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[Title] [Macular serous detachment revealing acute lymphoblastic leukemia].

BACKGROUND: Leukemias are a group of malignant diseases caused by immature hematopoietic cells proliferating in the blood marrow.

OBSERVATION: We report a case of a 42-year-old women presenting with loss of vision caused by serous macular detachment.

The investigations showed the diagnosis of acute lymphoblastic leukemia.

DISCUSSION: Ocular involvement is seen in 28%-80% of leukemia cases.

Serous detachment of the neuroepithelium is seldom reported, and can be the first symptom of the disease.

CONCLUSION: Ocular manifestations of leukemia are frequent but rarely reveal the disease.

However, the diagnosis of leukemia should be considered in case of pigmentary epithelium involvement.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Retinal Detachment / etiology

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(PMID = 15767897.001).

[ISSN] 0181-5512

[Journal-full-title] Journal français d'ophtalmologie

[ISO-abbreviation] J Fr Ophtalmol

[Language] fre

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] France

   

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The introduction of tyrosine kinase inhibitors in the treatment of BCR-ABL1-rearranged malignancies has revolutionized therapy, but the prognosis for acute leukemias remains suboptimal.

In this issue of Cancer Cell, Bueno et al. (2008) add a new dimension to the regulation of ABL1 expression.

The authors demonstrate that ABL1 is a direct target of miR-203, miR-203 is silenced by genetic and epigenetic mechanisms in hematopoietic malignancies expressing either ABL1 or BCR-ABL1, and restoration of miR-203 expression reduces ABL1 and BCR-ABL1 levels and inhibits cell proliferation.

[MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Proliferation. Gene Expression Regulation, Leukemic. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Lymphoma, T-Cell / pathology. Mice. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Protein Kinase Inhibitors / therapeutic use. Up-Regulation

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[CommentOn] Cancer Cell. 2008 Jun;13(6):496-506 [18538733.001]

(PMID = 18538729.001).

[ISSN] 1878-3686

[Journal-full-title] Cancer cell

[ISO-abbreviation] Cancer Cell

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / MicroRNAs; 0 / Protein Kinase Inhibitors; 0 / abl-bcr fusion protein, human; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl

   

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[Title] Insights from clinical studies into the role of the MLL gene in infant and childhood leukemia.

Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.

The use of DNA microarray analysis to distinguish a particular gene signature for MLL-rearranged leukemias is shedding light on the molecular mechanisms and potential therapeutic targets of these leukemias.

[MeSH-major] Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 17905612.001).

[ISSN] 1079-9796

[Journal-full-title] Blood cells, molecules & diseases

[ISO-abbreviation] Blood Cells Mol. Dis.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

[Number-of-references] 82

   

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BACKGROUND: The introduction of mAbs has changed the clinical approach to patients with lymphoma and leukemia.

RESULTS: Rituximab (anti-CD20) was the first mAb developed for the treatment of B-cell lymphomas.

Several randomized studies have demonstrated its efficacy in lymphomas and low toxicity profile; rituximab also has significant activity in chronic lymphocytic leukemia (CLL).

Alemtuzumab (anti-CD52) has shown efficacy in previously untreated or refractory CLL patients, while gemtuzumab ozogamicin (anti-CD33) appears to have significant activity in acute myeloid leukemias and myelodysplastic syndromes.

CONCLUSIONS: In the next few years, investigations will be concentrated on the improvement of the older mAbs, and the development of new mAbs, targeting molecules important for malignant cell cycle and survival in an attempt to further improve patient survival.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

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(PMID = 19236251.001).

[ISSN] 1744-7682

[Journal-full-title] Expert opinion on biological therapy

[ISO-abbreviation] Expert Opin Biol Ther

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents

[Number-of-references] 107

   

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[Title] [Effects of proteasome inhibitors on leukemias].

A lot of studies on effects of proteasome inhibitors on leukemias, including plasma cell leukemia; chronic lymphocytic leukemia, adult T cell lymphoma/leukemia, chronic myeloid leukemia and acute myeloid leukemia, were reviewed in this article.

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(PMID = 17708829.001).

[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; Review

[Publication-country] China

[Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib

[Number-of-references] 27

   

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We explored the impact of TEL-AML1 (ETV6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic phenotype.

These miRNAs blocked survivin expression and resulted in apoptosis in a similar manner as TEL-AML1 silencing by itself; this silencing was also shown to be Dicer-dependent. miRNAs-494 and -320a are expressed at lower levels in TEL-AML1+ leukemias compared with immunophenotype-matched nonTEL-AML1 acute lymphoblastic leukemia subtypes, and within TEL-AML1+ leukemias their expression is correlated to survivin levels.

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(PMID = 20807887.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA089032; United States / NCI NIH HHS / CA / R03-CA137829; United States / NCI NIH HHS / CA / R01 CA089032-06; United States / NCI NIH HHS / CA / R03 CA137829; United States / NCI NIH HHS / CA / R01-CA89032; United States / NCI NIH HHS / CA / CA137829-02; United States / NCI NIH HHS / CA / R03 CA137829-02; United States / NCI NIH HHS / CA / R01 CA089032-05; United States / NCI NIH HHS / CA / CA137829-01A1; United States / NCI NIH HHS / CA / R03 CA137829-01A1

[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 / BIRC5 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Inhibitor of Apoptosis Proteins; 0 / MicroRNAs; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / TEL-AML1 fusion protein

[Other-IDs] NLM/ PMC3265147

   

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[Title] Immunophenotyping of surface antigens in acute myeloid leukemia by flow cytometry after red blood cell lysis.

Immunophenotyping of acute leukemia using flow cytometry after density gradient separation (dg-sep) of mononuclear cells is the international gold standard.

Both methods revealed congruent results in phenotyping of 26 cases of acute myeloid leukemias by testing CD4, CD7, CD11b, CD11c, CD13, CD14, CD15, CD33, CD34, CD65s, Glycophorin A and HLA-DR antigens.

[MeSH-major] Antigens, CD / analysis. Antigens, Surface / analysis. Leukemia, Myeloid, Acute / genetics

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(PMID = 16730795.001).

[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 / Antigens, CD; 0 / Antigens, Surface; 0 / Glycophorin; 0 / HLA-DR Antigens

   

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[Title] Prognostic impact of c-KIT mutations in core binding factor leukemias: an Italian retrospective study.

Distinct forms of tyrosine kinase domain (TKD), juxtamembrane domain, exon 8, and internal tandem duplication (ITD) mutations of c-KIT, were observed in about 46% of core binding factor leukemia (CBFL) patients.

In acute myeloid leukemia (AML) with t(8;21), the presence of c-KIT TKD mutation at codon 816 (TKD(816)) was associated with a high white blood cell count at diagnosis (median, 29.60 x 10(9)/L) and a higher incidence (33%) of extramedullary leukemia (EML) during the course of the disease.

[MeSH-major] Core Binding Factors / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Proto-Oncogene Proteins c-kit / genetics

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(PMID = 16384925.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Core Binding Factors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

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[Title] Features and outcome of neonatal leukemia in Japan: experience of the Japan infant leukemia study group.

BACKGROUND: Neonatal leukemia characterized by early stem cell origin and extramedullary infiltration in the first 4 weeks of life is rare.

We analyzed the features and outcome of neonatal leukemia in Japan to establish an appropriate treatment strategy for this rare disorder.

PROCEDURE: Patients with infant leukemia registered and treated in the Japan Infant Leukemia Study between 1996 and 2001 were analyzed.

RESULTS: Among 162 infant leukemia patients, 11 exhibited neonatal leukemia; frequencies for all infant leukemias were 6.9% (8/116) for acute lymphoblastic leukemia (ALL) and 7.3% (3/41) for acute myeloid leukemia (AML).

Acute monoblastic leukemia was apparent in all three patients with AML (M5a in the FAB classification).

Four patients (one with AML, and three with ALL) have survived following stem cell transplantation (SCT); however, growth impairment related to SCT was observed in these patients.

CONCLUSIONS: These results suggest an improvement attributable to treatment of neonatal leukemia.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Myeloid / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Stem Cell Transplantation

[MeSH-minor] Acute Disease. Female. Histone-Lysine N-Methyltransferase. Humans. Infant. Infant, Newborn. Japan / epidemiology. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Registries. Survival Rate. Treatment Outcome

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[CommentIn] Pediatr Blood Cancer. 2006 Sep;47(3):234-5 [16206196.001]

(PMID = 16333820.001).

[ISSN] 1545-5009

[Journal-full-title] Pediatric blood & cancer

[ISO-abbreviation] Pediatr Blood Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

   

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By activating the glucocorticoid receptor (GR), GCs evoke apoptosis through transcriptional regulation of a complex, interactive gene network over a period of time preceding activation of the apoptotic enzymes.

Pediatric CD4+/CD8+ T-cell leukemia was represented by 3 CEM clones: two sensitive, CEM-C7-14 and CEM-C1-6, and one resistant, CEM-C1-15, to Dex.

GC-sensitive pediatric B-cell leukemia was represented by the SUP-B15 line and adult B-cell leukemia by RS4;11 cells.

Kasumi-1 cells gave an example of the rare Dex-sensitive acute myeloblastic leukemia (AML).

To test the generality of the correlations in malignant cell gene sets, we compared with GC effects on mouse non-transformed thymocytes.

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(PMID = 18045478.001).

[ISSN] 1475-2867

[Journal-full-title] Cancer cell international

[ISO-abbreviation] Cancer Cell Int.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA041407

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2228275

   

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[Title] The novel tryptamine derivative JNJ-26854165 induces wild-type p53- and E2F1-mediated apoptosis in acute myeloid and lymphoid leukemias.

The development of small-molecule activators of p53 is currently focused on malignancies containing a wild-type p53 genotype, which is present in most leukemias.

Here, we report the effects of JNJ-26854165 in acute leukemias.

JNJ-26854165 treatment induced p53-mediated apoptosis in acute leukemia cells with wild-type p53, in which p53 rapidly drives transcription-independent apoptosis followed by activation of a transcription-dependent pathway.

Apoptotic activity of JNJ-26854165 against primary acute leukemia cells was maintained in leukemia/stroma cocultures, unlike doxorubicin, which has reduced cytrotoxicity in coculture systems.

Our data suggest that JNJ-26854165 may provide a novel therapeutic approach for the treatment of acute leukemias.

[MeSH-major] Apoptosis / drug effects. E2F1 Transcription Factor / metabolism. Genes, p53. Leukemia, Myeloid, Acute / drug therapy. Tryptamines / pharmacology

[MeSH-minor] Cell Line, Tumor. Humans. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Transfection

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(PMID = 20736344.001).

[ISSN] 1538-8514

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA89346; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA089346-03; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / P01 CA049639-09A19007; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P01 CA055164-09; United States / NCI NIH HHS / CA / R01 CA089346; United States / NCI NIH HHS / CA / P30 CA016672-22S29015; United States / NCI NIH HHS / CA / P01 CA055164-08; United States / NCI NIH HHS / CA / CA55164; United States / NCI NIH HHS / CA / P01 CA049639; United States / NCI NIH HHS / CA / P01 CA055164

[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 / E2F1 Transcription Factor; 0 / Tryptamines

[Other-IDs] NLM/ NIHMS231527; NLM/ PMC2949269

   

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[Title] Acute leukemias in children with Down syndrome.

Children with Down syndrome have an increased risk for developing both acute myeloid as well as lymphoblastic leukemia.

These leukemias differ in presenting characteristics and underlying biology when compared with leukemias occurring in non-Down syndrome children.

Myeloid leukemia in children with Down syndrome is preceded by a preleukemic clone (transient leukemia or transient myeloproliferative disorder), which may disappear spontaneously, but may also need treatment in case of severe symptoms.

Twenty percent of children with transient leukemia subsequently develop myeloid leukemia.

This transition offers a unique model to study the stepwise development of leukemia, and of gene dosage effects mediated by aneuploidy.

[MeSH-major] Down Syndrome / complications. Leukemia, Myeloid / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Clinical Trials as Topic. Disease Progression. Humans. Infant. Infant, Newborn. Mutation

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(PMID = 18242315.001).

[ISSN] 0031-3955

[Journal-full-title] Pediatric clinics of North America

[ISO-abbreviation] Pediatr. Clin. North Am.

[Language] eng

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

[Publication-country] United States

[Number-of-references] 83

   

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[Title] Block of C/EBP alpha function by phosphorylation in acute myeloid leukemia with FLT3 activating mutations.

Mutations constitutively activating FLT3 kinase are detected in approximately 30% of acute myelogenous leukemia (AML) patients and affect downstream pathways such as extracellular signal-regulated kinase (ERK)1/2.

In contrast, there was no effect when serine 21 was mutated to aspartate (S21D), which mimics phosphorylation of C/EBPalpha.

Thus, our results suggest that therapies targeting the MEK/ERK cascade or development of protein therapies based on transduction of constitutively active C/EBPalpha may prove effective in treatment of FLT3 mutant leukemias resistant to the FLT3 inhibitor therapies.

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(PMID = 16446383.001).

[ISSN] 0022-1007

[Journal-full-title] The Journal of experimental medicine

[ISO-abbreviation] J. Exp. Med.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / K01 DK062064; United States / NCI NIH HHS / CA / P01 CA072009; United States / NIDDK NIH HHS / DK / DK62064; United States / NCI NIH HHS / CA / P01 CA72009

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

[Publication-country] United States

[Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Piperazines; 0 / Quinazolines; 452VLY9402 / Serine; E1IO3ICJ9A / tandutinib; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1

[Other-IDs] NLM/ PMC2118199

   

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[Title] A pharmacodynamic study of sorafenib in patients with relapsed and refractory acute leukemias.

We report the results of a phase I dose escalation trial of the multikinase inhibitor sorafenib in relapsed and refractory acute leukemia patients using an intermittent dosing regimen.

Fifteen patients with advanced leukemia (12 with acute myeloid leukemia, 2 with acute lymphoblastic leukemia, 1 with biphenotypic) and a median age of 63 (range 37-85) years were enrolled and treated on a dose escalation trial.

Out of 15 patients, 11 experienced stable disease as best response.

[MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyridines / therapeutic use

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(PMID = 20535150.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA128864; United States / NCI NIH HHS / CA / P30 CA006973-48; United States / NCRR NIH HHS / RR / UL1 RR025005; United States / NCI NIH HHS / CA / P30CA006973; United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CA / P50 CA100632; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCRR NIH HHS / RR / UL1 RR025005-04; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / P50 CA100632-06; United States / NCI NIH HHS / CA / R01 CA128864-04; United States / NCI NIH HHS / CA / U01 CA070095-17; United States / NCI NIH HHS / CA / U01CA70095

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases

[Other-IDs] NLM/ NIHMS201571; NLM/ PMC2921005

   

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[Title] Neuropilin-1 in acute myeloid leukemia: expression and role in proliferation and migration of leukemia cells.

The role of NRP-1 in the growth and progression of leukemia is unknown.

Our results showed that NRP-1 mRNA was expressed in six of seven leukemic cell lines and primary leukemias derived from all 24 patients with acute myeloid leukemia (AML).

Reduced NRP-1 expression by RNA interference led to a decrease of VEGF-mediated mitogenic and migration responses in acute myeloid leukemic cell line HEL.

Our data demonstrated that a higher level of NRP-1 mRNA was expressed in leukemias and NRP-1 promoted proliferation and chemotaxis of leukemic cells in response to VEGF.

[MeSH-major] Cell Movement. Cell Proliferation. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / pathology. Neuropilin-1 / analysis. Vascular Endothelial Growth Factor A / physiology

[MeSH-minor] Adolescent. Adult. Aged. Cell Survival. Chemotaxis. Child. Female. Humans. Male. Middle Aged. RNA, Messenger / analysis. RNA, Small Interfering / pharmacology. Tumor Cells, Cultured

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(PMID = 18231921.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 144713-63-3 / Neuropilin-1

   

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[Title] Patterns of leukemia incidence in the United States by subtype and demographic characteristics, 1997-2002.

OBJECTIVE: Efforts to prevent leukemia have been hampered by an inability to identify significant risk factors.

Exploring incidence patterns of leukemia subtypes by sex and race/ethnic group may generate new etiologic hypotheses and identify high-risk groups for further study.

METHODS: Data from the North American Association of Central Cancer Registries for 1997-2002 were used to assess patterns of leukemia incidence by subtype, sex, age, race and ethnicity.

RESULTS: A total of 144,559 leukemia cases were identified, including 66,067 (46%) acute and 71,860 (50%) chronic leukemias.

The highest rates of acute myeloid leukemia with and without maturation were observed in Asian-Pacific Islanders (API).

Hispanics had a higher incidence of acute lymphocytic leukemia, particularly in childhood, and promyelocytic leukemia than did non-Hispanics.

African-Americans had the highest rates of HTLV-1 positive adult T-cell leukemia/lymphoma.

A sharp increase in the incidence of chronic myeloid leukemia was observed for both APIs and Hispanics, 85 years and older.

CONCLUSION: Known risk factors are unlikely to explain the observed disparities in leukemia incidence.

Further studies of differences in environmental and genetic risk factors in these populations by specific leukemia subtype may provide clues to the etiologies of these malignancies.

[MeSH-major] Leukemia / ethnology

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(PMID = 18064533.001).

[ISSN] 0957-5243

[Journal-full-title] Cancer causes & control : CCC

[ISO-abbreviation] Cancer Causes Control

[Language] eng

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

[Publication-country] Netherlands

   

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To verify the expression of type 1 insulin-like growth factor receptor (IGF-IR) and its impact on hematopoietic cells apoptosis in myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML), marrow samples from 16 patients with MDS and 16 patients with AML were examined along with 16 healthy donors as controls.

Immunocytochemical methods (alkaline phosphatase anti-alkaline phosphatase) and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (fluorescence) were used simultaneously on nucleated cell cytospins.

In MDS nucleated cells, IGF-IR showed stronger expression in refractory anemia with excess blasts (RAEB)/RAEB in transformation/chronic myelomonocytic leukemia subgroup when compared to RA/RA with ringed sideroblasts cases (64.1+/-3.2 vs 53.5+/-16.2%) (P>0.05).

When analyzed by groups, cell number with IGF-IR expression showed a negative correlation to apoptotic cells amount (r=-0.852; P<0.01) but positive correlation to their blast count (r=0.677; P<0.01).

In conclusion, overexpression of IGF-IR existed in hematopoietic cells in MDS and AML marrows, which appeared to be contributed to disease progress.

[MeSH-major] Apoptosis. Bone Marrow Cells / cytology. Gene Expression Regulation, Neoplastic. Hematologic Neoplasms / metabolism. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Receptor, IGF Type 1 / biosynthesis

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Anemia / metabolism. Cell Transformation, Neoplastic. Child. Female. Humans. Male. Middle Aged

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(PMID = 16328478.001).

[ISSN] 0939-5555

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

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

[Publication-country] Germany

[Chemical-registry-number] EC 2.7.10.1 / Receptor, IGF Type 1

   

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[Title] 2-Methoxyestradiol blocks cell-cycle progression at the G2/M phase and induces apoptosis in human acute T lymphoblastic leukemia CEM cells.

The current study sought to determine the mechanism of anti-cancer activity of 2-ME2 in human acute T lymphoblastic leukemia CEM cells.

Exposure to 2-ME2 led to G(2)/M phase cell-cycle arrest, which preceded apoptosis characterized by the appearance of a sub-G(1) cell population.

Moreover, the expression level of p21 protein was upregulated, whereas Bcl-2 and dysfunctional p53 protein were downregulated, which also contributed to 2-ME2-induced apoptosis.

Our findings revealed that 2-ME2 might be a potent natural candidate for chemotherapeutic treatment of human acute T lymphoblastic leukemia when the precise effects of 2-ME2 were investigated further in other T leukemia cell lines and in primary T-cell leukemias.

[MeSH-major] Apoptosis / drug effects. Cell Cycle / drug effects. Estradiol / analogs & derivatives

[MeSH-minor] Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Cell Division / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. DNA Fragmentation / drug effects. Dose-Response Relationship, Drug. Flow Cytometry. G2 Phase / drug effects. Gene Expression Regulation, Leukemic / drug effects. Humans. Membrane Potential, Mitochondrial / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Time Factors. Tubulin Modulators / pharmacology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / metabolism

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(PMID = 20732853.001).

[ISSN] 1745-7270

[Journal-full-title] Acta biochimica et biophysica Sinica

[ISO-abbreviation] Acta Biochim. Biophys. Sin. (Shanghai)

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tubulin Modulators; 0 / Tumor Suppressor Protein p53; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol

   

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[Title] Cyclin D2 dysregulation by chromosomal translocations to TCR loci in T-cell acute lymphoblastic leukemias.

While the cyclin D1 and D3 genes (CCND1 and CCND3) are recurrently involved in genomic rearrangements, especially in B-cell lymphoid neoplasias, no clear involvement of the cyclin D2 gene (CCND2) has been reported to date.

Here, we identified chromosomal translocations targeting the CCND2 locus at 12p13, and the T-cell receptor beta (TCRB) or the TCRA/D loci in T-cell acute lymphoblastic leukemias (T-ALLs).

In order to evaluate dysregulation in T-ALL with respect to normal T-cell differentiation, we analyzed CCND2 expression in normal purified human thymic subpopulations.

CCND2 levels were downregulated through progression from the early stages of human T-cell differentiation, further suggesting that the massive and sustained expression in the CCND2-rearranged T-ALL cases was oncogenic.

This report is the first clear evidence of a direct involvement of cyclin D2 in human cancer due to recurrent somatic genetic alterations.

[MeSH-major] Chromosomes, Human, Pair 12 / genetics. Cyclins / biosynthesis. Cyclins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Receptors, Antigen, T-Cell / genetics. Translocation, Genetic

[MeSH-minor] Adult. Cell Separation. Child. Cyclin D2. Cytogenetic Analysis. DNA Mutational Analysis. Gene Rearrangement. Humans

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(PMID = 16270038.001).

[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 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Antigen, T-Cell

   

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[Title] PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2.

Leukemias and other cancers possess self-renewing stem cells that help to maintain the cancer.

Cancer stem cell eradication is thought to be crucial for successful anticancer therapy.

Using an acute myeloid leukemia (AML) model induced by the leukemia-associated monocytic leukemia zinc finger (MOZ)-TIF2 fusion protein, we show here that AML can be cured by the ablation of leukemia stem cells.

Cells expressing high amounts of CSF1R (CSF1R(high) cells), but not those expressing low amounts of CSF1R (CSF1R(low) cells), showed potent leukemia-initiating activity.

Moreover, induction of AML was suppressed in CSF1R-deficient mice and CSF1R inhibitors slowed the progression of MOZ-TIF2-induced leukemia.

Thus, in this subtype of AML, leukemia stem cells are contained within the CSF1R(high) cell population, and we suggest that targeting of PU.1-mediated upregulation of CSF1R expression might be a useful therapeutic approach.

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(PMID = 20418886.001).

[ISSN] 1546-170X

[Journal-full-title] Nature medicine

[ISO-abbreviation] Nat. Med.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA041456-24; United States / NCI NIH HHS / CA / R01 CA032551; United States / NCI NIH HHS / CA / P01 CA066996; United States / NCI NIH HHS / CA / 5P30-CA13330; United States / NCI NIH HHS / CA / CA041456-24; United States / NCI NIH HHS / CA / R01-CA41456; United States / NCI NIH HHS / CA / CA32551; United States / NCI NIH HHS / CA / R01 CA041456; United States / NCI NIH HHS / CA / P30 CA013330; United States / NHLBI NIH HHS / HL / R01 HL112719

[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 / Colony-Stimulating Factors; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Proto-Oncogene Proteins; 0 / Receptors, Colony-Stimulating Factor; 0 / Recombinant Fusion Proteins; 0 / Trans-Activators; 0 / proto-oncogene protein Spi-1; 81627-83-0 / Macrophage Colony-Stimulating Factor; EC 2.7.10.1 / Receptor, Macrophage Colony-Stimulating Factor

[Other-IDs] NLM/ NIHMS265702; NLM/ PMC3039870

   

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[Title] Loss of Ubr1 promotes aneuploidy and accelerates B-cell lymphomagenesis in TLX1/HOX11-transgenic mice.

The TLX1/HOX11 homeobox gene was originally identified at the recurrent t(10;14)(q24;q11) translocation breakpoint, a chromosomal abnormality observed in 5-7% of T-cell acute lymphoblastic leukemias (T-ALLs).

Proviral insertional mutagenesis studies performed on transgenic mice ectopically expressing TLX1/HOX11 in B lymphocytes (IgHmu-HOX11(Tg) mice) revealed the Ubr1 gene locus as a frequent site of proviral insertion, concomitant with accelerated development of diffuse large B-cell lymphoma.

Loss or reduced levels of Ubr1 expression was associated with 5/14 spontaneous B-cell lymphomas in IgHmu-HOX11(Tg) mice and one of nine primary human T-ALLs.

IgHmu-HOX11(Tg)/Ubr1(-/-) mice exhibited a modest but statistically significant acceleration of disease onset relative to IgHmu-HOX11(Tg)/Ubr1(+/-) mice.

Moreover, micronucleus assays to detect for chromosome missegregation were conducted and revealed increased presence of micronuclei in IgHmu-HOX11(Tg)/Ubr1(-/-) primary B lymphocyte cultures, and in both TLX1/HOX11-overexpressing T cell lines and fibroblast cultures following transfection with short interfering RNAs (siRNAs) targeting Ubr1.

[MeSH-major] Homeodomain Proteins / genetics. Lymphoma, B-Cell / genetics. Proto-Oncogene Proteins / genetics. Ubiquitin-Protein Ligases / deficiency

[MeSH-minor] Animals. Blotting, Southern. DNA Primers. Genome, Viral. Humans. Lymphocytes / physiology. Mice. Mice, Inbred C57BL. Mice, Knockout. Mice, Transgenic. Micronucleus Tests. Mitosis. RNA, Small Interfering / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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(PMID = 16862188.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United States / NIGMS NIH HHS / GM / GM69482

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

[Publication-country] England

[Chemical-registry-number] 0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Small Interfering; 143275-75-6 / TLX1 protein, human; EC 6.3.2.19 / UBR1 protein, mouse; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

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[Title] KIR ligands and prediction of relapse after unrelated donor hematopoietic cell transplantation for hematologic malignancy.

Recurrent malignancy remains a significant complication after allogeneic hematopoietic cell transplantation (HCT).

Efforts to decrease relapse have included donor lymphocyte infusion to stimulate donor anti-recipient T-cell allorecognition of major and minor histocompatibility differences.

Recently, alloreactive effects of donor natural killer cell-mediated inhibitory killer immunoglobulin-like receptor (KIR) recognition of recipient HLA-C and -B ligands have been described.

We examined KIR ligand effects on risk of relapse in 1770 patients undergoing myeloablative T-replete HCT from HLA-matched or -mismatched unrelated donors for the treatment of myeloid and lymphoid leukemias.

The decrease in hazard of relapse in patients with acute myelogenous leukemia was similar to that in patients with chronic myelogenous leukemia and acute lymphoblastic leukemia (P = .95).

Recipient homozygosity for HLA-B or -C epitopes that define KIR ligands is likely to be a predictive factor for leukemia relapse after myeloablative HCT from HLA-mismatched unrelated donors.

[MeSH-major] HLA-B Antigens / genetics. Hematologic Neoplasms / genetics. Hematopoietic Stem Cell Transplantation. Isoantigens / genetics. Living Donors. Lymphocyte Transfusion

[MeSH-minor] Disease-Free Survival. Epitopes / genetics. Epitopes / immunology. Female. Follow-Up Studies. HLA-C Antigens / genetics. HLA-C Antigens / immunology. Humans. Killer Cells, Natural / immunology. Ligands. Male. Receptors, Immunologic / agonists. Receptors, Immunologic / genetics. Receptors, Immunologic / immunology. Receptors, KIR. Recurrence. Risk Factors. Survival Rate. T-Lymphocytes / immunology. Transplantation, Homologous

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(PMID = 16864053.001).

[ISSN] 1083-8791

[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

[Grant] United States / NCI NIH HHS / CA / P01 CA 023766; United States / NIAID NIH HHS / AI / U24 AI 49215; United States / NIAID NIH HHS / AI / U24 AI49213; United States / NIAID NIH HHS / AI / UO1 AI 069197

[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

[Chemical-registry-number] 0 / Epitopes; 0 / HLA-B Antigens; 0 / HLA-Bw4 antigen; 0 / HLA-C Antigens; 0 / Isoantigens; 0 / Ligands; 0 / Receptors, Immunologic; 0 / Receptors, KIR

   

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[Title] Up-regulation of survivin by the E2A-HLF chimera is indispensable for the survival of t(17;19)-positive leukemia cells.

The E2A-HLF fusion transcription factor generated by t(17;19)(q22;p13) translocation is found in a small subset of pro-B cell acute lymphoblastic leukemias (ALLs) and promotes leukemogenesis by substituting for the antiapoptotic function of cytokines.

Forced expression of E2A-HLF in t(17;19)(-) leukemia cells up-regulated Survivin expression, suggesting that Survivin is a downstream target of E2A-HLF.

Analysis using a counterflow centrifugal elutriator revealed that t(17;19)+ ALL cells express Survivin throughout the cell cycle.

Reporter assays revealed that E2A-HLF induces survivin expression at the transcriptional level likely through indirect down-regulation of a cell cycle-dependent cis element in the promoter region.

Down-regulation of Survivin function by a dominant negative mutant of Survivin or reduction of Survivin expression induced massive apoptosis throughout the cell cycle in t(17;19)+ cells mainly through caspase-independent pathways involving translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus.

These data indicated that reversal of AIF translocation by Survivin, which is induced by E2A-HLF throughout the cell cycle, is one of the key mechanisms in the protection of t(17;19)+ leukemia cells from apoptosis.

[MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Basic-Leucine Zipper Transcription Factors / metabolism. Microtubule-Associated Proteins / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Recombinant Fusion Proteins / metabolism. Translocation, Genetic / genetics. Up-Regulation

[MeSH-minor] Animals. Apoptosis. Base Sequence. Caspases / metabolism. Cell Cycle / genetics. Cell Line, Tumor. Cell Survival / genetics. Chromosomes, Human, Pair 17 / genetics. Chromosomes, Human, Pair 19 / genetics. Humans. Inhibitor of Apoptosis Proteins. Mice. Molecular Sequence Data. Mutation. Precursor Cells, B-Lymphoid / cytology. Precursor Cells, B-Lymphoid / metabolism. Promoter Regions, Genetic / genetics. Transcriptional Activation

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(PMID = 19887369.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / HLF protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Recombinant Fusion Proteins; 0 / TCF3 protein, human; EC 3.4.22.- / Caspases

[Other-IDs] NLM/ PMC2804343

   

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[Title] Methylenetetrahydrofolate reductase gene polymorphisms and risk of acute lymphoblastic leukemia in children.

Leukemias are malignancies arising from rapidly proliferating hematopoietic cells having great requirement of DNA synthesis.

This case-control study was undertaken to analyze the association of the MTHFR gene polymorphisms 677 C"T and 1298 A"C and the risk of acute lymphoblastic leukemia in children.

MATERIALS AND METHODS: Eighty-six patients aged below 15 years with a confirmed diagnosis of acute lymphoblastic leukemia (ALL) and 99 matched controls were taken for this study.

[MeSH-major] Genetic Predisposition to Disease. Methylenetetrahydrofolate Reductase (NADPH2) / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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(PMID = 20071789.001).

[ISSN] 1998-4774

[Journal-full-title] Indian journal of cancer

[ISO-abbreviation] Indian J Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] India

[Chemical-registry-number] EC 1.5.1.20 / Methylenetetrahydrofolate Reductase (NADPH2)

   

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Arsenic, a natural substance that has been used as a drug for over 2000 years, has been revived because of its remarkable therapeutic efficacy in patients with acute promyelocytic leukemia (APL).

Specific degradation of the leukemogenic PML-RARalpha fusion protein induced by arsenic leads to the differentiation of leukemia cells.

Preliminary in vitro studies have also extended the potential anti-cancer effect of arsenic to non-APL leukemias, lymphoid malignancies and other cancers.

In vitro and in vivo studies demonstrate that arsenic exerts a broad spectrum of anti-cancer effects by induction of apoptosis, inhibition of cell proliferation, anti-angiogenesis and possible immunomodulation.

[MeSH-minor] Animals. Apoptosis / drug effects. Clinical Trials as Topic. Dose-Response Relationship, Drug. Humans. Leukemia / drug therapy. Lymphoma / drug therapy. Multiple Myeloma / drug therapy

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(PMID = 15655408.001).

[ISSN] 0959-4973

[Journal-full-title] Anti-cancer drugs

[ISO-abbreviation] Anticancer Drugs

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Arsenicals

[Number-of-references] 65

   

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The myeloid progenitor cell compartment (MPC) exhibits pronounced expansion in human myeloid leukemias.

It is becoming more apparent that progression of myelodysplastic syndromes and myeloproliferative diseases to acute myelogenous leukemia is the result of defects in progenitor cell maturation.

The MPC of bone marrow was analyzed in mice using a cell culture assay for measuring the relative frequency of proliferative myeloid progenitors.

Given the importance of this cell compartment in leukemia progression and the soon to be released genomic sequence of 15 mouse strains, these differences may provide a valuable tool for research into leukemia.

[MeSH-major] Cell Proliferation. Genetic Predisposition to Disease. Leukemia / genetics. Myeloid Progenitor Cells / metabolism

[MeSH-minor] Animals. Bone Marrow / growth & development. Cell Size. Chromosomes, Mammalian. Cytokines / metabolism. Flow Cytometry. Linkage Disequilibrium. Male. Mice. Mice, Inbred Strains. Stem Cells

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(PMID = 16897342.001).

[ISSN] 0938-8990

[Journal-full-title] Mammalian genome : official journal of the International Mammalian Genome Society

[ISO-abbreviation] Mamm. Genome

[Language] eng

[Grant] United States / NCI NIH HHS / CA / T32-CA09678

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cytokines

   

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[Title] Genetic stability of human embryonic stem cells: A first-step toward the development of potential hESC-based systems for modeling childhood leukemia.

Of interest, are the human childhood acute leukemias harboring specific fusion oncogenes such as MLL-AF4, TEL-AML1 or BCR-ABL wherein clinically significant manifestations arise in utero.

The mechanisms of transformation are not amenable to analysis with patient samples and, many mouse models for pediatric leukemias have fallen short in illuminating the human disease because they do not recapitulate key aspects of the actual disease, suggesting that the mouse models are missing essential components of oncogenesis present in the human embryo.

Prior to using hESCs as a tentative system for modeling leukemia, robust studies aimed at demonstrating their genetic stability are required; otherwise, cooperating mutations already present could prime hESCs susceptible to transformation.

This data should encourage stem cell researchers to implement robust cytogenetic tools when assessing hESC genetic stability, in order to detect tiny but relevant biological functional or structural chromosome abnormalities and, paves the way for generating fusion oncogene-expressing transgenic hESCs as a human-specific system for studying the early in utero events leading to normal hematopoietic specification versus childhood leukemic transformation.

[MeSH-major] Cell Differentiation / genetics. Cell Lineage / genetics. Disease Models, Animal. Embryo, Mammalian / cytology. Embryonic Stem Cells / physiology. Genomic Instability

[MeSH-minor] Acute Disease. Adult. Animals. Cells, Cultured. Child. Comparative Genomic Hybridization. Flow Cytometry. Humans. Immunoenzyme Techniques. Karyotyping. Leukemia / genetics. Male. Mice. Mice, SCID. Mutation / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Spectral Karyotyping. fms-Like Tyrosine Kinase 3 / genetics

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(PMID = 18930318.001).

[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 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

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[Title] Construction of doxycyline-dependent mini-HIV-1 variants for the development of a virotherapy against leukemias.

T-cell acute lymphoblastic leukemia (T-ALL) is a high-risk type of blood-cell cancer.

We describe the improvement of a candidate therapeutic virus for virotherapy of leukemic cells.

Virotherapy is based on the exclusive replication of a virus in leukemic cells, leading to the selective removal of these malignant cells.

These minimized HIV-rtTA variants contain up to 7 deletions/inactivating mutations (TAR, Tat, vif, vpR, vpU, nef and U3) and replicate efficiently in the leukemic SupT1 T cell line, but do not replicate in normal peripheral blood mononuclear cells.

The therapeutic viruses use CD4 and CXCR4 for cell entry and could potentially be used against CXCR4 expressing malignancies such as T-lymphoblastic leukemia/lymphoma, NK leukemia and some myeloid leukemias.

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(PMID = 17005036.001).

[ISSN] 1742-4690

[Journal-full-title] Retrovirology

[ISO-abbreviation] Retrovirology

[Language] ENG

[Grant] United States / PHS HHS / / R21-A147017-01

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

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antigens, CD4; 0 / Gene Products, tat; 0 / Receptors, CXCR4; 0 / tat Gene Products, Human Immunodeficiency Virus; N12000U13O / Doxycycline

[Other-IDs] NLM/ PMC1592508

   

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[Title] On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex.

The mixed lineage leukemia protein-1 (MLL1) is a member of the SET1 family of H3K4 methyltransferases and is frequently rearranged in acute leukemias.

Single turnover kinetic experiments reveal that the reaction leading to H3K4 dimethylation involves the transient accumulation of a monomethylated species, suggesting that the MLL1 core complex uses a non-processive mechanism to catalyze multiple lysine methylation.

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(PMID = 19556245.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA140522

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

[Publication-country] United States

[Chemical-registry-number] 0 / ASH2L protein, human; 0 / DNA-Binding Proteins; 0 / DPY30 protein, human; 0 / Histones; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / RBP5 protein, human; 0 / Retinol-Binding Proteins, Cellular; 0 / Transcription Factors; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine

[Other-IDs] NLM/ PMC2782018

   

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[Title] Cyclin A1 regulates WT1 expression in acute myeloid leukemia cells.

Cyclin A1 is a cell cycle protein that is expressed in testes, brain and CD34-positive hematopoietic progenitor cells.

Cyclin A1 is overexpressed in a variety of myeloid leukemic cell lines and in myeloid leukemic blasts.

Transgenic cyclin A1 overexpressing mice develop acute myeloid leukemia with low frequency.

Repression of WT1 expression was confirmed on the mRNA and protein level.

In addition, overexpression of the WT1-/+ isoform induced a G1 cell cycle arrest which was abrogated upon cotransfection with cyclin A1.

This study identified WT1 as a repressed target of cyclin A1 and suggests that the suppression of WT1 in cyclin A1-overexpressing leukemias might play a role in the growth and suppression of apoptosis in these leukemic cells.

[MeSH-minor] Animals. Blotting, Western. Bone Marrow / metabolism. Cell Line, Tumor. Colony-Forming Units Assay. Cyclin A1. G1 Phase / physiology. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Oligonucleotide Array Sequence Analysis. Protein Isoforms. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection. U937 Cells / metabolism

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(PMID = 19082485.001).

[ISSN] 1019-6439

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

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

[Publication-country] Greece

[Chemical-registry-number] 0 / CCNA1 protein, human; 0 / Ccna1 protein, mouse; 0 / Cyclin A; 0 / Cyclin A1; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / WT1 Proteins

   

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A phase 1 study was conducted to determine the maximum tolerated dose and toxicities of ABT-751 in patients with advanced myelodysplastic syndrome and relapsed or refractory acute leukemias.

RESULTS: Dose-limiting toxicity consisted of ileus in one patient at 200 mg/m(2), with a subsequent patient developing grade 2 constipation at the same dose level.

One patient with relapsed acute myelogenous leukemia achieved a complete remission that was sustained for 2 months.

Four other patients had transient hematologic improvements, consisting of a decrease in peripheral blood blasts and improvements in platelet counts.

CONCLUSION: Further assessment of ABT-751, especially in combination with other agents, in patients with acute leukemias is warranted.

[MeSH-minor] Acute Disease. Adult. Aged. Antigens, CD / analysis. Antigens, CD146. Antigens, CD31 / analysis. Antigens, CD45 / analysis. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Constipation / chemically induced. Diarrhea / chemically induced. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Endothelial Cells / chemistry. Female. Glycoproteins / analysis. Humans. Leukemia / blood. Leukemia / drug therapy. Leukemia / genetics. Male. Microtubules / metabolism. Middle Aged. Mutation. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / genetics. Nausea / chemically induced. Neoplasm Recurrence, Local. Neoplastic Cells, Circulating / chemistry. Neural Cell Adhesion Molecules / analysis. Peptides / analysis. Treatment Outcome. Tubulin / genetics. Vomiting / chemically induced

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(PMID = 16166440.001).

[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] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / ABT751; 0 / AC133 antigen; 0 / Antigens, CD; 0 / Antigens, CD146; 0 / Antigens, CD31; 0 / Antineoplastic Agents; 0 / Glycoproteins; 0 / Neural Cell Adhesion Molecules; 0 / Peptides; 0 / Sulfonamides; 0 / Tubulin; EC 3.1.3.48 / Antigens, CD45

   

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[Title] CXCR4 expression and biologic activity in acute myeloid leukemia are dependent on oxygen partial pressure.

In acute myeloid leukemia (AML), elevated expression of CXCR4 has been shown to correlate with shortened survival.

At this pO(2), CXCR4 surface and total expression were up-regulated within 10 hours in leukemic cell lines and patient samples as shown by Western blotting, fluorescence-activated cell sorting, and microscopy.

Given the importance of CXCR4 in cell signaling, survival, and adhesion in leukemia, the results suggest that pO(2) be considered a critical variable in conducting and interpreting studies of CXCR4 expression and regulation in leukemias.

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(PMID = 18957686.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P01 CA055164; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P01 CA55164

[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 / CXCL12 protein, human; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Receptors, CXCR4; S88TT14065 / Oxygen

[Other-IDs] NLM/ PMC2644078

   

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[Title] Survivin expression, apoptosis and proliferation in chronic myelomonocytic leukemia.

We analyzed the expression of the inhibitor of apoptosis survivin by immunocytochemistry in bone marrow cells from patients with chronic myelomonocytic leukemia (CMML) to evaluate possible abnormalities in comparison with other myelodysplastic (MDS) and myeloproliferative syndromes, and to investigate a possible correlation between survivin expression and altered apoptosis or proliferation, or relevant laboratory and clinical findings.

Thirty-four patients with CMML [18 MDS-CMML and 16 myeloproliferative disorder (MPD)-CMML], 90 with MDS, 41 with acute myeloid leukemia (AML), 19 with chronic MPD and 25 control subjects were studied.

In CMML and MDS apoptosis was significantly higher compared to normal controls and all other subtypes of leukemias (P < 0.0001).

In CMML there was no correlation between survivin expression and blast cell percentage, apoptosis or proliferation, FAB or WHO subgroup.

Survivin overexpression, by disrupting the balance between cell proliferation/differentiation and apoptosis, may play an important role in its pathophysiology.

[MeSH-major] Leukemia, Myelomonocytic, Chronic / pathology. Microtubule-Associated Proteins / physiology. Neoplasm Proteins / physiology

[MeSH-minor] Acute Disease. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis. Cell Division. Disease Progression. Female. Humans. Inhibitor of Apoptosis Proteins. Leukemia, Myeloid / classification. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Male. Middle Aged. Myelodysplastic Syndromes / metabolism. Myelodysplastic Syndromes / pathology

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(PMID = 16529600.001).

[ISSN] 0902-4441

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

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

[Publication-country] Denmark

[Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins

   

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Raf/MEK/Erk signaling is activated in the majority of acute myeloid leukemias (AMLs), providing rationale for targeting this pathway with therapeutic intent.

Our studies demonstrated that sorafenib significantly inhibited the phosphorylation levels of Raf downstream target proteins MEK1/2 and Erk, induced apoptosis and inhibited colony formation in AML cell lines and in primary AML samples.

Combination of sorafenib with cytarabine or the novel small molecule Bcl-2 inhibitor ABT-737 synergistically induced cell death in AML cell lines.

[MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / metabolism. Benzenesulfonates / pharmacology. Leukemia, Myeloid, Acute / drug therapy. Membrane Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Pyridines / pharmacology. Signal Transduction / drug effects

[MeSH-minor] Cell Line. Drug Synergism. Humans. Mitochondria / metabolism. Niacinamide / analogs & derivatives. Phenylurea Compounds

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(PMID = 18200035.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA100632; United States / NCI NIH HHS / CA / CA55164

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

[Publication-country] England

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Benzenesulfonates; 0 / Membrane Proteins; 0 / Phenylurea Compounds; 0 / Proto-Oncogene Proteins; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib

   

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[Title] Mucocutaneous findings in febrile neutropenic children with acute leukemias.

Febrile neutropenia is common in children with leukemia.

The authors prospectively examined children with fever with neutropenia in acute leukemia, aged 1-15 years, who were admitted to the Department of Pediatrics, King Chulalongkorn Memorial Hospital, between September 2000 and August 2001.

The prevalence of infection was found in severe neutropenia (absolute neutrophil count, ANC less than 500 cell/cu mm), moderate neutropenia (ANC, 500-1000 cell/cu mm) and mild neutropenia (ANC, 1001-1500 cell/cu mm) was 72%, 9% and 5%, respectively.

Daily physical examination of skin and mucous membrane are suggested for proper and prompt diagnosis and treatment of febrile neutropenic children with acute leukemia to reduce mortality and morbidity in these patients.

A Guideline for the use of antimicrobial agents in neutropenic patients with acute leukemia is proposed In conclusion, infection was commonly found in severe neutropenia.

Mucocutaneous infection was the most common site of infection infebrile neutropenia in children with leukemia.

[MeSH-major] Fever. Neutropenia / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Skin Diseases / etiology

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(PMID = 16083222.001).

[ISSN] 0125-2208

[Journal-full-title] Journal of the Medical Association of Thailand = Chotmaihet thangphaet

[ISO-abbreviation] J Med Assoc Thai

[Language] eng

[Publication-type] Journal Article

[Publication-country] Thailand

   

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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.

Virotherapy is based on the exclusive replication of a virus in leukemic cells, leading to the selective removal of these malignant cells.

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 mini-HIV variant that uses CD4 and CXCR4 for cell entry could potentially be used against CXCR4-expressing malignancies such as T-lymphoblastic leukemia/lymphoma, natural killer leukemia, and some myeloid leukemias.

[MeSH-major] HIV-1 / physiology. Leukemia-Lymphoma, Adult T-Cell / therapy. Leukemia-Lymphoma, Adult T-Cell / virology. T-Lymphocytes / virology

[MeSH-minor] Antigens, CD4 / biosynthesis. Cell Line, Tumor. Female. Gene Deletion. Genes, nef / genetics. Genes, vif / genetics. Genes, vpr / genetics. Genes, vpu / genetics. HIV Long Terminal Repeat / genetics. Humans. Jurkat Cells. Receptors, CXCR4 / biosynthesis. Virus Replication

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(PMID = 15833868.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NIAID NIH HHS / AI / R21-AI47017-01

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD4; 0 / Receptors, CXCR4

   

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[Title] An accurate and rapid flow cytometric diagnosis of BCR-ABL positive acute lymphoblastic leukemia.

Tyrosine kinase inhibitors have profoundly modified the treatment and prognosis of chronic myeloid leukemia and Ph(+) acute lymphoblastic leukemia.

A rapid and accurate detection of the BCR-ABL fusion protein is paramount today for an optimal management of Ph(+) acute lymphoblastic leukemia.

We have utilized a recently described and commercialized immunoassay that identifies qualitatively the presence of the BCR-ABL protein in leukemic cell lysates.

The assay was applied to 101 primary patient samples (94 acute leukemias and 7 chronic myeloid leukemia blast crisis) and the results of the immunoassay were concordant with those obtained by conventional molecular techniques.

This flow cytometric immunoassay has important implications for perfecting the management of Ph(+) acute lymphoblastic leukemia patients worldwide.

[MeSH-major] Flow Cytometry / methods. Fusion Proteins, bcr-abl / analysis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

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[Cites] N Engl J Med. 2000 Apr 6;342(14):998-1006 [10749961.001]

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[CommentIn] Haematologica. 2009 Dec;94(12):1639-41 [19996114.001]

(PMID = 19608682.001).

[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] EC 2.7.10.2 / Fusion Proteins, bcr-abl

[Other-IDs] NLM/ PMC2791932

   

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[Title] Phase I and pharmacologic study of infusional topotecan and Carboplatin in relapsed and refractory acute leukemia.

PURPOSE: To assess the maximum tolerated dose, toxicities, pharmacokinetics, and antileukemic activity of topotecan and carboplatin in adults with recurrent or refractory acute leukemias.

Among 45 evaluable patients, there were 7 complete remissions, 2 partial remissions, 1 incomplete complete remission, and 1 reversion to chronic-phase chronic myelogenous leukemia.

Leukemic cell levels of topoisomerase I, checkpoint kinase 1, checkpoint kinase 2, and Mcl-1 correlated with proliferating cell nuclear antigen but not with response.

Responses seem to correlate with low pretreatment blast cell Bcl-2 expression.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy

[MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Cells / drug effects. Bone Marrow Cells / metabolism. Carboplatin / administration & dosage. Carboplatin / adverse effects. Carboplatin / pharmacokinetics. Cell Cycle Proteins / metabolism. Combined Modality Therapy. DNA Topoisomerases, Type I / metabolism. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. HL-60 Cells. Hematopoietic Stem Cell Transplantation. Humans. Immunoblotting. Infusions, Intravenous. Male. Middle Aged. Neoplasm Recurrence, Local. Proliferating Cell Nuclear Antigen / metabolism. Topotecan / administration & dosage. Topotecan / adverse effects. Topotecan / pharmacokinetics. Treatment Outcome

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(PMID = 16166443.001).

[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

[Grant] United States / NCI NIH HHS / CA / R01 CA73709; United States / NCI NIH HHS / CA / U01 CA69854; United States / NCI NIH HHS / CA / U01 CA69912

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Proliferating Cell Nuclear Antigen; 7M7YKX2N15 / Topotecan; BG3F62OND5 / Carboplatin; EC 5.99.1.2 / DNA Topoisomerases, Type I

   

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Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem.

Thus, sorafenib may provide an effective therapeutic measure to treat Ph+ leukemias, particularly those expressing the T315I mutant, which is totally resistant to imatinib and the second generation BCR/ABL inhibitors.

[MeSH-major] Apoptosis / drug effects. Benzenesulfonates / pharmacology. Fusion Proteins, bcr-abl / antagonists & inhibitors. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Mitochondria / drug effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyridines / pharmacology

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(PMID = 19366808.001).

[ISSN] 1538-7445

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / ABT-737; 0 / Acetophenones; 0 / Benzamides; 0 / Benzenesulfonates; 0 / Benzopyrans; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Interleukin-3; 0 / Nitrophenols; 0 / Phenylurea Compounds; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrazines; 0 / Pyridines; 0 / Pyrimidines; 0 / Sulfonamides; 25X51I8RD4 / Niacinamide; 69G8BD63PP / Bortezomib; 8A1O1M485B / Imatinib Mesylate; 9ZOQ3TZI87 / sorafenib; E29LP3ZMUH / rottlerin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.4.22.- / Caspases

   

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[Title] Infant acute bilineal leukemia.

Most cases of acute leukemia can be assigned to the myeloid, B or T lineage.

There are rare cases of acute leukemia, which cannot be clearly classified, because either blasts express antigens of more than one lineage (acute biphenotypic leukemias) or distinct blast populations of two lineages co-exist (acute bilineal leukemias, aBLL).

We present a 10-month-old infant with de novo aBLL, characterized by blasts of monocytic and B-cell precursor lineages.

Despite poor initial response, both to acute lymphoblastic leukemia (ALL) induction treatment and acute myeloid leukemia induction blocks, the child reached complete clinical remission with minimal residual disease negative status and was transplanted.

This case report illustrates that aBLL is a very aggressive type of acute leukemia that should be individually treated and monitored, particularly in children less than 1 year of age.

[MeSH-major] B-Lymphocytes / pathology. Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Cell Lineage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Male. Remission Induction. Treatment Outcome

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(PMID = 19286255.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

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

[Publication-country] England

   

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[Title] KIS induces proliferation and the cell cycle progression through the phosphorylation of p27Kip1 in leukemia cells.

The mRNA expressions of KIS were successfully reduced in all cell lines.

We showed that KIS protein directly interacted with p27(Kip1) protein, and reduction of KIS inhibited the S10 phosphorylation of p27(Kip1) in leukemia cells.

On these cells transfected with siRNA KIS, the inhibition of S10 phosphorylation of p27(Kip1) was strongly suppressed cell proliferation in a time-dependent manner.

These data demonstrated that the KIS activity was induced during G0/G1, and it promotes cell cycle progression by phosphorylation of S10 on p27(Kip1).

We showed that KIS mRNA expression was increased in primary leukemia specimens (acute myelogenous leukemia (AML); 37, myelodysplastic syndrome (MDS); 72, acute lymphoblastic leukemia (ALL); 23), and the mean ratios of KIS to G3PDH in AML, MDS and ALL specimens were 3.62+/-0.68, 3.27+/-0.73 and 3.17+/-0.58, respectively.

Moreover, we found that KIS protein was overexpressed in all 132 adults cases of various leukemias, including 37 AML (8 M1, 12 M2, 2 M3, 7 M4, 8 M5), 72 MDS (42 RAEB-I, 30 REAB-II) and 23 ALL (23 L2).

This study demonstrates that the elevated levels of KIS protein in leukemia cells promote the cell cycle progression in leukemia cells.

[MeSH-major] Cell Cycle / physiology. Cell Proliferation. Intracellular Signaling Peptides and Proteins / metabolism. Intracellular Signaling Peptides and Proteins / physiology. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Protein-Serine-Threonine Kinases / physiology

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(PMID = 18384876.001).

[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 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / UHMK1 protein, human

   

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Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myeloid leukemia (CML) and Philadelphia-chromosome positive acute lymphoblastic leukemia (ALL), relapse with emerging imatinib-resistance mutations in the BCR/ABL kinase domain poses a significant problem.

Rottlerin also enhanced the cytotoxic effect of imatinib in leukemic cells from patients with CML blast crisis and Ph-positive ALL or a cell line expressing the imatinib-resistant E255K BCR/ABL mutant.

The present study indicates that rottlerin synergistically enhances imatinib-induced apoptosis through its mitochondrial uncoupling effect independent of PKCdelta and may contribute to the development of new treatment strategy to overcome the imatinib resistance and to cure the BCR/ABL expressing leukemias.

[MeSH-minor] Animals. Benzamides. Drug Synergism. Fusion Proteins, bcr-abl. Humans. Imatinib Mesylate. K562 Cells. Leukemia, Erythroblastic, Acute / drug therapy. Leukemia, Erythroblastic, Acute / enzymology. Mice. Mitochondria / drug effects. Mitochondria / enzymology. Mitochondria / metabolism. Up-Regulation / drug effects

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(PMID = 17130834.001).

[ISSN] 0950-9232

[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 / Acetophenones; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Benzopyrans; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Uncoupling Agents; 8A1O1M485B / Imatinib Mesylate; E29LP3ZMUH / rottlerin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 2.7.11.13 / Protein Kinase C-delta

   

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[Title] Therapeutic efficacy of the pan-cdk inhibitor PHA-793887 in vitro and in vivo in engraftment and high-burden leukemia models.

MATERIALS AND METHODS: Thirteen leukemic cell lines bearing different cytogenetic abnormalities and normal hematopoietic cells were used in cytotoxicity and colony assays.

The drug activity at the molecular level was analyzed by Western blotting.

PHA-793887 was also tested in vivo in several leukemia xenograft models.

RESULTS: PHA-793887 was cytotoxic for leukemic cell lines in vitro, with IC(50) ranging from 0.3 to 7 microM (mean: 2.9 microM), regardless of any specific chromosomal aberration.

Interestingly, in colony assays PHA-793887 showed very high activity against leukemia cell lines, with an IC(50) <0.1 microM (mean: 0.08 microM), indicating that it has efficient and prolonged antiproliferative activity.

PHA-793887 induced cell-cycle arrest, inhibited Rb and nucleophosmin phosphorylation, and modulated cyclin E and cdc6 expression at low doses (0.2-1 microM) and induced apoptosis at the highest dose (5 microM).

It was also effective in vivo in both subcutaneous xenograft and primary leukemic disseminated models that better mimic naturally occurring human disease.

Interestingly, in one disseminated model derived from a relapsed Philadelphia-positive acute lymphoid leukemia patient, PHA-793887 showed strong therapeutic activity also when treatment was started after establishment of high disease burden.

CONCLUSIONS: We conclude that PHA-793887 has promising therapeutic activity against acute leukemias in vitro and in vivo.

[MeSH-major] Antineoplastic Agents / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors. Leukemia / drug therapy

[MeSH-minor] Animals. Apoptosis. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Disease Models, Animal. Drug Screening Assays, Antitumor. Humans. Immunohistochemistry. Inhibitory Concentration 50. Mice. Mice, SCID

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(PMID = 20167248.001).

[ISSN] 1873-2399

[Journal-full-title] Experimental hematology

[ISO-abbreviation] Exp. Hematol.

[Language] eng

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

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.11.22 / Cyclin-Dependent Kinases