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1
b and t cell acute lymphoblastic leukemia 2005:2010[pubdate] *count=100
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Items 1 to 100 of about 2203
1.
Burmeister T, Meyer C, Schwartz S, Hofmann J, Molkentin M, Kowarz E, Schneider B, Raff T, Reinhardt R, Gökbuget N, Hoelzer D, Thiel E, Marschalek R:
The MLL recombinome of adult CD10-negative B-cell precursor acute lymphoblastic leukemia: results from the GMALL study group.
Blood
; 2009 Apr 23;113(17):4011-5
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[Title]
The MLL recombinome of adult CD10-negative B-
cell
precursor
acute lymphoblastic leukemia
: results from the GMALL study group.
MLL translocations in adult B-
cell
precursor (BCP)
acute lymphoblastic leukemia
(ALL) are largely restricted to the immature CD10(-) immunophenotypes.
Characteristic features of MLL(+) patients were significantly lower CD10 expression, expression of the NG2 antigen, a higher white blood count at
diagnosis
, and female sex.
[MeSH-major]
Myeloid
-
Lymphoid
Leukemia
Protein / metabolism. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Recombinant Fusion Proteins / metabolism
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(PMID = 19144982.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00198991/ NCT00199056
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 0 / Recombinant Fusion Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 3.4.24.11 / Neprilysin
2.
Mori A, Toyoshima N, Saito M, Oka T, Irie T, Morioka M:
[Hypercalcemia and multiple osteolytic lesions associated with proinflammatory cytokines in a patient with acute lymphoblastic leukemia].
Rinsho Ketsueki
; 2007 Jul;48(7):559-64
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[Title]
[Hypercalcemia and multiple osteolytic lesions associated with proinflammatory cytokines in a patient with
acute lymphoblastic leukemia
].
Bone marrow aspiration revealed increased lymphoblasts (48%), and the patient was diagnosed as having
acute lymphoblastic leukemia
(ALL, L2).
However, he died of
acute
pneumonia and gastrointestinal bleeding.
The postmortem findings showed leukemic
cell
involvement of the left tibia.
[MeSH-major]
Cytokines / physiology. Hypercalcemia / etiology. Osteolysis. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / physiopathology
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consumer health - Acute Lymphoblastic Leukemia
.
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(PMID = 17695305.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Cytokines; 0 / Interleukin-6; 0 / Parathyroid Hormone-Related Protein; 0 / Tumor Necrosis Factor-alpha
3.
Antillon F, de Maselli T, Garcia T, Rossi E, Sala A:
Nutritional status of children during treatment for acute lymphoblastic leukemia in the Central American Pediatric Hematology Oncology Association (AHOPCA): preliminary data from Guatemala.
Pediatr Blood Cancer
; 2008 Feb;50(2 Suppl):502-5; discussion 517
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[Title]
Nutritional status of children during treatment for
acute lymphoblastic leukemia
in the Central American Pediatric Hematology Oncology Association (AHOPCA): preliminary data from Guatemala.
Preliminary data reveal some degree of nutritional depletion in up to 54% of newly diagnosed children with
acute lymphoblastic leukemia
in Guatemala.
[MeSH-major]
Nutritional Status. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 18064654.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
15
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4.
Koyama N, Koschmieder S, Tyagi S, Portero-Robles I, Chromic J, Myloch S, Nürnberger H, Rossmanith T, Hofmann WK, Hoelzer D, Ottmann OG:
Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive leukemia cells to the ABL kinase inhibitor STI571.
Clin Cancer Res
; 2006 Apr 1;12(7 Pt 1):2025-31
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[Title]
Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive
leukemia
cells to the ABL kinase inhibitor STI571.
To investigate whether PTP1B modulates the biological effects of the abl kinase inhibitor STI571 in BCR-ABL-positive cells, we transfected Philadelphia chromosome-positive (Ph+) chronic
myeloid
leukemia cell
-derived K562 cells with either wild-type PTP1B (K562/PTP1B), a substrate-trapping dominant-negative mutant PTP1B (K562/D181A), or empty vector (K562/mock).
In both K562/mock and K562/PTP1B cells, 0.25 to 1 mumol/L STI571 induced dose-dependent growth arrest and apoptosis, as measured by a decrease of
cell
proliferation and an increase of Annexin V-positive cells and/or of cells in the sub-G(1) apoptotic phase.
Lastly, comparison of the STI571-sensitive Ph+
acute lymphoblastic leukemia cell
line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells.
In conclusion, functional PTP1B is involved in STI571-induced growth
and cell
cycle arrest, apoptosis, and differentiation, and attenuation of PTP1B function may contribute to resistance towards STI571.
[MeSH-minor]
Apoptosis / drug effects. Benzamides.
Cell
Differentiation / drug effects.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Imatinib Mesylate. K562 Cells. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 1. Structure-Activity Relationship. Vanadates / pharmacology
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IMATINIB MESYLATE
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(PMID = 16609011.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Enzyme Inhibitors; 0 / Piperazines; 0 / Pyrimidines; 0 / bis(N,N-dimethylhydroxamido)hydroxooxovanadate; 3WHH0066W5 / Vanadates; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.1.3.48 / PTPN1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases
5.
Nagai K, Hashimoto H, Itoh K, Matsushita A, Shimoji S, Kimura T, Inoue D, Mori M, Nagai Y, Tabata S, Yanagida M, Takahashi T:
[Graft-versus-leukemia effect by lymphocytes from the first donor after second cord blood transplantation in a patient with T-lymphoblastic lymphoma].
Rinsho Ketsueki
; 2010 Jun;51(6):413-21
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[Title]
[Graft-versus-
leukemia
effect by lymphocytes from the first donor after second cord blood transplantation in a patient with T-
lymphoblastic
lymphoma].
A 19-year-old girl with T-
lymphoblastic
lymphoma (T-LBL) was referred to our hospital because of refractory
disease
.
[MeSH-major]
Cord Blood Stem
Cell
Transplantation. Graft vs
Leukemia
Effect / immunology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy. T-Lymphocytes. T-Lymphocytes, Cytotoxic / immunology. Tissue Donors
[MeSH-minor]
Acute
Disease
. Asparaginase / therapeutic use. Bone Marrow Transplantation. Chronic
Disease
. Female. Graft vs Host
Disease
/ immunology. Humans. Minor Histocompatibility Antigens. Transplantation Conditioning. Young Adult
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(PMID = 20622488.001).
[ISSN]
0485-1439
[Journal-full-title]
[Rinshō ketsueki] The Japanese journal of clinical hematology
[ISO-abbreviation]
Rinsho Ketsueki
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Minor Histocompatibility Antigens; EC 3.5.1.1 / Asparaginase
6.
Intermesoli T, Mangili G, Salvi A, Biondi A, Bassan R:
Abnormally expanded pro-B hematogones associated with congenital cytomegalovirus infection.
Am J Hematol
; 2007 Oct;82(10):934-6
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We present the case of a newborn with an atypical, marked expansion of hematogones similar to the pro-B cells of infant
acute lymphoblastic leukemia
, which demonstrated their nonleukemic nature through gene rearrangement analysis and were associated with a congenital cytomegalovirus infection.
[MeSH-major]
Cytomegalovirus Infections /
diagnosis
. Infant, Premature, Diseases /
diagnosis
. Lymphocyte Subsets / pathology
[MeSH-minor]
Adult. Antiviral Agents / therapeutic use. Bone Marrow / pathology.
Diagnosis
, Differential. Female. Ganciclovir / therapeutic use. Hepatitis, Viral, Human / congenital. Hepatitis, Viral, Human / surgery. Humans. Infant, Newborn. Infant, Premature. Infectious
Disease
Transmission, Vertical. Liver Transplantation. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma /
diagnosis
. Pregnancy. Pregnancy Complications, Infectious /
diagnosis
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.
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.
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.
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.
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(PMID = 17617782.001).
[ISSN]
0361-8609
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antiviral Agents; P9G3CKZ4P5 / Ganciclovir
7.
Sharma VM, Calvo JA, Draheim KM, Cunningham LA, Hermance N, Beverly L, Krishnamoorthy V, Bhasin M, Capobianco AJ, Kelliher MA:
Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.
Mol Cell Biol
; 2006 Nov;26(21):8022-31
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[Title]
Notch1 contributes to mouse T-
cell leukemia
by directly inducing the expression of c-myc.
Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-
cell acute lymphoblastic leukemia
(T-ALL).
To identify Notch1 target genes in
leukemia
, we developed mouse T-
cell
leukemic lines that express intracellular Notch1 in a doxycycline-dependent manner.
Using gene expression profiling and chromatin immunoprecipitation, we identified c-myc as a novel, direct, and critical Notch1 target gene in T-
cell leukemia
. c-myc mRNA levels are increased in primary mouse T-
cell
tumors that harbor Notch1 mutations, and Notch1 inhibition decreases c-myc mRNA levels and inhibits leukemic
cell
growth.
Consistent with these findings, retroviral insertional mutagenesis screening of our T-
cell leukemia
mouse model revealed common insertions in either notch1 or c-myc genes.
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Cancer Res. 2005 Aug 15;65(16):7159-68
[
16103066.001
]
(PMID = 16954387.001).
[ISSN]
0270-7306
[Journal-full-title]
Molecular and cellular biology
[ISO-abbreviation]
Mol. Cell. Biol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA-096889
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Myc protein, mouse; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
[Other-IDs]
NLM/ PMC1636748
8.
Bram EE, Stark M, Raz S, Assaraf YG:
Chemotherapeutic drug-induced ABCG2 promoter demethylation as a novel mechanism of acquired multidrug resistance.
Neoplasia
; 2009 Dec;11(12):1359-70
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Herein, we explored the impact of drug treatment on the methylation status of the ABCG2 promoter and consequent reactivation of ABCG2 gene expression in parental tumor
cell
lines and their MDR sublines.
We demonstrate that ABCG2 promoter methylation is common in T-
cell acute lymphoblastic leukemia
(T-ALL) lines, also present in primary T-ALL lymphoblast specimens.
Furthermore, drug selection with sulfasalazine and topotecan induced a complete demethylation of the ABCG2 promoter in the T-ALL and ovarian carcinoma model
cell
lines CCRF-CEM and IGROV1, respectively.
Remarkably, mimicking cytotoxic bolus drug treatment through 12- to 24-hour pulse exposure of ABCG2-silenced
leukemia
cells, to clinically relevant concentrations of the chemotherapeutic agents daunorubicin and mitoxantrone, resulted in a marked transcriptional up-regulation of ABCG2.
[MeSH-minor]
ATP Binding Cassette Transporter, Sub-Family G, Member 2. Antineoplastic Agents / pharmacology. Azacitidine / analogs & derivatives. Azacitidine / pharmacology.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Cytidine / analogs & derivatives. Cytidine / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Humans. Jurkat Cells. K562 Cells. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / pathology. Reverse Transcriptase Polymerase Chain Reaction
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(PMID = 20019844.001).
[ISSN]
1476-5586
[Journal-full-title]
Neoplasia (New York, N.Y.)
[ISO-abbreviation]
Neoplasia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 5CSZ8459RP / Cytidine; 776B62CQ27 / decitabine; 7A9Y5SX0GY / pyrimidin-2-one beta-ribofuranoside; M801H13NRU / Azacitidine
[Other-IDs]
NLM/ PMC2794517
9.
Neudenberger J, Hotfilder M, Rosemann A, Langebrake C, Reinhardt D, Pieters R, Schrauder A, Schrappe M, Röttgers S, Harbott J, Vormoor J:
Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem cell populations in paediatric acute myeloid leukaemia/abn(11q23) and acute lymphoblastic leukaemia/t(4;11).
Br J Haematol
; 2006 May;133(3):337-44
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[Title]
Lack of expression of the chondroitin sulphate proteoglycan neuron-glial antigen 2 on candidate stem
cell
populations in paediatric
acute
myeloid leukaemia
/abn(11q23)
and acute lymphoblastic
leukaemia
/t(4;11).
Therefore, these leukaemic stem cells should be the target cells for therapy and for minimal residual
disease
(MRD) detection.
Six
acute
myeloid leukaemia
(AML)/abn(11q23) and three
acute lymphoblastic
leukaemia
(ALL)/t(4;11) samples were analysed by four-colour flow cytometry for NG2 expression on primitive
cell
populations.
Candidate leukaemic
cell
populations were defined by the antigen profiles CD34+CD38- in AML and CD34+CD19-CD117+ in ALL.
Surprisingly, in all patients these candidate stem
cell
populations were shown to lack expression of NG2.
Instead, a correlation between the expression of the
myeloid
differentiation marker CD33 and increasing levels of NG2 on maturing cells could be demonstrated.
Thus, NG2 appears to be upregulated with differentiation and not to be expressed on primitive
disease
-maintaining cells.
[MeSH-major]
Antigens / metabolism. Biomarkers, Tumor / metabolism.
Leukemia
,
Myeloid
/ metabolism. Neoplastic Stem Cells / metabolism. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Proteoglycans / metabolism
[MeSH-minor]
Acute
Disease
. Antigens, CD / metabolism. Antigens, Differentiation, Myelomonocytic / metabolism. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 4 / genetics. Flow Cytometry / methods. Humans. Neoplasm Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Sialic Acid Binding Ig-like Lectin 3. Translocation, Genetic
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(PMID = 16643437.001).
[ISSN]
0007-1048
[Journal-full-title]
British journal of haematology
[ISO-abbreviation]
Br. J. Haematol.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Biomarkers, Tumor; 0 / CD33 protein, human; 0 / Neoplasm Proteins; 0 / Proteoglycans; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / chondroitin sulfate proteoglycan 4
10.
Heuser M, Beutel G, Krauter J, Döhner K, von Neuhoff N, Schlegelberger B, Ganser A:
High meningioma 1 (MN1) expression as a predictor for poor outcome in acute myeloid leukemia with normal cytogenetics.
Blood
; 2006 Dec 1;108(12):3898-905
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[Title]
High meningioma 1 (MN1) expression as a predictor for poor outcome in
acute
myeloid
leukemia
with normal cytogenetics.
The translocation t(12;22) involves MN1 and TEL and is rarely found in
acute
myeloid
leukemia
(AML).
MN1 was highly expressed in some patients with
acute lymphoblastic
but not chronic
lymphocytic
or
myeloid
leukemia
.
[MeSH-major]
Biomarkers, Tumor / biosynthesis. Gene Expression Regulation, Leukemic.
Leukemia
,
Myeloid
,
Acute
/ metabolism. Tumor Suppressor Proteins / biosynthesis
[MeSH-minor]
Adolescent. Adult. Animals. Cytogenetic Analysis / methods.
Disease
-Free Survival. Female. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ genetics.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ metabolism.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ mortality.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ therapy.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / genetics.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / metabolism.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / mortality.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / therapy. Male. Mice. Middle Aged. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Predictive Value of Tests. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Transcription Factors / biosynthesis. Transcription Factors / genetics
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(PMID = 16912223.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Homeodomain Proteins; 0 / MN1 protein, human; 0 / MN1-TEL fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / homeobox protein HOXA9
11.
De Keersmaecker K, Lahortiga I, Mentens N, Folens C, Van Neste L, Bekaert S, Vandenberghe P, Odero MD, Marynen P, Cools J:
In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-cell acute lymphoblastic leukemia.
Haematologica
; 2008 Apr;93(4):533-42
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[Title]
In vitro validation of gamma-secretase inhibitors alone or in combination with other anti-cancer drugs for the treatment of T-
cell acute lymphoblastic leukemia
.
BACKGROUND: Activating NOTCH1 mutations are common in T-
cell acute lymphoblastic leukemia
.
Inhibition of NOTCH1 signaling with gamma-secretase inhibitors causes
cell
cycle block, but only after treatment for several days.
We further documented the effects of gamma-secretase inhibitor treatment on T-
cell acute lymphoblastic leukemia cell
lines and tested whether combining gamma-secretase inhibitors with other anti-cancer drugs offers a therapeutic advantage.
DESIGN AND METHODS: The effect of gamma-secretase inhibitor treatment and combinations of gamma-secretase inhibitors with chemotherapy or glucocorticoids was assessed on T-
cell acute lymphoblastic leukemia cell
lines.
We sequenced NOTCH1 in T-
cell acute lymphoblastic leukemia
cases with ABL1 fusions and tested combinations of gamma-secretase inhibitors and the ABL1 inhibitor imatinib in a T-
cell acute lymphoblastic leukemia cell
line.
RESULTS: gamma-secretase inhibitor treatment for 5-7 days reversibly inhibited
cell
proliferation, caused
cell
cycle block in sensitive T-
cell acute lymphoblastic leukemia cell
lines, and caused differentiation of some T-
cell acute lymphoblastic leukemia cell
lines.
The cytotoxic effects of the chemotherapeutic agent vincristine were not significantly enhanced by addition of gamma-secretase inhibitors to T-
cell acute lymphoblastic leukemia cell
lines, but gamma-secretase inhibitor treatment sensitized cells to the effect of dexamethasone.
NOTCH1 mutations were identified in all T-
cell acute lymphoblastic leukemia
patients with ABL1 fusions and in a T-
cell acute lymphoblastic leukemia cell
line expressing NUP214-ABL1.
In this
cell
line, the anti-proliferative effect of imatinib was increased by pre-treatment with gamma-secretase inhibitors.
CONCLUSIONS: Short-term treatment of T-
cell acute lymphoblastic leukemia cell
lines with gamma-secretase inhibitors had limited effects on
cell
proliferation and survival.
Combinations of gamma-secretase inhibitors with other drugs may be required to obtain efficient therapeutic effects in T-
cell acute lymphoblastic leukemia
, and not all combinations may be useful.
[MeSH-major]
Amyloid Precursor Protein Secretases / antagonists & inhibitors. Antineoplastic Agents / pharmacology. Benzodiazepinones / pharmacology. Carbamates / pharmacology. Dipeptides / pharmacology. Enzyme Inhibitors / pharmacology.
Leukemia
-Lymphoma, Adult T-
Cell
/ drug therapy. Neoplasm Proteins / antagonists & inhibitors. Receptor, Notch1 / antagonists & inhibitors
[MeSH-minor]
Apoptosis / drug effects. Benzamides.
Cell
Cycle / drug effects.
Cell
Division / drug effects.
Cell
Line, Tumor / drug effects.
Cell
Line, Tumor / enzymology. DNA, Neoplasm / genetics. Daunorubicin / administration & dosage. Daunorubicin / pharmacology. Dexamethasone / administration & dosage. Dexamethasone / pharmacology. Drug Screening Assays, Antitumor. Drug Synergism. Humans. Imatinib Mesylate. In Vitro Techniques. Mutation. Oncogene Proteins, Fusion / antagonists & inhibitors. Oncogene Proteins, Fusion / genetics. Piperazines / administration & dosage. Piperazines / pharmacology. Pyrimidines / administration & dosage. Pyrimidines / pharmacology. Sequence Analysis, DNA. Vincristine / administration & dosage. Vincristine / pharmacology
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[CommentIn]
Haematologica. 2008 Apr;93(4):493-7
[
18379008.001
]
(PMID = 18322257.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzodiazepinones; 0 / Carbamates; 0 / DNA, Neoplasm; 0 / Dipeptides; 0 / Enzyme Inhibitors; 0 / L 685458; 0 / NOTCH1 protein, human; 0 / NUP214-ABL1 fusion protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8A1O1M485B / Imatinib Mesylate; EC 3.4.- / Amyloid Precursor Protein Secretases; ZS7284E0ZP / Daunorubicin
12.
Muzzafar T, Medeiros LJ, Wang SA, Brahmandam A, Thomas DA, Jorgensen JL:
Aberrant underexpression of CD81 in precursor B-cell acute lymphoblastic leukemia: utility in detection of minimal residual disease by flow cytometry.
Am J Clin Pathol
; 2009 Nov;132(5):692-8
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[Title]
Aberrant underexpression of CD81 in precursor B-
cell acute lymphoblastic leukemia
: utility in detection of minimal residual
disease
by flow cytometry.
We studied CD81 expression by flow cytometry (FC) on benign precursor B cells (hematogones) and leukemic blasts in precursor B-
cell acute lymphoblastic leukemia
(pre-B-ALL) and established its usefulness in minimal residual
disease
(MRD) assays.
In 98 pre-B-ALLs at
diagnosis
or overt relapse, 80 (82%) showed aberrantly decreased CD81 intensity.
[MeSH-major]
Antigens, CD / biosynthesis. Biomarkers, Tumor / analysis. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / pathology
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(PMID = 19846809.001).
[ISSN]
1943-7722
[Journal-full-title]
American journal of clinical pathology
[ISO-abbreviation]
Am. J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD81; 0 / Biomarkers, Tumor; 0 / CD81 protein, human
13.
Suzuki N, Yumura-Yagi K, Yoshida M, Hara J, Nishimura S, Kudoh T, Tawa A, Usami I, Tanizawa A, Hori H, Ito Y, Miyaji R, Oda M, Kato K, Hamamoto K, Osugi Y, Hashii Y, Nakahata T, Horibe K, Japan Association of Childhood Leukemia Study (JACLS):
Outcome of childhood acute lymphoblastic leukemia with induction failure treated by the Japan Association of Childhood Leukemia study (JACLS) ALL F-protocol.
Pediatr Blood Cancer
; 2010 Jan;54(1):71-8
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[Title]
Outcome of childhood
acute lymphoblastic leukemia
with induction failure treated by the Japan Association of Childhood
Leukemia
study (JACLS) ALL F-protocol.
BACKGROUND: Children with
acute lymphoblastic leukemia
(ALL) who fail to achieve complete remission (CR) after induction therapy (induction failure: IF) have a poor prognosis; however, there have been few prospective studies in patients with IF.
Twenty-three of these patients entered the F-protocol study, which mainly consisted of
acute
-
myeloid
-
leukemia
-oriented chemotherapy followed by scheduled hematopoietic
cell
transplantation (HCT).
RESULTS: Seventeen (73.9%) of the 23 patients responded to
re
-induction chemotherapy with CR.
The 5-year OS rate of the 17 patients who obtained CR by
re
-induction therapy and the 6 who did not were 47.1 +/- 12.1% and 0%, respectively (P < 0.001).
CONCLUSION:
Acute
-
myeloid
-
leukemia
-oriented chemotherapy followed by scheduled HCT is a promising treatment strategy for non-Ph(+) ALL patients with IF.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Transplantation. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia, Childhood
.
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consumer health - Bone Marrow Transplantation
.
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[Copyright]
Copyright 2009 Wiley-Liss, Inc.
(PMID = 19813250.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
14.
Cho J, Hur M, Moon HW, Yun YM, Lee CH, Lee HG:
A case of therapy-related ALL with MLL gene rearrangement following treatment of breast cancer.
Korean J Lab Med
; 2010 Jun;30(3):255-9
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However, the patient's complete blood
cell
count indicated
acute leukemia
: white blood
cell
count, 174.1 x 10(9)/L with 88% blasts; Hb level, 12.5 g/dL; and platelet count, 103.0 x 10(9)/L.
Following consolidation chemotherapy, she underwent allogenic peripheral blood stem
cell
transplantation and has been clinically stable.
[MeSH-major]
Breast Neoplasms / drug therapy.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / etiology. Translocation, Genetic
[MeSH-minor]
Antibiotics, Antineoplastic / therapeutic use. Blood
Cell
Count. Bone Marrow / pathology. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Cytogenetic Analysis. Epirubicin / therapeutic use. Female. Fluorouracil / therapeutic use. Gene Rearrangement. Hematopoietic Stem
Cell
Transplantation. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence
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(PMID = 20603585.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; U3P01618RT / Fluorouracil
15.
Bornhauser BC, Bonapace L, Lindholm D, Martinez R, Cario G, Schrappe M, Niggli FK, Schäfer BW, Bourquin JP:
Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway.
Blood
; 2007 Sep 15;110(6):2084-91
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[Title]
Low-dose arsenic trioxide sensitizes glucocorticoid-resistant
acute lymphoblastic leukemia
cells to dexamethasone via an Akt-dependent pathway.
Incorporation of apoptosis-inducing agents into current therapeutic regimens is an attractive strategy to improve treatment for drug-resistant
leukemia
.
We tested the potential of arsenic trioxide (ATO) to restore the response to dexamethasone in glucocorticoid (GC)-resistant
acute lymphoblastic leukemia
(ALL).
Low-dose ATO markedly increased in vitro GC sensitivity of ALL cells from T-
cell and
precursor B-
cell
ALL patients with poor in vivo response to prednisone.
In GC-resistant
cell
lines, this effect was mediated, at least in part, by inhibition of Akt and affecting downstream Akt targets such as Bad, a proapoptotic Bcl-2 family member, and the X-linked inhibitor of apoptosis protein (XIAP).
[MeSH-major]
Antineoplastic Agents / pharmacology. Arsenicals / administration & dosage. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Glucocorticoids / pharmacology. Oxides / administration & dosage. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction
[MeSH-minor]
Apoptosis / drug effects. Blotting, Western. Caspases.
Cell
Line, Tumor / drug effects.
Cell
Survival / drug effects. Drug Synergism. Humans. Neoplasm, Residual /
diagnosis
. Phosphorylation / drug effects. Prednisone / pharmacology. RNA, Small Interfering / pharmacology. Reactive Oxygen Species / metabolism. Remission Induction. Sirolimus / pharmacology. Transfection. X-Linked Inhibitor of Apoptosis Protein / metabolism. bcl-Associated Death Protein / metabolism
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.
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.
PhosphoSitePlus.
gene/protein/disease-specific - PhosphoSitePlus® - comprehensive post-translational modification resource
.
Hazardous Substances Data Bank.
ARSENIC TRIOXIDE
.
Hazardous Substances Data Bank.
DEXAMETHASONE
.
Hazardous Substances Data Bank.
PREDNISONE
.
Hazardous Substances Data Bank.
SIROLIMUS
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 17537996.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Arsenicals; 0 / BAD protein, human; 0 / Glucocorticoids; 0 / Oxides; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / bcl-Associated Death Protein; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Caspases; S7V92P67HO / arsenic trioxide; VB0R961HZT / Prednisone; W36ZG6FT64 / Sirolimus
16.
Vilimas T, Mascarenhas J, Palomero T, Mandal M, Buonamici S, Meng F, Thompson B, Spaulding C, Macaroun S, Alegre ML, Kee BL, Ferrando A, Miele L, Aifantis I:
Targeting the NF-kappaB signaling pathway in Notch1-induced T-cell leukemia.
Nat Med
; 2007 Jan;13(1):70-7
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[Title]
Targeting the NF-kappaB signaling pathway in Notch1-induced T-
cell leukemia
.
T-
cell acute lymphoblastic leukemia
(T-ALL), unlike other ALL types, is only infrequently associated with chromosomal aberrations, but it was recently shown that most individuals with T-ALL carry activating mutations in the NOTCH1 gene.
[MeSH-major]
Leukemia
, T-
Cell
/ pathology. NF-kappa B / metabolism. Receptor, Notch1 / metabolism
[MeSH-minor]
Animals. Antigens, CD4 / analysis. Antigens, CD8 / analysis. Boronic Acids / pharmacology. Bortezomib. COS Cells.
Cell
Line.
Cell
Line, Tumor.
Cell
Survival / drug effects. Cercopithecus aethiops. DNA-Binding Proteins / genetics. Gene Expression Profiling. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Interleukin Receptor Common gamma Subunit / genetics.
Leukemia
, Experimental / genetics.
Leukemia
, Experimental / metabolism.
Leukemia
, Experimental / pathology. Mice. Mice, Inbred C57BL. Mice, Knockout. Microscopy, Confocal. Mutation. Pyrazines / pharmacology. Signal Transduction / genetics. Signal Transduction / physiology. Survival Analysis
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Mouse Genome Informatics (MGI)
.
SciCrunch.
OMIM: Data: Gene Annotation
.
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(PMID = 17173050.001).
[ISSN]
1078-8956
[Journal-full-title]
Nature medicine
[ISO-abbreviation]
Nat. Med.
[Language]
eng
[Grant]
United States / NIA NIH HHS / AG / P01AG025531; United States / NCI NIH HHS / CA / R01CA105129; United States / NCI NIH HHS / CA / R01CA84065
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD4; 0 / Antigens, CD8; 0 / Boronic Acids; 0 / DNA-Binding Proteins; 0 / Il2rg protein, mouse; 0 / Interleukin Receptor Common gamma Subunit; 0 / NF-kappa B; 0 / NOTCH1 protein, human; 0 / Pyrazines; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 147336-22-9 / Green Fluorescent Proteins; 69G8BD63PP / Bortezomib
17.
Betts DR, Stanchescu R, Niggli FK, Cohen N, Rechavi G, Amariglio N, Trakhtenbrot L:
SKY reveals a high frequency of unbalanced translocations involving chromosome 6 in t(12;21)-positive acute lymphoblastic leukemia.
Leuk Res
; 2008 Jan;32(1):39-43
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[Title]
SKY reveals a high frequency of unbalanced translocations involving chromosome 6 in t(12;21)-positive
acute lymphoblastic leukemia
.
The G-band cryptic t(12;21)(p13;q22) is the most common chromosomal rearrangement in childhood
acute lymphoblastic leukemia
(ALL).
[MeSH-major]
Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 6. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Spectral Karyotyping. Translocation, Genetic
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[CommentIn]
Leuk Res. 2007 Dec;31(12):1761-2
[
17560648.001
]
(PMID = 17418891.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Validation Studies
[Publication-country]
England
18.
Yang Y, Takeuchi S, Hofmann WK, Ikezoe T, van Dongen JJ, Szczepański T, Bartram CR, Yoshino N, Taguchi H, Koeffler HP:
Aberrant methylation in promoter-associated CpG islands of multiple genes in acute lymphoblastic leukemia.
Leuk Res
; 2006 Jan;30(1):98-102
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[Title]
Aberrant methylation in promoter-associated CpG islands of multiple genes in
acute lymphoblastic leukemia
.
Methylation profile was analyzed in 10 childhood
acute lymphoblastic leukemia
(ALL) and nine adult ALL cases.
[MeSH-major]
CpG Islands. DNA Methylation. Neoplasm Proteins / metabolism. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
NCI CPTC Antibody Characterization Program.
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.
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NCI CPTC Antibody Characterization Program
.
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(PMID = 16039715.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Neoplasm Proteins
19.
Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL):
Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
Eur J Haematol
; 2010 Oct;85(4):300-8
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[Title]
Childhood near-tetraploid
acute lymphoblastic leukemia
: an EGIL study on 36 cases.
OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes)
acute lymphoblastic leukemia
(NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
METHODS: The members of the European Group for Immunophenotyping of
Leukemias
(EGIL) searched retrospectively their databases for NT-ALL patients.
Ten children were diagnosed as T-
cell
ALL (T-ALL) EGIL categories (T-I n=2, T-II n=2, T-III n=3, T-IV n=3) and four displayed various structural chromosomal abnormalities.
B-
cell
precursor (BCP) ALL was diagnosed in 26 children.
One girl with hypodiploid and NT metaphases and ETV6-RUNX1-negative BCP-ALL and one of two boys with NT-BCP-ALL not examined for ETV6-RUNX1 died of infection after stem
cell
transplantation in 2nd/3rd CR.
[MeSH-major]
Precursor
Cell Lymphoblastic Leukemia
-Lymphoma
Genetic Alliance.
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[Copyright]
© 2010 John Wiley & Sons A/S.
(PMID = 20561032.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
20.
Infante-Rivard C, Vermunt JK, Weinberg CR:
Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia.
Am J Epidemiol
; 2007 Jun 1;165(11):1248-54
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[Title]
Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with
acute lymphoblastic leukemia
.
Topoisomerase II is a DNA-processing enzyme, and secondary
acute
myeloid
leukemia
has been associated with exposure to drugs that inhibit its action.
Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood
leukemia
.
To assess its role in the etiology of childhood
acute lymphoblastic leukemia
, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000).
[MeSH-major]
Family Health. Inheritance Patterns. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / epidemiology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
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[Cites]
BMJ. 2002 Feb 2;324(7332):283-7
[
11823363.001
]
(PMID = 17332311.001).
[ISSN]
0002-9262
[Journal-full-title]
American journal of epidemiology
[ISO-abbreviation]
Am. J. Epidemiol.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 ES045005-11
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; J64922108F / Benzene
[Other-IDs]
NLM/ NIHMS33454; NLM/ PMC2080583
21.
O'Brien S, Ravandi F, Riehl T, Wierda W, Huang X, Tarrand J, O'Neal B, Kantarjian H, Keating M:
Valganciclovir prevents cytomegalovirus reactivation in patients receiving alemtuzumab-based therapy.
Blood
; 2008 Feb 15;111(4):1816-9
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Alemtuzumab is an immunosuppressive antibody that depletes normal T cells
and B
cells.
Diagnoses included chronic
lymphocytic
leukemia
(29), T-
cell
prolymphocytic
leukemia
(3), hairy
cell leukemia
(1), adult T-
cell leukemia
/lymphoma (ATLL) (1), marginal zone
leukemia
(1), large granular lymphocyte
leukemia
(2),
acute lymphoblastic leukemia
(1),
and T
-
cell
lymphoma (2).
[MeSH-major]
Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Cytomegalovirus / physiology. Cytomegalovirus Infections / prevention & control. Ganciclovir / analogs & derivatives.
Leukemia
,
Lymphocytic
, Chronic, B-
Cell
/ drug therapy. Virus Activation / physiology
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.
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.
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[CommentIn]
Blood. 2008 Sep 1;112(5):2167
[
18725576.001
]
(PMID = 18039954.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00562770
[Publication-type]
Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / valganciclovir; 3A189DH42V / alemtuzumab; P9G3CKZ4P5 / Ganciclovir
22.
Benketira A, Tichit R, Tenenbaum J, Margueritte G, Bernard F:
[BK virus infection in a child after an hematopoietic stem cell transplantation].
Arch Pediatr
; 2005 Apr;12 Suppl 1:S64-6
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[Title]
[BK virus infection in a child after an hematopoietic stem
cell
transplantation].
[Transliterated title]
Infection à BK Virus après allogreffe
de cellules
hématopoïétiques. A propos d'un cas.
A 10-year old boy with poor-prognosis
acute T lymphoblastic
leukaemia
underwent cord blood allogeneic stem
cell
transplantation while in his first relapse.
Macroscopic haematuria and low back pain occurred by day 95, in the context of
acute
graft versus host
disease
and pulmonary aspergillosis.
Histopathologic examination showed a cytopathogenetic effect consistent with the
diagnosis
of BKV infection.
The current understanding,
diagnosis
, and treatment of BKV-associated infection is discussed.
[MeSH-major]
BK Virus / pathogenicity. Cytosine / analogs & derivatives. Hematopoietic Stem
Cell
Transplantation / adverse effects. Polyomavirus Infections / etiology
[MeSH-minor]
Antiviral Agents / therapeutic use. Child. Humans.
Leukemia
-Lymphoma, Adult T-
Cell
/ therapy. Male. Organophosphonates / therapeutic use. Prognosis
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.
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(PMID = 15893243.001).
[ISSN]
0929-693X
[Journal-full-title]
Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
[ISO-abbreviation]
Arch Pediatr
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Antiviral Agents; 0 / Organophosphonates; 8J337D1HZY / Cytosine; JIL713Q00N / cidofovir
23.
Goto H, Naruto T, Tanoshima R, Kato H, Yokosuka T, Yanagimachi M, Fujii H, Yokota S, Komine H:
Chemo-sensitivity in a panel of B-cell precursor acute lymphoblastic leukemia cell lines, YCUB series, derived from children.
Leuk Res
; 2009 Oct;33(10):1386-91
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[Title]
Chemo-sensitivity in a panel of B-
cell
precursor
acute lymphoblastic leukemia cell
lines, YCUB series, derived from children.
Sensitivity to 10 anticancer drugs was evaluated in 6 childhood B-
cell
precursor
acute lymphoblastic leukemia
(BCP-ALL)
cell
lines.
Authenticity of newly established
cell
lines was confirmed by genomic fingerprinting.
The line YCUB-5R established at relapse was more resistant to 4-hydroperoxy-cyclophosphamide, cytarabine, L-asparaginase, topotecan, fludarabine, and etoposide than YCUB-5 from the same patient at
diagnosis
.
This
cell
line panel offers an in vitro model for the development of new therapies for childhood BCP-ALL.
[MeSH-major]
B-Lymphocytes / pathology. DNA Fingerprinting / methods. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
[MeSH-minor]
Antineoplastic Agents / therapeutic use.
Cell
Division / drug effects.
Cell
Line, Tumor / drug effects.
Cell
Survival / drug effects. Child. Child, Preschool. Flow Cytometry. Humans. Immunophenotyping. Leukocyte Count. Male. Prednisolone / pharmacology
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.
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.
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(PMID = 19157546.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents; 9PHQ9Y1OLM / Prednisolone
24.
Yoshimi A, Ito M, Kojima S:
Leukemic cell death induced by antithymocyte globulin.
Leuk Res
; 2005 Jul;29(7):821-7
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[Title]
Leukemic
cell
death induced by antithymocyte globulin.
We studied the cytotoxic effects of antithymocyte globulin (ATG) in leukemic cells obtained from five patients with
acute T lymphoblastic leukemia
or precursor
T lymphoblastic leukemia
.
We also examined apoptotic
cell
death using Annexin-V.
Cell
incubation with ATG increased Annexin-V binding significantly compared with horse IgG (50.3+/-7.6% versus 95.7+/-1.8%, p = or < 0.0001).
However, ATG did not induce apparent DNA fragmentation in a human T-ALL
cell
line.
These results suggest that ATG induces leukemic
cell
death in a Fas/Fas-ligand- and caspase-independent manner.
[MeSH-major]
Antilymphocyte Serum / pharmacology.
Cell
Death / drug effects. Immunosuppressive Agents / pharmacology.
Leukemia
-Lymphoma, Adult T-
Cell
/ pathology
[MeSH-minor]
Animals.
Cell
Line, Tumor. Horses. Humans. Immunoglobulin G / pharmacology
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(PMID = 15893374.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antilymphocyte Serum; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents
25.
Bosch FJ, Badenhorst L, Le Roux JA, Louw VJ:
Successful treatment of Chromobacterium violaceum sepsis in South Africa.
J Med Microbiol
; 2008 Oct;57(Pt 10):1293-5
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As far as could be ascertained, this infection has never been reported in a patient with
leukaemia
.
We describe what we believe to be the first such case of C. violaceum sepsis, in a 16-year-old female patient with
acute
biphenotypic leukaemia
, which developed during the neutropenic phase after intensive chemotherapy.
[MeSH-minor]
Adolescent. Antifungal Agents / pharmacology. Candidiasis / complications. Candidiasis / drug therapy. Female. Humans.
Leukemia
/ complications. Neutropenia / complications. South Africa / epidemiology. Treatment Outcome
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.
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.
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(PMID = 18809561.001).
[ISSN]
0022-2615
[Journal-full-title]
Journal of medical microbiology
[ISO-abbreviation]
J. Med. Microbiol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-Bacterial Agents; 0 / Antifungal Agents
26.
van Brussel M, Takken T, Lucia A, van der Net J, Helders PJ:
Is physical fitness decreased in survivors of childhood leukemia? A systematic review.
Leukemia
; 2005 Jan;19(1):13-7
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[Title]
Is physical fitness decreased in survivors of childhood
leukemia
? A systematic review.
The aim of this review is to determine whether physical fitness, assessed by peak oxygen uptake (VO(2peak)) measurement, is reduced in survivors of
acute lymphoblastic leukemia
(ALL) compared to healthy children.
[MeSH-major]
Physical Fitness. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / physiopathology. Survivors
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.
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(PMID = 15526028.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
38
27.
Bayrak IK, Yalin T, Ozmen Z, Aksoz T, Doughanji R:
Acute lymphoblastic leukemia presented as multiple breast masses.
Korean J Radiol
; 2009 Sep-Oct;10(5):508-10
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[Title]
Acute lymphoblastic leukemia
presented as multiple breast masses.
Breast metastases in cases
leukemia
are very rare and occur primarily in patients with
acute
myeloid
leukemia
.
We report the involvement of breast metastases in a 30-year-old woman with
acute T cell lymphoblastic leukemia
.
[MeSH-major]
Breast Neoplasms / secondary. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology
[MeSH-minor]
Adult.
Diagnosis
, Differential. Female. Humans. Mammography. Ultrasonography, Mammary
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.
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[Cites]
Radiol Clin North Am. 1982 Sep;20(3):561-8
[
7111707.001
]
[Cites]
AJR Am J Roentgenol. 1983 Oct;141(4):685-90
[
6604418.001
]
[Cites]
AJR Am J Roentgenol. 1999 Feb;172(2):343-8
[
9930779.001
]
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Clin Pediatr (Phila). 1999 Sep;38(9):545-6
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10500889.001
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J Clin Ultrasound. 2002 Nov-Dec;30(9):552-6
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Semin Ultrasound CT MR. 2000 Oct;21(5):375-94
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]
[Cites]
Eur Radiol. 2000;10(6):1031
[
10879725.001
]
(PMID = 19721836.001).
[ISSN]
2005-8330
[Journal-full-title]
Korean journal of radiology
[ISO-abbreviation]
Korean J Radiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Korea (South)
[Number-of-references]
10
[Other-IDs]
NLM/ PMC2731869
[Keywords]
NOTNLM ; Acute lymphoblastic leukemia / Breast metastasis / Mammography / Ultrasonography
28.
Cohen MH, Johnson JR, Justice R, Pazdur R:
FDA drug approval summary: nelarabine (Arranon) for the treatment of T-cell lymphoblastic leukemia/lymphoma.
Oncologist
; 2008 Jun;13(6):709-14
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[Title]
FDA drug approval summary: nelarabine (Arranon) for the treatment of T-
cell lymphoblastic leukemia
/lymphoma.
Food and Drug Administration (FDA) approval of nelarabine (Arranon), a new purine analogue, for the treatment of patients with T-
cell acute lymphoblastic leukemia
(T-ALL)
and T
-
cell lymphoblastic
lymphoma (T-LBL) whose
disease
has not responded to or has relapsed following treatment with at least two chemotherapy regimens.
[MeSH-major]
Arabinonucleosides / therapeutic use. Drug Approval / legislation & jurisprudence.
Leukemia
-Lymphoma, Adult T-
Cell
/ drug therapy. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy
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.
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(PMID = 18586926.001).
[ISSN]
1083-7159
[Journal-full-title]
The oncologist
[ISO-abbreviation]
Oncologist
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Arabinonucleosides; 60158CV180 / nelarabine
29.
Ausserlechner MJ, Obexer P, Geley S, Kofler R:
G1 arrest by p16INK4A uncouples growth from cell cycle progression in leukemia cells with deregulated cyclin E and c-Myc expression.
Leukemia
; 2005 Jun;19(6):1051-7
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[Title]
G1 arrest by p16INK4A uncouples growth from
cell
cycle progression in
leukemia
cells with deregulated cyclin E and c-Myc expression.
The
cell
cycle inhibitor p16(INK4A) is frequently inactivated in
acute lymphoblastic
T-
cell leukemia
(T-ALL).
CCRF-CEM cells with tetracycline-regulated p16(INK4A) expression underwent stable G1-phase
cell
cycle arrest for 72 h followed by massive apoptosis. p16(INK4A) expression caused pRB hypophosphorylation and repression of certain E2F target genes.
Thus, p16(INK4A), although unable to repress the expression of deregulated cyclin E and c-Myc, functionally inactivated these potential oncogenes. p16(INK4A)-arrested cells showed
morphologic
changes, induction of T-
cell
-specific surface markers and repression of telomerase activity, suggesting differentiation.
Taken together, p16(INK4A) reconstitution in p16(INK4A)-deficient T-ALL cells induced
cell
cycle arrest in the presence of cyclin E and c-Myc expression, uncoupled growth from
cell
cycle progression and caused a sequential process of growth, differentiation and apoptosis.
[MeSH-major]
Cyclin E / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Genes, myc / physiology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / physiopathology
[MeSH-minor]
Apoptosis / physiology. Biomarkers, Tumor.
Cell
Differentiation / physiology.
Cell
Division / physiology. Child. G1 Phase / physiology. Gene Expression Regulation, Leukemic. Humans. Nuclear Proteins / genetics. Nuclear Proteins / metabolism. Phosphorylation. Retinoblastoma-Like Protein p107. T-Lymphocytes / pathology. T-Lymphocytes / physiology. Telomerase / metabolism. Transcriptional Activation / physiology
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(PMID = 15800668.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Cyclin E; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Nuclear Proteins; 0 / RBL1 protein, human; 0 / Retinoblastoma-Like Protein p107; EC 2.7.7.49 / Telomerase
30.
Mitchell L, Lambers M, Flege S, Kenet G, Li-Thiao-Te V, Holzhauer S, Bidlingmaier C, Frühwald MC, Heller C, Schmidt W, Pautard B, Nowak-Göttl U:
Validation of a predictive model for identifying an increased risk for thromboembolism in children with acute lymphoblastic leukemia: results of a multicenter cohort study.
Blood
; 2010 Jun 17;115(24):4999-5004
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[Title]
Validation of a predictive model for identifying an increased risk for thromboembolism in children with
acute lymphoblastic leukemia
: results of a multicenter cohort study.
Among risk factors for developing thromboembolism (VTE) in children with
acute lymphoblastic leukemia
were Escherichia coli asparaginase, concomitant steroid use, presence of central venous lines, and thrombophilic abnormalities.
In multivariate analysis adjusted for age, duration of asparaginase administration, enoxaparin prophylaxis,
and T
-immunophenotype, the HRG was significantly associated with VTE compared with the LRG (hazard/95% confidence interval [CI], 8.22/1.85-36.53).
On the basis of the high specificity, the model may identify children with
leukemia
at risk of VTE.
[MeSH-major]
Models, Statistical. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / epidemiology. Thromboembolism /
diagnosis
. Thromboembolism / epidemiology
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.
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commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
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[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Validation Studies
[Publication-country]
United States
[Chemical-registry-number]
0 / Anticoagulants; 0 / Enoxaparin; 0 / Steroids; EC 3.5.1.1 / Asparaginase
[Other-IDs]
NLM/ PMC2890143
31.
Inukai T, Zhang X, Kameyama T, Suzuki Y, Yoshikawa K, Kuroda I, Nemoto A, Akahane K, Sato H, Goi K, Nakamoto K, Hamada J, Tada M, Moriuchi T, Sugita K:
A specific linkage between the incidence of TP53 mutations and type of chromosomal translocations in B-precursor acute lymphoblastic leukemia cell lines.
Am J Hematol
; 2010 Jul;85(7):535-7
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[Title]
A specific linkage between the incidence of TP53 mutations and type of chromosomal translocations in B-precursor
acute lymphoblastic leukemia cell
lines.
[MeSH-major]
Mutation. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Translocation, Genetic. Tumor Suppressor Protein p53 / genetics
[MeSH-minor]
Cell
Line, Tumor. Humans. Oncogene Proteins, Fusion
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(PMID = 20575032.001).
[ISSN]
1096-8652
[Journal-full-title]
American journal of hematology
[ISO-abbreviation]
Am. J. Hematol.
[Language]
eng
[Publication-type]
Letter
[Publication-country]
United States
[Chemical-registry-number]
0 / Oncogene Proteins, Fusion; 0 / Tumor Suppressor Protein p53
32.
Wu S, Gessner R, Taube T, von Stackelberg A, Henze G, Seeger K:
Expression of interleukin-10 splicing variants is a positive prognostic feature in relapsed childhood acute lymphoblastic leukemia.
J Clin Oncol
; 2005 May 1;23(13):3038-42
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[Title]
Expression of interleukin-10 splicing variants is a positive prognostic feature in relapsed childhood
acute lymphoblastic leukemia
.
This study aimed to determine the expression of a splicing-derived variant of interleukin (IL) -10 in leukemic cells and its clinical relevance in children with
acute lymphoblastic leukemia
(ALL) at first relapse.
PATIENTS AND METHODS: Between January 1997 and December 2001, bone marrow (BM) samples were collected from 98 children with first relapse of ALL at
diagnosis
.
CONCLUSION: These results indicate that splicing-derived IL-10 isoforms may modulate IL-10-mediated biologic effects and therapeutic efficacy in lymphatic
disease
, and expression of IL-10delta3 is a positive prognostic feature in relapsed childhood ALL.
[MeSH-major]
Gene Expression Profiling. Genetic Variation. Interleukin-10 / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology
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(PMID = 15860861.001).
[ISSN]
0732-183X
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
130068-27-8 / Interleukin-10
33.
Zweier-Renn LA, Hawley TS, Burkett S, Ramezani A, Riz I, Adler RL, Hickstein DD, Hawley RG:
Hematopoietic immortalizing function of the NKL-subclass homeobox gene TLX1.
Genes Chromosomes Cancer
; 2010 Feb;49(2):119-31
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Translocations resulting in ectopic expression of the TLX1 homeobox gene (previously known as HOX11) are recurrent events in human T-
cell acute lymphoblastic leukemia
(T-ALL).
Transduction of primary murine hematopoietic stem/progenitor cells with retroviral vectors expressing TLX1 readily yields immortalized hematopoietic progenitor
cell
lines.
Additionally, the generation of murine hematopoietic progenitor
cell
lines due to retroviral integrations into Evi1 or Prdm16 has also been recently reported.
Here, we determined by linker-mediated nested polymerase chain reaction the integration sites in eight TLX1-immortalized hematopoietic
cell
lines.
Notably, no common integration site was observed among the
cell
lines.
However, neither Lmo2 nor any of the other genes examined surrounding the integration sites showed differential vector-influenced expression compared to the
cell
lines lacking such insertions.
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(PMID = 19862821.001).
[ISSN]
1098-2264
[Journal-full-title]
Genes, chromosomes & cancer
[ISO-abbreviation]
Genes Chromosomes Cancer
[Language]
ENG
[Grant]
United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01 HL065519-08; United States / NHLBI NIH HHS / HL / R01 HL066305-05; United States / NHLBI NIH HHS / HL / HL065519-08; United States / NHLBI NIH HHS / HL / R01 HL065519; United States / Intramural NIH HHS / / ; United States / NHLBI NIH HHS / HL / R01 HL066305; United States / NHLBI NIH HHS / HL / HL066305-05; United States / NHLBI NIH HHS / HL / R01HL66305
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 143275-75-6 / TLX1 protein, human
[Other-IDs]
NLM/ NIHMS155591; NLM/ PMC2795049
34.
Trentin L, Giordan M, Dingermann T, Basso G, Te Kronnie G, Marschalek R:
Two independent gene signatures in pediatric t(4;11) acute lymphoblastic leukemia patients.
Eur J Haematol
; 2009 Nov;83(5):406-19
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[Title]
Two independent gene signatures in pediatric t(4;11)
acute lymphoblastic leukemia
patients.
METHOD: In our study we sought to overcome these limitations and for proof of principle, we analyzed the rare t(4;11)
leukemia
disease
entity.
First, gene expression data of each t(4;11)
leukemia
patient were normalized by pairwise subtraction against normal bone marrow (n = 3) to identify significantly deregulated gene sets for each patient.
RESULT: A 'core signature' of 186 commonly deregulated genes present in each investigated t(4;11)
leukemia
patient was defined.
Linking the obtained gene sets to four biological discriminators (HOXA gene expression, age at
diagnosis
, fusion gene transcripts and chromosomal breakpoints) divided patients into two distinct subgroups: the first one comprised infant patients with low HOXA genes expression and the MLL breakpoints within introns 11/12.
CONCLUSION: A yet homogeneous
leukemia
entity was further subdivided, based on distinct genetic properties.
This approach provided a simplified way to obtain robust and
disease
-specific gene signatures even in smaller cohorts.
[MeSH-major]
Chromosomes, Human, Pair 11 / metabolism. Chromosomes, Human, Pair 4 / metabolism. Gene Expression Regulation, Leukemic. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Translocation, Genetic
[MeSH-minor]
Female. Gene Expression Profiling / methods. Histone-Lysine N-Methyltransferase. Homeodomain Proteins / biosynthesis. Homeodomain Proteins / genetics. Humans. Male.
Myeloid
-
Lymphoid
Leukemia
Protein / biosynthesis.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Oligonucleotide Array Sequence Analysis / methods. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics
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(PMID = 19558506.001).
[ISSN]
1600-0609
[Journal-full-title]
European journal of haematology
[ISO-abbreviation]
Eur. J. Haematol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 157907-48-7 / HoxA protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
35.
Wang Z, Hu T, Cao LZ, Kang R, Zhao MY, Yu Y, Xu WQ:
[Expression of WAVE1 in childhood acute lymphocytic leukemia and in the apoptosis of Jurkat cells induced by adriamycin].
Zhongguo Dang Dai Er Ke Za Zhi
; 2008 Oct;10(5):620-4
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[Title]
[Expression of WAVE1 in childhood
acute
lymphocytic
leukemia and
in the apoptosis of Jurkat cells induced by adriamycin].
OBJECTIVE: To investigate whether WASP/Verprolin homologous protein 1 (WAVE1) plays a role in the pathogenesis of childhood
acute lymphoblastic leukemia
(ALL).
The
cell
proliferation was detected with MTT.
[MeSH-major]
Antibiotics, Antineoplastic / pharmacology. Apoptosis / drug effects. Doxorubicin / pharmacology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / metabolism. Wiskott-Aldrich Syndrome Protein Family / physiology
[MeSH-minor]
Adolescent. Blotting, Western.
Cell
Proliferation / drug effects. Child. Child, Preschool. Female. Humans. Infant. Jurkat Cells. Male. RNA, Messenger / analysis
Hazardous Substances Data Bank.
DOXORUBICIN
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 18947485.001).
[ISSN]
1008-8830
[Journal-full-title]
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
[ISO-abbreviation]
Zhongguo Dang Dai Er Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; 0 / RNA, Messenger; 0 / WASF1 protein, human; 0 / Wiskott-Aldrich Syndrome Protein Family; 80168379AG / Doxorubicin
36.
Jelinek J, Oki Y, Gharibyan V, Bueso-Ramos C, Prchal JT, Verstovsek S, Beran M, Estey E, Kantarjian HM, Issa JP:
JAK2 mutation 1849G>T is rare in acute leukemias but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic leukemia.
Blood
; 2005 Nov 15;106(10):3370-3
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[Title]
JAK2 mutation 1849G>T is rare in
acute
leukemias
but can be found in CMML, Philadelphia chromosome-negative CML, and megakaryocytic
leukemia
.
The mutation was frequent in polycythemia vera (PV) (86%) and myelofibrosis (95%) but less prevalent in
acute
myeloid
leukemia
(AML) with an antecedent PV or myelofibrosis (5 [36%] of 14 patients).
JAK2 mutation was also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic myelogenous
leukemia
(CML), 2 (18%) of 11 patients with megakaryocytic AML, 7 (13%) of 52 patients with chronic myelomonocytic
leukemia
, and 1 (1%) of 68 patients with myelodysplastic syndromes.
No mutation was found in Ph(+)CML (99 patients), AML M0-M6 (28 patients), or
acute lymphoblastic leukemia
(20 patients).
We conclude that the JAK2 1849G>T mutation is common in Ph(-) MPD but not critical for transformation to the
acute
phase of these diseases and that it is generally rare in aggressive
leukemias
.
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Blood. 2002 Feb 1;99(3):840-9
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(PMID = 16037387.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P50CA100632
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
[Other-IDs]
NLM/ PMC1895065
37.
Rezvani K, Yong AS, Savani BN, Mielke S, Keyvanfar K, Gostick E, Price DA, Douek DC, Barrett AJ:
Graft-versus-leukemia effects associated with detectable Wilms tumor-1 specific T lymphocytes after allogeneic stem-cell transplantation for acute lymphoblastic leukemia.
Blood
; 2007 Sep 15;110(6):1924-32
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[Title]
Graft-versus-
leukemia
effects associated with detectable Wilms tumor-1 specific T lymphocytes after allogeneic stem-
cell
transplantation for
acute lymphoblastic leukemia
.
To determine whether the
leukemia
-associated Wilms tumor antigen (WT1) contributes to a graft-versus-
leukemia
(GVL) effect after allogeneic stem-
cell
transplantation (SCT) for
acute lymphoblastic leukemia
(ALL), we studied CD8(+) T-
cell
responses to WT1 in 10 human lymphocyte antigen (HLA)-A*0201-positive ALL patients during the early phase of immune recovery after SCT (days 30-120).
Using WT1/HLA-A*0201 tetramers and intracellular interferon-gamma (IFN-gamma) staining, WT1(+) CD8(+) T-
cell
responses after SCT were found only in patients with detectable WT1 expression before SCT (5 of 7 vs. 0 of 3; P < .05).
To monitor the kinetics of WT1(+) CD8(+) T-
cell
responses and
disease
regression after SCT, absolute WT1(+) CD8(+) T-
cell
numbers and WT1 expression were studied for each time point.
Loss of WT1(+) CD8(+) T-
cell
responses was associated with reappearance of WT1 transcripts, consistent with a molecular relapse (P < .001).
[MeSH-major]
Burkitt Lymphoma / therapy. Graft vs
Leukemia
Effect. Immunologic Memory. Stem
Cell
Transplantation. T-Lymphocytes / metabolism. WT1 Proteins / metabolism
[MeSH-minor]
Adolescent. Adult. CD8-Positive T-Lymphocytes. Child. Cytomegalovirus / pathogenicity. Cytomegalovirus Infections / immunology. Cytomegalovirus Infections / therapy. Cytomegalovirus Infections / virology. Female. Graft vs Host
Disease
. HLA-A Antigens / metabolism. HLA-A2 Antigen. Humans. Male. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tissue Donors. Transplantation, Homologous
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[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Grant]
United Kingdom / Medical Research Council / / G0501963
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / WT1 Proteins
[Other-IDs]
NLM/ PMC1976363
38.
Winter SS, Jiang Z, Khawaja HM, Griffin T, Devidas M, Asselin BL, Larson RS, Children's Oncology Group:
Identification of genomic classifiers that distinguish induction failure in T-lineage acute lymphoblastic leukemia: a report from the Children's Oncology Group.
Blood
; 2007 Sep 1;110(5):1429-38
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[Title]
Identification of genomic classifiers that distinguish induction failure in T-
lineage
acute lymphoblastic leukemia
: a report from the Children's Oncology Group.
The clinical and cytogenetic features associated with T-
cell acute lymphoblastic leukemia
(T-ALL) are not predictive of early treatment failure.
Seven genes were similarly upregulated in both the genomic classifier for IF patients
and T
-ALL
cell
lines having acquired resistance to neoplastic agents, identifying potential target genes for further study in drug resistance.
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[ErratumIn]
Blood. 2008 May 1;111(9):4830
(PMID = 17495134.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U10 CA29139; United States / NCI NIH HHS / CA / R21 CA098251; United States / NCI NIH HHS / CA / U10 CA98543-03-14305; United States / NCI NIH HHS / CA / R01 CA114589; United States / NCI NIH HHS / CA / U10 CA029139; United States / NCI NIH HHS / CA / U10 CA098543; United States / NCI NIH HHS / CA / R01 CA114589-01; United States / NCI NIH HHS / CA / R21 CA098251-01
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Other-IDs]
NLM/ PMC1975833
39.
Pottier N, Yang W, Assem M, Panetta JC, Pei D, Paugh SW, Cheng C, Den Boer ML, Relling MV, Pieters R, Evans WE, Cheok MH:
The SWI/SNF chromatin-remodeling complex and glucocorticoid resistance in acute lymphoblastic leukemia.
J Natl Cancer Inst
; 2008 Dec 17;100(24):1792-803
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[Title]
The SWI/SNF chromatin-remodeling complex and glucocorticoid resistance in
acute lymphoblastic leukemia
.
BACKGROUND: Glucocorticoids are used in the curative treatment of
acute lymphoblastic leukemia
(ALL).
Prednisolone resistance was higher in SMARCA4 shRNA-transfected Jurkat cells (drug concentration lethal to 50% of the
leukemia
cells [LC(50)] = 277 microM) than in control shRNA-transfected cells (LC(50) = 174 microM, difference = 103 microM, 95% confidence interval of the difference = 100 to 106 microM; P < .001, t test).
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J Clin Endocrinol Metab. 2005 Jun;90(6):3505-9
[
15755863.001
]
(PMID = 19066270.001).
[ISSN]
1460-2105
[Journal-full-title]
Journal of the National Cancer Institute
[ISO-abbreviation]
J. Natl. Cancer Inst.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / R01 CA78224; United States / NCI NIH HHS / CA / R37 CA36401; United States / NIGMS NIH HHS / GM / U01 GM61393
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Chromosomal Proteins, Non-Histone; 0 / Glucocorticoids; 0 / Nuclear Proteins; 0 / SWI-SNF-B chromatin-remodeling complex; 0 / Transcription Factors; 9PHQ9Y1OLM / Prednisolone; EC 3.6.1.- / SMARCA4 protein, human; EC 3.6.4.- / DNA Helicases
[Other-IDs]
NLM/ PMC2639326
40.
Pluta A, Nyman U, Joseph B, Robak T, Zhivotovsky B, Smolewski P:
The role of p73 in hematological malignancies.
Leukemia
; 2006 May;20(5):757-66
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Thus, p73 is involved in the regulation of
cell
cycle,
cell
death and development.
Overexpression of p73 protein and aberrant expression of its particular isoforms, with very low frequency of P73 hypermethylation or mutations, were found in malignant myeloproliferations, including
acute
myeloblastic
leukemia
.
In contrast, hypermethylation and subsequent inactivation of the P73 gene are the most common findings in malignant lymphoproliferative disorders, especially
acute lymphoblastic leukemia
(ALL) and non-Hodgkin's lymphomas.
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(PMID = 16541141.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73
[Number-of-references]
99
41.
Damnjanovic T, Milicevic R, Novkovic T, Jovicic O, Bunjevacki V, Jekic B, Lukovic L, Novakovic I, Redzic D, Milasin J:
Association between the methylenetetrahydrofolate reductase polymorphisms and risk of acute lymphoblastic leukemia in Serbian children.
J Pediatr Hematol Oncol
; 2010 May;32(4):e148-50
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[Title]
Association between the methylenetetrahydrofolate reductase polymorphisms and risk of
acute lymphoblastic leukemia
in Serbian children.
We investigated a possible association of MTHFR polymorphisms (677C>
T and
1298A>C) and increased risk for
acute lymphoblastic leukemia
in 78 affected children.
A significant association between CT/TT individuals and reduced risk of
acute lymphoblastic leukemia
was found.
[MeSH-major]
Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Polymorphism, Genetic / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
[MeSH-minor]
Adolescent. Case-Control Studies. Child. Child, Preschool. Female. Genetic Predisposition to
Disease
. Genotype. Humans. Infant. Male. Prognosis. Risk Factors. Serbia
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(PMID = 20445408.001).
[ISSN]
1536-3678
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)
42.
Li X, Gounari F, Protopopov A, Khazaie K, von Boehmer H:
Oncogenesis of T-ALL and nonmalignant consequences of overexpressing intracellular NOTCH1.
J Exp Med
; 2008 Nov 24;205(12):2851-61
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Mutations resulting in overexpression of intracellular Notch1 (ICN1) are frequently observed in human
T cell acute lymphoblastic leukemia
(T-ALL).
Early consequences are the generation of polyclonal nontumorigenic CD4(+)8(+)
T cell
receptor (TCR)-alphabeta(+) cells that do not qualify as tumor precursors despite the observation that they overexpress Notch 1 and c-Myc and degrade the tumor suppressor E2A by posttranslational modification.
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J Exp Med. 2007 Aug 6;204(8):1825-35
[
17646408.001
]
(PMID = 18981238.001).
[ISSN]
1540-9538
[Journal-full-title]
The Journal of experimental medicine
[ISO-abbreviation]
J. Exp. Med.
[Language]
ENG
[Databank-accession-numbers]
GEO/ GSE12948
[Grant]
United States / NIAID NIH HHS / AI / R01 AI045846; United States / NCI NIH HHS / CA / P01 CA109901; United States / NCI NIH HHS / CA / T32 CA070083; United States / NCI NIH HHS / CA / T32-CA70083; United States / NIAID NIH HHS / AI / R01 AI45846; United States / NCI NIH HHS / CA / CA109901
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Tumor Suppressor Protein p53
[Other-IDs]
NLM/ PMC2585834
43.
Klingebiel T, Cornish J, Labopin M, Locatelli F, Darbyshire P, Handgretinger R, Balduzzi A, Owoc-Lempach J, Fagioli F, Or R, Peters C, Aversa F, Polge E, Dini G, Rocha V, Pediatric Diseases and Acute Leukemia Working Parties of the European Group for Blood and Marrow Transplantation (EBMT):
Results and factors influencing outcome after fully haploidentical hematopoietic stem cell transplantation in children with very high-risk acute lymphoblastic leukemia: impact of center size: an analysis on behalf of the Acute Leukemia and Pediatric Disease Working Parties of the European Blood and Marrow Transplant group.
Blood
; 2010 Apr 29;115(17):3437-46
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[Title]
Results and factors influencing outcome after fully haploidentical hematopoietic stem
cell
transplantation in children with very high-risk
acute lymphoblastic leukemia
: impact of center size: an analysis on behalf of the
Acute Leukemia
and Pediatric
Disease
Working Parties of the European Blood and Marrow Transplant group.
T cell
-depleted haploidentical hematopoietic stem
cell
transplantation (haploHSCT) is an option to treat children with very high-risk
acute lymphoblastic leukemia
(ALL) lacking an HLA-identical donor.
The 5-year
leukemia
-free survival (LFS) was 30%, 34%, 22%, and 0%, respectively.
In a multivariate analysis, haploHSCT performed in larger centers (performing > or = 231 allotransplantations in the studied period) was associated with improved LFS rate and decreased RI (adjusted P = .01 and P = .04, respectively), adjusting for different patient-,
disease
-, and transplant-related factors such as number of previous autotransplantations, cytomegalovirus serology status, type of T-
cell
depletion, and use of total body irradiation and antithymocyte globulin.
In conclusion, higher CD34(+)
cell
dose and better patient selection may improve outcomes of children with ALL who undergo a haploHSCT.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation. Hospitals, Pediatric. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
[MeSH-minor]
Adolescent. Adult. Child. Child, Preschool.
Disease
-Free Survival. Europe. Female. Humans. Infant. Male. Remission Induction. Risk Factors. Survival Rate. Transplantation, Homologous
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[CommentIn]
Blood. 2010 Apr 29;115(17):3420-1
[
20430960.001
]
(PMID = 20040760.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article; Multicenter Study
[Publication-country]
United States
44.
Huang XJ, Liu DH, Liu KY, Xu LP, Chen H, Han W, Chen YH, Zhang XH, Lu DP:
Treatment of acute leukemia with unmanipulated HLA-mismatched/haploidentical blood and bone marrow transplantation.
Biol Blood Marrow Transplant
; 2009 Feb;15(2):257-65
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[Title]
Treatment of
acute leukemia
with unmanipulated HLA-mismatched/haploidentical blood and bone marrow transplantation.
Allogeneic hematopoietic stem
cell
transplantation (allo-HSCT) remains one of the best therapeutic options to cure
acute leukemia
(AL).
Recently, we developed a new method for HLA-mismatched/haploidentical transplantation without in vitro
T cell
depletion (TCD).
The incidence of grade 2-4
acute
graft-versus-host
disease
(aGVHD) was 45.8%, and that of grades 3 and 4 was 13.4%, which was not associated with the extent of HLA disparity.
One hundred forty-one of the 250 patients survived free of
disease
recurrence at a median of 1092 days (range: 442-2437 days) of follow-up.
Seventeen patients received DLI as a treatment for relapse after transplantation and 7 patients achieved
leukemia
-free survival (LFS).
The 3-year probability of LFS for
acute
myelogenous
leukemia
(AML) was 70.7% and 55.9%, and for
acute lymphoblastic leukemia
(ALL) it was 59.7% and 24.8% in standard-risk and high-risk groups, respectively.
Lower LFS were associated with
diagnosis
of
acute leukemia
in the high-risk group (P= .001, relative risk [RR], 95% confidence interval [CI]: 2.94[1.535-5.631]) and the occurrence of aGVHD of grades 3 and 4 (P= .004).
[MeSH-major]
Bone Marrow Transplantation / methods. HLA Antigens / immunology. Haplotypes / immunology. Histocompatibility / immunology.
Leukemia
/ therapy. Peripheral Blood Stem
Cell
Transplantation / methods
[MeSH-minor]
Acute
Disease
. Adolescent. Adult. Child. Child, Preschool.
Disease
-Free Survival. Female. Graft vs Host
Disease
/ immunology. HLA-A Antigens. HLA-B Antigens. HLA-DR Antigens. Humans.
Leukemia
,
Myeloid
,
Acute
/ mortality.
Leukemia
,
Myeloid
,
Acute
/ therapy. Male. Middle Aged. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / mortality. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy. Transplantation, Homologous / immunology. Treatment Outcome. Young Adult
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(PMID = 19167686.001).
[ISSN]
1523-6536
[Journal-full-title]
Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
[ISO-abbreviation]
Biol. Blood Marrow Transplant.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / HLA Antigens; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / HLA-DR Antigens
45.
Fischer G S, Neira L L, Ferreiro M M, Torres C MT, Giadrosich R V, Milinarsky T A, Arriagada M M, Arinoviche S R:
[Bone mineral density in leukemic children after completing one month of chemotherapy].
Rev Med Chil
; 2005 Jan;133(1):71-6
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[Transliterated title]
Densitometría ósea
en
niños leucémicos al completar el primer mes
de
quimioterapia.
BACKGROUND: An important loss of bone mineral density, associated to pain and fractures, has been reported in children with
acute lymphoblastic leukemia
(ALL).
AIM: To measure bone mineral density among children with
acute lymphoblastic leukemia
(ALL) that completed the remission induction phase with chemotherapy, that lasts 30 days.
[MeSH-major]
Bone Density. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy
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(PMID = 15768152.001).
[ISSN]
0034-9887
[Journal-full-title]
Revista médica de Chile
[ISO-abbreviation]
Rev Med Chil
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Chile
46.
Ozbek U, Kandilci A, van Baal S, Bonten J, Boyd K, Franken P, Fodde R, Grosveld GC:
SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice.
Am J Pathol
; 2007 Aug;171(2):654-66
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[Title]
SET-CAN, the product of the t(9;9) in
acute
undifferentiated
leukemia
, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic mice.
Leukemia
-specific chromosome translocations involving the nucleoporin CAN/NUP214 lead to expression of different fusion genes including DEK-CAN, CAN-ABL, and SET-CAN.
DEK-CAN and CAN-ABL1 are associated with
acute
myeloid
leukemia and
T-
cell acute lymphoblastic leukemia
, respectively, whereas SET-CAN was identified in a patient with
acute
undifferentiated
leukemia
.
Although SET-CAN mice showed expansion of an early progenitor
cell
pool and partial depletion of lymphocytes, the animals were not
leukemia
-prone and did not show shortening of
disease
latency after retroviral tagging.
This suggests that SET-CAN expression in
acute
undifferentiated
leukemia
might determine the primitive phenotype of the
disease
, whereas secondary genetic lesions are necessary for
disease
development.
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gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
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.
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.
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Marmoset Gene list: Data: Gene Annotation
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Blood. 1976 May;47(5):705-21
[
1260131.001
]
(PMID = 17569777.001).
[ISSN]
0002-9440
[Journal-full-title]
The American journal of pathology
[ISO-abbreviation]
Am. J. Pathol.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-76480
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Chromosomal Proteins, Non-Histone; 0 / Ki-67 Antigen; 0 / Nuclear Pore Complex Proteins; 0 / Nup214 protein, mouse; 0 / Oncogene Proteins, Fusion
[Other-IDs]
NLM/ PMC1934515
47.
Xu T, Gu J, Zhou Y, Du L:
Improving detection of differentially expressed gene sets by applying cluster enrichment analysis to Gene Ontology.
BMC Bioinformatics
; 2009;10:240
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When used with two
acute leukemia
(ALL and ALL/AML) microarray expression datasets, CeaGO correctly identified specifically enriched GO groups that were overlooked by other individual test methods.
CeaGO is currently available at http://chgc.sh.cn/
en
/software/CeaGO/.
[MeSH-minor]
Cell
Cycle. Cluster Analysis.
Leukemia
,
Myeloid
,
Acute
/ genetics. Phenotype. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
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[Cites]
Cancer Cell. 2004 Mar;5(3):275-85
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BMC Bioinformatics. 2004 Mar 29;5:34
[
15050037.001
]
(PMID = 19653916.001).
[ISSN]
1471-2105
[Journal-full-title]
BMC bioinformatics
[ISO-abbreviation]
BMC Bioinformatics
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Other-IDs]
NLM/ PMC2731756
48.
Cauwelier B, Cavé H, Gervais C, Lessard M, Barin C, Perot C, Van den Akker J, Mugneret F, Charrin C, Pagès MP, Grégoire MJ, Jonveaux P, Lafage-Pochitaloff M, Mozzicconacci MJ, Terré C, Luquet I, Cornillet-Lefebvre P, Laurence B, Plessis G, Lefebvre C, Leroux D, Antoine-Poirel H, Graux C, Mauvieux L, Heimann P, Chalas C, Clappier E, Verhasselt B, Benoit Y, Moerloose BD, Poppe B, Van Roy N, Keersmaecker KD, Cools J, Sigaux F, Soulier J, Hagemeijer A, Paepe AD, Dastugue N, Berger R, Speleman F:
Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone de Cytogénétique Hématologique.
Leukemia
; 2007 Jan;21(1):121-8
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[Title]
Clinical, cytogenetic and molecular characteristics of 14 T-ALL patients carrying the TCRbeta-HOXA rearrangement: a study of the Groupe Francophone
de
Cytogénétique Hématologique.
Recently, we and others described a new chromosomal rearrangement, that is, inv(7)(p15q34)
and t
(7;7)(p15;q34) involving the T-
cell
receptor beta (TCRbeta) (7q34) and the HOXA gene locus (7p15) in 5% of T-
cell acute lymphoblastic leukemia
(T-ALL) patients leading to transcriptional activation of especially HOXA10.
[MeSH-major]
Homeodomain Proteins / genetics.
Leukemia
-Lymphoma, Adult T-
Cell
/ genetics. Receptors, Antigen, T-
Cell
, alpha-beta / genetics
COS Scholar Universe.
author profiles
.
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(PMID = 17039236.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Receptors, Antigen, T-Cell, alpha-beta; 140441-81-2 / HOXA10 protein, human
49.
Mandal C, Srinivasan GV, Chowdhury S, Chandra S, Mandal C, Schauer R, Mandal C:
High level of sialate-O-acetyltransferase activity in lymphoblasts of childhood acute lymphoblastic leukaemia (ALL): enzyme characterization and correlation with disease status.
Glycoconj J
; 2009 Jan;26(1):57-73
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[Title]
High level of sialate-O-acetyltransferase activity in lymphoblasts of childhood
acute lymphoblastic
leukaemia
(ALL): enzyme characterization and correlation with
disease
status.
Previous studies had established an over-expression of 9-O-acetylated sialoglycoproteins (Neu5,9Ac(2)-GPs) on lymphoblasts of childhood
acute lymphoblastic
leukaemia
(ALL).
Here, we report the discovery and characterization of sialate-O-acetyltransferase enzyme in ALL-
cell
lines and lymphoblasts from bone marrow of children diagnosed with B-
and T
-ALL.
Sialate-O-acetyltransferase activity in
cell
lysates or microsomal fractions of lymphoblasts of patients was always higher than that in healthy donors reaching up to 22-fold in microsomes.
Sialate-O-acetyltransferase activity increased at the
diagnosis
of
leukaemia
, decreased with clinical remission and sharply increased again in relapsed patients as determined by radiometric-assay.
[MeSH-major]
Acetyltransferases / metabolism. Bone Marrow / enzymology. Microsomes / enzymology. Neoplasm Proteins / metabolism. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / enzymology. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / enzymology
[MeSH-minor]
Acetyl Coenzyme A / metabolism. Adolescent.
Cell
Line, Tumor. Child. Child, Preschool. Cytidine Monophosphate / metabolism. Humans. Infant. Male. N-Acetylneuraminic Acid / metabolism
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(PMID = 18677580.001).
[ISSN]
1573-4986
[Journal-full-title]
Glycoconjugate journal
[ISO-abbreviation]
Glycoconj. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Neoplasm Proteins; 72-89-9 / Acetyl Coenzyme A; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.- / N-acylneuraminate-9(7)-O-acetyltransferase; F469818O25 / Cytidine Monophosphate; GZP2782OP0 / N-Acetylneuraminic Acid
50.
Nakazawa H, Ito T, Makishima H, Misawa N, Okiyama W, Uehara T, Hidaka E, Kiyosawa K, Ishida F:
Adenovirus fulminant hepatic failure: disseminated adenovirus disease after unrelated allogeneic stem cell transplantation for acute lymphoblastic leukemia.
Intern Med
; 2006;45(16):975-80
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[Title]
Adenovirus fulminant hepatic failure: disseminated adenovirus
disease
after unrelated allogeneic stem
cell
transplantation for
acute lymphoblastic leukemia
.
Adenovirus is one of the major causes of non-relapse morbidity and mortality after allogeneic hematopoietic stem
cell
transplantation for hematological malignancy.
Extremely high mortality and aggressiveness of the clinical course have been posing clinical challenges for the
diagnosis
as well as for the treatment.
Here, we report a case with disseminated adenovirus
disease
presenting with fulminant hepatic failure after bone marrow transplantation for
acute lymphoblastic leukemia
.
[MeSH-major]
Adenoviridae Infections / complications. Adenoviridae Infections / etiology. Hematopoietic Stem
Cell
Transplantation / adverse effects. Liver Failure,
Acute
/ virology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / surgery. Stem
Cell
Transplantation / adverse effects
Genetic Alliance.
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.
Genetic Alliance.
consumer health - Transplantation
.
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(PMID = 16974062.001).
[ISSN]
1349-7235
[Journal-full-title]
Internal medicine (Tokyo, Japan)
[ISO-abbreviation]
Intern. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Japan
[Number-of-references]
47
51.
Szczepanek J, Pogorzala M, Konatkowska B, Juraszewska E, Badowska W, Olejnik I, Kuzmicz M, Stanczak E, Malinowska I, Stefaniak J, Sobol G, Szczepanski T, Czyzewski K, Wysocki M, Styczynski J:
Differential ex vivo activity of bortezomib in newly diagnosed paediatric acute lymphoblastic and myeloblastic leukaemia.
Anticancer Res
; 2010 Jun;30(6):2119-24
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[Title]
Differential ex vivo activity of bortezomib in newly diagnosed paediatric
acute lymphoblastic
and myeloblastic
leukaemia
.
The objective of this study was the analysis of the ex vivo activity of bortezomib in paediatric
acute lymphoblastic
leukaemia
(ALL), in comparison to paediatric
acute
myeloid leukaemia
(AML).
A total of 159 patients entered the study, including 106 ALL (including 86 precursor-B-
cell
ALL, and 20 T-
cell
ALL) and 53 AML children.
With respect to immunophenotype, ex vivo drug resistance in T-
cell
ALL (T-ALL) was higher for most of the drugs.
No differences in drug resistance between T-ALL and common/pre-B-
cell
-ALL were found for daunorubicin, mitoxantrone and 6-thioguanine.
[MeSH-major]
Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use.
Leukemia
,
Myeloid
,
Acute
/ drug therapy. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Pyrazines / therapeutic use
MedlinePlus Health Information.
consumer health - Acute Myeloid Leukemia
.
MedlinePlus Health Information.
consumer health - Cancer Chemotherapy
.
Hazardous Substances Data Bank.
BORTEZOMIB
.
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(PMID = 20651360.001).
[ISSN]
1791-7530
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib
52.
Tirado CA, Meloni-Ehrig AM, Edwards T, Scheerle J, Burks K, Repetti C, Christacos NC, Kelly JC, Greenberg J, Murphy C, Croft CD, Heritage D, Mowrey PN:
Cryptic ins(4;11)(q21;q23q23) detected by fluorescence in situ hybridization: a variant of t(4;11)(q21;q23) in an infant with a precursor B-cell acute lymphoblastic leukemia report of a second case.
Cancer Genet Cytogenet
; 2007 Apr 15;174(2):166-9
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[Title]
Cryptic ins(4;11)(q21;q23q23) detected by fluorescence in situ hybridization: a variant of t(4;11)(q21;q23) in an infant with a precursor B-
cell acute lymphoblastic leukemia
report of a second case.
We report the chromosomal findings in a 4-year-old female with precursor B-
cell acute lymphoblastic leukemia
(ALL).
Our case exemplifies the importance of FISH in the further characterization of precursor B-
cell
ALL cases without any apparent prognostically significant chromosomal abnormalities.
[MeSH-major]
Burkitt Lymphoma / genetics. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 4. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Translocation, Genetic
[MeSH-minor]
Child, Preschool. Chromosome Banding. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Mutagenesis, Insertional.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics
Genetic Alliance.
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.
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(PMID = 17452260.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
53.
Panagopoulos I, Lilljebjörn H, Strömbeck B, Hjorth L, Olofsson T, Johansson B:
MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-cell acute lymphoblastic leukemia.
Haematologica
; 2006 Sep;91(9):1287-8
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[Title]
MLL/GAS7 fusion in a pediatric case of t(11;17)(q23;p13)-positive precursor B-
cell acute lymphoblastic leukemia
.
MLL/GAS7, resulting from t(11;17)(q23;p13), has been reported in one case of treatment-related
acute
myeloid
leukemia
(AML).
We present
a de
novo case of t(11;17)-positive pediatric
acute lymphoblastic leukemia
.
[MeSH-major]
Oncogene Proteins, Fusion / genetics. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Translocation, Genetic
[MeSH-minor]
Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 17. Female. Humans. Infant.
Myeloid
-
Lymphoid
Leukemia
Protein / genetics. Nerve Tissue Proteins / genetics
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
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(PMID = 16956839.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
Italy
[Chemical-registry-number]
0 / GAS7 protein, human; 0 / MLL-GAS7 fusion protein; 0 / Nerve Tissue Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein
54.
Fujiwara S, Yamashita Y, Choi YL, Watanabe H, Kurashina K, Soda M, Enomoto M, Hatanaka H, Takada S, Ozawa K, Mano H:
Transforming activity of purinergic receptor P2Y, G protein coupled, 8 revealed by retroviral expression screening.
Leuk Lymphoma
; 2007 May;48(5):978-86
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Biphenotypic
acute leukemia
(BAL) is a relatively rare subtype of
acute leukemia
characterized by the presence of both
myeloid
and
lymphoid
cell
surface antigens.
Quantitation of P2RY8 mRNA in CD34(+) cells of bone marrow showed that P2RY8 expression is frequently increased in
leukemia
patients, especially in those with refractory
disease
.
Our data thus reveal an abundant expression of P2RY8 in leukemic cells and its unexpected role in the pathogenesis of
acute leukemia
.
[MeSH-major]
Gene Expression Regulation, Leukemic.
Leukemia
/ genetics.
Leukemia
/ metabolism. Receptors, Purinergic / physiology. Receptors, Purinergic P2 / metabolism. Receptors, Purinergic P2Y / metabolism. Receptors, Purinergic P2Y / physiology. Retroviridae / metabolism
[MeSH-minor]
3T3 Cells. Animals. Antigens, CD34 / biosynthesis. Bone Marrow Cells / metabolism.
Cell
Line, Tumor. DNA, Complementary / genetics. Gene Library. Humans. Mice. Mice, Nude. Transcription, Genetic
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.
Guide to Pharmacology.
gene/protein/disease-specific - P2RY8 - data and references
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 17487742.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, CD34; 0 / DNA, Complementary; 0 / P2RY8 protein, human; 0 / P2RY9 receptor, human; 0 / P2RY9 receptor, mouse; 0 / Receptors, Purinergic; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2Y
55.
Tragiannidis A, Athanassiadou F, Papageorgiou T, Petsatodis G:
Severe skeletal complications in a child with acute lymphoblastic leukemia.
Pediatr Hematol Oncol
; 2006 Sep;23(6):523-5; author reply 527-8
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[Title]
Severe skeletal complications in a child with
acute lymphoblastic leukemia
.
[MeSH-major]
Osteoporosis / chemically induced. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / complications
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.
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consumer health - Osteoporosis
.
Hazardous Substances Data Bank.
Alendronic acid
.
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[CommentOn]
Pediatr Hematol Oncol. 2005 Oct-Nov;22(7):543-50
[
16166046.001
]
(PMID = 16849284.001).
[ISSN]
1521-0669
[Journal-full-title]
Pediatric hematology and oncology
[ISO-abbreviation]
Pediatr Hematol Oncol
[Language]
eng
[Publication-type]
Case Reports; Comment; Letter
[Publication-country]
England
[Chemical-registry-number]
X1J18R4W8P / Alendronate
56.
Liu Z, Liu XL, Du QF, Xu N, Zhong M, Song LL, Yi ZS, Liu QF, Meng FY, Zhou SY:
[Clinical characteristics and outcomes of 59 patients with acute lymphoblastic leukemia positive for BCR/ABL].
Nan Fang Yi Ke Da Xue Xue Bao
; 2009 Mar;29(3):512-5
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[Title]
[Clinical characteristics and outcomes of 59 patients with
acute lymphoblastic leukemia
positive for BCR/ABL].
OBJECTIVE: To study the clinical characteristics and outcomes of BCR/ABL-positive
acute lymphoblastic leukemia
(BCR/ABL360888725-ALL) and screen the prognostic factors for BCR/ABL360888725-ALL.
METHODS: From January 2001 to May 2008, 59 patients (median age of 32 years ranging from 3 to 69 years) with the
diagnosis
of BCR/ABL360888725-ALL by fluorescence in situ hybridization received induction chemotherapy with VDLP-/+Ara-C regimen.
The patients who failed to respond to the chemotherapy received subsequent consolidation chemotherapy with imatinib (400-800 mg/day) (17 cases) or allogeneic hematopoietic stem
cell
transplantation (allo-HSCT) (16 cases).
In patients with peripheral white blood
cell
(WBC) count <30=10(9)/L, 30-99.9(9)/L and > or =100(9)/L, the CR rates were 75.0% (18/24), 56.3% (9/15) and 26.3% (5/19) (P=0.006), and the overall survival probability of 2 years ( OSs of 2-yrs) was 24.7%, 22.5% and 21.1%, respectively (P=0.180).
According to the FAB classification, 56 cases were divided into L1, L2 and
biphenotypic
acute leukemia
(BAL) subgroups, and their CR rates were 66.7% (6/9), 63.2% (24/38) and 22.2% (2/9) (P=0.029), with OSs of 2-yrs of 22.2%, 27.0% and 22.0%, respectively (P=0.623).
In terms of immunophenotype grouping by EGIL, the patients with ALL,
myeloid
antigen-positive ALL and BAL had CR rates of 61.1% (11/18), 60.6% (20/33) and 12.5% (1/8) (P=0.039), and the OSs of 2-yrs of 22.7%, 21.0% and 18.8%, respectively (P=0.643).
In 55 patients with known karyotype, the CR rates were 71.4%(5/7), 70.8% (17/24) and 37.5% (9/24) in normal, sole t(9;22)
abnormality
, t(9;22) with additional abnormalities groups (P=0.046), with the OSs of 2-yrs of 42.9%, 34.0% and 7.3%, respectively (P=0.000).
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Genes, abl / genetics. Hematopoietic Stem
Cell
Transplantation. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
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.
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IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 19304540.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
57.
Papaemmanuil E, Hosking FJ, Vijayakrishnan J, Price A, Olver B, Sheridan E, Kinsey SE, Lightfoot T, Roman E, Irving JA, Allan JM, Tomlinson IP, Taylor M, Greaves M, Houlston RS:
Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood acute lymphoblastic leukemia.
Nat Genet
; 2009 Sep;41(9):1006-10
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[Title]
Loci on 7p12.2, 10q21.2 and 14q11.2 are associated with risk of childhood
acute lymphoblastic leukemia
.
To identify risk variants for childhood
acute lymphoblastic leukemia
(ALL), we conducted a genome-wide association study of two case-control series, analyzing the genotypes with respect to 291,423 tagging SNPs in a total of 907 ALL cases and 2,398 controls.
The 10q21.2 (ARID5B) risk association appears to be selective for the subset of B-
cell
precursor ALL with hyperdiploidy.
These data show that common low-penetrance susceptibility alleles contribute to the risk of developing childhood ALL and provide new insight into
disease
causation of this specific hematological cancer.
Notably, all three risk variants map to genes involved in transcriptional regulation and differentiation of B-
cell
progenitors.
[MeSH-major]
Chromosomes, Human, Pair 10. Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 7. Genetic Predisposition to
Disease
. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / etiology
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consumer health - Acute Lymphoblastic Leukemia, Childhood
.
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[ISSN]
1546-1718
[Journal-full-title]
Nature genetics
[ISO-abbreviation]
Nat. Genet.
[Language]
eng
[Grant]
United Kingdom / Bloodwise / / 13027; United Kingdom / Medical Research Council / / G0000934; United Kingdom / Cancer Research UK / / C1298/A8362
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ARID5B protein, human; 0 / CCAAT-Enhancer-Binding Proteins; 0 / DNA-Binding Proteins; 0 / IKZF1 protein, human; 0 / Transcription Factors; 142805-41-2 / CEBPE protein, human; 148971-36-2 / Ikaros Transcription Factor
[Other-IDs]
NLM/ EMS27409; NLM/ PMC4915548
58.
Dong X, Xiong L, Jiang X, Wang Y:
Quantitative proteomic analysis reveals the perturbation of multiple cellular pathways in jurkat-T cells induced by doxorubicin.
J Proteome Res
; 2010 Nov 5;9(11):5943-51
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Doxorubicin remains an important part of chemotherapy regimens in the clinic and is considered an effective agent in the treatment of
acute lymphoblastic leukemia
(ALL).
Here we utilized mass spectrometry, together with stable isotope labeling by amino acids in
cell
culture (SILAC), to analyze comparatively the protein expression in Jurkat-T cells before and after treatment with a clinically relevant concentration of doxorubicin.
Hazardous Substances Data Bank.
DOXORUBICIN
.
Hazardous Substances Data Bank.
CHOLESTEROL
.
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[ISSN]
1535-3907
[Journal-full-title]
Journal of proteome research
[ISO-abbreviation]
J. Proteome Res.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA116522; United States / NCI NIH HHS / CA / R01 CA 116522
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
80168379AG / Doxorubicin; 97C5T2UQ7J / Cholesterol
[Other-IDs]
NLM/ NIHMS235911; NLM/ PMC2974774
59.
Bacher U, Schnittger S, Haferlach C, Haferlach T:
Molecular diagnostics in acute leukemias.
Clin Chem Lab Med
; 2009;47(11):1333-41
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[Title]
Molecular diagnostics in
acute
leukemias
.
Acute
myeloid
leukemia
(AML)
and acute lymphoblastic leukemia
(ALL) both represent highly heterogeneous entities on the basis of diverse cyto- and molecular genetic alterations with considerable influence on prognosis and therapeutic decisions.
Thus, molecular analysis based on various techniques, such as polymerase chain reaction (PCR) has become an essential part of the diagnostic panel for
acute leukemia
.
In addition, cytomorphology, cytogenetics, fluorescence in situ hybridization (FISH), and immunophenotyping with multiparameter flow cytometry (MFC) need to be applied for
diagnosis
.
During the course of
disease
, the residual leukemic
cell
load can be monitored by highly sensitive quantitative PCR techniques ("real-time PCR").
This demonstrates that molecular diagnostics for
acute
leukemias
are in continuous development.
This review summarizes the most important recurrent molecular markers seen in
acute
leukemias
, their role in prognosis and therapy and provides an overview on the relevant PCR techniques.
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.
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(PMID = 19817644.001).
[ISSN]
1437-4331
[Journal-full-title]
Clinical chemistry and laboratory medicine
[ISO-abbreviation]
Clin. Chem. Lab. Med.
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
78
60.
Baldazzi C, Iacobucci I, Luatti S, Ottaviani E, Marzocchi G, Paolini S, Stacchini M, Papayannidis C, Gamberini C, Martinelli G, Baccarani M, Testoni N:
B-cell acute lymphoblastic leukemia as evolution of a 8p11 myeloproliferative syndrome with t(8;22)(p11;q11) and BCR-FGFR1 fusion gene.
Leuk Res
; 2010 Oct;34(10):e282-5
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[Title]
B-
cell acute lymphoblastic leukemia
as evolution of a 8p11 myeloproliferative syndrome with t(8;22)(p11;q11) and BCR-FGFR1 fusion gene.
[MeSH-major]
Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 8. Gene Fusion. Myeloproliferative Disorders / genetics. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Proto-Oncogene Proteins c-bcr / genetics. Receptor, Fibroblast Growth Factor, Type 1 / genetics. Translocation, Genetic
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.
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(PMID = 20594995.001).
[ISSN]
1873-5835
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
EC 2.7.10.1 / FGFR1 protein, human; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; EC 2.7.11.1 / BCR protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-bcr
61.
Braun FK, Fecker LF, Schwarz C, Walden P, Assaf C, Dürkop H, Sterry W, Eberle J:
Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells.
J Invest Dermatol
; 2007 Oct;127(10):2425-37
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[Title]
Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-
cell
lymphoma cells.
In this study, cutaneous T-
cell
lymphoma (CTCL)
cell
lines revealed pronounced resistance to death ligands as compared to
cell
lines of T-
cell acute lymphoblastic leukemia
(T-ALL).
The proapoptotic activity of tumor necrosis factor (TNF)-alpha was blocked, sensitivity to TNF-related apoptosis-inducing ligand was significantly reduced, and 1/4 CTCL
cell
lines was resistant to CD95 activation.
No indication for a responsibility of typical downstream regulators of apoptosis was obtained, but loss of CD95 was found in 1/4, loss of TNF-R1 in 3/4, loss of caspase-10 in 2/4, loss of Bid in 1/4, and overexpression of cellular flice inhibitory protein was found in 4/4 CTCL
cell
lines.
[MeSH-major]
Apoptosis / physiology. Lymphoma, T-
Cell
, Cutaneous / pathology. Receptors, Death Domain / antagonists & inhibitors. Signal Transduction / physiology. Skin Neoplasms / pathology
[MeSH-minor]
Aged. Antigens, CD95 / physiology. BH3 Interacting Domain Death Agonist Protein / physiology. CASP8 and FADD-Like Apoptosis Regulating Protein / physiology. Caspase 10 / physiology.
Cell
Line, Tumor. Female. Humans.
Leukemia
-Lymphoma, Adult T-
Cell
/ pathology.
Leukemia
-Lymphoma, Adult T-
Cell
/ physiopathology. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology
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.
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.
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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
62.
Huang X, Chen S, Shen Q, Yang L, Li B, Zhong L, Geng S, Du X, Li Y:
Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-cell acute lymphoblastic leukemia.
J Hematol Oncol
; 2010;3(1):44
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[Title]
Analysis of the expression pattern of the BCL11B gene and its relatives in patients with T-
cell acute lymphoblastic leukemia
.
BACKGROUND: In a human T-
cell acute lymphoblastic leukemia
(T-ALL)
cell
line (Molt-4), siRNA-mediated suppression of BCL11B expression was shown to inhibit proliferation and induce apoptosis, functions which may be related to genes involved in apoptosis (such as TNFSF10 and BCL2L1) and TGF-β pathways (such as SPP1and CREBBP).
[MeSH-major]
CREB-Binding Protein / biosynthesis. Gene Expression Regulation, Neoplastic / genetics. Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Repressor Proteins / biosynthesis. Tumor Suppressor Proteins / biosynthesis. bcl-X Protein / biosynthesis
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[Cites]
Methods. 2001 Dec;25(4):402-8
[
11846609.001
]
[Cites]
Am J Physiol Renal Physiol. 2010 Jul;299(1):F234-42
[
20392802.001
]
[Cites]
Nat Immunol. 2003 Jun;4(6):525-32
[
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]
[Cites]
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]
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Leukemia. 1997 Dec;11(12):2087-96
[
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]
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[
9446631.001
]
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[
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]
[Cites]
FASEB J. 2004 Dec;18(15):1826-33
[
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]
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Leukemia. 2005 Feb;19(2):201-8
[
15668700.001
]
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Trends Cell Biol. 2006 Feb;16(2):79-87
[
16406521.001
]
[Cites]
Blood. 2006 Jun 1;107(11):4500-7
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]
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]
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]
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[
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]
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[
17173069.001
]
[Cites]
Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1087-97
[
17548669.001
]
[Cites]
Oncogene. 2007 Aug 30;26(40):5840-50
[
17369851.001
]
[Cites]
J Cell Physiol. 2008 Jan;214(1):192-200
[
17579344.001
]
[Cites]
BMC Cancer. 2007;7:195
[
17941976.001
]
[Cites]
J Immunotoxicol. 2008 Apr;5(2):235-48
[
18569395.001
]
[Cites]
Nat Rev Drug Discov. 2009 Feb;8(2):129-38
[
19180106.001
]
[Cites]
Adv Drug Deliv Rev. 2009 Aug 10;61(10):850-62
[
19422869.001
]
[Cites]
Nucleic Acids Res. 2002 May 1;30(9):e36
[
11972351.001
]
(PMID = 21080944.001).
[ISSN]
1756-8722
[Journal-full-title]
Journal of hematology & oncology
[ISO-abbreviation]
J Hematol Oncol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / BCL11B protein, human; 0 / BCL2L1 protein, human; 0 / CREBBP protein, human; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / bcl-X Protein; EC 2.3.1.48 / CREB-Binding Protein
[Other-IDs]
NLM/ PMC2992472
63.
Gumy-Pause F, Wacker P, Maillet P, Betts DR, Sappino AP:
ATM variants and predisposition to childhood T-lineage acute lymphoblastic leukaemia.
Leukemia
; 2006 Mar;20(3):526-7; author reply 527
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[Title]
ATM variants and predisposition to childhood T-
lineage
acute lymphoblastic
leukaemia
.
[MeSH-major]
Cell
Cycle Proteins / genetics. DNA-Binding Proteins / genetics. Genetic Predisposition to
Disease
.
Leukemia
-Lymphoma, Adult T-
Cell
/ genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Protein-Serine-Threonine Kinases / genetics. Tumor Suppressor Proteins / genetics
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[CommentOn]
Leukemia. 2005 Nov;19(11):1887-95
[
16167060.001
]
(PMID = 16408093.001).
[ISSN]
0887-6924
[Journal-full-title]
Leukemia
[ISO-abbreviation]
Leukemia
[Language]
eng
[Publication-type]
Comment; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
64.
Slavov SN, Gimenes Teixeira HL, Rego EM:
The role of micro-ribonucleic acids in normal hematopoiesis and leukemic T-lymphogenesis.
Braz J Med Biol Res
; 2010 Jul;43(7):619-26
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Although many data are available about the role of microRNAs in various lymphoproliferative disorders, their impact on the development of
acute lymphoblastic leukemia
of T-
cell
progenitors is largely unknown.
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.
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(PMID = 20549139.001).
[ISSN]
1414-431X
[Journal-full-title]
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
[ISO-abbreviation]
Braz. J. Med. Biol. Res.
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
Brazil
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / MicroRNAs; 0 / RNA, Neoplasm
65.
Amakawa R, Hiramoto N, Kawano S, Hyo A, Nakamichi N, Tajima K, Ito T, Mori S, Kishimoto Y, Fukuhara S:
Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.
J Clin Exp Hematop
; 2010;50(1):51-8
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[Title]
Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with
de
novo
mixed
-
lineage
leukemia
.
We report a case of
acute
mixed
-
lineage
leukemia
, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.
The
diagnosis
was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-
lineage
antigens and
myeloid
antigens accompanied by clonal rearrangements of IgH gene.
Add (11q23)
abnormality
was found in sideline karyotypes as well as the stemline
abnormality
of dic(17;20) (p11;q11).
[MeSH-major]
Gene Amplification.
Leukemia
,
Biphenotypic
,
Acute
/ genetics. Translocation, Genetic
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(PMID = 20505276.001).
[ISSN]
1880-9952
[Journal-full-title]
Journal of clinical and experimental hematopathology : JCEH
[ISO-abbreviation]
J Clin Exp Hematop
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
66.
Tie LJ, Gu LJ, Jiang LM, Zhao JC, Chen J, Pan C, Dong L, Chen J, Xue HL, Tang JY, Wang YP:
[Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual disease in childhood acute lymphoblastic leukemia].
Zhongguo Dang Dai Er Ke Za Zhi
; 2009 Apr;11(4):246-50
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[Title]
[Tandem application of flow cytometry and polymerase chain reaction for choice targets of minimal residual
disease
in childhood
acute lymphoblastic leukemia
].
OBJECTIVE: Minimal residual
disease
(MRD) is one of the most important prognostic factors in childhood
acute lymphoblastic leukemia
(ALL).
Using sets of combined antibodies, immunophenotypic expression of
leukemia
cells was observed in 95 of 106 B-
lineage
ALL cases (89.6%).
Only one aberrant immunophenotype was observed in 11 cases (11.6%) and most patients with B-
lineage
ALL (88.4%) expressed at least two suitable targets.
2. Using PCR technique, T-
cell
receptor (TCR) or immunoglobulin gene rearrangements were identified in 26 of 27 patients (96.3%).
The majority (70%) of T-
lineage
ALL cases contained TCRVgammaI-Jgamma1.3/2.3.
Cross-
lineage
TCR rearrangements were found in 57.1% of cases with B-
lineage
ALL.
Cross-
lineage
TCR rearrangements and bi-allelic gene rearrangements were observed in many patients.
[MeSH-major]
Flow Cytometry / methods. Polymerase Chain Reaction / methods. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / immunology
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.
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(PMID = 19374803.001).
[ISSN]
1008-8830
[Journal-full-title]
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
[ISO-abbreviation]
Zhongguo Dang Dai Er Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
67.
Osugi Y, Yamada H, Hosoi G, Noma H, Ikemiya M, Ishii T, Sako M:
Treatment with candesartan combined with angiotensin-converting enzyme inhibitor for immunosuppressive treatment-resistant nephrotic syndrome after allogeneic stem cell transplantation.
Int J Hematol
; 2006 Jun;83(5):454-8
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[Title]
Treatment with candesartan combined with angiotensin-converting enzyme inhibitor for immunosuppressive treatment-resistant nephrotic syndrome after allogeneic stem
cell
transplantation.
Most cases of nephrotic syndrome following stem
cell
transplantation (SCT) occur 6 months after SCT.
A 15-year-old boy with
acute lymphoblastic leukemia
underwent allogeneic peripheral blood SCT from a completely HLA-matched sibling after completion of a conditioning regimen composed of 12-Gy doses of total-body irradiation, 600 mg/m2 thiotepa, and 140 mg/m2 melphalan.
[MeSH-major]
Angiotensin-Converting Enzyme Inhibitors / administration & dosage. Antihypertensive Agents / administration & dosage. Benzimidazoles / administration & dosage. Nephrotic Syndrome / drug therapy. Stem
Cell
Transplantation. Tetrazoles / administration & dosage
[MeSH-minor]
Adolescent. Drug Resistance / drug effects. Humans. Immunosuppressive Agents / administration & dosage. Male. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / complications. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / pathology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy. Proteinuria / drug therapy. Proteinuria / etiology. Proteinuria / pathology. Time Factors. Transplantation, Homologous
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.
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.
Hazardous Substances Data Bank.
CANDESARTAN
.
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[Cites]
Int J Hematol. 2004 Feb;79(2):193-7
[
15005351.001
]
[Cites]
Pediatr Nephrol. 2004 Sep;19(9):956-61
[
15278690.001
]
[Cites]
Am J Kidney Dis. 2005 Sep;46(3):550-6
[
16129218.001
]
[Cites]
Nephrol Dial Transplant. 1999 Oct;14(10):2461-3
[
10528673.001
]
[Cites]
Diabetes Care. 2003 Aug;26(8):2268-74
[
12882847.001
]
[Cites]
Am J Kidney Dis. 2000 Sep;36(3):474-80
[
10977778.001
]
[Cites]
Nephrol Dial Transplant. 1997 Nov;12(11):2433-5
[
9394341.001
]
[Cites]
Int J Hematol. 2003 Oct;78(3):262-5
[
14604287.001
]
[Cites]
Bone Marrow Transplant. 1995 Aug;16(2):303-5
[
7581152.001
]
[Cites]
Am J Nephrol. 2001 Sep-Oct;21(5):351-6
[
11684793.001
]
[Cites]
J Hum Hypertens. 1999 Jan;13 Suppl 1:S57-60; discussion S61
[
10076922.001
]
[Cites]
J Nephrol. 2002 Jan-Feb;15(1):79-82
[
11936432.001
]
(PMID = 16787879.001).
[ISSN]
0925-5710
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antihypertensive Agents; 0 / Benzimidazoles; 0 / Immunosuppressive Agents; 0 / Tetrazoles; S8Q36MD2XX / candesartan
68.
Kolenova A, Hikkel I, Ilencikova D, Hikkelova M, Sejnova D, Kaiserova E, Cizmar A, Puskacova J, Bubanska E, Oravkinova I, Gencik M:
Minimal residual disease detection using real-time quantitative PCR analysis of immunoglobulin and T-cell receptor gene rearrangements in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: Slovak experience.
Neoplasma
; 2010;57(6):552-61
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[Title]
Minimal residual
disease
detection using real-time quantitative PCR analysis of immunoglobulin
and T
-
cell
receptor gene rearrangements in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: Slovak experience.
Acute lymphoblastic leukemia
is the most common form of cancer in children.
An intense effort has been made to develop methods to determine the degree of minimal residual
leukemia
cells present in patients considered to be in morphological remission.
Because of the strong correlation between minimal residual
disease
(MRD) levels and risk of relapse, monitoring of MRD provides unique information regarding treatment response.
The MRD monitoring based on real-time quantitative PCR detection of patient-specific immunoglobulin
and T
-
cell
receptor (Ig/TCR) gene rearrangements is currently considered to be the most reliable tool for MRD-based
diagnosis
in ALL.
A total of 40 patients with BCP-ALL (
B cell
precursor ALL) and 4 patients with T ALL were analyzed for Ig/TCR rearrangement.
[MeSH-major]
Gene Rearrangement. Gene Rearrangement, T-Lymphocyte. Genes, Immunoglobulin. Polymerase Chain Reaction / methods. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma /
diagnosis
[MeSH-minor]
Adolescent. Child. Child, Preschool. Female. Humans. Immunophenotyping. Infant. Leukocyte Count. Male. Neoplasm, Residual /
diagnosis
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(PMID = 20845994.001).
[ISSN]
0028-2685
[Journal-full-title]
Neoplasma
[ISO-abbreviation]
Neoplasma
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Slovakia
69.
Ercan TE, Soycan LY, Apak H, Celkan T, Ozkan A, Akdenizli E, Kasapçopur O, Yildiz I:
Antibody titers and immune response to diphtheria-tetanus-pertussis and measles-mumps-rubella vaccination in children treated for acute lymphoblastic leukemia.
J Pediatr Hematol Oncol
; 2005 May;27(5):273-7
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[Title]
Antibody titers and immune response to diphtheria-tetanus-pertussis and measles-mumps-rubella vaccination in children treated for
acute lymphoblastic leukemia
.
The objective of this study was to investigate the diphtheria-tetanus-pertussis and/or measles-mumps antibody titers before and after vaccination at various time points of
acute lymphoblastic leukemia
(ALL) therapy and to suggest an appropriate vaccination approach for ALL patients.
[MeSH-major]
Antibody Formation. Diphtheria-Tetanus-Pertussis Vaccine / therapeutic use. Measles Vaccine / therapeutic use. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / immunology. Rubella Vaccine / therapeutic use
Genetic Alliance.
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.
Genetic Alliance.
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.
Genetic Alliance.
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.
Genetic Alliance.
consumer health - Mumps
.
Genetic Alliance.
consumer health - Rubella
.
Genetic Alliance.
consumer health - Tetanus
.
MedlinePlus Health Information.
consumer health - Tetanus, Diphtheria, and Pertussis Vaccines
.
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(PMID = 15891564.001).
[ISSN]
1077-4114
[Journal-full-title]
Journal of pediatric hematology/oncology
[ISO-abbreviation]
J. Pediatr. Hematol. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Diphtheria-Tetanus-Pertussis Vaccine; 0 / Measles Vaccine; 0 / Rubella Vaccine
70.
Ek T, Mellander L, Andersson B, Abrahamsson J:
Immune reconstitution after childhood acute lymphoblastic leukemia is most severely affected in the high risk group.
Pediatr Blood Cancer
; 2005 May;44(5):461-8
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[Title]
Immune reconstitution after childhood
acute lymphoblastic leukemia
is most severely affected in the high risk group.
OBJECTIVE: The aim was to examine the immune reconstitution after current chemotherapy for childhood ALL, with a special focus on
finding
immunologic variables that predict a poor immune response to vaccinations.
PROCEDURE: In a cross-sectional study of 31 children after treatment with the NOPHO ALL-1992 protocol peripheral blood lymphocyte subsets, T-
and B
-
cell
function in vitro and serum immunoglobulins (Ig) were measured.
Naive T-
cell
subsets were more reduced than memory subsets.
Total B-
cell
number was low at 1 month, but normal at 6 months.
Antigen-independent T-
and B
-
cell
function in vitro were affected at 1 month, but virtually normalized at 6 months.
The most intensively treated patients still have persistent abnormalities in T-, B-, and NK-
cell
subsets at 6 months post therapy and show a poor response to immunization with T-
cell
dependent antigens.
In the HR group, routine
re
-immunizations before this time point are of limited benefit, and the effect of repeated vaccinations should be evaluated.
[MeSH-major]
Immune System / physiology. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Regeneration. Vaccination
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia, Childhood
.
MedlinePlus Health Information.
consumer health - Immune System and Disorders
.
MedlinePlus Health Information.
consumer health - Immunization
.
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[Copyright]
2004 Wiley-Liss, Inc.
(PMID = 15558707.001).
[ISSN]
1545-5009
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antineoplastic Agents; 0 / Immunoglobulins
71.
Giebel S, Krawczyk-Kuliś M, Adamczyk-Cioch M, Czyz A, Lech-Marańda E, Piatkowska-Jakubas B, Paluszewska M, Pałynyczko G, Piszcz J, Hołowiecki J, Polish Adult Leukemia Group:
Prophylaxis and therapy of central nervous system involvement in adult acute lymphoblastic leukemia: recommendations of the Polish Adult Leukemia Group.
Pol Arch Med Wewn
; 2008 Jun;118(6):356-61
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[Title]
Prophylaxis and therapy of central nervous system involvement in adult
acute lymphoblastic leukemia
: recommendations of the Polish Adult
Leukemia
Group.
The central nervous system (CNS) is one of the most frequent extramedullary locations of adult
acute lymphoblastic leukemia
(ALL), affecting approximately 5% of patients at
diagnosis
.
T-
lineage
ALL, high initial leukocyte counts and mediastinal involvement are the predisposing factors.
As the prognosis of patients with isolated or
mixed
CNS relapse is particularly poor, adequate prophylaxis seems critical.
[MeSH-major]
Central Nervous System Neoplasms / prevention & control. Central Nervous System Neoplasms / therapy. Neoplasm Recurrence, Local. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Quality of Life
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(PMID = 18619191.001).
[Journal-full-title]
Polskie Archiwum Medycyny Wewnetrznej
[ISO-abbreviation]
Pol. Arch. Med. Wewn.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Poland
[Number-of-references]
28
72.
Yoshida K, Hasegawa D, Takusagawa A, Kato I, Ogawa C, Echizen N, Ohkoshi K, Yamaguchi T, Hosoya R, Manabe A:
Bullous exudative retinal detachment due to infiltration of leukemic cells in a child with acute lymphoblastic leukemia.
Int J Hematol
; 2010 Oct;92(3):535-7
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[Title]
Bullous exudative retinal detachment due to infiltration of leukemic cells in a child with
acute lymphoblastic leukemia
.
Acute lymphoblastic leukemia
(ALL) is known to cause several ocular involvements, but exudative retinal detachment is a rare complication.
We describe a case report of a 4-year-old boy with
T cell
ALL who developed bilateral exudative retinal detachment caused by leukemic infiltration in the retinas after achieving hematological remission.
Intravenous steroid pulse therapy and local irradiation reversed the condition, but it recurred concurrently with
disease
progression after a second relapse in the bone marrow.
It is suggested that ophthalmic examination is crucial for ALL patients, especially for those whose white blood
cell
count is very high at onset.
[MeSH-major]
Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / complications. Retinal Detachment / etiology. Retinal Detachment / pathology
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.
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[Cites]
J Pediatr Ophthalmol Strabismus. 2001 Jul-Aug;38(4):242-4
[
11495313.001
]
[Cites]
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]
(PMID = 20838956.001).
[ISSN]
1865-3774
[Journal-full-title]
International journal of hematology
[ISO-abbreviation]
Int. J. Hematol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
73.
Gao YJ, Zhu XH, Yang Y, Wu Y, Lu FJ, Zhai XW, Wang HS:
Prevalence of ETV6-RUNX1 fusion gene in children with acute lymphoblastic leukemia in China.
Cancer Genet Cytogenet
; 2007 Oct 1;178(1):57-60
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[Title]
Prevalence of ETV6-RUNX1 fusion gene in children with
acute lymphoblastic leukemia
in China.
A series of 92 Chinese children newly diagnosed with
acute lymphoblastic leukemia
(ALL) were examined for the ETV6-RUNX1 (previously TEL-AML1) fusion gene by using a nested reverse transcriptase-polymerase chain reaction.
ETV6-RUNX1 fusion transcripts were detected in 21 of 92 patients (22.8%): 16 with common ALL, 4 with precursor B-
cell
ALL, and 1 with T-ALL.
The prevalence of ETV6-RUNX1 positivity was 24.7% (20/81) in childhood B-
lineage
ALL.
[MeSH-major]
Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Proto-Oncogene Proteins c-ets / biosynthesis. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / biosynthesis. Repressor Proteins / genetics
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(PMID = 17889709.001).
[ISSN]
0165-4608
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Core Binding Factor Alpha 2 Subunit; 0 / ETS translocation variant 6 protein; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-ets; 0 / RUNX1 protein, human; 0 / Repressor Proteins
74.
Lazić J, Dokmanović L, Krstovski N, Predojević J, Tosić N, Pavlović S, Janić D:
[Immunoglobulin genes and T-cell receptors as molecular markers in children with acute lymphoblastic leukaemia].
Srp Arh Celok Lek
; 2009 Jul-Aug;137(7-8):384-90
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[Title]
[Immunoglobulin genes
and T
-
cell
receptors as molecular markers in children with
acute lymphoblastic
leukaemia
].
INTRODUCTION:
Acute lymphoblastic
leukaemia
(ALL) is a malignant clonal
disease
, one of the most common malignancies in childhood.
The ability of molecular genetic methods help to establish submicroscopic classification and minimal residual
disease
(MRD) follow up, in major percent responsible for relapse.
METHODS: Forty-one children with ALL were enrolled in the study group, with initial
diagnosis
of IgH and TCR gene rearrangements by polimerase chain reaction (PCR).
RESULTS: In the study group IgH rearrangement was detected in 82.9% of children at the
diagnosis
, while TCR rearrangement was seen in 56.1%.
MRD stands out as a precise predictive factor for the relapse of
disease
.
[MeSH-major]
Gene Rearrangement. Immunoglobulin Heavy Chains / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Receptors, Antigen, T-
Cell
/ genetics
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(PMID = 19764592.001).
[ISSN]
0370-8179
[Journal-full-title]
Srpski arhiv za celokupno lekarstvo
[ISO-abbreviation]
Srp Arh Celok Lek
[Language]
srp
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Serbia
[Chemical-registry-number]
0 / Immunoglobulin Heavy Chains; 0 / Receptors, Antigen, T-Cell
75.
Matsuzaki A, Suminoe A, Koga Y, Kusuhara K, Hara T, Ogata R, Sata T, Hara T:
Fatal visceral varicella-zoster virus infection without skin involvement in a child with acute lymphoblastic leukemia.
Pediatr Hematol Oncol
; 2008 Apr-May;25(3):237-42
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[Title]
Fatal visceral varicella-zoster virus infection without skin involvement in a child with
acute lymphoblastic leukemia
.
A 5-year-old girl with
acute lymphoblastic leukemia
in remission suffered from fatal visceral varicella-zoster virus (VZV) infection after the oral administration of a high-dose dexamethasone.
[MeSH-major]
Chickenpox / etiology. Herpesvirus 3, Human. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / complications
[MeSH-minor]
Antigens, Viral / blood. Antineoplastic Agents, Hormonal / administration & dosage. Child, Preschool. DNA, Viral / blood. Dexamethasone / administration & dosage. Disseminated Intravascular Coagulation / etiology. Fatal Outcome. Female. Humans. Liver Failure,
Acute
/ etiology
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(PMID = 18432508.001).
[ISSN]
1521-0669
[Journal-full-title]
Pediatric hematology and oncology
[ISO-abbreviation]
Pediatr Hematol Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antigens, Viral; 0 / Antineoplastic Agents, Hormonal; 0 / DNA, Viral; 7S5I7G3JQL / Dexamethasone
76.
Chen LJ, Li JY, Wu YJ, Yang H, Qian SX, Wu HX, Lu H, Xu W, Sheng RL:
[Immunophenotyping characteristics of T-cell acute lymphoblastic leukemia].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2007 Aug;15(4):692-5
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[Title]
[Immunophenotyping characteristics of T-
cell acute lymphoblastic leukemia
].
The objective of this study was to investigate the immunophenotypic characteristics of T-
cell acute lymphoblastic leukemia
(T-ALL).
The results showed that the T-
lineage
-associated antigen expressions were CD7 > CD2 > CD3 > CD5 successively.
Among 140 cases of T-ALL, 12 (8.57%) was accompanied by B-
lineage
associated antigen expression.
Myeloid
antigen expression was identified in 31 out of 136 cases (22.79%).
The positive rate of
myeloid
antigen expression in CD34(+) T-ALL (36.58%) was significantly higher than that in CD34(-) T-ALL (15.38%) (p < 0.01).
It is concluded that immunophenotyping is an important tool for
diagnosis
of T-ALL.
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(PMID = 17708784.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD; 0 / Antigens, CD3; 0 / Antigens, CD34; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3
77.
Bacher U, Kohlmann A, Haferlach T:
Perspectives of gene expression profiling for diagnosis and therapy in haematological malignancies.
Brief Funct Genomic Proteomic
; 2009 May;8(3):184-93
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[Title]
Perspectives of gene expression profiling for
diagnosis
and therapy in haematological malignancies.
Considering the heterogeneity of
leukaemias
and the widening spectrum of therapeutic strategies, novel diagnostic methods are urgently needed for haematological malignancies.
For a decade, gene expression profiling (GEP) has been applied in
leukaemia
research.
Thus, various studies demonstrated worldwide that the majority of genetically defined
leukaemia
subtypes are accurately predictable by GEP, for example, with respect to reciprocal rearrangements in
acute
myeloid leukaemia
(AML).
Considering the lymphatic malignancies, GEP studies defined novel clinically relevant subtypes in diffuse large
B cell
lymphoma (DLBCL), and improved the discrimination of Burkitt lymphoma and DLBCL cases, overcoming considerable overlaps of these entities that exist from morphological and genetic perspectives.
Treatment-specific sensitivity assays are being developed for targeted drugs such as farnesyl transferase inhibitors in AML or imatinib in BCR-ABL1 positive
acute lymphoblastic
leukaemia
(ALL).
Large multicentre studies such as the MILE Study (Microarray Innovations in
LEukemia
) aim at translating this methodology into clinical routine workflows and to catalyze this process.
[MeSH-major]
Gene Expression Profiling. Hematologic Neoplasms /
diagnosis
. Hematologic Neoplasms / therapy
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(PMID = 19474126.001).
[ISSN]
1477-4062
[Journal-full-title]
Briefings in functional genomics & proteomics
[ISO-abbreviation]
Brief Funct Genomic Proteomic
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Number-of-references]
90
78.
Matsuno N, Hoshino K, Nanri T, Kawakita T, Suzushima H, Kawano F, Mitsuya H, Asou N:
p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult acute leukemia.
Leuk Res
; 2005 May;29(5):557-64
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[Title]
p15 mRNA expression detected by real-time quantitative reverse transcriptase-polymerase chain reaction correlates with the methylation density of the gene in adult
acute leukemia
.
Cyclin-dependent kinase inhibitor p15 is frequently inactivated by either methylation or deletion in patients with
acute leukemia
.
To examine pathologic and clinical significance of the p15 gene inactivation, we established a quantitative assay of p15 mRNA expression in the bone marrow cells by real-time quantitative reverse transcriptase-polymerase chain reaction. p15 mRNA expression in 14 patients with precursor B-
cell acute lymphoblastic leukemia
(PBC-ALL) well correlated with status of deletion and methylation in the p15 gene analyzed by Southern blotting.
Furthermore, two patients with PBC-ALL and 11
acute
myeloblastic
leukemia
(AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
Among 108 AML patients, p15 mRNA expression was significantly lower in the
myeloid lineage
(M1, M2, M3) than the monocytic
lineage
(M4, M5) (P = 0.0019).
[MeSH-major]
Burkitt Lymphoma / genetics.
Cell
Cycle Proteins / genetics. DNA Methylation. Gene Expression Regulation, Leukemic.
Leukemia
,
Myeloid
/ genetics. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. RNA, Messenger / metabolism. Tumor Suppressor Proteins / genetics
[MeSH-minor]
Acute
Disease
. Adult. Bone Marrow Cells / metabolism. Bone Marrow Cells / pathology.
Cell
Lineage
. CpG Islands. Cyclin-Dependent Kinase Inhibitor p15. Humans. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Tumor Cells, Cultured
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(PMID = 15755508.001).
[ISSN]
0145-2126
[Journal-full-title]
Leukemia research
[ISO-abbreviation]
Leuk. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / CDKN2B protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / RNA, Messenger; 0 / Tumor Suppressor Proteins
79.
Porkka K, Koskenvesa P, Lundán T, Rimpiläinen J, Mustjoki S, Smykla R, Wild R, Luo R, Arnan M, Brethon B, Eccersley L, Hjorth-Hansen H, Höglund M, Klamova H, Knutsen H, Parikh S, Raffoux E, Gruber F, Brito-Babapulle F, Dombret H, Duarte RF, Elonen E, Paquette R, Zwaan CM, Lee FY:
Dasatinib crosses the blood-brain barrier and is an efficient therapy for central nervous system Philadelphia chromosome-positive leukemia.
Blood
; 2008 Aug 15;112(4):1005-12
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[Title]
Dasatinib crosses the blood-brain barrier and is an efficient therapy for central nervous system Philadelphia chromosome-positive
leukemia
.
Although imatinib, a BCR-ABL tyrosine kinase inhibitor, is used to treat
acute
Philadelphia chromosome-positive (Ph(+))
leukemia
, it does not prevent central nervous system (CNS) relapses resulting from poor drug penetration through the blood-brain barrier.
Imatinib and dasa-tinib (a dual-specific SRC/BCR-ABL kinase inhibitor) were compared in a preclinical mouse model of intracranial Ph(+)
leukemia
.
Clinical dasatinib treatment in patients with CNS Ph(+)
leukemia
was assessed.
Stabilization and regression of CNS
disease
were achieved with continued dasa-tinib administration.
The drug also demonstrated substantial activity in 11 adult and pediatric patients with CNS Ph(+)
leukemia
.
Dasatinib has promising therapeutic potential in managing intracranial leukemic
disease
and substantial clinical activity in patients who experience CNS relapse while on imatinib therapy.
[MeSH-major]
Blood-Brain Barrier / metabolism. Central Nervous System Neoplasms / drug therapy.
Leukemia
, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Pyrimidines / administration & dosage. Pyrimidines / pharmacokinetics. Thiazoles / administration & dosage. Thiazoles / pharmacokinetics
[MeSH-minor]
Adolescent. Adult. Aged. Animals. Child. Cytogenetic Analysis. Dasatinib.
Disease
Models, Animal. Drug Evaluation, Preclinical. Drug Monitoring. Female. Humans. Male. Mice. Middle Aged. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma. Remission Induction. Spinal Puncture. Survival Rate. Treatment Outcome. Tumor Burden / drug effects
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(PMID = 18477770.001).
[ISSN]
1528-0020
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00108719/ NCT00110097
[Publication-type]
Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
80.
Baeumler J, Szuhai K, Falkenburg JH, van Schie ML, Ottmann OG, Nijmeijer BA:
Establishment and cytogenetic characterization of a human acute lymphoblastic leukemia cell line (ALL-VG) with ETV6/ABL1 rearrangement.
Cancer Genet Cytogenet
; 2008 Aug;185(1):37-42
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[Title]
Establishment and cytogenetic characterization of a human
acute lymphoblastic leukemia cell
line (ALL-VG) with ETV6/ABL1 rearrangement.
Here we present the generation of an ETV6/ABL1 positive human
acute lymphoblastic leukemia
(ALL)
cell
line, ALL-VG.
The
cell
line expressed ETV6/ABL1 fusion transcripts and displayed sensitivity to imatinib with an IC(50) of 0.1 microM.
The ALL-VG
cell
line may serve as a tool for the study of ETV6/ABL1.
[MeSH-major]
Cell
Line, Tumor. Chromosomes, Human, Pair 6. Genes, abl. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Translocation, Genetic
[MeSH-minor]
Adult. Benzamides.
Cell
Survival / drug effects. Chromosome Deletion. Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 12. Cytogenetic Analysis. Dose-Response Relationship, Drug. Humans. Imatinib Mesylate. Inhibitory Concentration 50. Male. Piperazines / pharmacology. Protein-Tyrosine Kinases / pharmacology. Pyrimidines / pharmacology. Remission Induction. Sensitivity and Specificity
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(PMID = 18656692.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases
81.
Novara F, Beri S, Bernardo ME, Bellazzi R, Malovini A, Ciccone R, Cometa AM, Locatelli F, Giorda R, Zuffardi O:
Different molecular mechanisms causing 9p21 deletions in acute lymphoblastic leukemia of childhood.
Hum Genet
; 2009 Oct;126(4):511-20
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[Title]
Different molecular mechanisms causing 9p21 deletions in
acute lymphoblastic leukemia
of childhood.
Deletion of chromosome 9p21 is a crucial event for the development of several cancers including
acute lymphoblastic leukemia
(ALL).
[MeSH-major]
Chromosomes, Human, Pair 9 / genetics. Cyclin-Dependent Kinase Inhibitor p15 / genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Sequence Deletion / genetics
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Nat Genet. 2004 Sep;36(9):949-51
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(PMID = 19484265.001).
[ISSN]
1432-1203
[Journal-full-title]
Human genetics
[ISO-abbreviation]
Hum. Genet.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / CDKN2B protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p15; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / DNA Primers
[Other-IDs]
NLM/ PMC2762534
82.
Huh J, Chung W:
[A Case of Acute Lymphoblastic Leukemia with ider(9)(q10)t(9;22)(q34;q11.2).].
Korean J Lab Med
; 2006 Jun;26(3):223-6
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[Title]
[A Case of
Acute Lymphoblastic Leukemia
with ider(9)(q10)t(9;22)(q34;q11.2).].
It is known to be rarely observed in
acute lymphoblastic leukemia
(ALL) or
lymphoblastic
crisis transformed from chronic myelogenous
leukemia
.
We herein describe a 26-year-old female patient with precursor B-
cell
ALL, cytogenetically characterized by ider(9)(q10)t(9;22).
Although a t(9;22) and a deletion of the short arm of chromosome 9 are known to be associated with a poor prognostic factor in
acute lymphoblastic leukemia
, a larger study is needed to determine the prognosis of ider(9)(q10)t(9;22) cases.
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(PMID = 18156729.001).
[ISSN]
1598-6535
[Journal-full-title]
The Korean journal of laboratory medicine
[ISO-abbreviation]
Korean J Lab Med
[Language]
kor
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Korea (South)
83.
Jeeninga RE, Jan B, van der Linden B, van den Berg H, Berkhout B:
Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-cell lines: towards a new virotherapy approach.
Cancer Res
; 2005 Apr 15;65(8):3347-55
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[Title]
Construction of a minimal HIV-1 variant that selectively replicates in leukemic derived T-
cell
lines: towards a new virotherapy approach.
T-
cell acute lymphoblastic leukemia
is a high-risk type of blood-
cell
cancer.
We analyzed the possibility of developing virotherapy for T-
cell acute lymphoblastic leukemia
.
This mini-HIV virus has five deletions (vif, vpR, vpU, nef, and U3) and replicated in the SupT1
cell
line, but did not replicate in normal peripheral blood mononuclear cells.
The stripped down mini-HIV variant was also able to efficiently remove leukemic cells from
a mixed
culture with untransformed control cells.
In contrast to wild-type HIV-1, we did not observe bystander killing in
mixed
culture experiments with the mini-HIV variant.
The mini-HIV variant that uses CD4 and CXCR4 for
cell
entry could potentially be used against CXCR4-expressing malignancies such as T-
lymphoblastic leukemia
/lymphoma, natural killer
leukemia
, and some
myeloid leukemias
.
[MeSH-major]
HIV-1 / physiology.
Leukemia
-Lymphoma, Adult T-
Cell
/ therapy.
Leukemia
-Lymphoma, Adult T-
Cell
/ virology. T-Lymphocytes / virology
[MeSH-minor]
Antigens, CD4 / biosynthesis.
Cell
Line, Tumor. Female. Gene Deletion. Genes, nef / genetics. Genes, vif / genetics. Genes, vpr / genetics. Genes, vpu / genetics. HIV Long Terminal Repeat / genetics. Humans. Jurkat Cells. Receptors, CXCR4 / biosynthesis. Virus Replication
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.
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treatment guidelines - Human Herpesvirus-8
.
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(PMID = 15833868.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / R21-AI47017-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD4; 0 / Receptors, CXCR4
84.
Li HL, Xiang Z, Zhao T:
[Expressions of surviving, MMP2, TIMP1, CD44 and nm23 of two tumors originating from different immunosurveillance in the same patient].
Nan Fang Yi Ke Da Xue Xue Bao
; 2010 Jun;30(6):1291-4
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METHODS: The expressions of survivin, MMP2, TIMP1, CD44, and nm23 proteins were detected immunohistochemically in a patient with
acute lymphoblastic leukemia and
lymphoma after allogeneic blood stem
cell
transplantation.
RESULTS: Survivin, MMP2, TIMP1, CD44, and nm23 proteins were positive in
acute lymphoblastic leukemia
samples obtained before transplantation and negative in the lymphoma tissue occurring after the transplantation.
[MeSH-major]
Hematopoietic Stem
Cell
Transplantation / adverse effects. Inhibitor of Apoptosis Proteins / metabolism. Lymphoma, Large B-
Cell
, Diffuse / metabolism. Neoplasms, Second Primary / metabolism. Tissue Inhibitor of Metalloproteinase-1 / metabolism
[MeSH-minor]
Adult. Antigens, CD44 / metabolism. Female. Humans. Matrix Metalloproteinase 2 / metabolism. NM23 Nucleoside Diphosphate Kinases / metabolism. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / therapy
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NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 20584660.001).
[ISSN]
1673-4254
[Journal-full-title]
Nan fang yi ke da xue xue bao = Journal of Southern Medical University
[ISO-abbreviation]
Nan Fang Yi Ke Da Xue Xue Bao
[Language]
chi
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Antigens, CD44; 0 / BIRC5 protein, human; 0 / CD44 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / TIMP1 protein, human; 0 / Tissue Inhibitor of Metalloproteinase-1; EC 2.7.4.6 / NME1 protein, human; EC 3.4.24.24 / MMP2 protein, human; EC 3.4.24.24 / Matrix Metalloproteinase 2
85.
Matsunaga T, Kamiya T, Sumi D, Kumagai Y, Kalyanaraman B, Hara A:
L-Xylulose reductase is involved in 9,10-phenanthrenequinone-induced apoptosis in human T lymphoma cells.
Free Radic Biol Med
; 2008 Mar 15;44(6):1191-202
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9,10-Phenanthrenequinone (9,10-PQ), a major component in diesel exhaust particles, is suggested to generate reactive oxygen species (ROS) through its redox cycling, leading to
cell
toxicity. l-Xylulose reductase (XR), a NADPH-dependent enzyme in the uronate pathway, strongly reduces alpha-dicarbonyl compounds and was thought to act as a detoxification enzyme against reactive carbonyl compounds.
Here, we have investigated the role of intracellular ROS generation in apoptotic signaling in human
acute T
-
lymphoblastic leukemia
MOLT-4 cells treated with 9,10-PQ and the role of XR in the generation of ROS.
Surprisingly, the ROS generation and cytotoxicity by 9,10-PQ were augmented in an XR-transformed
cell
line.
[MeSH-minor]
Blotting, Western. Caspases / drug effects. Caspases / metabolism.
Cell
Line, Tumor. Flow Cytometry. Humans. Membrane Potential, Mitochondrial / drug effects. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes
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(PMID = 18206670.001).
[ISSN]
0891-5849
[Journal-full-title]
Free radical biology & medicine
[ISO-abbreviation]
Free Radic. Biol. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Air Pollutants; 0 / Phenanthrenes; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; EC 1.- / Oxidoreductases; EC 3.4.22.- / Caspases
86.
Hubeek I, Peters GJ, Broekhuizen R, Zwaan CM, Kaaijk P, van Wering ES, Gibson BE, Creutzig U, Janka-Schaub GE, den Boer ML, Pieters R, Kaspers GJ:
In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood acute leukemia.
Haematologica
; 2006 Jan;91(1):17-23
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[Title]
In vitro sensitivity and cross-resistance to deoxynucleoside analogs in childhood
acute leukemia
.
BACKGROUND AND OBJECTIVES: Cytarabine (ara-C) is a key drug in the treatment of
acute leukemia
.
DESIGN AND METHODS: Using the MTT assay, we determined in vitro sensitivity and cross-resistance to deoxynucleoside analogs in 362
acute leukemia
samples from untreated children and 32 normal bone marrow mononuclear
cell
samples.
RESULTS: Normal bone marrow samples were significantly more resistant to ara-C, cladribine and fludarabine than were
acute
myeloid
leukemia
(AML) samples and significantly more resistant to ara-C and fludarabine than were
acute lymphoblastic leukemia
(ALL) samples.
T-ALL was significantly more resistant to cladribine than B-
cell
precursor ALL.
We observed cross-resistance between ara-C and other deoxynucleoside analogs, as well as between ara-C and drugs with different modes of action in childhood
acute leukemia
.
[MeSH-major]
Drug Resistance, Multiple.
Leukemia
/ drug therapy. Nucleosides / therapeutic use
[MeSH-minor]
Acute
Disease
. Child. Cytarabine / therapeutic use. Drug Screening Assays, Antitumor. Humans
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(PMID = 16434366.001).
[ISSN]
1592-8721
[Journal-full-title]
Haematologica
[ISO-abbreviation]
Haematologica
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Nucleosides; 04079A1RDZ / Cytarabine
87.
Aventín A, Sánchez J, Nomdedéu JF, Estany C, Forcada P, La Starza R, Mecucci C:
Novel IGHalpha translocations, t(2;14)(q14.3;q32) and t(14;17)(q32;q21), in B-cell precursor acute lymphoblastic leukemia.
Cancer Genet Cytogenet
; 2008 Aug;185(1):57-9
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[Title]
Novel IGHalpha translocations, t(2;14)(q14.3;q32)
and t
(14;17)(q32;q21), in B-
cell
precursor
acute lymphoblastic leukemia
.
[MeSH-major]
Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 2. Genes, Immunoglobulin Heavy Chain / genetics. Precursor B-
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Translocation, Genetic
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(PMID = 18656697.001).
[ISSN]
1873-4456
[Journal-full-title]
Cancer genetics and cytogenetics
[ISO-abbreviation]
Cancer Genet. Cytogenet.
[Language]
eng
[Publication-type]
Case Reports; Letter; Research Support, Non-U.S. Gov't
[Publication-country]
United States
88.
Yamasaki N, Miyazaki K, Nagamachi A, Koller R, Oda H, Miyazaki M, Sasaki T, Honda ZI, Wolff L, Inaba T, Honda H:
Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop acute B-lineage leukemia.
Oncogene
; 2010 Apr 1;29(13):1963-75
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[Title]
Identification of Zfp521/ZNF521 as a cooperative gene for E2A-HLF to develop
acute B
-
lineage
leukemia
.
E2A-hepatic
leukemia
factor (HLF) is a chimeric protein found in B-
lineage
acute lymphoblastic leukemia
(ALL) with t(17;19).
To analyze the leukemogenic process and to create model mice for t(17;19)-positive
leukemia
, we generated inducible knock-in (iKI) mice for E2A-HLF.
Despite the induced expression of E2A-HLF in the hematopoietic tissues, no
disease
was developed during the long observation period, indicating that additional gene alterations are required to develop
leukemia
.
Virus infection induced
acute
leukemias
in E2A-HLF iKI mice with higher morbidity and mortality than in control mice.
Interestingly, tumors with Zfp521 integration exclusively showed B-
lineage
ALL, which corresponds to the phenotype of human t(17;19)-positive
leukemia
.
In addition, ZNF521 (human counterpart of Zfp521) was found to be overexpressed in human leukemic
cell
lines harboring t(17;19).
Moreover, both iKI for E2A-HLF and transgenic for Zfp521 mice frequently developed B-
lineage
ALL.
These results indicate that a set of transcription factors promote leukemic transformation of E2A-HLF-expressing hematopoietic progenitors and suggest that aberrant expression of Zfp521/ZNF521 may be clinically relevant to t(17;19)-positive B-
lineage
ALL.
[MeSH-major]
Basic-Leucine Zipper Transcription Factors / genetics. DNA-Binding Proteins / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
[MeSH-minor]
Animals.
Cell
Transformation, Neoplastic. Humans. Mice. Mutation. Nuclear Proteins. Transcriptional Activation / genetics
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(subscription/membership/fee required).
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.
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Marmoset Gene list: Data: Gene Annotation
.
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(PMID = 20062079.001).
[ISSN]
1476-5594
[Journal-full-title]
Oncogene
[ISO-abbreviation]
Oncogene
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Basic-Leucine Zipper Transcription Factors; 0 / COPRS protein, human; 0 / DNA-Binding Proteins; 0 / E2a-Hlf fusion protein, mouse; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / zinc finger protein 521, human
89.
Segal I, Rassekh SR, Bond MC, Senger C, Schreiber RA:
Abnormal liver transaminases and conjugated hyperbilirubinemia at presentation of acute lymphoblastic leukemia.
Pediatr Blood Cancer
; 2010 Sep;55(3):434-9
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[Title]
Abnormal liver transaminases and conjugated hyperbilirubinemia at presentation of
acute lymphoblastic leukemia
.
BACKGROUND:
Acute lymphoblastic leukemia
(ALL) is the most common malignancy in childhood.
While hepatitis is a well-known complication during the treatment phase of ALL, the association of abnormal liver biochemistries at initial presentation of
leukemia
is poorly described.
The aim of this study is to examine the prevalence and assess the clinical impact of hepatitis at
diagnosis
in children with ALL.
Risk factors for elevated transaminases included a high WBC count at
diagnosis
, older age, bulky
disease
,
and T
-
cell leukemia
.
[MeSH-major]
Alanine Transaminase / blood. Aspartate Aminotransferases / blood. Hepatitis / complications. Hyperbilirubinemia / complications. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / complications
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.
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.
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[Copyright]
2010 Wiley-Liss, Inc.
(PMID = 20658613.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
EC 2.6.1.1 / Aspartate Aminotransferases; EC 2.6.1.2 / Alanine Transaminase; RFM9X3LJ49 / Bilirubin
90.
Chen P, Chen YZ, Wu Y, Huang HF, Li NN:
[Identification of the isoform in type II receptor of transforming growth factor-beta in patients with acute leukemia and its clinical significance].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2006 Apr;14(2):221-4
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[Title]
[Identification of the isoform in type II receptor of transforming growth factor-beta in patients with
acute leukemia
and its clinical significance].
To identify the mutation of TbetaR-II in patients with
acute leukemia
, the bone marrow samples from 6 patients with
acute leukemia
and 11 normal individuals as control were detected by long-range RT-PCR.
The results showed that there was existance of the isoform of TbetaR-II in 2 cases out of 6 patients with
acute leukemia
.
In conclusion, there was the isoform of TbetaR-II in partial patients with
acute leukemia
, and the isoform may be related with prognosis.
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(PMID = 16638184.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
CHI
[Publication-type]
English Abstract; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Protein Isoforms; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
91.
Kanazawa T, Ogawa C, Taketani T, Taki T, Hayashi Y, Morikawa A:
TLS/FUS-ERG fusion gene in acute lymphoblastic leukemia with t(16;21)(p11;q22) and monitoring of minimal residual disease.
Leuk Lymphoma
; 2005 Dec;46(12):1833-5
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[Title]
TLS/FUS-ERG fusion gene in
acute lymphoblastic leukemia
with t(16;21)(p11;q22) and monitoring of minimal residual
disease
.
This study reports a 1-year-old boy with precursor
B cell acute lymphoblastic leukemia
(ALL) carrying t(16;21)(p11;q22).
Complete remission (CR) was achieved by chemotherapy oriented for
acute
myeloid
leukemia
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 21. Neoplasm, Residual / genetics. Oncogene Proteins, Fusion / genetics. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. RNA-Binding Protein FUS / genetics. Translocation, Genetic
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.
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CYTARABINE
.
Hazardous Substances Data Bank.
ETOPOSIDE
.
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(PMID = 16263589.001).
[ISSN]
1042-8194
[Journal-full-title]
Leukemia & lymphoma
[ISO-abbreviation]
Leuk. Lymphoma
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Oncogene Proteins, Fusion; 0 / RNA-Binding Protein FUS; 0 / TLS-ERG fusion protein, human; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin
92.
Riz I, Hawley TS, Luu TV, Lee NH, Hawley RG:
TLX1 and NOTCH coregulate transcription in T cell acute lymphoblastic leukemia cells.
Mol Cancer
; 2010 Jul 09;9:181
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[Title]
TLX1 and NOTCH coregulate transcription in
T cell acute lymphoblastic leukemia
cells.
BACKGROUND: The homeobox gene TLX1 (for T-
cell leukemia
homeobox 1, previously known as HOX11) is inappropriately expressed in a major subgroup of
T cell acute lymphoblastic leukemia
(T-ALL) where it is strongly associated with activating NOTCH1 mutations.
In addition, the TLX1/NOTCH/MYC transcriptional network coregulates genes involved in
T cell
development, such as CD1 and RAG family members, and therefore may prescribe the early cortical stage of differentiation arrest characteristic of the TLX1 subgroup of T-ALL.
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(PMID = 20618946.001).
[ISSN]
1476-4598
[Journal-full-title]
Molecular cancer
[ISO-abbreviation]
Mol. Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01CA120316; United States / NHLBI NIH HHS / HL / R01HL65519; United States / NHLBI NIH HHS / HL / R01HL66305
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 143275-75-6 / TLX1 protein, human
[Other-IDs]
NLM/ PMC2913983
93.
Pfeifer H, Wassmann B, Pavlova A, Wunderle L, Oldenburg J, Binckebanck A, Lange T, Hochhaus A, Wystub S, Brück P, Hoelzer D, Ottmann OG:
Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with de novo Philadelphia-positive acute lymphoblastic leukemia (Ph+ ALL).
Blood
; 2007 Jul 15;110(2):727-34
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[Title]
Kinase domain mutations of BCR-ABL frequently precede imatinib-based therapy and give rise to relapse in patients with
de
novo Philadelphia-positive
acute lymphoblastic leukemia
(Ph+ ALL).
Acquired imatinib resistance in advanced Philadelphia-positive
acute lymphoblastic leukemia
(Ph(+) ALL) has been associated with mutations in the kinase domain (KD) of BCR-ABL.
Patients enrolled in the German Multicenter Study Group for Adult
Acute Lymphoblastic Leukemia
(GMALL) trial ADE10 for newly diagnosed elderly Ph(+) ALL were retrospectively examined for the presence of BCR-ABL KD mutations by denaturing high-performance liquid chromatography (D-HPLC), cDNA sequencing, and allele-specific polymerase chain reaction (PCR).
At relapse, the dominant
cell
clone harbored an identical mutation in 90% of cases, the overall prevalence of mutations at relapse was 80%.
BCR-ABL mutations conferring high-level imatinib resistance are present in a substantial proportion of patients with
de
novo Ph(+) ALL and eventually give rise to relapse.
[MeSH-major]
Fusion Proteins, bcr-abl / genetics. Mutation. Piperazines / therapeutic use. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / drug therapy. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics. Pyrimidines / therapeutic use
Genetic Alliance.
consumer health - Acute Lymphoblastic Leukemia
.
Hazardous Substances Data Bank.
IMATINIB MESYLATE
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 17405907.001).
[ISSN]
0006-4971
[Journal-full-title]
Blood
[ISO-abbreviation]
Blood
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl
94.
Friedman AD, Cook JR, Scharpf J:
Precursor T-cell acute lymphoblastic lymphoma presenting as a tongue mass.
J Otolaryngol Head Neck Surg
; 2009 Feb;38(1):E16-8
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[Title]
Precursor T-
cell acute lymphoblastic
lymphoma presenting as a tongue mass.
[MeSH-major]
Precursor T-
Cell Lymphoblastic Leukemia
-Lymphoma / pathology. Tongue Neoplasms / pathology
Genetic Alliance.
consumer health - Lymphoblastic lymphoma
.
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(PMID = 19344598.001).
[ISSN]
1916-0216
[Journal-full-title]
Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale
[ISO-abbreviation]
J Otolaryngol Head Neck Surg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Canada
[Chemical-registry-number]
0 / Antineoplastic Agents
95.
Jiang XJ, Wang JS, Fang Q:
[Gene expression of breast cancer resistance protein in adult acute lymphocytic leukemia and its clinical significance].
Zhongguo Shi Yan Xue Ye Xue Za Zhi
; 2008 Feb;16(1):31-4
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[Title]
[Gene expression of breast cancer resistance protein in adult
acute
lymphocytic
leukemia and
its clinical significance].
The objective of this study was to investigate the relationship between the expressions of breast cancer resistance protein (BCRP) gene and drug resistance as well as prognosis in adult patients with
acute
lymphocytic
leukemia
(ALL).
Semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the expression of BCRP gene in 97 adult patients with
acute
lymphocytic
leukemia
(ALL) and 30 normal subjects.
In immune types the BCRP gene expression of B-ALL was higher than that of
T cell
type, especially in mature
B cell
type with obviously statistical significance (p<0.01).
It is concluded that the high expression of BCRP gene may induce clinical drug resistance, and may be an unfavorable factor for prognosis in adult patients with
acute
lymphocytic
leukemia
.
[MeSH-major]
ATP-Binding Cassette Transporters / metabolism. Drug Resistance, Neoplasm / genetics. Neoplasm Proteins / metabolism. Precursor
Cell Lymphoblastic Leukemia
-Lymphoma / genetics
Genetic Alliance.
consumer health - Breast Cancer
.
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(PMID = 18315895.001).
[ISSN]
1009-2137
[Journal-full-title]
Zhongguo shi yan xue ye xue za zhi
[ISO-abbreviation]
Zhongguo Shi Yan Xue Ye Xue Za Zhi
[Language]
chi
[Publication-type]
Journal Article
[Publication-country]
China
[Chemical-registry-number]
0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Neoplasm Proteins
96.
Bryant J, Picot J, Levitt G, Sullivan I, Baxter L, Clegg A:
Cardioprotection against the toxic effects of anthracyclines given to children with cancer: a systematic review.
Health Technol Assess
; 2007 Jul;11(27):iii, ix-x, 1-84
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RESULTS: Four randomised controlled trials (RCTs) met the inclusion criteria of the review, each considering a different cardioprotective intervention; all trials included children with
acute lymphoblastic