.
Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA:
WT1 mutations in T-ALL.
Blood
; 2009 Jul 30;114(5):1038-45
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The molecular mechanisms involved in
disease
progression and relapse in T-
cell
acute
lymphoblastic
leukemia
(T-ALL) are poorly understood.
This analysis showed that
diagnosis
and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at
diagnosis
, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at
diagnosis
.
[MeSH-major]
Genes, Wilms Tumor. Mutation.
Precursor
T-
Cell Lymphoblastic
Leukemia
-
Lymphoma
/ genetics
[MeSH-minor]
Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics.
Disease
Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics
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]
(PMID = 19494353.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Databank-accession-numbers]
GEO/ GSE15931
[Grant]
United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
[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 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
[Other-IDs]
NLM/ PMC2721784
39.
Romana SP, Radford-Weiss I, Ben Abdelali R, Schluth C, Petit A, Dastugue N, Talmant P, Bilhou-Nabera C, Mugneret F, Lafage-Pochitaloff M, Mozziconacci MJ, Andrieu J, Lai JL, Terre C, Rack K, Cornillet-Lefebvre P, Luquet I, Nadal N, Nguyen-Khac F, Perot C, Van den Akker J, Fert-Ferrer S, Cabrol C, Charrin C, Tigaud I, Poirel H, Vekemans M, Bernard OA, Berger R, Groupe Francophone de Cytogénétique Hématologique:
NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique.
Leukemia
; 2006 Apr;20(4):696-706
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[Title]
NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone
de
Cytogénétique Hématologique.
In order to gain additional clinico-hematological data and to identify new partners of NUP98, the Groupe Francophone
de
Cytogénétique Hématologique (GFCH) collected cases of hematological malignancies where a 11p15 rearrangement was detected.
Genes of the HOXA cluster and the nuclear-receptor set domain (NSD) genes were frequently fused to NUP98, mainly in
de
novo myeloid malignancies whereas the DDX10 and TOP1 genes were equally rearranged in
de
novo and in therapy-related myeloid proliferations.
Involvement of ADD3 and C6ORF80 genes were detected, respectively, in myeloid disorders and in T-
cell
acute
lymphoblastic
leukemia
(T-ALL), whereas the RAP1GDS1 gene was fused to NUP98 in T-ALL.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
HGNC: Data: Gene Annotation
.
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(PMID = 16467868.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Receptors, Cytoplasmic and Nuclear; 157907-48-7 / HoxA protein
40.
Jagani Z, Song K, Kutok JL, Dewar MR, Melet A, Santos T, Grassian A, Ghaffari S, Wu C, Yeckes-Rodin H, Ren R, Miller K, Khosravi-Far R:
Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors.
Cancer Res
; 2009 Aug 15;69(16):6546-55
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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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.
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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
41.
Bruenke J, Barbin K, Kunert S, Lang P, Pfeiffer M, Stieglmaier K, Niethammer D, Stockmeyer B, Peipp M, Repp R, Valerius T, Fey GH:
Effective lysis of lymphoma cells with a stabilised bispecific single-chain Fv antibody against CD19 and FcgammaRIII (CD16).
Br J Haematol
; 2005 Jul;130(2):218-28
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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
42.
Hagemeijer A, Graux C:
ABL1 rearrangements in T-cell acute lymphoblastic leukemia.
Genes Chromosomes Cancer
; 2010 Apr;49(4):299-308
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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
43.
Nahimana A, Attinger A, Aubry D, Greaney P, Ireson C, Thougaard AV, Tjørnelund J, Dawson KM, Dupuis M, Duchosal MA:
The NAD biosynthesis inhibitor APO866 has potent antitumor activity against hematologic malignancies.
Blood
; 2009 Apr 2;113(14):3276-86
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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
44.
Horino S, Rikiishi T, Niizuma H, Abe H, Watanabe Y, Onuma M, Hoshi Y, Sasahara Y, Yoshinari M, Kazama T, Hayashi Y, Kumaki S, Tsuchiya S:
Refractory chronic immune thrombocytopenic purpura in a child with acute lymphoblastic leukemia.
Int J Hematol
; 2009 Nov;90(4):483-5
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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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Pediatr Hematol Oncol. 2000 Dec;17(8):719-20
[
11127406.001
]
(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
45.
Chiarini F, Grimaldi C, Ricci F, Tazzari PL, Evangelisti C, Ognibene A, Battistelli M, Falcieri E, Melchionda F, Pession A, Pagliaro P, McCubrey JA, Martelli AM:
Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.
Cancer Res
; 2010 Oct 15;70(20):8097-107
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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
46.
Chan WY, Follows GA, Lacaud G, Pimanda JE, Landry JR, Kinston S, Knezevic K, Piltz S, Donaldson IJ, Gambardella L, Sablitzky F, Green AR, Kouskoff V, Göttgens B:
The paralogous hematopoietic regulators Lyl1 and Scl are coregulated by Ets and GATA factors, but Lyl1 cannot rescue the early Scl-/- phenotype.
Blood
; 2007 Mar 1;109(5):1908-16
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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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.
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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
47.
De Keersmaecker K, Rocnik JL, Bernad R, Lee BH, Leeman D, Gielen O, Verachtert H, Folens C, Munck S, Marynen P, Fornerod M, Gilliland DG, Cools J:
Kinase activation and transformation by NUP214-ABL1 is dependent on the context of the nuclear pore.
Mol Cell
; 2008 Jul 11;31(1):134-42
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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
48.
Taki T, Taniwaki M:
Chromosomal translocations in cancer and their relevance for therapy.
Curr Opin Oncol
; 2006 Jan;18(1):62-8
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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
49.
Carulli G, Marini A, Baccelli E, Lambelet P, Lari T, Azzarà A:
Association of B-chronic lymphocytic leukemia and acute myeloid leukemia.
J Exp Clin Cancer Res
; 2007 Sep;26(3):421-4
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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
50.
Beesley AH, Firth MJ, Ford J, Weller RE, Freitas JR, Perera KU, Kees UR:
Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism.
Br J Cancer
; 2009 Jun 16;100(12):1926-36
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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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]
[ErratumIn]
Br J Cancer. 2010 Mar 30;102(7):1200
(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
51.
Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M:
Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
Int J Hematol
; 2007 Apr;85(3):212-8
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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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Blood. 2001 Dec 15;98(13):3793-9
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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
52.
Dohda T, Maljukova A, Liu L, Heyman M, Grandér D, Brodin D, Sangfelt O, Lendahl U:
Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines.
Exp Cell Res
; 2007 Aug 15;313(14):3141-52
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[Title]
Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-
cell
acute
lymphoblastic
leukemia
cell
lines.
In T-
cell
acute
lymphoblastic
leukemia
(T-ALL) NOTCH 1 receptors are frequently mutated.
This leads to aberrantly high Notch signaling, but how this translates into deregulated
cell
cycle control and the transformed
cell type
is poorly understood.
Notch activity, measured immediately downstream of the NOTCH 1 receptor, is high, but expression of the canonical downstream Notch response genes HES 1 and HEY 2 is low both in primary cells from T-ALL patients and in T-
ALL cell
lines.
We show that in T-
ALL cell
lines, recruitment of NOTCH 1 intracellular domain (ICD) to the SKP2 promoter was accompanied by high SKP2 and low p27Kip1 protein levels.
T-ALL cells show a rapid G1-S
cell
cycle transition, while blocked Notch signaling resulted in G0/G1
cell
cycle arrest, also observed by transfection of p27Kip1 or, to a smaller extent, a dominant negative SKP2 allele.
Collectively, our data suggest that the aberrantly high Notch signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid
cell
cycle progression.
[MeSH-major]
Intracellular Signaling Peptides and Proteins / metabolism.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ metabolism. Receptor, Notch1 / metabolism. S-Phase Kinase-Associated Proteins / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism
[MeSH-minor]
Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism.
Cell
Cycle / physiology.
Cell
Cycle Proteins / genetics.
Cell
Cycle Proteins / metabolism.
Cell
Line, Tumor. Child. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Repressor Proteins / genetics. Repressor Proteins / metabolism
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(PMID = 17560996.001).
[ISSN]
0014-4827
[Journal-full-title]
Experimental cell research
[ISO-abbreviation]
Exp. Cell Res.
[Language]
eng
[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 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / HEY2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Repressor Proteins; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
53.
Akiyama S, Dhavan D, Yi T:
PRL-2 increases Epo and IL-3 responses in hematopoietic cells.
Blood Cells Mol Dis
; 2010 Apr 15;44(4):209-14
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Dual specificity protein tyrosine phosphatase PRL-2 is overexpressed in pediatric
acute
myeloid
leukemia
(AML) and is located at human chromosome 1p35, a region often rearranged or amplified in malignant
lymphoma
and B-
cell
chronic
lymphocytic leukemia
(B-CLL).
Herein we demonstrated that ectopic expression of PRL-2 in murine
pre
-B-
cell
line Baf3ER and mouse bone marrow cells induced key features associated with malignant progression and metastasis.
PRL-2-transfected Baf3ER cells had augmented growth responses to hematopoietic growth factors Epo or IL-3 with shortened
cell
cycle, reduced requirement (5x) for Epo in
cell
survival, increased
cell
migration (3x), reduced
cell
adhesion (5x), and conversion to an immature
cell
morphology in association with increased expression (3x) of stem
cell
marker Bmi-1.
Hazardous Substances Data Bank.
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.
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9514946.001
]
(PMID = 20226699.001).
[ISSN]
1096-0961
[Journal-full-title]
Blood cells, molecules & diseases
[ISO-abbreviation]
Blood Cells Mol. Dis.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA102481-03; United States / NCI NIH HHS / CA / R01 CA096636; United States / NCI NIH HHS / CA / R01 CA102481; United States / NCI NIH HHS / CA / R01 CA096636-05; United States / NCI NIH HHS / CA / CA102481-03; United States / NCI NIH HHS / CA / CA096636-05
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Interleukin-3; 0 / Recombinant Fusion Proteins; 0 / Recombinant Proteins; 0 / STAT5 Transcription Factor; 11096-26-7 / Erythropoietin; 64FS3BFH5W / Epoetin Alfa; EC 3.1.3.48 / PTP4A2 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatases
[Other-IDs]
NLM/ NIHMS182540; NLM/ PMC2847026
54.
Kreitman RJ:
Recombinant immunotoxins for the treatment of chemoresistant hematologic malignancies.
Curr Pharm Des
; 2009;15(23):2652-64
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[Source]
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No agents of this class are approved yet for medical use, although a related molecule, denileukin diftitox, composed of interleukin-2 fused to truncated diphtheria toxin, is approved for relapsed/refractory cutaneous T-
cell lymphoma
.
Major responses were observed with LMB-2 in adult T-
cell
leukemia
, chronic
lymphocytic leukemia
(CLL), cutaneous T-
cell lymphoma
, Hodgkin's
disease
, and hairy
cell
leukemia
(HCL).
HA22, an improved version of BL22 with higher affinity to CD22, is now undergoing phase I testing in HCL, CLL, non-Hodgkin's
lymphoma
, and pediatric
acute
lymphoblastic
leukemia
.
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(PMID = 19689336.001).
[ISSN]
1873-4286
[Journal-full-title]
Current pharmaceutical design
[ISO-abbreviation]
Curr. Pharm. Des.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Diphtheria Toxin; 0 / Immunotoxins; 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Recombinant Proteins; 0 / Toxins, Biological
[Number-of-references]
190
55.
Xu W, Li JY, Qian SX, Wu HX, Lu H, Chen LJ, Zhang SJ, Lu RL, Sheng RL:
Outcome of treatment with Hyper-CVAD regimen in Chinese patients with acute lymphocytic leukemia.
Leuk Res
; 2008 Jun;32(6):930-5
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[Title]
Outcome of treatment with Hyper-CVAD regimen in Chinese patients with
acute lymphocytic leukemia
.
Modern intensive chemotherapy regimens have improved the prognosis for adult patients with
acute lymphocytic leukemia
(ALL).
With these regimens, the complete response (CR) rates are approximately 75% and long-term
disease
-free survival (DFS) rates are about 20-35%.
However, patients with mediastinal
disease
had lower CR rates (P<0.05), with the presence of hepatomegaly and t(9;22) abnormalities had poor survival (P<0.05).
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ drug therapy
Hazardous Substances Data Bank.
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.
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.
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(PMID = 18061665.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
56.
Rapanotti MC, Caruso R, Ammatuna E, Zaza S, Trotta L, Divona M, Cicconi L, Funaro D, Federici G, Amadori S, De Rossi G, Lo-Coco F:
Molecular characterization of paediatric idiopathic hypereosinophilia.
Br J Haematol
; 2010 Dec;151(5):440-6
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Early identification of pHES that may evolve towards a lymphomyeloproliferative
disease
is relevant in light of prognostic and therapeutic implications.
Molecular features of 10 pHES patients were analysed at presentation and during their clinical course, including analysis of BCR-ABL1 and FIP1L1/PDGFRA fusion genes, quantitation of WT1 gene copy number and clonality of T-
cell
receptor (TCR) and immunoglobulin heavy chain (IGH).
Five children showed IGH clonality at presentation: of these, two developed a B non-Hodgkin
lymphoma
and a B-lineage
acute lymphocytic
leukaemia
at six and 12 months respectively, two spontaneously reverted to a polyclonal IGH profile during the follow-up, and the last one persisted with pHES without B-clonal evolution after 19 months.
IGH rearrangement was observed to be a frequent molecular feature of pHES and may precede B-
cell
clonal expansion and evolution into B-
cell
malignancies in children.
[MeSH-minor]
Adolescent. Child. Child, Preschool. Female. Follow-Up Studies. Gene Rearrangement. Humans. Immunoglobulin Heavy Chains / genetics. Immunophenotyping. Infant.
Lymphoma
, B-
Cell
/ etiology. Male.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ etiology. Prognosis
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[Copyright]
© 2010 Blackwell Publishing Ltd.
(PMID = 20955401.001).
[ISSN]
1365-2141
[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 / Immunoglobulin Heavy Chains
57.
Ngamphaiboon N, Sweeney R, Wetzler M, Wang ES:
Pyridoxine treatment of vincristine-induced cranial polyneuropathy in an adult patient with acute lymphocytic leukemia: Case report and review of the literature.
Leuk Res
; 2010 Aug;34(8):e194-6
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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
Hazardous Substances Data Bank.
VINCRISTINE
.
Hazardous Substances Data Bank.
PYRIDOXINE HYDROCHLORIDE
.
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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
58.
Spokoini R, Kfir-Erenfeld S, Yefenof E, Sionov RV:
Glycogen synthase kinase-3 plays a central role in mediating glucocorticoid-induced apoptosis.
Mol Endocrinol
; 2010 Jun;24(6):1136-50
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It is still unclear how glucocorticoids (GCs) induce apoptosis of thymocytes and T
lymphoma
cells.
Emergence of GC-resistant
lymphoma
cells is a major obstacle in GC therapy, emphasizing the need for novel strategies that maintain the sensitivity of
lymphoma
cells to the proapoptotic effects of GC.
Chemical inhibition of GSK3 by SB216763, BIO-Acetoxime, or LiCl and GSK3 inhibition using a dominant-negative mutant of GSK3 impede this
cell
death process, indicating that GSK3 is involved in transmitting the apoptotic signal.
GC resistance in
lymphoma
cells can be relieved by inhibiting the phosphatidylinositol-3 kinase-Akt survival pathway, which inactivates GSK3.
Notch1, a transcription factor frequently activated in
T acute
lymphoblastic
leukemia
cells, confers GC resistance through activation of Akt.
[MeSH-minor]
Animals. Apoptosis Regulatory Proteins / metabolism. Bcl-2-Like Protein 11.
Cell
Line. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Enzyme Activation / drug effects. Glycogen Synthase Kinase 3 beta. Humans. Ligands. Membrane Proteins / metabolism. Mice. Models, Biological. Protein Binding / drug effects. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Glucocorticoid / metabolism. Receptors, Notch / metabolism
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.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
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Mouse Genome Informatics (MGI)
.
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.
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(PMID = 20371704.001).
[ISSN]
1944-9917
[Journal-full-title]
Molecular endocrinology (Baltimore, Md.)
[ISO-abbreviation]
Mol. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Ligands; 0 / Membrane Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Glucocorticoid; 0 / Receptors, Notch; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / GSK3B protein, human; EC 2.7.11.1 / Glycogen Synthase Kinase 3 beta; EC 2.7.11.1 / Gsk3b protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 2.7.11.26 / glycogen synthase kinase 3 alpha
59.
Nowak AK, Lake RA, Robinson BW:
Combined chemoimmunotherapy of solid tumours: improving vaccines?
Adv Drug Deliv Rev
; 2006 Oct 1;58(8):975-90
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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
60.
Zhang Y, Payne KJ, Zhu Y, Price MA, Parrish YK, Zielinska E, Barsky LW, Crooks GM:
SCL expression at critical points in human hematopoietic lineage commitment.
Stem Cells
; 2005 Jun-Jul;23(6):852-60
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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
61.
Dourado M, Sarmento AB, Pereira SV, Alves V, Silva T, Pinto AM, Rosa MS:
CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture.
Pathophysiology
; 2007 May;14(1):3-10
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[Title]
CD26/DPPIV expression and 8-azaguanine response in T-
acute
lymphoblastic leukaemia cell
lines in culture.
Dipeptidyl peptidase IV,
a cell
membrane surface protease also known as CD26 (CD26/DPPIV), is known to play multiple functions in human organism, where it is largely expressed, for instance, in the development of human cancer and metastasis as well as in chemotherapy response.
The objective of this work was to study the CD26 membrane expression and DPPIV activity in T-
acute
leukaemia cell
lines (CEM and MOLT3) in culture, in order to observe the modification of its expression under the 8-azaguanine treatment.
Cell
line samples were incubated, some without different azaguanine concentration and others with, ranging from 10 to 100muM.
Cell
surface CD26 expression has been identified by flow cytometry and DPPIV activity, in cultured medium, was fluorimetrically measured.
Results we have observed showed that 8-azaguanine induced a decrease in
cell
viability in a dose, time and
cell type
dependent manner with MOLT3 cells being the most sensitive to 8-azaguanine citotoxic effects (24h IC50: +/-10muM) when compared with CEM cells (24h IC50: +/-100muM).
In the same experimental conditions, MOLT3
cell
treated with 8-azaguanine shows an increase in CD26 expression (MIF) compared with that of CEM
cell
submitted to the same conditions (65.4+/-1.3 versus 18.7+/-1.7).
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(PMID = 17055708.001).
[ISSN]
0928-4680
[Journal-full-title]
Pathophysiology : the official journal of the International Society for Pathophysiology
[ISO-abbreviation]
Pathophysiology
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
Netherlands
62.
Santamaría-Quesada C, Vargas M, Venegas P, Calvo M, Obando C, Valverde B, Cartín W, Carrillo JM, Jimenez R, González M:
Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.
J Pediatr Hematol Oncol
; 2009 Feb;31(2):131-5
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[Title]
Molecular and epidemiologic findings of childhood
acute leukemia
in Costa Rica.
In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially
acute
lymphoblastic
leukemia
(ALL).
Preliminary studies have described a high incidence of childhood
leukemia
in these countries; however, no molecular analyses of these malignancies have yet been carried out.
We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65
precursor
B-ALL, 5 T-
cell ALL
, and 14
acute
myeloblastic
leukemia
).
The observed rate of
leukemia
was 52.2 cases per million children per year.
Twelve out of 65 (18.4%)
precursor
B-ALL tested positive for TEL-AML1 and 3 cases for BCR-ABL (4.6%).
None of the T-
cell ALL
cases were positive for either SIL-TAL1 or HOX11L2.
Within 14
acute
myeloblastic
leukemia
patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.
The present study confirms the relatively high incidence of pediatric
leukemia
in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood
leukemia
in our region.
[MeSH-major]
Leukemia
/ epidemiology.
Leukemia
/ genetics
[MeSH-minor]
Acute
Disease
. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis
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(PMID = 19194200.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Oncogene Proteins, Fusion
63.
Malcovati L:
Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia.
Haematologica
; 2006 Mar;91(3):290A
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[Title]
Novel homeobox gene recombination in T-
cell
acute
lymphoblastic
leukemia
.
[MeSH-major]
Genes, Homeobox / genetics.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ genetics. Recombination, Genetic / genetics
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[CommentOn]
Haematologica. 2006 Mar;91(3):317-21
[
16531254.001
]
(PMID = 16531247.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Comment; Journal Article
[Publication-country]
Italy
64.
Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A:
A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.
Leukemia
; 2007 Jan;21(1):72-8
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[Title]
A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-
cell
acute
lymphoblastic
leukemia
.
Fanconi anemia (FA) is an autosomal recessive
disease
characterized by pancitopenia, congenital malformations, predisposition to cancers and chromosomal instability.
We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage
acute
lymphoblastic
leukemia
(ALL).
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ drug therapy.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ genetics. Mutation
[MeSH-minor]
Amino Acid Substitution. Antigens, CD. Antigens, CD13. Antigens, Differentiation, Myelomonocytic. Child. Chromosomal Instability.
Disease
Progression. Fanconi Anemia / genetics. Humans. Infection / etiology. Infection / genetics. Male. Pancytopenia / chemically induced. Pancytopenia / genetics. Remission Induction. Sialic Acid Binding Ig-like Lectin 3
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(PMID = 17096012.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Grant]
Italy / Telethon / / TGM06S01
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
65.
Nishimura S, Takahashi S, Kamikatahira H, Kuroki Y, Jaalouk DE, O'Brien S, Koivunen E, Arap W, Pasqualini R, Nakayama H, Kuniyasu A:
Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells.
J Biol Chem
; 2008 Apr 25;283(17):11752-62
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[Title]
Combinatorial targeting of the macropinocytotic pathway in
leukemia
and
lymphoma
cells.
Ligand-directed delivery of agents to
leukemia
and
lymphoma
cells has the potential to yield new mechanistic
disease
insights and targeted therapies.
From the screening of
acute T
-
lymphoblastic
leukemia
Molt-4 cells with a random phage-display peptide library, we isolated a phage displaying the sequence CAYHRLRRC.
This peptide contains a lymph node-homing motif (Cys-Ala-Tyr) and
a cell
-penetrating motif (Arg-Leu-Arg-Arg).
Binding of this ligand-directed phage to a large panel of
leukemia
/
lymphoma
cells and to patient-
derived
samples was much higher than to non-
leukemia
control cells.
Flow cytometry with fluorescein-labeled peptide and endocytosis blocking with specific inhibitors revealed that CAYHRLRRC is indeed taken up through macropinocytosis in Molt-4 and K562 human
leukemia
cells.
Unexpectedly, the
cell
surface receptor for the CAYHRLRRC peptide is not a heparan sulfate proteoglycan as it would be predicted for other
cell
-penetrating peptides.
Confirming this interpretation, a CAYHRLRRC-directed peptidomimetic-induced
cell
death in all the
leukemia
and
lymphoma
cells was evaluated, whereas a control transactivator of transcription protein (tat)-directed proapoptotic peptidomimetic was non-selective.
In summary, the targeting peptide CAYHRLRRC is selectively internalized through macropinocytosis in
leukemia
and
lymphoma
cells and has potential as a drug lead for ligand-directed anti-
leukemia
therapies.
[MeSH-major]
Antineoplastic Agents / pharmacology. Gene Expression Regulation, Leukemic.
Leukemia
/ metabolism.
Lymphoma
/ metabolism
[MeSH-minor]
Catalysis.
Cell
Line, Tumor.
Cell
Survival. Chemistry, Pharmaceutical / methods. Drug Design. Humans. K562 Cells. Ligands. Peptide Library. Peptides / chemistry. Pinocytosis
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(PMID = 18292083.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[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 / Antineoplastic Agents; 0 / Ligands; 0 / Peptide Library; 0 / Peptides
[Other-IDs]
NLM/ PMC3762554
66.
Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A:
Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
Blood
; 2007 Jan 15;109(2):674-82
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[Title]
Characterization of a progenitor
cell
population in childhood T-
cell
acute
lymphoblastic
leukemia
.
A significant proportion of children with T-
cell
acute
lymphoblastic
leukemia
(T-ALL) continue to fail therapy.
Consequently, characterization of the cells that proliferate to maintain the
disease
should provide valuable information on the most relevant therapeutic targets.
The majority of cells capable of long-term proliferation in vitro were
derived
from the CD34+/CD4- and CD34+/CD7- subfractions.
The immunophenotype and genotype of the original
leukemia
cells were preserved with serial passage in the NOD/SCID mice.
These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that
a cell
with a more primitive phenotype was the target for leukemic transformation in these cases.
[MeSH-major]
Leukemia
-
Lymphoma
, Adult T-
Cell
/ immunology.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ immunology. Stem Cells / immunology. Stem Cells / pathology
[MeSH-minor]
Adolescent. Animals.
Cell
Culture Techniques.
Cell
Proliferation.
Cell
Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-
Cell
Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays
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(PMID = 17003368.001).
[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
67.
Te Boekhorst PA, Lamers CH, Schipperus MR, Hintzen RQ, van der Holt B, Cornelissen JJ, Löwenberg B, Gratama JW:
T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants.
Bone Marrow Transplant
; 2006 Apr;37(8):763-72
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[Title]
T-lymphocyte reconstitution following rigorously T-
cell
-depleted versus unmodified autologous stem
cell
transplants.
We compared the kinetics of T-
cell
recovery after extensive ex vivo and in vivo T-
cell
depleted autologous stem
cell
transplantation (SCT) for multiple sclerosis (MS; n=8) with unmodified SCT for hematological malignancies (HM; n=39).
Unexpectedly, the kinetics of T-
cell
recovery between 3 and 12 months post transplant was similar in T-depleted and unmodified SCT.
Before SCT, the HM patients showed lymphopenia of all T-
cell
subsets, upregulated HLA-DR and CD95 expression and increased cytokine responses.
We suggest that the similar kinetics of T-
cell
recovery in the two patient groups may be explained by the susceptibility to apoptosis of the activated CD4(+) T-cells in the autografts of the HM patients.
This susceptibility to apoptosis would interfere with a swift and sustained CD4(+) T-
cell
regeneration post SCT.
[MeSH-major]
Multiple Sclerosis / blood. Multiple Sclerosis / therapy. Stem
Cell
Transplantation / methods. T-Lymphocytes / metabolism. Transplantation, Autologous / methods
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(PMID = 16518423.001).
[ISSN]
0268-3369
[Journal-full-title]
Bone marrow transplantation
[ISO-abbreviation]
Bone Marrow Transplant.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD27; 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD95; 0 / Cytokines; 0 / Interleukin-2; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma; EC 3.1.3.48 / Antigens, CD45
68.
Ratei R, Karawajew L, Lacombe F, Jagoda K, Del Poeta G, Kraan J, De Santiago M, Kappelmayer J, Björklund E, Ludwig WD, Gratama J, Orfao A, European Working Group of Clinical Cell Analysis (EWGCCA):
Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias.
Cytometry B Clin Cytom
; 2006 Jan;70(1):1-9
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[Title]
Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of
acute
leukemias
.
BACKGROUND: Multiparametric flow cytometry has become an indispensable but complex tool for the
diagnosis
of
acute
leukemias
.
METHODS: Eight laboratories participated in the study and recruited a total of 151 individuals including 29 patients with B-
cell precursor
acute
lymphoblastic
leukemia
(BCP-ALL), 77 with
acute
myeloid
leukemia
(AML), 10 with T-
cell precursor
acute
lymphoblastic
leukemia
(T-ALL), and 35 normal bone marrow donors.
CONCLUSION: Residual normal lymphocytes can serve as internal quality control for studies addressing fluorescence intensity in the setting of immunophenotyping of
acute
leukemias
.
[MeSH-major]
Flow Cytometry / methods. Immunophenotyping / methods.
Leukemia
. Lymphocytes / cytology. Lymphocytes / metabolism
[MeSH-minor]
Acute
Disease
. Case-Control Studies. Fluorescence. Humans. Quality Control. Reference Standards
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[Copyright]
Copyright (c) 2005 Wiley-Liss, Inc.
(PMID = 16278833.001).
[ISSN]
1552-4949
[Journal-full-title]
Cytometry. Part B, Clinical cytometry
[ISO-abbreviation]
Cytometry B Clin Cytom
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
69.
Mustjoki S, Ekblom M, Arstila TP, Dybedal I, Epling-Burnette PK, Guilhot F, Hjorth-Hansen H, Höglund M, Kovanen P, Laurinolli T, Liesveld J, Paquette R, Pinilla-Ibarz J, Rauhala A, Shah N, Simonsson B, Sinisalo M, Steegmann JL, Stenke L, Porkka K:
Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy.
Leukemia
; 2009 Aug;23(8):1398-405
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Fifteen patients had a cytotoxic T-
cell
and seven patients had an NK-
cell
phenotype.
All T-
cell
expansions were clonal.
Responses to dasatinib were good and included complete, unexpectedly long-lasting remissions in patients with advanced
leukemia
.
In a phase II clinical study on 46 Philadelphia chromosome-positive
acute
lymphoblastic
leukemia
, patients with lymphocytosis had superior survival compared with patients without lymphocytosis.
[MeSH-major]
Antineoplastic Agents / pharmacology. Killer Cells, Natural / drug effects.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Cytotoxic / drug effects. Thiazoles / pharmacology
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[CommentIn]
Acta Haematol. 2016;136(4):219-228
[
27656875.001
]
(PMID = 19295545.001).
[ISSN]
1476-5551
[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 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
70.
Asnafi V, Buzyn A, Thomas X, Huguet F, Vey N, Boiron JM, Reman O, Cayuela JM, Lheritier V, Vernant JP, Fiere D, Macintyre E, Dombret H:
Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study.
Blood
; 2005 Apr 15;105(8):3072-8
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[Title]
Impact of TCR status and genotype on outcome in adult T-
cell
acute
lymphoblastic
leukemia
: a LALA-94 study.
Patients with T-
cell
acute
lymphoblastic leukemias
(T-
ALLs
) within the Leucemies Aigues Lymphoblastiques
de
l'Adulte-94 (LALA-94) prospective trial were treated with a 4-drug per 4-week induction, with intermediate-dose cytarabine and mitoxantrone salvage treatment for patients not achieving complete remission (CR) in 1 course.
Representative patients with T-ALL (91 patients) were classified into surface T-
cell
receptor (TCR)-expressing T-ALL patients (TCRalphabeta+ or TCRgammadelta+),
pre
-alphabeta T-ALL patients (cTCRbeta+, TCR-), and immature (IM) cTCRbeta-, TCR- T-ALL patients; 81 patients underwent genotyping for SIL-TAL1, CALM-AF10, HOX11, and HOX11L2.
Once CR was obtained, cumulative relapse rates were similar for IM,
pre
-alphabeta, and TCR+ T-ALL patients (P = .51), but were higher in HOX11L2 (83%) and SIL-TAL1 (82%) T-ALL patients compared with other genetic subgroups (48%; P = .05).
This was associated with an inferior OS for HOX11L2 T-
ALLs
(13% vs 47% in HOX11L2-T-
ALLs
; P = .009).
Both TCR and genotypic stratification can therefore contribute to risk-adapted management of adult T-
ALLs
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / administration & dosage.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ drug therapy.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ genetics. Receptors, Antigen, T-
Cell
/ genetics
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.
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.
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(PMID = 15637138.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Receptors, Antigen, T-Cell; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
71.
Malani AK, Gupta C, Rangineni R, Singh J, Ammar H:
Concomitant presentation of acute myeloid leukemia with T-cell large granular lymphocytic leukemia.
Acta Oncol
; 2007;46(2):247-9
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[Title]
Concomitant presentation of
acute
myeloid
leukemia
with T-
cell
large granular
lymphocytic leukemia
.
T-
cell
large granular lymphocyte
leukemia
(T-LGL) also known as T-
cell
chronic
lymphocytic leukemia
is rare and comprises a small minority of all small
lymphocytic
leukemias
.
The concomitant presentation of T-LGL with
acute
myeloid
leukemia
(AML) has not been previously reported.
We present an elderly gentleman with concomitant T-LGL and AML (non-M3) diagnosed by a combination of
morphologic
evaluation, immunophenotyping by flow cytometry, and T-
cell
gene rearrangement studies.
He remains alive and well seven months after initial
diagnosis
.
[MeSH-major]
Leukemia
, Myeloid /
diagnosis
.
Leukemia
, Prolymphocytic, T-
Cell
/
diagnosis
[MeSH-minor]
Acute
Disease
. Aged, 80 and over. Antigens, CD / analysis. Flow Cytometry. Humans. Male
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(PMID = 17453377.001).
[ISSN]
0284-186X
[Journal-full-title]
Acta oncologica (Stockholm, Sweden)
[ISO-abbreviation]
Acta Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Norway
[Chemical-registry-number]
0 / Antigens, CD
[Number-of-references]
17
72.
Perseghin P, Terruzzi E, Dassi M, Baldini V, Parma M, Coluccia P, Accorsi P, Confalonieri G, Tavecchia L, Verga L, Ravagnani F, Iacone A, Pogliani EM, Pioltelli P:
Management of poor peripheral blood stem cell mobilization: incidence, predictive factors, alternative strategies and outcome. A retrospective analysis on 2177 patients from three major Italian institutions.
Transfus Apher Sci
; 2009 Aug;41(1):33-7
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[Title]
Management of poor peripheral blood stem
cell
mobilization: incidence, predictive factors, alternative strategies and outcome. A retrospective analysis on 2177 patients from three major Italian institutions.
Patients' characteristics, including age, sex, stage of the underlying
disease
(complete or partial remission),
diagnosis
, previously administered radio/chemotherapy regimens, time-lapse from last chemotherapy before mobilization and mobilization schedule (including dose of GF) were considered as possibly predictive of poor or failed mobilization.
Therefore, a patient who fails a first mobilization (and when an HLA-compatible related on unrelated donor is not available) could undergo a second attempt either with different mobilization schedule or by using different GF, such as stem
cell
factor, growth hormone (GH), or more recently newly introduced drugs such as AMD3100, alone or in combination with rHuG- or -rHuGM-CSF.
[MeSH-major]
Neoplasms / surgery. Peripheral Blood Stem
Cell
Transplantation / methods
[MeSH-minor]
Adult. Antigens, CD34 / blood. Follow-Up Studies. Hematopoiesis. Hematopoietic Stem
Cell
Mobilization / methods. Humans.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ surgery.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / surgery.
Leukemia
, Myeloid,
Acute
/ surgery.
Lymphoma
, Non-Hodgkin / surgery. Multiple Myeloma / surgery. Retrospective Studies. Survival Analysis
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(PMID = 19540167.001).
[ISSN]
1473-0502
[Journal-full-title]
Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis
[ISO-abbreviation]
Transfus. Apher. Sci.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD34
73.
Rolny C, Lu L, Agren N, Nilsson I, Roe C, Webb GC, Welsh M:
Shb promotes blood vessel formation in embryoid bodies by augmenting vascular endothelial growth factor receptor-2 and platelet-derived growth factor receptor-beta signaling.
Exp Cell Res
; 2005 Aug 15;308(2):381-93
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[Title]
Shb promotes blood vessel formation in embryoid bodies by augmenting vascular endothelial growth factor receptor-2 and platelet-
derived
growth factor receptor-beta signaling.
To elucidate a possible role of Shb in embryonic vascular development, wild-
type
and SH2 domain mutated (R522K) Shb were overexpressed in murine embryonic stem (ES) cells.
This response may be the consequence of an increased number of VEGFR-2 positive cells at an early stage of EB development,
a finding
corroborated by both immunostaining and real-time RT-PCR.
The findings suggest that Shb may play a crucial role during early ES
cell
differentiation to vascular structures by transducing VEGFR-2 and PDGFR-beta signals.
[MeSH-major]
Blood Vessels / embryology. Blood Vessels / metabolism. Neovascularization, Physiologic / physiology. Pluripotent Stem Cells / metabolism. Proto-Oncogene Proteins / metabolism. Receptor, Platelet-
Derived
Growth Factor beta / metabolism. Up-Regulation / physiology. Vascular Endothelial Growth Factor Receptor-2 / metabolism
[MeSH-minor]
Animals. Antigens, CD31 / metabolism. Basic Helix-Loop-Helix Transcription Factors.
Cell
Differentiation / physiology.
Cell
Line. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Embryo Culture Techniques. Endothelial Cells / cytology. Endothelial Cells / metabolism. Gene Expression Profiling. Gene Expression Regulation, Developmental / physiology. Mice. Mutation / genetics. Oligonucleotide Array Sequence Analysis. Phenotype. Platelet Membrane Glycoprotein IIb / genetics. Platelet Membrane Glycoprotein IIb / metabolism. RNA, Messenger / metabolism. Signal Transduction / physiology. Transcription Factors / genetics. Transcription Factors / metabolism
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
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(PMID = 15919073.001).
[ISSN]
0014-4827
[Journal-full-title]
Experimental cell research
[ISO-abbreviation]
Exp. Cell Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD31; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / Platelet Membrane Glycoprotein IIb; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Shb protein, mouse; 0 / Tal1 protein, mouse; 0 / Transcription Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
74.
Leung KT, Li KK, Sun SS, Chan PK, Ooi VE, Chiu LC:
Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-cell acute lymphoblastic leukemia.
Carcinogenesis
; 2008 Mar;29(3):544-51
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[Title]
Activation of the JNK pathway promotes phosphorylation and degradation of BimEL--a novel mechanism of chemoresistance in T-
cell
acute
lymphoblastic
leukemia
.
T-
cell
acute
lymphoblastic leukemias
(T-
ALLs
) are highly malignant tumors with 20% of patients continues to fail therapy, in part due to chemoresistance of T-ALL cells via largely unknown mechanisms.
Here, we showed that lack of Bcl-2-interacting mediator of
cell
death (Bim)(EL) protein expression, a BH3-only member of the Bcl-2 family proteins, conferred resistance of a T-
ALL cell
line, Sup-T1, to etoposide-induced apoptosis.
[MeSH-major]
Apoptosis Regulatory Proteins / metabolism. Drug Resistance, Neoplasm.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ metabolism. MAP Kinase Kinase 4 / metabolism. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism
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.
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ETOPOSIDE
.
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.
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(PMID = 18174237.001).
[ISSN]
1460-2180
[Journal-full-title]
Carcinogenesis
[ISO-abbreviation]
Carcinogenesis
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 6PLQ3CP4P3 / Etoposide; EC 2.7.12.2 / MAP Kinase Kinase 4
75.
Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP:
Cooperative genetic defects in TLX3 rearranged pediatric T-ALL.
Leukemia
; 2008 Apr;22(4):762-70
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T-
cell
acute
lymphoblastic
leukemia
(T-ALL) is an aggressive neoplastic
disorder
, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
[MeSH-major]
Chromosome Aberrations. Homeodomain Proteins / genetics.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ genetics. Sequence Deletion
[MeSH-minor]
Cell
Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics
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(PMID = 18185524.001).
[ISSN]
1476-5551
[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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
81.
Lin YW, Beharry ZM, Hill EG, Song JH, Wang W, Xia Z, Zhang Z, Aplan PD, Aster JC, Smith CD, Kraft AS:
A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma.
Blood
; 2010 Jan 28;115(4):824-33
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[Title]
A small molecule inhibitor of Pim protein kinases blocks the growth of
precursor
T-
cell lymphoblastic
leukemia
/
lymphoma
.
We demonstrate that SMI-4a, a novel benzylidene-thiazolidine-2, 4-dione small molecule inhibitor of the Pim kinases, kills a wide range of both myeloid and lymphoid
cell
lines with
precursor
T-
cell lymphoblastic
leukemia
/
lymphoma
(
pre
-T-LBL/T-ALL) being highly sensitive.
Incubation of
pre
-T-LBL cells with SMI-4a induced G1 phase
cell
-cycle arrest secondary to a dose-dependent induction of p27(Kip1), apoptosis through the mitochondrial pathway, and inhibition of the mammalian target of rapamycin C1 (mTORC1) pathway based on decreases in phospho-p70 S6K and phospho-4E-BP1, 2 substrates of this enzyme.
In addition, treatment of these cells with SMI-4a was found to induce phosphorylation of extracellular signal-related kinase1/2 (ERK1/2), and the combination of SMI-4a and a mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor was highly synergistic in killing
pre
-T-LBL cells.
In immunodeficient mice carrying subcutaneous
pre
-T-LBL tumors, treatment twice daily with SMI-4a caused a significant delay in the tumor growth without any change in the weight, blood counts, or chemistries.
Our data suggest that inhibition of the Pim protein kinases may be developed as a therapeutic strategy for the treatment of
pre
-T-LBL.
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(PMID = 19965690.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA138313; United States / NCRR NIH HHS / RR / UL1 RR029882; United States / NCI NIH HHS / CA / P30 CA 138313
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Intracellular Signaling Peptides and Proteins; 0 / MYC protein, human; 0 / PIM2 protein, human; 0 / Pim2 protein, mouse; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / PIM1 protein, human; EC 2.7.11.1 / PIM3 protein, human; EC 2.7.11.1 / Pim1 protein, mouse; EC 2.7.11.1 / Pim3 protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-pim-1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
[Other-IDs]
NLM/ PMC2941996
82.
Chiu PP, Jiang H, Dick JE:
Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance.
Blood
; 2010 Dec 9;116(24):5268-79
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[Title]
Leukemia
-initiating cells in human T-
lymphoblastic
leukemia
exhibit glucocorticoid resistance.
T-
cell
acute
lymphoblastic
leukemia
(T-ALL) is associated with a significant risk of
disease
relapse, but the biological basis for relapse is poorly understood.
Here, we identify leukemiainitiating cells (L-ICs) on the basis of functional assays and prospective isolation and report a role for L-ICs in T-
ALL disease
and relapse.
Long-term proliferation in response to NOTCH1 activating signals in OP9-DL1 coculture system or capacity to initiate
leukemia
in xenografts by the CD7(+)CD1a(-) subset of primary T-ALL samples was superior to other subsets, refining the identity of T-ALL L-ICs.
T-ALL engraftment was improved in nonobese diabetic/severe combined immunodeficiency (NOD/scid)IL2Rγ(null) (NSG) mice compared with NOD/scid with anti-CD122 treatment (NS122), but both showed changes in
leukemia
immunophenotype.
Our results establish that primary CD1a(-) T-ALL cells are functionally distinct from CD1a(+) cells and that the CD7(+)CD1a(-) subset is enriched for L-IC activity that may be involved in mediating
disease
relapse after therapy.
[MeSH-minor]
Animals. Antigens, CD1. Antigens, CD7. Antineoplastic Agents, Hormonal / pharmacology.
Cell
Proliferation. Clone Cells / pathology. Coculture Techniques. Dexamethasone / pharmacology. Humans. Immunophenotyping. Mice. Mice, SCID. Receptor, Notch1 / metabolism. Recurrence. Transplantation, Heterologous
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(PMID = 20810926.001).
[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 / Antigens, CD1; 0 / Antigens, CD7; 0 / Antineoplastic Agents, Hormonal; 0 / CD1a antigen; 0 / Glucocorticoids; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone
83.
Choi J, Foss F:
Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia.
Yale J Biol Med
; 2006 Dec;79(3-4):169-72
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[Title]
Efficacy of low dose clofarabine in refractory
precursor
T-
acute
lymphoblastic
leukemia
.
Refractory T-
lymphoblastic
leukemia
in adults has a poor prognosis in patients who relapse after allogeneic stem
cell
transplantation, and relatively few new agents have demonstrated activity.
We used low dose clofarabine and induced a remission in a patient who relapsed in the skin and marrow after allogeneic transplant and was refractory to nelarabine and report a near complete response, suggesting significant activity for low intermittent dose clofarabine in patients with relapsed T-
cell leukemias
.
[MeSH-major]
Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use.
Leukemia
-
Lymphoma
, Adult T-
Cell
/ drug therapy
[MeSH-minor]
Adult. Bone Marrow Neoplasms / drug therapy. Bone Marrow Neoplasms / secondary. Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Humans. Immunophenotyping. Male. Recurrence. Skin Neoplasms / drug therapy. Skin Neoplasms / secondary. Stem
Cell
Transplantation. Transplantation, Homologous. Treatment Outcome
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12791647.001
]
[Cites]
Blood. 2004 Feb 1;103(3):784-9
[
14551141.001
]
(PMID = 17940627.001).
[ISSN]
1551-4056
[Journal-full-title]
The Yale journal of biology and medicine
[ISO-abbreviation]
Yale J Biol Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Adenine Nucleotides; 0 / Arabinonucleosides; 60158CV180 / nelarabine; 762RDY0Y2H / clofarabine
[Other-IDs]
NLM/ PMC1994805
84.
Gong H, Liu WL, Zhou JF, Xu HZ:
[Expression of mitosis checkpoint gene CHFR in acute leukemia].
Zhonghua Yi Xue Za Zhi
; 2005 Apr 27;85(16):1085-8
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[Title]
[Expression of mitosis checkpoint gene CHFR in
acute leukemia
].
OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with
acute leukemia
(AL) and its clinical significance.
METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with
acute
myelocytic
leukemia
(AML) and 22 with
acute lymphocytic leukemia
(ALL), 45
de
novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
The
cell
cycle was examined by flow cytometric analysis.
(1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent
acute
lymphoblastic
leukemia
(ALL) was 0.71, significantly higher than that of the
de
novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with
acute leukemia
.
Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of
acute leukemia
to chemotherapy.
[MeSH-major]
Cell
Cycle Proteins / biosynthesis.
Leukemia
, Myeloid,
Acute
/ genetics. Neoplasm Proteins / biosynthesis.
Precursor Cell Lymphoblastic
Leukemia
-
Lymphoma
/ genetics
[MeSH-minor]
Adolescent. Adult. Antineoplastic Agents / pharmacology.
Cell
Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics
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(PMID = 16029562.001).
[ISSN]
0376-2491
[Journal-full-title]
Zhonghua yi xue za zhi
[ISO-abbreviation]
Zhonghua Yi Xue Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
85.
Malissen B, Luche H:
Immunology: Egocentric pre-T-cell receptors.
Nature
; 2010 Oct 14;467(7317):793-4
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[Title]
Immunology: Egocentric
pre
-T-
cell
receptors.
[MeSH-major]
Protein Multimerization. Receptors, Antigen, T-
Cell
, alpha-beta / chemistry. Receptors, Antigen, T-
Cell
, alpha-beta / metabolism
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[CommentOn]
Nature. 2010 Oct 14;467(7317):844-8
[
20944746.001
]
(PMID = 20944732.001).
[ISSN]
1476-4687
[Journal-full-title]
Nature
[ISO-abbreviation]
Nature
[Language]
eng
[Publication-type]
Comment; News
[Publication-country]
England
[Chemical-registry-number]
0 / Receptors, Antigen, T-Cell, alpha-beta
86.
Ikezoe T, Yang Y, Bandobashi K, Saito T, Takemoto S, Machida H, Togitani K, Koeffler HP, Taguchi H:
Oridonin, a diterpenoid purified from Rabdosia rubescens, inhibits the proliferation of cells from lymphoid malignancies in association with blockade of the NF-kappa B signal pathways.
Mol Cancer Ther
; 2005 Apr;4(4):578-86
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This study found that oridonin, a natural diterpenoid purified from Rabdosia rubescens, inhibited growth of multiple myeloma (MM; U266, RPMI8226),
acute
lymphoblastic
T-
cell
leukemia
(Jurkat), and adult T-
cell
leukemia
(MT-1) cells with an effective dose that inhibited 50% of target cells (ED50) ranging from 0.75 to 2.7 microg/mL.
Of note, oridonin decreased survival of freshly isolated adult T-
cell
leukemia
(three samples),
acute
lymphoblastic
leukemia
(one sample), chronic
lymphocytic leukemia
(one sample), non-Hodgkin's
lymphoma
(three samples), and MM (four samples) cells from patients in association with inhibition of NF-kappa B DNA-binding activity.
Taken together, oridonin might be useful as adjunctive therapy for individuals with lymphoid malignancies, including the lethal
disease
adult T-
cell
leukemia
.
[MeSH-major]
Cell
Proliferation / drug effects. Diterpenes / pharmacology. Isodon / metabolism. NF-kappa B / metabolism. Phytotherapy / methods. Plant Extracts / pharmacology
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Animals. Apoptosis. Blotting, Western.
Cell
Line.
Cell
Line, Tumor. Diterpenes, Kaurane. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Genes, Reporter. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / metabolism. Humans. In Situ Nick-End Labeling. Jurkat Cells.
Leukemia
/ drug therapy.
Leukemia
/ pathology. Lipopolysaccharides / metabolism. Male. Mice. Middle Aged. Models, Chemical. Multiple Myeloma / drug therapy. Multiple Myeloma / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Signal Transduction. T-Lymphocytes / metabolism. T-Lymphocytes / virology. Thymidine / chemistry. Thymidine / metabolism. Time Factors. Transfection. Trypan Blue / pharmacology. bcl-X Protein
MedlinePlus Health Information.
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.
Hazardous Substances Data Bank.
Trypan blue
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
The Lens.
Cited by Patents in
.
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(PMID = 15827331.001).
[ISSN]
1535-7163
[Journal-full-title]
Molecular cancer therapeutics
[ISO-abbreviation]
Mol. Cancer Ther.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / BCL2L1 protein, human; 0 / Bcl2l1 protein, mouse; 0 / Diterpenes; 0 / Diterpenes, Kaurane; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein; 0APJ98UCLQ / oridonin; I2ZWO3LS3M / Trypan Blue; VC2W18DGKR / Thymidine
87.
Maruo T, Namikawa K, Kunihiro A, Lynch J, Shida T, Kishikawa S:
Large granular lymphocytic leukaemia complicated with histiocytic sarcoma in a dog.
J S Afr Vet Assoc
; 2009 Dec;80(4):261-3
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[Title]
Large granular
lymphocytic
leukaemia
complicated with histiocytic sarcoma in a dog.
Based on these findings this case was diagnosed as LGL
leukaemia
.
Shortly after
diagnosis
, the dog developed sudden onset of central nervous system signs and died on day 270.
A common outcome of canine LGL is the development of
acute
blast crisis or
lymphoma
.
[MeSH-major]
Antineoplastic Agents / administration & dosage. Histiocytic Sarcoma / veterinary.
Leukemia
, Large Granular
Lymphocytic
/ veterinary
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(PMID = 20458870.001).
[ISSN]
1019-9128
[Journal-full-title]
Journal of the South African Veterinary Association
[ISO-abbreviation]
J S Afr Vet Assoc
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
South Africa
[Chemical-registry-number]
0 / Antineoplastic Agents
88.
Hensel M, Zoz M, Giesecke C, Benner A, Neben K, Jauch A, Stilgenbauer S, Ho AD, Krämer A:
High rate of centrosome aberrations and correlation with proliferative activity in patients with untreated B-cell chronic lymphocytic leukemia.
Int J Cancer
; 2007 Sep 1;121(5):978-83
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[Title]
High rate of centrosome aberrations and correlation with proliferative activity in patients with untreated B-
cell
chronic
lymphocytic leukemia
.
B-
cell
chronic
lymphocytic leukemia
(CLL) is characterized by a high rate of clonal genomic alterations and a low proliferative activity with
cell
cycle arrest in G(0)/G(1) phase.
To investigate whether centrosome aberrations do occur in CLL and whether they correlate with common prognostic factors and
disease
activity, we examined peripheral blood mononuclear cells (PBMC) from 70 patients with previously untreated CLL using an antibody to gamma-tubulin.
Accordingly, more centrosome aberrations were found in PHA-stimulated T lymphocytes from healthy individuals as well as in B cells from surgically removed tonsil tissue of patients with
acute
tonsillitis as compared to the peripheral blood B lymphocytes from the control group.
[MeSH-major]
Cell
Proliferation. Centrosome.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ pathology
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.
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consumer health - Leukemia, B-cell, chronic
.
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 17417785.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
89.
Papalambros E, Felekouras E, Karavokyros IG, Diamantis T, Androulaki A, Boutsis D, Sigala F, Tsavaris N, Pangalis G:
Acute abdomen as initial manifestation of M4 - acute non-lymphocytic leukemia.
J BUON
; 2005 Apr-Jun;10(2):277-80
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[Title]
Acute
abdomen as initial manifestation of M4 -
acute
non-
lymphocytic leukemia
.
Visceral involvement in
acute
non-
lymphocytic leukemia
(ANLL) seldom precedes hematological manifestation.
We report on a patient with M4 - ANLL presenting with
acute
abdomen without any evidence of blood
disorder
.
We discuss the contrast between histology and short
disease
duration, the unusual presentation and the bad prognosis, and attempt to correlate the clinical course with the coexpression of markers.
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(PMID = 17343343.001).
[ISSN]
1107-0625
[Journal-full-title]
Journal of B.U.ON. : official journal of the Balkan Union of Oncology
[ISO-abbreviation]
J BUON
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
90.
Dalmas DA, Tierney LA, Zhang C, Narayanan PK, Boyce RW, Schwartz LW, Frazier KS, Scicchitano MS:
Effects of p38 MAP kinase inhibitors on the differentiation and maturation of erythroid progenitors.
Toxicol Pathol
; 2008 Dec;36(7):958-71
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To identify target
cell
populations affected, a differentiating primary liquid erythroid culture system using sca-1(+)cells from mouse bone marrow was developed and challenged with p38is SB-203580, SB-226882, and SB-267030.
Drug-related alterations in genes involved at different stages of erythropoiesis,
cell
-surface antigen expression (CSAE), burst-forming unit erythroid (BFU-E) colony formation, and cellular morphology (CM), growth (CG), and viability were evaluated.
[MeSH-minor]
Animals. Antigens, Ly / metabolism. Basic Helix-Loop-Helix Transcription Factors / metabolism. Bone Marrow Cells / drug effects.
Cell
Culture Techniques.
Cell
Survival / drug effects. Cells, Cultured. Colony-Forming Units Assay. Erythroid
Precursor
Cells / drug effects. GATA2 Transcription Factor / metabolism. Immunophenotyping. Male. Membrane Proteins / metabolism. Mice. Proto-Oncogene Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction
NCI CPTC Antibody Characterization Program.
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.
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(PMID = 19126791.001).
[ISSN]
1533-1601
[Journal-full-title]
Toxicologic pathology
[ISO-abbreviation]
Toxicol Pathol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Ly; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / GATA2 Transcription Factor; 0 / Gata2 protein, mouse; 0 / Imidazoles; 0 / Ly6a protein, mouse; 0 / Membrane Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 0 / SB 203580; 0 / Tal1 protein, mouse; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
91.
Gran B, Yu S, Zhang GX, Rostami A:
Accelerated thymocyte maturation in IL-12Rβ2-deficient mice contributes to increased susceptibility to autoimmune inflammatory demyelination.
Exp Mol Pathol
; 2010 Oct;89(2):126-34
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Accelerated maturation is observed in mice injected with anti-CD3 to mimic
pre
-T-
cell
receptor stimulation, and also in mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide to induce EAE.
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
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[ISSN]
1096-0945
[Journal-full-title]
Experimental and molecular pathology
[ISO-abbreviation]
Exp. Mol. Pathol.
[Language]
ENG
[Grant]
United States / NIAID NIH HHS / AI / R01 AI061818; United States / NINDS NIH HHS / NS / R01 NS048435; United States / NIAID NIH HHS / AI / U19 AI082726
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Antigens, CD3; 0 / Mog protein, mouse; 0 / Myelin Proteins; 0 / Myelin-Associated Glycoprotein; 0 / Myelin-Oligodendrocyte Glycoprotein; 187348-17-0 / Interleukin-12
[Other-IDs]
NLM/ NIHMS218212; NLM/ PMC2939283
92.
Yamasaki S, Saito T:
Molecular basis for pre-TCR-mediated autonomous signaling.
Trends Immunol
; 2007 Jan;28(1):39-43
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