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16. Braun FK, Fecker LF, Schwarz C, Walden P, Assaf C, Dürkop H, Sterry W, Eberle J: Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells. J Invest Dermatol; 2007 Oct;127(10):2425-37
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  • [Title] Blockade of death receptor-mediated pathways early in the signaling cascade coincides with distinct apoptosis resistance in cutaneous T-cell lymphoma cells.
  • Control of apoptosis via death ligands plays a basic role for lymphocyte homeostasis and lymphoma development.
  • In this study, cutaneous T-cell lymphoma (CTCL) cell lines revealed pronounced resistance to death ligands as compared to cell lines of T-cell acute lymphoblastic leukemia (T-ALL).
  • The proapoptotic activity of tumor necrosis factor (TNF)-alpha was blocked, sensitivity to TNF-related apoptosis-inducing ligand was significantly reduced, and 1/4 CTCL cell lines was resistant to CD95 activation.
  • No indication for a responsibility of typical downstream regulators of apoptosis was obtained, but loss of CD95 was found in 1/4, loss of TNF-R1 in 3/4, loss of caspase-10 in 2/4, loss of Bid in 1/4, and overexpression of cellular flice inhibitory protein was found in 4/4 CTCL cell lines.
  • [MeSH-major] Apoptosis / physiology. Lymphoma, T-Cell, Cutaneous / pathology. Receptors, Death Domain / antagonists & inhibitors. Signal Transduction / physiology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD95 / physiology. BH3 Interacting Domain Death Agonist Protein / physiology. CASP8 and FADD-Like Apoptosis Regulating Protein / physiology. Caspase 10 / physiology. Cell Line, Tumor. Female. Humans. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Male. Middle Aged. TNF-Related Apoptosis-Inducing Ligand / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / physiology. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / physiology

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  • (PMID = 17495957.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / BH3 Interacting Domain Death Agonist Protein; 0 / BID protein, human; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / Receptors, Death Domain; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 3.4.22.- / Caspase 10
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17. Dzhagalov I, Dunkle A, He YW: The anti-apoptotic Bcl-2 family member Mcl-1 promotes T lymphocyte survival at multiple stages. J Immunol; 2008 Jul 1;181(1):521-8
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  • Genetic studies have demonstrated that the Bcl-2 family member Mcl-1 is an important anti-apoptotic protein in the development of multiple cell types including T lymphocytes.
  • In this study, we examined the expression pattern of Mcl-1 in different populations of T cells at the single-cell level and found that Mcl-1 protein is constitutively expressed in all T cell populations and up-regulated upon TCR stimulation.
  • We then investigated the role of Mcl-1 in the survival of these different populations by conditionally deleting Mcl-1 at various T cell stages.

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  • (PMID = 18566418.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI074754; United States / NIAID NIH HHS / AI / AI054658-05; United States / NCI NIH HHS / CA / R01 CA092123; United States / NCI NIH HHS / CA / CA092123-05; United States / NIAID NIH HHS / AI / R01 AI054658-05; United States / NIAID NIH HHS / AI / AI54683; United States / NCI NIH HHS / CA / R01 CA092123-05; United States / NCI NIH HHS / CA / CA92123; United States / NIAID NIH HHS / AI / R01 AI054658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-X Protein
  • [Other-IDs] NLM/ NIHMS66462; NLM/ PMC2561902
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18. Look AT: Investigator profile. An interview with A. Thomas Look, M.D. Interview by Vicki Glaser. Zebrafish; 2005;2(4):231-6
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  • Work in Dr. Look's laboratory focuses on the molecular pathogenesis of leukemia.
  • His group has been credited with the identification and functional analysis of several chimeric oncogenes activated by chromosomal translocations, including the E2A-HLF transcription factor, which was shown to act through an evolutionarily conserved genetic pathway to promote leukemia cell survival.
  • Their efforts in human T-cell acute lymphoblastic leukemia have revealed key multistep mutational pathways that drive the pathogenesis of this disease and demonstrated that NOTCH1 receptors are mutationally activated in a majority of these cases.
  • Look's laboratory developed the first transgenic model of leukemia in the zebrafish, opening the way for chemical and genome-wide genetic modifier screens in a vertebrate disease model.

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  • (PMID = 18248181.001).
  • [ISSN] 1557-8542
  • [Journal-full-title] Zebrafish
  • [ISO-abbreviation] Zebrafish
  • [Language] eng
  • [Publication-type] Interview
  • [Publication-country] United States
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19. Verbeek WH, Van De Water JM, Al-Toma A, Oudejans JJ, Mulder CJ, Coupé VM: Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands. Scand J Gastroenterol; 2008;43(11):1322-8
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  • [Title] Incidence of enteropathy--associated T-cell lymphoma: a nation-wide study of a population-based registry in The Netherlands.
  • OBJECTIVE: Enteropathy-associated T-cell lymphomas (EATLs) are T-cell non-Hodgkin lymphomas of the small bowel, which are specifically associated with coeliac disease (CD).
  • We included all T-cell lymphomas detected between January 2000 and December 2006 that initially presented in the small bowel.
  • Finally, the distribution of characteristics such as the localization, the Marsh classification and method of diagnosis are described.
  • Most EATLs were localized in the proximal small intestine and the diagnosis was made by surgical resection in the majority of cases.
  • CONCLUSIONS: EATL is a rare disease with an incidence of 0.10 per 100,000 inhabitants per year, occurring in older age, with a peak incidence in the 7th decade.
  • [MeSH-major] Celiac Disease / epidemiology. Lymphoma, T-Cell / epidemiology

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  • (PMID = 18618372.001).
  • [ISSN] 1502-7708
  • [Journal-full-title] Scandinavian journal of gastroenterology
  • [ISO-abbreviation] Scand. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
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20. Yu Q, Sharma A, Sen JM: TCF1 and beta-catenin regulate T cell development and function. Immunol Res; 2010 Jul;47(1-3):45-55
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  • [Title] TCF1 and beta-catenin regulate T cell development and function.
  • T cell factor-1 (TCF1) critically regulates T cell development.
  • We have genetically manipulated the beta-catenin gene and generated mutant mice that have shown an essential role for beta-catenin and TCF1 during pre-T cell receptor (TCR) and TCR-dependent stages of T cell development.
  • [MeSH-major] Cell Differentiation. Gene Expression Regulation. T Cell Transcription Factor 1 / metabolism. T-Lymphocytes / cytology. T-Lymphocytes / immunology. beta Catenin / metabolism
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / immunology. Humans. Mice. Receptors, Antigen, T-Cell / genetics. Receptors, Antigen, T-Cell / metabolism. Signal Transduction

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  • (PMID = 20082155.001).
  • [ISSN] 1559-0755
  • [Journal-full-title] Immunologic research
  • [ISO-abbreviation] Immunol. Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 AG000768-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell; 0 / T Cell Transcription Factor 1; 0 / beta Catenin
  • [Other-IDs] NLM/ NIHMS172600; NLM/ PMC2891409
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21. Hwang C, Jang S, Choi DK, Kim S, Lee JH, Lee Y, Kim CD, Lee JH: The role of nkx2.5 in keratinocyte differentiation. Ann Dermatol; 2009 Nov;21(4):376-81
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  • BACKGROUND: Nkx2.5 is a homeodomain-containing nuclear transcription protein that has been associated with acute T-lymphoblastic leukemia.
  • In addition, the expression of Nkx2.5 was significantly increased in psoriasis and squamous cell carcinoma, but was barely detected in atopic dermatitis and basal cell carcinoma.
  • CONCLUSION: These results suggest that Nkx2.5 may play a role in the change from proliferation to differentiation of keratinocytes and in the pathogenesis of skin disease with aberrant keratinocyte differentiation.

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  • (PMID = 20523827.001).
  • [ISSN] 2005-3894
  • [Journal-full-title] Annals of dermatology
  • [ISO-abbreviation] Ann Dermatol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2861273
  • [Keywords] NOTNLM ; Keratinocyte differentiation / Nkx2.5 / Transcription factor
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22. Chen W, Wang E, Lu Y, Gaal KK, Huang Q: Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review. Am J Clin Pathol; 2010 Jan;133(1):75-82
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  • [Title] Therapy-related acute lymphoblastic leukemia without 11q23 abnormality: report of six cases and a literature review.
  • Therapy-related acute lymphoblastic leukemia (t-ALL) is a rare secondary leukemia following chemotherapy and/or radiotherapy for primary malignancies.
  • Chromosomal 11q23 abnormality, frequently detected in therapy-related acute myeloid leukemia, is the most common cytogenetic alteration in t-ALL.
  • However, t-ALL cases without 11q23 abnormality have been rarely described.
  • In the 48 cases, an 11q23 abnormality involving the MLL gene locus was the predominant chromosomal aberration (32 [67%]), followed by t(9;22) (6 [13%]) and a normal karyotype (4 [8%]).
  • Compared with t-ALL cases with an 11q23 abnormality, cases without an 11q23 abnormality had a relatively longer latency period (median, 36 vs 19 months) and a different primary malignancy spectrum.
  • The t(8;14)(q11.2;q32), a rare, nonrandom, balanced chromosomal translocation differing from the more common translocation involving c-MYC on chromosome 8q24, was seen in 1 adult t-ALL case, which may suggest another possible pathogenesis of this disease.
  • [MeSH-major] Chromosomes, Human, Pair 11. Combined Modality Therapy / adverse effects. Neoplasms / therapy. Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / etiology

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  • (PMID = 20023261.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 42
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23. Brewer JL, Ericson SG: An improved methodology to detect human T cell receptor beta variable family gene expression patterns. J Immunol Methods; 2005 Jul;302(1-2):54-67
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  • [Title] An improved methodology to detect human T cell receptor beta variable family gene expression patterns.
  • Comprehensive gene expression analysis of the T cell receptor repertoire of an individual can be very useful in evaluating the immune response in a variety of conditions.
  • Antibody-based analysis methods can detect approximately 60% of the human T cell receptor beta variable (TCRBV) proteins, while gene expression analysis, primarily through employment of the polymerase chain reaction (PCR), has had somewhat greater success in the detection of additional TCRBV families.
  • We describe here a real-time reverse transcription polymerase chain reaction-based method, which allows efficient automation and integration of amplification, detection, and analysis with sequence-specific detection of all T cell receptor beta variable gene families, subfamilies, and alleles.
  • [MeSH-major] Gene Expression Profiling / methods. Multigene Family. Receptors, Antigen, T-Cell, alpha-beta / biosynthesis. Receptors, Antigen, T-Cell, alpha-beta / genetics
  • [MeSH-minor] DNA Primers. Fluorometry / methods. Genetic Variation. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Humans. Polymerase Chain Reaction / methods. RNA, Messenger / biosynthesis

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  • (PMID = 16038929.001).
  • [ISSN] 0022-1759
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 P20 RR16440-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 0 / Receptors, Antigen, T-Cell, alpha-beta
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2
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4. Geurts JJ, Blezer EL, Vrenken H, van der Toorn A, Castelijns JA, Polman CH, Pouwels PJ, Bö L, Barkhof F: Does high-field MR imaging improve cortical lesion detection in multiple sclerosis? J Neurol; 2008 Feb;255(2):183-91
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  • [Title] Does high-field MR imaging improve cortical lesion detection in multiple sclerosis?
  • OBJECTIVE: Cortical lesions in multiple sclerosis (MS) are notoriously difficult to visualize with standard MR imaging (MRI) techniques.
  • However, the use of higher field-strengths with intrinsically higher signal-to-noise, which can partly be used to increase spatial resolution, may improve cortical lesion detection.
  • Therefore, in this post mortem study, the sensitivity of high field-strength MRI (4.7 T) for cortical lesions was investigated, and compared to that of standard field-strength (1.5 T).
  • Proteolipid protein (PLP)-stained tissue sections (10 microm) of the same brain slices were matched to the corresponding MR images, and cortical lesions were scored on all three MR sequences (blinded to histology) and in tissue sections (blinded to MRI).
  • Sensitivity of the sequences for four cortical lesion types was calculated.
  • RESULTS: Sensitivity for purely intracortical lesions (histological lesion types II, III, and IV; n = 128) was below 10 % for both 1.5 T and 4.7 T MRI, while mixed gray matter-white matter (type I) lesions (n = 5) were detected in four out of five cases.
  • CONCLUSIONS: MRI sensitivity for post mortem detection of cortical lesions is low, even when a higher field-strength was used.
  • It varies, however, for different subtypes of cortical lesions.

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  • (PMID = 18231704.001).
  • [ISSN] 0340-5354
  • [Journal-full-title] Journal of neurology
  • [ISO-abbreviation] J. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Fixatives; 1HG84L3525 / Formaldehyde
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25. Tosello V, Mansour MR, Barnes K, Paganin M, Sulis ML, Jenkinson S, Allen CG, Gale RE, Linch DC, Palomero T, Real P, Murty V, Yao X, Richards SM, Goldstone A, Rowe J, Basso G, Wiernik PH, Paietta E, Pieters R, Horstmann M, Meijerink JP, Ferrando AA: WT1 mutations in T-ALL. Blood; 2009 Jul 30;114(5):1038-45
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  • The molecular mechanisms involved in disease progression and relapse in T-cell acute lymphoblastic leukemia (T-ALL) are poorly understood.
  • This analysis showed that diagnosis and relapsed cases have common genetic alterations, but also that relapsed samples frequently lose chromosomal markers present at diagnosis, suggesting that relapsed T-ALL emerges from an ancestral clone different from the major leukemic population at diagnosis.
  • [MeSH-major] Genes, Wilms Tumor. Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adult. Child. Chromosome Aberrations. Clone Cells / chemistry. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. Disease Progression. Genes, Homeobox. Humans. Kaplan-Meier Estimate. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Oncogenes. Polymorphism, Single Nucleotide. Prognosis. Recurrence. WT1 Proteins / chemistry. WT1 Proteins / genetics. Zinc Fingers / genetics

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  • (PMID = 19494353.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE15931
  • [Grant] United States / NCI NIH HHS / CA / CA114737; United Kingdom / Medical Research Council / / MC/ U137686856; United States / NCI NIH HHS / CA / R01 CA129382; United Kingdom / Medical Research Council / / ; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01CA120196; United States / NCI NIH HHS / CA / R01CA129382; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA120196-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / WT1 Proteins
  • [Other-IDs] NLM/ PMC2721784
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26. Romana SP, Radford-Weiss I, Ben Abdelali R, Schluth C, Petit A, Dastugue N, Talmant P, Bilhou-Nabera C, Mugneret F, Lafage-Pochitaloff M, Mozziconacci MJ, Andrieu J, Lai JL, Terre C, Rack K, Cornillet-Lefebvre P, Luquet I, Nadal N, Nguyen-Khac F, Perot C, Van den Akker J, Fert-Ferrer S, Cabrol C, Charrin C, Tigaud I, Poirel H, Vekemans M, Bernard OA, Berger R, Groupe Francophone de Cytogénétique Hématologique: NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique. Leukemia; 2006 Apr;20(4):696-706
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  • [Title] NUP98 rearrangements in hematopoietic malignancies: a study of the Groupe Francophone de Cytogénétique Hématologique.
  • In order to gain additional clinico-hematological data and to identify new partners of NUP98, the Groupe Francophone de Cytogénétique Hématologique (GFCH) collected cases of hematological malignancies where a 11p15 rearrangement was detected.
  • Genes of the HOXA cluster and the nuclear-receptor set domain (NSD) genes were frequently fused to NUP98, mainly in de novo myeloid malignancies whereas the DDX10 and TOP1 genes were equally rearranged in de novo and in therapy-related myeloid proliferations.
  • Involvement of ADD3 and C6ORF80 genes were detected, respectively, in myeloid disorders and in T-cell acute lymphoblastic leukemia (T-ALL), whereas the RAP1GDS1 gene was fused to NUP98 in T-ALL.

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  • (PMID = 16467868.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Nuclear Pore Complex Proteins; 0 / Nup98 protein, human; 0 / Receptors, Cytoplasmic and Nuclear; 157907-48-7 / HoxA protein
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27. Hagemeijer A, Graux C: ABL1 rearrangements in T-cell acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2010 Apr;49(4):299-308
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  • [Title] ABL1 rearrangements in T-cell acute lymphoblastic leukemia.
  • T-cell acute lymphoblastic leukemia (T-ALL) is the result of multiple oncogenic insults of thymocytes.
  • [MeSH-major] Gene Rearrangement. Oncogene Proteins, Fusion / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-abl / genetics

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  • (PMID = 20073070.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  • [Number-of-references] 60
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28. Cai Y, Xu Z, Xie J, Ham AJ, Koury MJ, Hiebert SW, Brandt SJ: Eto2/MTG16 and MTGR1 are heteromeric corepressors of the TAL1/SCL transcription factor in murine erythroid progenitors. Biochem Biophys Res Commun; 2009 Dec 11;390(2):295-301
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  • The TAL1 (or SCL) gene, originally discovered through its involvement by a chromosomal translocation in T-cell acute lymphoblastic leukemia, encodes a basic helix-loop-helix (bHLH) transcription factor essential for hematopoietic and vascular development.

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  • (PMID = 19799863.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL049118; United States / NHLBI NIH HHS / HL / HL049118-15; United States / NHLBI NIH HHS / HL / R01 HL49118; United States / NHLBI NIH HHS / HL / R01 HL049118-15; United States / NCI NIH HHS / CA / 5P30CA068485; United States / NCI NIH HHS / CA / P30 CA068485
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CBFA2T2 myeloid-transforming gene-related protein; 0 / Cbfa2t3 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tal1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS151956; NLM/ PMC2774815
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29. Chiarini F, Grimaldi C, Ricci F, Tazzari PL, Evangelisti C, Ognibene A, Battistelli M, Falcieri E, Melchionda F, Pession A, Pagliaro P, McCubrey JA, Martelli AM: Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia. Cancer Res; 2010 Oct 15;70(20):8097-107
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  • [Title] Activity of the novel dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor NVP-BEZ235 against T-cell acute lymphoblastic leukemia.
  • Recent findings have highlighted that constitutively active phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival, and drug resistance.
  • Here, we have analyzed the therapeutic potential of the novel dual PI3K/mTOR inhibitor NVP-BEZ235, an orally bioavailable imidazoquinoline derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples.
  • NVP-BEZ235 was cytotoxic to a panel of T-ALL cell lines as determined by MTT assays.
  • NVP-BEZ235 treatment resulted in cell cycle arrest and apoptosis.
  • Remarkably, NVP-BEZ235 targeted the side population of both T-ALL cell lines and patient lymphoblasts, which might correspond to leukemia-initiating cells, and synergized with chemotherapeutic agents (cyclophosphamide, cytarabine, dexamethasone) currently used for treating T-ALL patients.
  • Taken together, our findings indicate that longitudinal inhibition at two nodes of the PI3K/Akt/mTOR network with NVP-BEZ235, either alone or in combination with chemotherapeutic drugs, may be an efficient treatment of those T-ALLs that have aberrant upregulation of this signaling pathway for their proliferation and survival.
  • [MeSH-major] Imidazoles / therapeutic use. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Quinolines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Autophagy / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Coculture Techniques. Flow Cytometry. Humans. Jurkat Cells / drug effects. Mice. Stromal Cells / drug effects


30. Reckard JM, Chung MH, Varma MK, Zagorski SM: Management of intraabdominal hypertension by percutaneous catheter drainage. J Vasc Interv Radiol; 2005 Jul;16(7):1019-21
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  • The authors report a case of an 18-year-old man with T-cell acute lymphocytic leukemia who developed hemorrhagic pancreatitis after chemotherapy.
  • [MeSH-minor] Acute Disease. Adolescent. Hemorrhage / complications. Humans. Leukemia-Lymphoma, Adult T-Cell / complications. Male. Pancreatitis / complications. Ultrasonics. Ultrasonography

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  • (PMID = 16002511.001).
  • [ISSN] 1051-0443
  • [Journal-full-title] Journal of vascular and interventional radiology : JVIR
  • [ISO-abbreviation] J Vasc Interv Radiol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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31. Chang PY, Draheim K, Kelliher MA, Miyamoto S: NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cells. Cancer Res; 2006 Jun 15;66(12):6008-13
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  • [Title] NFKB1 is a direct target of the TAL1 oncoprotein in human T leukemia cells.
  • We recently showed that a subset of human T acute lymphoblastic leukemia (T-ALL) cell lines expresses low basal levels of p50, a nuclear factor-kappaB (NF-kappaB)/Rel family member, resulting in their capacity to activate the atypical p65:cRel complex rather than the classic p50:p65 dimer.
  • When TAL1 expression is reduced in CEM T leukemia cells, basal NFKB1 expression is increased, and the levels of p65:cRel complex and transcription of its target gene, such as intercellular adhesion molecule-1 (ICAM-1), are reduced in response to etoposide treatment.
  • Moreover, a significant negative correlation between NFKB1 and TAL1 or LMO1 was found in primary human TAL1/LMO1 double-positive T-ALL samples previously described by Ferrando et al. Thus, TAL1 modulates NFKB1 expression and an NF-kappaB-dependent transcriptional program in a subset of human T-cell leukemia cells.

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  • (PMID = 16778171.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / R01-CA077474; United States / NCI NIH HHS / CA / R01-CA081065
  • [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 / NF-kappa B p50 Subunit; 0 / NFKB1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Transcription Factor RelA; 135471-20-4 / TAL1 protein, human; 6PLQ3CP4P3 / Etoposide
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32. De Keersmaecker K, Rocnik JL, Bernad R, Lee BH, Leeman D, Gielen O, Verachtert H, Folens C, Munck S, Marynen P, Fornerod M, Gilliland DG, Cools J: Kinase activation and transformation by NUP214-ABL1 is dependent on the context of the nuclear pore. Mol Cell; 2008 Jul 11;31(1):134-42
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  • We show that NUP214-ABL1 displays attenuated transforming capacity as compared to BCR-ABL1 and that NUP214-ABL1 preferentially transforms T cells, which is in agreement with its unique occurrence in T cell acute lymphoblastic leukemia.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Nuclear Pore / enzymology. Oncogene Proteins, Fusion / metabolism. Protein-Tyrosine Kinases / metabolism
  • [MeSH-minor] Animals. Cell Line. Enzyme Activation. Humans. Mice. Nuclear Pore Complex Proteins / metabolism

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  • (PMID = 18614052.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA8484
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NUP214-ABL1 fusion protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; EC 2.7.10.1 / Protein-Tyrosine Kinases
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33. Taki T, Taniwaki M: Chromosomal translocations in cancer and their relevance for therapy. Curr Opin Oncol; 2006 Jan;18(1):62-8
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  • Observation of high frequencies of mutations in NOTCH1, NPM and JAK2 in T-cell acute lymphoblastic leukemia, acute myeloid leukemia with normal karyotype and myeloproliferative disorders (polycythemia vera, essential thrombocythemia and idiopathic myelofibrosis) have provided important suggestions for a better understanding of chromosomal translocations.

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  • (PMID = 16357566.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 46
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34. Beesley AH, Firth MJ, Ford J, Weller RE, Freitas JR, Perera KU, Kees UR: Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism. Br J Cancer; 2009 Jun 16;100(12):1926-36
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  • [Title] Glucocorticoid resistance in T-lineage acute lymphoblastic leukaemia is associated with a proliferative metabolism.
  • Glucocorticoids (GCs) are among the most important drugs for acute lymphoblastic leukaemia (ALL), yet despite their clinical importance, the exact mechanisms involved in GC cytotoxicity and the development of resistance remain uncertain.
  • We examined the baseline profile of a panel of T-ALL cell lines to determine factors that contribute to GC resistance without prior drug selection.
  • The data also provide the first evidence that altered expression of wild-type MLL may contribute to GC-resistant phenotypes.
  • [MeSH-major] Cell Proliferation / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Methylprednisolone / pharmacology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Signal Transduction / drug effects


35. Shimizu D, Taki T, Utsunomiya A, Nakagawa H, Nomura K, Matsumoto Y, Nishida K, Horiike S, Taniwaki M: Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma. Int J Hematol; 2007 Apr;85(3):212-8
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  • [Title] Detection of NOTCH1 mutations in adult T-cell leukemia/lymphoma and peripheral T-cell lymphoma.
  • We analyzed NOTCH1 gene mutation in 53 adults with mature T-cell leukemia/lymphoma: 21 patients with adult T-cell leukemia (ATL), 25 with T-cell non-Hodgkin's lymphoma (T-NHL), and 7 with T-cell prolymphocytic leukemia.
  • We detected a nonsense mutation, C7249T (resulting in Q2417X, where X is a termination codon) in the PEST domain of NOTCH1 in an ATL patient and detected a 3-bp deletion (positions 7234-7236) that resulted in deletion of a proline codon at codon 2412 in the PEST domain of NOTCH1 in a patient with a T-NHL, peripheral T-cell lymphoma-unspecified (PTCL-u).
  • These findings suggest that nonsense mutation in the PEST domain in the ATL case was associated with NOTCH1 signaling through a pathway different from that for T-cell acute lymphoblastic leukemia (T-ALL).
  • Although NOTCH1 mutation occurs infrequently in mature T-cell leukemia/lymphoma, NOTCH1 may be involved in leukemogenesis associated with various forms of T-cell leukemia/lymphoma rather than only with T-ALL.
  • [MeSH-major] Codon, Nonsense. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Peripheral / genetics. Receptor, Notch1 / genetics

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  • (PMID = 17483057.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Codon, Nonsense; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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36. Dohda T, Maljukova A, Liu L, Heyman M, Grandér D, Brodin D, Sangfelt O, Lendahl U: Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines. Exp Cell Res; 2007 Aug 15;313(14):3141-52
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  • [Title] Notch signaling induces SKP2 expression and promotes reduction of p27Kip1 in T-cell acute lymphoblastic leukemia cell lines.
  • In T-cell acute lymphoblastic leukemia (T-ALL) NOTCH 1 receptors are frequently mutated.
  • This leads to aberrantly high Notch signaling, but how this translates into deregulated cell cycle control and the transformed cell type is poorly understood.
  • Notch activity, measured immediately downstream of the NOTCH 1 receptor, is high, but expression of the canonical downstream Notch response genes HES 1 and HEY 2 is low both in primary cells from T-ALL patients and in T-ALL cell lines.
  • We show that in T-ALL cell lines, recruitment of NOTCH 1 intracellular domain (ICD) to the SKP2 promoter was accompanied by high SKP2 and low p27Kip1 protein levels.
  • T-ALL cells show a rapid G1-S cell cycle transition, while blocked Notch signaling resulted in G0/G1 cell cycle arrest, also observed by transfection of p27Kip1 or, to a smaller extent, a dominant negative SKP2 allele.
  • Collectively, our data suggest that the aberrantly high Notch signaling in T-ALL maintains SKP2 at a high level and reduces p27Kip1, leading to more rapid cell cycle progression.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. S-Phase Kinase-Associated Proteins / metabolism. Signal Transduction / physiology. T-Lymphocytes / metabolism
  • [MeSH-minor] Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Cycle / physiology. Cell Cycle Proteins / genetics. Cell Cycle Proteins / metabolism. Cell Line, Tumor. Child. Cyclin-Dependent Kinase Inhibitor p27. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic. Repressor Proteins / genetics. Repressor Proteins / metabolism

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  • (PMID = 17560996.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CDKN1B protein, human; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / HEY2 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / Repressor Proteins; 0 / S-Phase Kinase-Associated Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
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37. Rainis L, Toki T, Pimanda JE, Rosenthal E, Machol K, Strehl S, Göttgens B, Ito E, Izraeli S: The proto-oncogene ERG in megakaryoblastic leukemias. Cancer Res; 2005 Sep 1;65(17):7596-602
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  • [Title] The proto-oncogene ERG in megakaryoblastic leukemias.
  • Acquired additions of chromosome 21 are a common finding in leukemias, suggesting a contributory role to leukemogenesis.
  • About 10% of patients with a germ line trisomy 21 (Down syndrome) are born with transient megakaryoblastic leukemia.
  • We show that ERG is expressed in hematopoietic stem cells, megakaryoblastic cell lines, and in primary leukemic cells from Down syndrome patients.
  • ERG expression is induced upon megakaryocytic differentiation of the erythroleukemia cell lines K562 and UT-7, and forced expression of ERG in K562 cells induces erythroid to megakaryoblastic phenotypic switch.
  • Furthermore, both ERG and ETS2 bind in vivo the hematopoietic enhancer of SCL/TAL1, a key regulator of hematopoietic stem cell and megakaryocytic development.
  • We propose that trisomy 21 facilitates the occurrence of megakaryoblastic leukemias through a shift toward the megakaryoblastic lineage caused by the excess expression of ERG, and possibly by other chromosome 21 genes, such as RUNX1 and ETS2, in hematopoietic progenitor cells, coupled with a differentiation arrest caused by the acquisition of mutations in GATA1.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Megakaryoblastic, Acute / genetics. Oncogene Proteins / genetics. Trans-Activators / genetics
  • [MeSH-minor] Base Sequence. Basic Helix-Loop-Helix Transcription Factors. Cell Lineage. Chromosomes, Human, Pair 21 / genetics. Erythroid-Specific DNA-Binding Factors. GATA1 Transcription Factor. HeLa Cells. Hematopoietic Stem Cells / metabolism. Humans. K562 Cells. Leukemia, Erythroblastic, Acute / genetics. Leukemia, Erythroblastic, Acute / pathology. Molecular Sequence Data. Promoter Regions, Genetic. Proto-Oncogene Proteins / metabolism. Transcription Factors / genetics. Transcription Factors / metabolism

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  • (PMID = 16140924.001).
  • [ISSN] 0008-5472
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / ERG protein, human; 0 / Erythroid-Specific DNA-Binding Factors; 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / Oncogene Proteins; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human
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38. Spokoini R, Kfir-Erenfeld S, Yefenof E, Sionov RV: Glycogen synthase kinase-3 plays a central role in mediating glucocorticoid-induced apoptosis. Mol Endocrinol; 2010 Jun;24(6):1136-50
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  • It is still unclear how glucocorticoids (GCs) induce apoptosis of thymocytes and T lymphoma cells.
  • Emergence of GC-resistant lymphoma cells is a major obstacle in GC therapy, emphasizing the need for novel strategies that maintain the sensitivity of lymphoma cells to the proapoptotic effects of GC.
  • Chemical inhibition of GSK3 by SB216763, BIO-Acetoxime, or LiCl and GSK3 inhibition using a dominant-negative mutant of GSK3 impede this cell death process, indicating that GSK3 is involved in transmitting the apoptotic signal.
  • GC resistance in lymphoma cells can be relieved by inhibiting the phosphatidylinositol-3 kinase-Akt survival pathway, which inactivates GSK3.
  • Notch1, a transcription factor frequently activated in T acute lymphoblastic leukemia cells, confers GC resistance through activation of Akt.
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Bcl-2-Like Protein 11. Cell Line. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Enzyme Activation / drug effects. Glycogen Synthase Kinase 3 beta. Humans. Ligands. Membrane Proteins / metabolism. Mice. Models, Biological. Protein Binding / drug effects. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptors, Glucocorticoid / metabolism. Receptors, Notch / metabolism

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  • (PMID = 20371704.001).
  • [ISSN] 1944-9917
  • [Journal-full-title] Molecular endocrinology (Baltimore, Md.)
  • [ISO-abbreviation] Mol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BCL2L11 protein, human; 0 / Bcl-2-Like Protein 11; 0 / Bcl2l11 protein, mouse; 0 / Glucocorticoids; 0 / Ligands; 0 / Membrane Proteins; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Glucocorticoid; 0 / Receptors, Notch; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.1 / GSK3B protein, human; EC 2.7.11.1 / Glycogen Synthase Kinase 3 beta; EC 2.7.11.1 / Gsk3b protein, mouse; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 2.7.11.26 / glycogen synthase kinase 3 alpha
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39. Nowak AK, Lake RA, Robinson BW: Combined chemoimmunotherapy of solid tumours: improving vaccines? Adv Drug Deliv Rev; 2006 Oct 1;58(8):975-90
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  • It is now clear that the way a chemotherapeutic drug kills a tumour cell determines how that dying cell interacts with the immune system and whether the interaction leads to an immune response.
  • Furthermore, lymphodepletion triggers homeostatic T cell reconstitution, creating new populations of pre-T cells that need education in the thymic environment.

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  • (PMID = 17005292.001).
  • [ISSN] 0169-409X
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines
  • [Number-of-references] 105
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40. Dourado M, Sarmento AB, Pereira SV, Alves V, Silva T, Pinto AM, Rosa MS: CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture. Pathophysiology; 2007 May;14(1):3-10
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  • [Title] CD26/DPPIV expression and 8-azaguanine response in T-acute lymphoblastic leukaemia cell lines in culture.
  • Dipeptidyl peptidase IV, a cell membrane surface protease also known as CD26 (CD26/DPPIV), is known to play multiple functions in human organism, where it is largely expressed, for instance, in the development of human cancer and metastasis as well as in chemotherapy response.
  • The objective of this work was to study the CD26 membrane expression and DPPIV activity in T-acute leukaemia cell lines (CEM and MOLT3) in culture, in order to observe the modification of its expression under the 8-azaguanine treatment.
  • Cell line samples were incubated, some without different azaguanine concentration and others with, ranging from 10 to 100muM.
  • Cell surface CD26 expression has been identified by flow cytometry and DPPIV activity, in cultured medium, was fluorimetrically measured.
  • Results we have observed showed that 8-azaguanine induced a decrease in cell viability in a dose, time and cell type dependent manner with MOLT3 cells being the most sensitive to 8-azaguanine citotoxic effects (24h IC50: +/-10muM) when compared with CEM cells (24h IC50: +/-100muM).
  • In the same experimental conditions, MOLT3 cell treated with 8-azaguanine shows an increase in CD26 expression (MIF) compared with that of CEM cell submitted to the same conditions (65.4+/-1.3 versus 18.7+/-1.7).

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  • (PMID = 17055708.001).
  • [ISSN] 0928-4680
  • [Journal-full-title] Pathophysiology : the official journal of the International Society for Pathophysiology
  • [ISO-abbreviation] Pathophysiology
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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41. Santamaría-Quesada C, Vargas M, Venegas P, Calvo M, Obando C, Valverde B, Cartín W, Carrillo JM, Jimenez R, González M: Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica. J Pediatr Hematol Oncol; 2009 Feb;31(2):131-5
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  • [Title] Molecular and epidemiologic findings of childhood acute leukemia in Costa Rica.
  • In Central America, nearly 70% of pediatric cancer is related to hemato-oncologic disorders, especially acute lymphoblastic leukemia (ALL).
  • Preliminary studies have described a high incidence of childhood leukemia in these countries; however, no molecular analyses of these malignancies have yet been carried out.
  • We studied diagnostic samples from 84 patients from the National Children's Hospital in San Jose, Costa Rica (65 precursor B-ALL, 5 T-cell ALL, and 14 acute myeloblastic leukemia).
  • The observed rate of leukemia was 52.2 cases per million children per year.
  • Twelve out of 65 (18.4%) precursor B-ALL tested positive for TEL-AML1 and 3 cases for BCR-ABL (4.6%).
  • None of the T-cell ALL cases were positive for either SIL-TAL1 or HOX11L2.
  • Within 14 acute myeloblastic leukemia patients, we confirmed 2 cases with FLT3-internal tandem duplication+, 1 patient with AML1-ETO, and only 1 case carrying a PML-RARalpha rearrangement.
  • The present study confirms the relatively high incidence of pediatric leukemia in Costa Rica and constitutes the first report regarding the incidence of the main molecular alterations of childhood leukemia in our region.
  • [MeSH-major] Leukemia / epidemiology. Leukemia / genetics
  • [MeSH-minor] Acute Disease. Child. Costa Rica / epidemiology. Cytogenetic Analysis. Gene Rearrangement. Humans. Mutation. Oncogene Proteins, Fusion / analysis

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  • (PMID = 19194200.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins, Fusion
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42. Malcovati L: Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia. Haematologica; 2006 Mar;91(3):290A
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  • [Title] Novel homeobox gene recombination in T-cell acute lymphoblastic leukemia.
  • [MeSH-major] Genes, Homeobox / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Recombination, Genetic / genetics

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  • [CommentOn] Haematologica. 2006 Mar;91(3):317-21 [16531254.001]
  • (PMID = 16531247.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] Italy
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43. Borriello A, Locasciulli A, Bianco AM, Criscuolo M, Conti V, Grammatico P, Cappellacci S, Zatterale A, Morgese F, Cucciolla V, Delia D, Della Ragione F, Savoia A: A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia. Leukemia; 2007 Jan;21(1):72-8
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  • [Title] A novel Leu153Ser mutation of the Fanconi anemia FANCD2 gene is associated with severe chemotherapy toxicity in a pediatric T-cell acute lymphoblastic leukemia.
  • Fanconi anemia (FA) is an autosomal recessive disease characterized by pancitopenia, congenital malformations, predisposition to cancers and chromosomal instability.
  • We report the clinical and molecular features of a patient initially identified as a potential FA case only because of chemotherapy toxicity during the treatment of a T-lineage acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Fanconi Anemia Complementation Group D2 Protein / genetics. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation
  • [MeSH-minor] Amino Acid Substitution. Antigens, CD. Antigens, CD13. Antigens, Differentiation, Myelomonocytic. Child. Chromosomal Instability. Disease Progression. Fanconi Anemia / genetics. Humans. Infection / etiology. Infection / genetics. Male. Pancytopenia / chemically induced. Pancytopenia / genetics. Remission Induction. Sialic Acid Binding Ig-like Lectin 3

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  • (PMID = 17096012.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] Italy / Telethon / / TGM06S01
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / FANCD2 protein, human; 0 / Fanconi Anemia Complementation Group D2 Protein; 0 / Sialic Acid Binding Ig-like Lectin 3; EC 3.4.11.2 / Antigens, CD13
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44. Nishimura S, Takahashi S, Kamikatahira H, Kuroki Y, Jaalouk DE, O'Brien S, Koivunen E, Arap W, Pasqualini R, Nakayama H, Kuniyasu A: Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells. J Biol Chem; 2008 Apr 25;283(17):11752-62
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  • [Title] Combinatorial targeting of the macropinocytotic pathway in leukemia and lymphoma cells.
  • Ligand-directed delivery of agents to leukemia and lymphoma cells has the potential to yield new mechanistic disease insights and targeted therapies.
  • From the screening of acute T-lymphoblastic leukemia Molt-4 cells with a random phage-display peptide library, we isolated a phage displaying the sequence CAYHRLRRC.
  • This peptide contains a lymph node-homing motif (Cys-Ala-Tyr) and a cell-penetrating motif (Arg-Leu-Arg-Arg).
  • Binding of this ligand-directed phage to a large panel of leukemia/lymphoma cells and to patient-derived samples was much higher than to non-leukemia control cells.
  • Flow cytometry with fluorescein-labeled peptide and endocytosis blocking with specific inhibitors revealed that CAYHRLRRC is indeed taken up through macropinocytosis in Molt-4 and K562 human leukemia cells.
  • Unexpectedly, the cell surface receptor for the CAYHRLRRC peptide is not a heparan sulfate proteoglycan as it would be predicted for other cell-penetrating peptides.
  • Confirming this interpretation, a CAYHRLRRC-directed peptidomimetic-induced cell death in all the leukemia and lymphoma cells was evaluated, whereas a control transactivator of transcription protein (tat)-directed proapoptotic peptidomimetic was non-selective.
  • In summary, the targeting peptide CAYHRLRRC is selectively internalized through macropinocytosis in leukemia and lymphoma cells and has potential as a drug lead for ligand-directed anti-leukemia therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Gene Expression Regulation, Leukemic. Leukemia / metabolism. Lymphoma / metabolism
  • [MeSH-minor] Catalysis. Cell Line, Tumor. Cell Survival. Chemistry, Pharmaceutical / methods. Drug Design. Humans. K562 Cells. Ligands. Peptide Library. Peptides / chemistry. Pinocytosis

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  • (PMID = 18292083.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Peptide Library; 0 / Peptides
  • [Other-IDs] NLM/ PMC3762554
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45. Xue SL, Wu DP, Sun AN, Tang XW: CAG regimen enables relapsed or refractory T-cell acute lymphocytic leukemia patients to achieve complete remission: a report of six cases. Am J Hematol; 2008 Feb;83(2):167-70
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  • [Title] CAG regimen enables relapsed or refractory T-cell acute lymphocytic leukemia patients to achieve complete remission: a report of six cases.
  • Patients with either relapsed or refractory T-cell acute lymphocytic leukemia (T-ALL) are candidates for allogeneic hematopoietic stem cell transplantation (allo-HSCT).
  • The CAG regimen (cytosine arabinoside 10 mg/m(2) subcutaneously every 12 hr, day 1-14; aclarubicin 5-7 mg/m(2) intravenously daily, day 1-8; and concurrent use of G-CSF 200 microg/m(2)/day subcutaneously) was devised originally for the treatment of relapsed acute myelogenous leukemia.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy

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  • (PMID = 17874449.001).
  • [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 / Antigens, CD; 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 74KXF8I502 / Aclarubicin; CAG protocol
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46. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
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  • [Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
  • A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.
  • Consequently, characterization of the cells that proliferate to maintain the disease should provide valuable information on the most relevant therapeutic targets.
  • The majority of cells capable of long-term proliferation in vitro were derived from the CD34+/CD4- and CD34+/CD7- subfractions.
  • The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.
  • These data demonstrate the long-term repopulating ability of the CD34+/CD4- and CD34+/CD7- subfractions in T-ALL and suggest that a cell with a more primitive phenotype was the target for leukemic transformation in these cases.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology
  • [MeSH-minor] Adolescent. Animals. Cell Culture Techniques. Cell Proliferation. Cell Separation. Cells, Cultured. Child. Child, Preschool. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor / genetics. Genotype. Humans. Immunophenotyping. Infant. Male. Mice. Mice, Inbred NOD. Mice, SCID. Xenograft Model Antitumor Assays


47. Te Boekhorst PA, Lamers CH, Schipperus MR, Hintzen RQ, van der Holt B, Cornelissen JJ, Löwenberg B, Gratama JW: T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants. Bone Marrow Transplant; 2006 Apr;37(8):763-72
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  • [Title] T-lymphocyte reconstitution following rigorously T-cell-depleted versus unmodified autologous stem cell transplants.
  • We compared the kinetics of T-cell recovery after extensive ex vivo and in vivo T-cell depleted autologous stem cell transplantation (SCT) for multiple sclerosis (MS; n=8) with unmodified SCT for hematological malignancies (HM; n=39).
  • Unexpectedly, the kinetics of T-cell recovery between 3 and 12 months post transplant was similar in T-depleted and unmodified SCT.
  • Before SCT, the HM patients showed lymphopenia of all T-cell subsets, upregulated HLA-DR and CD95 expression and increased cytokine responses.
  • We suggest that the similar kinetics of T-cell recovery in the two patient groups may be explained by the susceptibility to apoptosis of the activated CD4(+) T-cells in the autografts of the HM patients.
  • This susceptibility to apoptosis would interfere with a swift and sustained CD4(+) T-cell regeneration post SCT.
  • [MeSH-major] Multiple Sclerosis / blood. Multiple Sclerosis / therapy. Stem Cell Transplantation / methods. T-Lymphocytes / metabolism. Transplantation, Autologous / methods

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  • (PMID = 16518423.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD27; 0 / Antigens, CD3; 0 / Antigens, CD4; 0 / Antigens, CD95; 0 / Cytokines; 0 / Interleukin-2; 126880-86-2 / L-Selectin; 82115-62-6 / Interferon-gamma; EC 3.1.3.48 / Antigens, CD45
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48. Ratei R, Karawajew L, Lacombe F, Jagoda K, Del Poeta G, Kraan J, De Santiago M, Kappelmayer J, Björklund E, Ludwig WD, Gratama J, Orfao A, European Working Group of Clinical Cell Analysis (EWGCCA): Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias. Cytometry B Clin Cytom; 2006 Jan;70(1):1-9
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  • [Title] Normal lymphocytes from leukemic samples as an internal quality control for fluorescence intensity in immunophenotyping of acute leukemias.
  • BACKGROUND: Multiparametric flow cytometry has become an indispensable but complex tool for the diagnosis of acute leukemias.
  • METHODS: Eight laboratories participated in the study and recruited a total of 151 individuals including 29 patients with B-cell precursor acute lymphoblastic leukemia (BCP-ALL), 77 with acute myeloid leukemia (AML), 10 with T-cell precursor acute lymphoblastic leukemia (T-ALL), and 35 normal bone marrow donors.
  • CONCLUSION: Residual normal lymphocytes can serve as internal quality control for studies addressing fluorescence intensity in the setting of immunophenotyping of acute leukemias.
  • [MeSH-major] Flow Cytometry / methods. Immunophenotyping / methods. Leukemia. Lymphocytes / cytology. Lymphocytes / metabolism
  • [MeSH-minor] Acute Disease. Case-Control Studies. Fluorescence. Humans. Quality Control. Reference Standards

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  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16278833.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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49. Mustjoki S, Ekblom M, Arstila TP, Dybedal I, Epling-Burnette PK, Guilhot F, Hjorth-Hansen H, Höglund M, Kovanen P, Laurinolli T, Liesveld J, Paquette R, Pinilla-Ibarz J, Rauhala A, Shah N, Simonsson B, Sinisalo M, Steegmann JL, Stenke L, Porkka K: Clonal expansion of T/NK-cells during tyrosine kinase inhibitor dasatinib therapy. Leukemia; 2009 Aug;23(8):1398-405
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  • Fifteen patients had a cytotoxic T-cell and seven patients had an NK-cell phenotype.
  • All T-cell expansions were clonal.
  • Responses to dasatinib were good and included complete, unexpectedly long-lasting remissions in patients with advanced leukemia.
  • In a phase II clinical study on 46 Philadelphia chromosome-positive acute lymphoblastic leukemia, patients with lymphocytosis had superior survival compared with patients without lymphocytosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Killer Cells, Natural / drug effects. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Lymphocytosis / chemically induced. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Protein Kinase Inhibitors / pharmacology. Pyrimidines / pharmacology. T-Lymphocyte Subsets / drug effects. T-Lymphocytes, Cytotoxic / drug effects. Thiazoles / pharmacology

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  • [CommentIn] Acta Haematol. 2016;136(4):219-228 [27656875.001]
  • (PMID = 19295545.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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50. Asnafi V, Buzyn A, Thomas X, Huguet F, Vey N, Boiron JM, Reman O, Cayuela JM, Lheritier V, Vernant JP, Fiere D, Macintyre E, Dombret H: Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study. Blood; 2005 Apr 15;105(8):3072-8
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  • [Title] Impact of TCR status and genotype on outcome in adult T-cell acute lymphoblastic leukemia: a LALA-94 study.
  • Patients with T-cell acute lymphoblastic leukemias (T-ALLs) within the Leucemies Aigues Lymphoblastiques de l'Adulte-94 (LALA-94) prospective trial were treated with a 4-drug per 4-week induction, with intermediate-dose cytarabine and mitoxantrone salvage treatment for patients not achieving complete remission (CR) in 1 course.
  • Representative patients with T-ALL (91 patients) were classified into surface T-cell receptor (TCR)-expressing T-ALL patients (TCRalphabeta+ or TCRgammadelta+), pre-alphabeta T-ALL patients (cTCRbeta+, TCR-), and immature (IM) cTCRbeta-, TCR- T-ALL patients; 81 patients underwent genotyping for SIL-TAL1, CALM-AF10, HOX11, and HOX11L2.
  • Once CR was obtained, cumulative relapse rates were similar for IM, pre-alphabeta, and TCR+ T-ALL patients (P = .51), but were higher in HOX11L2 (83%) and SIL-TAL1 (82%) T-ALL patients compared with other genetic subgroups (48%; P = .05).
  • This was associated with an inferior OS for HOX11L2 T-ALLs (13% vs 47% in HOX11L2-T-ALLs; P = .009).
  • Both TCR and genotypic stratification can therefore contribute to risk-adapted management of adult T-ALLs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 15637138.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Receptors, Antigen, T-Cell; 04079A1RDZ / Cytarabine; BZ114NVM5P / Mitoxantrone
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56. Lin YW, Beharry ZM, Hill EG, Song JH, Wang W, Xia Z, Zhang Z, Aplan PD, Aster JC, Smith CD, Kraft AS: A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma. Blood; 2010 Jan 28;115(4):824-33
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  • [Title] A small molecule inhibitor of Pim protein kinases blocks the growth of precursor T-cell lymphoblastic leukemia/lymphoma.
  • We demonstrate that SMI-4a, a novel benzylidene-thiazolidine-2, 4-dione small molecule inhibitor of the Pim kinases, kills a wide range of both myeloid and lymphoid cell lines with precursor T-cell lymphoblastic leukemia/lymphoma (pre-T-LBL/T-ALL) being highly sensitive.
  • Incubation of pre-T-LBL cells with SMI-4a induced G1 phase cell-cycle arrest secondary to a dose-dependent induction of p27(Kip1), apoptosis through the mitochondrial pathway, and inhibition of the mammalian target of rapamycin C1 (mTORC1) pathway based on decreases in phospho-p70 S6K and phospho-4E-BP1, 2 substrates of this enzyme.
  • In addition, treatment of these cells with SMI-4a was found to induce phosphorylation of extracellular signal-related kinase1/2 (ERK1/2), and the combination of SMI-4a and a mitogen-activated protein kinase kinase 1/2 (MEK1/2) inhibitor was highly synergistic in killing pre-T-LBL cells.
  • In immunodeficient mice carrying subcutaneous pre-T-LBL tumors, treatment twice daily with SMI-4a caused a significant delay in the tumor growth without any change in the weight, blood counts, or chemistries.
  • Our data suggest that inhibition of the Pim protein kinases may be developed as a therapeutic strategy for the treatment of pre-T-LBL.


57. Chiu PP, Jiang H, Dick JE: Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance. Blood; 2010 Dec 9;116(24):5268-79
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  • [Title] Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a significant risk of disease relapse, but the biological basis for relapse is poorly understood.
  • Here, we identify leukemiainitiating cells (L-ICs) on the basis of functional assays and prospective isolation and report a role for L-ICs in T-ALL disease and relapse.
  • Long-term proliferation in response to NOTCH1 activating signals in OP9-DL1 coculture system or capacity to initiate leukemia in xenografts by the CD7(+)CD1a(-) subset of primary T-ALL samples was superior to other subsets, refining the identity of T-ALL L-ICs.
  • T-ALL engraftment was improved in nonobese diabetic/severe combined immunodeficiency (NOD/scid)IL2Rγ(null) (NSG) mice compared with NOD/scid with anti-CD122 treatment (NS122), but both showed changes in leukemia immunophenotype.
  • Our results establish that primary CD1a(-) T-ALL cells are functionally distinct from CD1a(+) cells and that the CD7(+)CD1a(-) subset is enriched for L-IC activity that may be involved in mediating disease relapse after therapy.
  • [MeSH-minor] Animals. Antigens, CD1. Antigens, CD7. Antineoplastic Agents, Hormonal / pharmacology. Cell Proliferation. Clone Cells / pathology. Coculture Techniques. Dexamethasone / pharmacology. Humans. Immunophenotyping. Mice. Mice, SCID. Receptor, Notch1 / metabolism. Recurrence. Transplantation, Heterologous

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  • (PMID = 20810926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD7; 0 / Antineoplastic Agents, Hormonal; 0 / CD1a antigen; 0 / Glucocorticoids; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone
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58. Choi J, Foss F: Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia. Yale J Biol Med; 2006 Dec;79(3-4):169-72
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  • [Title] Efficacy of low dose clofarabine in refractory precursor T- acute lymphoblastic leukemia.
  • Refractory T-lymphoblastic leukemia in adults has a poor prognosis in patients who relapse after allogeneic stem cell transplantation, and relatively few new agents have demonstrated activity.
  • We used low dose clofarabine and induced a remission in a patient who relapsed in the skin and marrow after allogeneic transplant and was refractory to nelarabine and report a near complete response, suggesting significant activity for low intermittent dose clofarabine in patients with relapsed T-cell leukemias.
  • [MeSH-major] Adenine Nucleotides / therapeutic use. Arabinonucleosides / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Adult. Bone Marrow Neoplasms / drug therapy. Bone Marrow Neoplasms / secondary. Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Humans. Immunophenotyping. Male. Recurrence. Skin Neoplasms / drug therapy. Skin Neoplasms / secondary. Stem Cell Transplantation. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 17940627.001).
  • [ISSN] 1551-4056
  • [Journal-full-title] The Yale journal of biology and medicine
  • [ISO-abbreviation] Yale J Biol Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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  • [Other-IDs] NLM/ PMC1994805
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59. Malissen B, Luche H: Immunology: Egocentric pre-T-cell receptors. Nature; 2010 Oct 14;467(7317):793-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunology: Egocentric pre-T-cell receptors.
  • [MeSH-major] Protein Multimerization. Receptors, Antigen, T-Cell, alpha-beta / chemistry. Receptors, Antigen, T-Cell, alpha-beta / metabolism

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  • [CommentOn] Nature. 2010 Oct 14;467(7317):844-8 [20944746.001]
  • (PMID = 20944732.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Publication-type] Comment; News
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell, alpha-beta
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60. Terme JM, Mocquet V, Kuhlmann AS, Zane L, Mortreux F, Wattel E, Duc Dodon M, Jalinot P: Inhibition of the hTERT promoter by the proto-oncogenic protein TAL1. Leukemia; 2009 Nov;23(11):2081-9
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  • In this report, we show that the basic helix-loop-helix factor, TAL1 (T-cell acute lymphoblastic leukemia 1), is a negative regulator of the hTERT promoter.
  • Considering the relationship recently established between TAL1 and the human T-cell leukemia virus type 1 (HTLV-1) Tax protein, which was confirmed in T lymphocyte clones derived from adult T-cell leukemia patients, we analyzed the effect of TAL1 with respect to the earlier characterized effects of Tax and HBZ (HTLV-1 basic leucine zipper) on hTERT expression.
  • [MeSH-major] Basic Helix-Loop-Helix Transcription Factors / metabolism. Gene Expression Regulation, Leukemic / physiology. Leukemia, T-Cell / genetics. Proto-Oncogene Proteins / metabolism. Telomerase / genetics. Telomerase / metabolism

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  • (PMID = 19587703.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / Proto-Oncogene Proteins; 0 / Sp1 Transcription Factor; 0 / Viral Proteins; 0 / tax protein, Human T-lymphotrophic virus 1; 135471-20-4 / TAL1 protein, human; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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61. Gran B, Yu S, Zhang GX, Rostami A: Accelerated thymocyte maturation in IL-12Rβ2-deficient mice contributes to increased susceptibility to autoimmune inflammatory demyelination. Exp Mol Pathol; 2010 Oct;89(2):126-34
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  • Accelerated maturation is observed in mice injected with anti-CD3 to mimic pre-T-cell receptor stimulation, and also in mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide to induce EAE.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20599940.001).
  • [ISSN] 1096-0945
  • [Journal-full-title] Experimental and molecular pathology
  • [ISO-abbreviation] Exp. Mol. Pathol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI061818; United States / NINDS NIH HHS / NS / R01 NS048435; United States / NIAID NIH HHS / AI / U19 AI082726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Mog protein, mouse; 0 / Myelin Proteins; 0 / Myelin-Associated Glycoprotein; 0 / Myelin-Oligodendrocyte Glycoprotein; 187348-17-0 / Interleukin-12
  • [Other-IDs] NLM/ NIHMS218212; NLM/ PMC2939283
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62. Yamasaki S, Saito T: Molecular basis for pre-TCR-mediated autonomous signaling. Trends Immunol; 2007 Jan;28(1):39-43
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular basis for pre-TCR-mediated autonomous signaling.
  • The pre-T-cell receptor (pre-TCR) is a multimeric complex composed of a nascent TCRbeta chain, an invariant pre-TCRalpha (pTalpha) chain and CD3 molecules, and is crucial for early T-cell development.
  • Despite its structural similarity to the mature alphabetaTCR, which requires MHC-antigen for receptor triggering, the pre-TCR is proposed to initiate signals in a ligand-independent manner.
  • In this review, we summarize current data relating to the molecular mechanism underlying the initiation of pre-TCR-mediated autonomous signaling.
  • [MeSH-major] Lymphoma / immunology. Membrane Glycoproteins / immunology. Receptors, Antigen, T-Cell, alpha-beta / immunology. Signal Transduction / immunology

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  • (PMID = 17126602.001).
  • [ISSN] 1471-4906
  • [Journal-full-title] Trends in immunology
  • [ISO-abbreviation] Trends Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / pre-T cell receptor alpha
  • [Number-of-references] 48
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63. Benito JM, López M, Lozano S, Ballesteros C, Martinez P, González-Lahoz J, Soriano V: Differential upregulation of CD38 on different T-cell subsets may influence the ability to reconstitute CD4+ T cells under successful highly active antiretroviral therapy. J Acquir Immune Defic Syndr; 2005 Apr 1;38(4):373-81
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  • [Title] Differential upregulation of CD38 on different T-cell subsets may influence the ability to reconstitute CD4+ T cells under successful highly active antiretroviral therapy.
  • BACKGROUND: Immune activation is an independent surrogate marker of CD4 T-cell depletion in HIV-infected patients.
  • Highly active antiretroviral therapy (HAART) reduces disease progression as a direct consequence of suppressing HIV replication.
  • So far, it is unclear to what extent immune activation may influence the evolution of CD4 T-cell counts in patients on HAART.
  • In patients on successful HAART, immune activation declined in all T-cell subsets, particularly among memory CD8+ cells.
  • There was a significant correlation between the CD8+ T-cell activation decay and the increase of CD4+ T cells on HAART.
  • Patients with the highest decline in CD8 activation were those showing the highest CD4 T-cell gains after 12 months of therapy.
  • CONCLUSIONS: The level of CD38 expression on different T-cell subsets is differentially upregulated in drug-naive HIV-infected patients.
  • After successful HAART, immune activation decreases in all T-cell subsets, although it still remains elevated in most cases after 12 months of HAART.

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  • (PMID = 15764953.001).
  • [ISSN] 1525-4135
  • [Journal-full-title] Journal of acquired immune deficiency syndromes (1999)
  • [ISO-abbreviation] J. Acquir. Immune Defic. Syndr.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Membrane Glycoproteins; EC 3.2.2.5 / ADP-ribosyl Cyclase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human
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64. Bellavia D, Mecarozzi M, Campese AF, Grazioli P, Gulino A, Screpanti I: Notch and Ikaros: not only converging players in T cell leukemia. Cell Cycle; 2007 Nov 15;6(22):2730-4
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  • [Title] Notch and Ikaros: not only converging players in T cell leukemia.
  • Notch3 overexpression has been observed in virtually 100% of T cell acute lymphoblastic leukemia (T-ALL).
  • A high percentage of infant B- and T-ALLs also display an increased expression of non DNA-binding Ikaros isoforms.
  • We recently suggested that pre-TCR is the missing link between Notch and Ikaros in T cell leukemogenesis.
  • Our studies demonstrate that the presence of pre-TCR is required to sustain a Notch3-induced altered expression of spliced Ikaros isoforms.
  • Moreover, we identified HuD, an RNA-binding protein able to regulate both mRNA stability and alternative splicing, as the potential pre-TCR-dependent mediator of Notch3 activity.
  • Our findings may help in clarifying the regulatory mechanism of Ikaros alternative splicing and suggest a crosstalk among Notch3, pre-TCR signalling and spliced Ikaros variants in T cell leukemogenesis, mediated by HuD.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Leukemia, T-Cell / metabolism. Receptors, Notch / physiology

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  • (PMID = 18032925.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Notch; 148971-36-2 / Ikaros Transcription Factor
  • [Number-of-references] 66
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65. Dufner-Beattie J, Huang ZL, Geiser J, Xu W, Andrews GK: Generation and characterization of mice lacking the zinc uptake transporter ZIP3. Mol Cell Biol; 2005 Jul;25(13):5607-15
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  • EGFP fluorescence revealed that ZIP3 was expressed in the inner cell mass of the blastocyst and later during embryonic development in many tissues.
  • In knockout mice stressed with a zinc-deficient diet during pregnancy or at weaning, a subtle increase in the sensitivity to abnormal morphogenesis of the embryo and to depletion of thymic pre-T cells, respectively, was noted.

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  • (PMID = 15964816.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK50181
  • [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 / Carrier Proteins; 0 / Cation Transport Proteins; 0 / Slc39a3 protein, mouse; 0 / zinc-binding protein; 147336-22-9 / Green Fluorescent Proteins; J41CSQ7QDS / Zinc
  • [Other-IDs] NLM/ PMC1156975
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66. Chadwick N, Zeef L, Portillo V, Boros J, Hoyle S, van Doesburg JC, Buckle AM: Notch protection against apoptosis in T-ALL cells mediated by GIMAP5. Blood Cells Mol Dis; 2010 Oct 15;45(3):201-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have highlighted the role of Notch signalling in the development of T cell acute lymphoblasic leukaemia (T-ALL).
  • The aims of this study were to determine the effect of Notch signalling on apoptosis in human T-ALL cell lines and to identify targets of Notch signalling that may mediate this effect.
  • Microarray analysis revealed that GIMAP5, a gene coding for an anti-apoptotic intracellular protein, is upregulated by Notch in T-ALL cell lines.
  • [MeSH-major] Apoptosis. GTP-Binding Proteins / biosynthesis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptor, Notch1 / metabolism. Receptors, Notch / metabolism. Signal Transduction

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20817506.001).
  • [ISSN] 1096-0961
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GIMAP5 protein, human; 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / NOTCH3 protein, human; 0 / Protease Inhibitors; 0 / Receptor, Notch1; 0 / Receptors, Notch; EC 3.6.1.- / GTP-Binding Proteins
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67. Wu XC, Andrews P, Chen VW, Groves FD: Incidence of extranodal non-Hodgkin lymphomas among whites, blacks, and Asians/Pacific Islanders in the United States: anatomic site and histology differences. Cancer Epidemiol; 2009 Nov;33(5):337-46
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  • BACKGROUND: Extranodal non-Hodgkin lymphoma (NHL) accounts for much of the increase in NHL incidence in the past three decades in the United States, but its descriptive epidemiology is scarce in the literature.
  • We grouped anatomic sites of extranodal NHLs according to the Surveillance, Epidemiology, and End Results (SEER) site recodes, and histology subtypes according to the nested classification of lymphoid neoplasms developed by the Pathology Working Group of the International Lymphoma Epidemiology Consortium.
  • RESULTS: Blacks and Asians/Pacific Islanders (APIs) experienced incidence rates about the same as or lower than whites' for B-cell extranodal NHL as a whole and most of its histologic subtypes.
  • The significant exceptions are: API men had a 40% higher rate of marginal zone lymphoma (MZL) than white men, and API women had a 12% higher rate of diffuse large B-cell lymphoma (DLBCL) than white women.
  • The rates of all T-cell extranodal NHLs combined and peripheral T-cell lymphoma (PTCL) among black women exceeded those of white women by 46% and 18%, respectively.
  • Blacks had higher rates of the two most common types of T-cell extranodal NHL and APIs had higher rate of the two common types of B-cell types than whites.
  • [MeSH-major] Lymphoma, Non-Hodgkin / epidemiology. Lymphoma, Non-Hodgkin / pathology

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  • (PMID = 19853554.001).
  • [ISSN] 1877-783X
  • [Journal-full-title] Cancer epidemiology
  • [ISO-abbreviation] Cancer Epidemiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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68. Gordon WR, Roy M, Vardar-Ulu D, Garfinkel M, Mansour MR, Aster JC, Blacklow SC: Structure of the Notch1-negative regulatory region: implications for normal activation and pathogenic signaling in T-ALL. Blood; 2009 Apr 30;113(18):4381-90
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  • The NRR includes the 3 Lin12/Notch repeats and the juxtamembrane heterodimerization domain, the region of Notch1 most frequently mutated in T-cell acute lymphoblastic leukemia lymphoma (T-ALL).
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / chemistry. Receptor, Notch1 / metabolism. Regulatory Sequences, Nucleic Acid. Signal Transduction

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  • (PMID = 19075186.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R56 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-030003; United States / NCI NIH HHS / CA / R01 CA092433-05S1; United States / NCI NIH HHS / CA / CA092433; United States / NCI NIH HHS / CA / R56 CA092433-06A1; United States / NCI NIH HHS / CA / R01 CA092433; United States / NCI NIH HHS / CA / P01 CA119070-03; United States / NCI NIH HHS / CA / P01 CA119070-039001; United States / NCI NIH HHS / CA / P01 CA119070-029001; United States / NCI NIH HHS / CA / P01 CA119070-020003; United States / NCI NIH HHS / CA / R01 CA092433-05; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / R01 CA092433-04; United States / NCI NIH HHS / CA / P01 CA119070
  • [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, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC2676092
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69. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.
  • Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL).
  • To identify Notch1 target genes in leukemia, we developed mouse T-cell leukemic lines that express intracellular Notch1 in a doxycycline-dependent manner.
  • Using gene expression profiling and chromatin immunoprecipitation, we identified c-myc as a novel, direct, and critical Notch1 target gene in T-cell leukemia. c-myc mRNA levels are increased in primary mouse T-cell tumors that harbor Notch1 mutations, and Notch1 inhibition decreases c-myc mRNA levels and inhibits leukemic cell growth.
  • Consistent with these findings, retroviral insertional mutagenesis screening of our T-cell leukemia mouse model revealed common insertions in either notch1 or c-myc genes.

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  • (PMID = 16954387.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA-096889
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Myc protein, mouse; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC1636748
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70. Quintás-Cardama A, Tong W, Manshouri T, Vega F, Lennon PA, Cools J, Gilliland DG, Lee F, Cortes J, Kantarjian H, Garcia-Manero G: Activity of tyrosine kinase inhibitors against human NUP214-ABL1-positive T cell malignancies. Leukemia; 2008 Jun;22(6):1117-24
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  • [Title] Activity of tyrosine kinase inhibitors against human NUP214-ABL1-positive T cell malignancies.
  • Amplification of the NUP214-ABL1 oncogene can be detected in patients with T cell acute lymphoblastic leukemia (T-ALL).
  • We screened 29 patients with T cell malignancies for the expression of NUP214-ABL1 by reverse transcription-polymerase chain reaction (RT-PCR).
  • We also studied the activity of imatinib, nilotinib and dasatinib against the human NUP214-ABL1-positive cell lines PEER and BE-13.
  • In contrast, the NUP214-ABL-negative T-ALL cell line Jurkat, was remarkably resistant to tyrosine kinase inhibition.
  • Moreover, dasatinib was active in a NUP214-ABL1-positive leukemia xenograft murine model and in marrow lymphoblasts from a patient with NUP214-ABL1-positive T-ALL.
  • On the basis of these results, ABL1 kinase inhibitors warrant clinical investigation in patients with NUP214-ABL1-positive T-cell malignancies.

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  • (PMID = 18401417.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA100067; United States / Howard Hughes Medical Institute / / ; United States / NCI NIH HHS / CA / CA105771
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide; 0 / Adaptor Proteins, Signal Transducing; 0 / Benzamides; 0 / CRKL protein; 0 / NUP214-ABL1 fusion protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / STAT5 Transcription Factor; 0 / Thiazoles; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; RBZ1571X5H / Dasatinib
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71. Weerkamp F, Luis TC, Naber BA, Koster EE, Jeannotte L, van Dongen JJ, Staal FJ: Identification of Notch target genes in uncommitted T-cell progenitors: No direct induction of a T-cell specific gene program. Leukemia; 2006 Nov;20(11):1967-77
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  • [Title] Identification of Notch target genes in uncommitted T-cell progenitors: No direct induction of a T-cell specific gene program.
  • During normal lymphoid development, activation of the Notch signaling pathway poses a T-cell fate on hematopoietic progenitors.
  • We confirmed HES1, NOTCH1 and NRARP as Notch target genes, but other reported Notch targets, including the genes for Deltex1, pre-T-cell receptor alpha and E2A, were not found to be differentially expressed.
  • Remarkably, no induction of T-cell receptor gene rearrangements or transcription of known T-cell specific genes was found after activation of the Notch pathway.
  • Apparently, Notch signaling is essential to open the T-cell pathway, but does not initiate the T-cell program itself.
  • [MeSH-major] Cell Lineage / physiology. Hematopoietic Stem Cells / physiology. Receptor, Notch1 / metabolism. T-Lymphocytes / physiology

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  • (PMID = 16990763.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Homeodomain Proteins; 0 / Hoxa5 protein, mouse; 0 / NOTCH1 protein, human; 0 / Nrarp protein, mouse; 0 / Phosphoproteins; 0 / Proteins; 0 / Receptor, Notch1; 0 / TCFL5 protein, human; 0 / Triglycerides; 149348-15-2 / HES1 protein, human; 56-12-2 / gamma-Aminobutyric Acid; 93349-26-9 / 1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol
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72. Lee SY, Kumano K, Nakazaki K, Sanada M, Matsumoto A, Yamamoto G, Nannya Y, Suzuki R, Ota S, Ota Y, Izutsu K, Sakata-Yanagimoto M, Hangaishi A, Yagita H, Fukayama M, Seto M, Kurokawa M, Ogawa S, Chiba S: Gain-of-function mutations and copy number increases of Notch2 in diffuse large B-cell lymphoma. Cancer Sci; 2009 May;100(5):920-6
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  • [Title] Gain-of-function mutations and copy number increases of Notch2 in diffuse large B-cell lymphoma.
  • Gain of Notch1 function results in the development of T-cell acute lymphoblastic leukemia in a number of mouse experimental models, and activating Notch1 mutations deregulate Notch1 signaling in the majority of human T-cell acute lymphoblastic leukemias.
  • Notch2, another member of the Notch gene family, is preferentially expressed in mature B cells and is essential for marginal zone B-cell generation.
  • Here, we report that 5 of 63 (approximately 8%) diffuse large B-cell lymphomas, a subtype of mature B-cell lymphomas, have Notch2 mutations.
  • Furthermore, high-density oligonucleotide microarray analysis revealed that some diffuse large B-cell lymphoma cases also have increased copies of the mutated Notch2 allele.
  • In the Notch activation-sensitive luciferase reporter assay in vitro, mutant Notch2 receptors show increased activity compared with wild-type Notch2.
  • These findings implicate Notch2 gain-of-function mutations in the pathogenesis of a subset of B-cell lymphomas, and suggest broader roles for Notch gene mutations in human cancers.
  • [MeSH-major] Gene Dosage / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Receptor, Notch2 / metabolism

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  • (PMID = 19445024.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / NOTCH2 protein, human; 0 / Receptor, Notch2; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
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73. Oble DA, Mino-Kenudson M, Goldsmith J, Hodi FS, Seliem RM, Dranoff G, Mihm M, Hasserjian R, Lauwers GY: Alpha-CTLA-4 mAb-associated panenteritis: a histologic and immunohistochemical analysis. Am J Surg Pathol; 2008 Aug;32(8):1130-7
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  • Immunohistochemical analysis revealed a marked increase of all T-cell subsets (CD3+, CD4+, and CD8+) and of CD4CD25 regulatory T cells.


74. Falà F, Blalock WL, Tazzari PL, Cappellini A, Chiarini F, Martinelli G, Tafuri A, McCubrey JA, Cocco L, Martelli AM: Proapoptotic activity and chemosensitizing effect of the novel Akt inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-cell acute lymphoblastic leukemia. Mol Pharmacol; 2008 Sep;74(3):884-95
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  • [Title] Proapoptotic activity and chemosensitizing effect of the novel Akt inhibitor (2S)-1-(1H-Indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) in T-cell acute lymphoblastic leukemia.
  • Constitutively activated AKT kinase is a common feature of T-cell acute lymphoblastic leukemia (T-ALL).
  • Here, we report that the novel AKT inhibitor (2S)-1-(1H-indol-3-yl)-3-[5-(3-methyl-2H-indazol-5-yl)pyridin-3-yl]oxypropan2-amine (A443654) leads to rapid cell death of T-ALL lines and patient samples.
  • Effects were time- and dose-dependent, resulting in apoptotic cell death.
  • Apoptotic cell death was mostly dependent on caspase-2 activation, as demonstrated by preincubation with a selective pharmacological inhibitor.
  • It is remarkable that A443654 was highly effective against the drug-resistant cell line CEM-VBL100, which expresses 170-kDa P-glycoprotein.
  • Moreover, A443654 synergized with the DNA-damaging agent etoposide in both drug-sensitive and drug-resistant cell lines when coadministered [combination index (CI) = 0.39] or when pretreated with etoposide followed by A443654 (CI = 0.689).
  • At 1 microM, the inhibitor was able to induce apoptotic cell death of T-ALL blast cells, as indicated by flow cytometric analysis of samples immunostained for active (cleaved) caspase-3.

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  • (PMID = 18577685.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098195-05; United States / NCI NIH HHS / CA / R01 CA098195-05; United States / NCI NIH HHS / CA / R01-CA091025
  • [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 / A 443654; 0 / Indazoles; 0 / Indoles; 1114-81-4 / Phosphothreonine; 17885-08-4 / Phosphoserine; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ NIHMS79780; NLM/ PMC2659779
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75. Dictor M, Warenholt J, Isinger A: Resolving T-cell receptor clonality in two and genotype in four multiplex polymerase chain reactions. Haematologica; 2005 Nov;90(11):1524-32
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  • [Title] Resolving T-cell receptor clonality in two and genotype in four multiplex polymerase chain reactions.
  • BACKGROUND AND OBJECTIVES: The diagnosis of T-cell neoplasia requires the use of immunohistochemistry on tumor sections or molecular genetic analysis of T-cell receptor (TCR) clonality.
  • DESIGN AND METHODS: Template DNA was derived from frozen or formalin-fixed tissue and from imprints of aspirates or cut tissue surface on a FTA MicroCard.
  • Two hundred and eleven clinically and immunohistochemically well-characterized benign and malignant non-T-cell lymphoid proliferations, including 138 B-cell lymphomas, were analyzed to determine specificity.
  • The results were compared with those of 28 peripheral and immature T-cell neoplasms and two NK/T-cell lymphomas to determine sensitivity and compute predictive values.
  • RESULTS: In all T-cell tumors, one or more TCR loci showed clonal rearrangement, which was not evident in two NK/T-cell lymphomas.
  • Multiplex PCR targeting of TCRG and TCRD together resolved clonality in all T-cell neoplasms, whereas the TCRB locus was clonal in two of three cases with polyclonal TCRG.
  • Unexpectedly, in B-cell lymphomas single clonal incomplete TCRB (Dbeta-Jbeta) peaks were 20 times more likely to occur than clonal TCRG.
  • INTERPRETATION AND CONCLUSIONS: Clonality can be accurately determined in nodal T-cell lymphoma with two single-tube multiplex PCR targeting TCRG and TCRD.
  • TCRB analysis should be considered in equivocal cases in which a polyclonal background may obscure clonal TCRD, but clonal incomplete TCRB rearrangement alone is insufficient for presuming T-cell lineage.
  • In the absence of objective evidence of B-cell neoplasia, multiplex PCR of T-cell receptor genes may be used early in the diagnostic work-up, including for fine needle aspirates.
  • [MeSH-major] Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / pathology. Polymerase Chain Reaction / methods. Receptors, Antigen, T-Cell / genetics

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  • (PMID = 16266900.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Receptors, Antigen, T-Cell
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76. Lu J, Quearry B, Harada H: p38-MAP kinase activation followed by BIM induction is essential for glucocorticoid-induced apoptosis in lymphoblastic leukemia cells. FEBS Lett; 2006 Jun 12;580(14):3539-44
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  • [Title] p38-MAP kinase activation followed by BIM induction is essential for glucocorticoid-induced apoptosis in lymphoblastic leukemia cells.
  • Treatment of CCRF-CEM (T cell acute lymphoblastic leukemia) cells with the GC, dexamethasone (Dex), activates p38-mitogen activated protein kinase (p38-MAPK) and then induces mRNA transcription and synthesis levels of BIM, a BH3-only pro-apoptotic BCL-2 family member.
  • These findings indicate that BIM induction through p38-MAPK activation is a critical pathway in GC-induced cell death.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / biosynthesis. Dexamethasone / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Membrane Proteins / biosynthesis. Proto-Oncogene Proteins / biosynthesis. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Base Sequence. Blotting, Western. Cell Line, Tumor. DNA Primers. Enzyme Activation. Humans

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  • (PMID = 16730715.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / DNA Primers; 0 / Membrane Proteins; 0 / Proto-Oncogene Proteins; 7S5I7G3JQL / Dexamethasone; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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77. Ramoglu SI, Sari Z: Maxillary expansion in the mixed dentition: rapid or semi-rapid? Eur J Orthod; 2010 Feb;32(1):11-8
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  • A splint type tooth- and tissue-borne modified bonded RME appliance was used, with the patients activating the screw two-quarter turns per day for the first week, followed by one-quarter turn every other day in the SRME group and two-quarter turns per day throughout treatment in the RME group.
  • A Wilcoxon signed rank test was used to evaluate the treatment effects [pre-(T(0)) - post-(T(1)) treatment changes] for both the SRME and RME groups and a Mann-Whitney U-test to determine the differences between the two groups (T(0)-T(1) changes SRME versus T(0)-T(1) changes RME).

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  • (PMID = 19797410.001).
  • [ISSN] 1460-2210
  • [Journal-full-title] European journal of orthodontics
  • [ISO-abbreviation] Eur J Orthod
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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78. Masui N, Tani-ichi S, Maki K, Ikuta K: Transcriptional activation of mouse TCR Jgamma4 germline promoter by STAT5. Mol Immunol; 2008 Feb;45(3):849-55
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  • Here, we showed that cytokine stimulation induced Jgamma4-Cgamma4 germline transcripts in a pre-T cell line, Scid.adh, and a hematopoietic cell line, Ba/F3.
  • [MeSH-major] Interleukin-7 / immunology. Precursor Cells, T-Lymphoid / metabolism. Receptors, Antigen, T-Cell, gamma-delta / biosynthesis. Response Elements / physiology. STAT5 Transcription Factor / metabolism. Transcription, Genetic / physiology
  • [MeSH-minor] Acetylation. Animals. Cell Line. Chromatin / genetics. Chromatin / immunology. Chromatin / metabolism. Histones / genetics. Histones / immunology. Histones / metabolism. Membrane Proteins / genetics. Membrane Proteins / immunology. Membrane Proteins / metabolism. Mice. Phosphoproteins / genetics. Phosphoproteins / immunology. Phosphoproteins / metabolism. Quantitative Trait Loci / physiology. Transcriptional Activation / physiology. p300-CBP Transcription Factors / genetics. p300-CBP Transcription Factors / immunology. p300-CBP Transcription Factors / metabolism

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  • (PMID = 17664008.001).
  • [ISSN] 0161-5890
  • [Journal-full-title] Molecular immunology
  • [ISO-abbreviation] Mol. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Chromatin; 0 / Histones; 0 / Interleukin-7; 0 / Membrane Proteins; 0 / Pag1 protein, mouse; 0 / Phosphoproteins; 0 / Receptors, Antigen, T-Cell, gamma-delta; 0 / STAT5 Transcription Factor; EC 2.3.1.48 / p300-CBP Transcription Factors
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79. Miao K, Li J, Qiu H, Zhang R, Chen L, Wu H, Wang R, Zhang J: The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia. Onkologie; 2010;33(7):385-7
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  • [Title] The chromosomal translocation (11;14) (p13; q11) in acute B-Cell lymphocytic leukemia.
  • BACKGROUND: Cytogenetic abnormalities are the most important independent prognostic factors of acute leukemia and imply the potential molecular mechanism of the disease.
  • Translocation (11;14)(p13;q11) has been predominantly found in T-cell acute lymphocytic leukemia (ALL) but is rare in B-cell ALL.
  • CONCLUSIONS: Translocation (11;14) (p13;q11) in B-cell ALL is rare, but it is worth exploring the molecular mechanisms and discovering the prognostic value in more B-cell ALL patients.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Leukemia, B-Cell / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Chromosome Banding. Disease Progression. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Male. Prognosis. Remission Induction

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  • [Copyright] Copyright 2010 S. Karger AG, Basel.
  • (PMID = 20631486.001).
  • [ISSN] 1423-0240
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
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80. Schweneker M, Favre D, Martin JN, Deeks SG, McCune JM: HIV-induced changes in T cell signaling pathways. J Immunol; 2008 May 15;180(10):6490-500
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  • [Title] HIV-induced changes in T cell signaling pathways.
  • Infection with HIV usually results in chronic activation of the immune system, with profound quantitative and qualitative changes in the T cell compartment.
  • To better understand the mechanistic basis for T cell dysfunction and to discern whether such mechanisms are reversed after effective antiviral treatment, we analyzed changes in signaling pathways of human CD4(+) and CD8(+) T cells from 57 HIV-infected subjects in varying stages of disease progression and treatment, including long-term nonprogressors, progressors, and chronically infected subjects provided effective antiretroviral therapy (responders).
  • T cell signaling induced by TCR cross-linking, IL-2, or PMA/ionomycin was found to be blunted within all T cell subpopulations in those with progressive HIV disease compared with long-term nonprogressors and responders.
  • Notably, provision of effective antiretroviral therapy was associated with a normalization of both basal phosphorylation levels and T cell signaling.
  • These data, in aggregate, suggest that generalized dysfunction of the T cell compartment during progressive HIV disease may be in part dependent upon an increased basal level of phosphorylation, which itself may be due to the heightened state of immune activation found in advanced disease.

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  • (PMID = 18453567.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI 52745; United States / NCRR NIH HHS / RR / UL1 RR 024131; United States / NIAID NIH HHS / AI / R01 AI047062-09; United States / NIAID NIH HHS / AI / AI047062-08; United States / NCRR NIH HHS / RR / UL1 RR024131-010001; United States / NIAID NIH HHS / AI / R37 AI040312-09; United States / NIAID NIH HHS / AI / R37 AI040312-10; United States / NIH HHS / OD / DPI OD 00329; United States / NIAID NIH HHS / AI / R37 AI040312-12; United States / NIAID NIH HHS / AI / K24 AI069994; United States / NIAID NIH HHS / AI / R01 AI052745; United States / NCRR NIH HHS / RR / UL1 RR024131; United States / NIH HHS / OD / DP1 OD000329; United States / NCRR NIH HHS / RR / UL1 RR024131-010004; United States / NIAID NIH HHS / AI / R01 AI 40312; United States / NIAID NIH HHS / AI / R37 AI040312-11; United States / NCRR NIH HHS / RR / RR024131-010004; United States / NIAID NIH HHS / AI / R01 AI047062-08; United States / NCRR NIH HHS / RR / RR024131-010001; United States / NCRR NIH HHS / RR / UL1 RR024131-01S2; United States / NIAID NIH HHS / AI / R37 AI040312-08; United States / NIAID NIH HHS / AI / K24 AI 69994; United States / NCRR NIH HHS / RR / M01 RR 00083; United States / NIAID NIH HHS / AI / R01 AI047062-06; United States / NIAID NIH HHS / AI / P30 AI027763; United States / NIAID NIH HHS / AI / AI 47062; United States / NIAID NIH HHS / AI / R37 AI040312; United States / NIMH NIH HHS / MH / P30 MH 59037; United States / NIAID NIH HHS / AI / R01 AI040312; United States / NIAID NIH HHS / AI / AI047062-09; United States / NIAID NIH HHS / AI / AI047062-06; United States / NCRR NIH HHS / RR / M01 RR000083; United States / NIAID NIH HHS / AI / AI047062-07; United States / NIAID NIH HHS / AI / R01 AI047062; United States / NIAID NIH HHS / AI / P30 AI 27763; United States / NIAID NIH HHS / AI / R01 AI047062-07
  • [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 / Anti-Retroviral Agents; 0 / Antigens, CD; 0 / Cross-Linking Reagents; 0 / RNA, Viral
  • [Other-IDs] NLM/ NIHMS88354; NLM/ PMC2648824
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81. Rodig SJ, Payne EG, Degar BA, Rollins B, Feldman AL, Jaffe ES, Androkites A, Silverman LB, Longtine JA, Kutok JL, Fleming MD, Aster JC: Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1. Am J Hematol; 2008 Feb;83(2):116-21
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  • [Title] Aggressive Langerhans cell histiocytosis following T-ALL: clonally related neoplasms with persistent expression of constitutively active NOTCH1.
  • Langerhans cell histiocytosis (LCH) and related entities are neoplasms of unknown pathogenesis.
  • Here, we describe studies assessing the role of NOTCH1 mutations in LCH, which were based on a case of fatal Langerhans cell tumor after T-cell acute lymphoblastic leukemia (T-ALL).
  • Although the two types of neoplasm in this patient were temporally and pathologically distinct, molecular analyses showed that they harbored the same T-cell receptor gene rearrangements and two activating NOTCH1 mutations involving exons 27 and 34.
  • Analysis of cDNA prepared from the aggressive Langerhans cell tumor showed that the NOTCH1 mutations were aligned in cis, a configuration that caused synergistic increases in NOTCH1 signal strength in reporter gene assays.
  • Immunohistochemistry confirmed that the Langerhans cell tumor also expressed NOTCH1 protein.
  • Although these data suggested that NOTCH1 mutations might contribute to the pathogenesis of typical sporadic LCH and related neoplasms occurring in the absence of T-ALL, an analysis of 24 cases of LCH and Rosai-Dorfman Disease occurring in patients without an antecedent history of T-ALL revealed no mutations.
  • Thus, activating NOTCH1 mutations appear to be unique to aggressive Langerhans cell tumors occurring after T-ALL.

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  • (PMID = 17874453.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI050225; United States / NCI NIH HHS / CA / CA082308; United States / NCI NIH HHS / CA / CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070-02; United States / NCI NIH HHS / CA / P01 CA119070
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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82. Lopez MC, Watson RR: Alterations in mesenteric lymph node T cell phenotype and cytokine secretion are associated with changes in thymocyte phenotype after LP-BM5 retrovirus infection. Clin Dev Immunol; 2005 Dec;12(4):249-57
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  • [Title] Alterations in mesenteric lymph node T cell phenotype and cytokine secretion are associated with changes in thymocyte phenotype after LP-BM5 retrovirus infection.
  • Simultaneous analysis of surface markers and cytokine secretion was done in an attempt to understand whether the deregulation of IFN-gamma secretion could be ascribed to a defined cell phenotype, concluding that all T cell subsets studied increased IFN-gamma secretion after retrovirus infection.
  • Finally, thymocyte phenotype was further analyzed trying to correlate changes in thymocyte phenotype with MLN cell phenotype.
  • In summary, we can conclude that LP-BM5 uses the immune system to reach the thymus where it interferes with the generation of functionally mature T cells, favoring the development of T cells with an abnormal phenotype.

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  • (PMID = 16584110.001).
  • [ISSN] 1740-2522
  • [Journal-full-title] Clinical & developmental immunology
  • [ISO-abbreviation] Clin. Dev. Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL 63667
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Egypt
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / Receptors, Interleukin-7; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II
  • [Other-IDs] NLM/ PMC2270737
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83. Dixon DN, Izon DJ, Dagger S, Callow MJ, Taplin RH, Kees UR, Greene WK: TLX1/HOX11 transcription factor inhibits differentiation and promotes a non-haemopoietic phenotype in murine bone marrow cells. Br J Haematol; 2007 Jul;138(1):54-67
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  • The TLX/HOX11 subfamily of divergent homeobox genes are involved in various aspects of embryogenesis and, in the case of TLX1/HOX11 and TLX3/HOX11L2, feature prominently as oncogenes in human T-cell acute lymphoblastic leukaemia.
  • TLX1 possesses immortalising activity in a wide variety of blood cell lineages, however, the effect of this oncogene on haemopoietic cell differentiation has not been fully investigated.
  • TLX1 was found to dramatically alter haemopoiesis, promoting the emergence of a non-haemopoietic CD45(-) CD31(+) cell population while markedly inhibiting erythroid and granulocytic cell differentiation.
  • This may account for its ability to promote the pre-leukaemic state via perturbation of specific gene expression programs.
  • [MeSH-minor] 3T3 Cells. Animals. Cell Differentiation / genetics. Female. Flow Cytometry. Gene Expression. Gene Expression Profiling. Hematopoiesis / genetics. Liver / embryology. Luciferases / genetics. Mice. Mice, Inbred C57BL. Oligonucleotide Array Sequence Analysis. Proto-Oncogene Proteins c-kit / genetics. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / pathology. Transduction, Genetic. Vascular Endothelial Growth Factor C / genetics. beta-Galactosidase / genetics

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  • (PMID = 17555447.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Tlx1 protein, mouse; 0 / Vascular Endothelial Growth Factor C; EC 1.13.12.- / Luciferases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.2.1.23 / beta-Galactosidase
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84. Piernas S, Xicoy B, Grifols JR, Ribera JM: [Autoimmune hemolytic anemia with positive direct antiglobulin test associated with T cell acute lymphoblastic leukemia]. Med Clin (Barc); 2006 May 6;126(17):678-9
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  • [Title] [Autoimmune hemolytic anemia with positive direct antiglobulin test associated with T cell acute lymphoblastic leukemia].
  • [Transliterated title] Anemia hemolítica autoinmunitaria con prueba de la antiglobulina directa positiva, sociada a leucemia aguda linfoblástica de origen T.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / diagnosis. Anemia, Hemolytic, Autoimmune / epidemiology. Coombs Test. Leukemia-Lymphoma, Adult T-Cell / epidemiology


85. Uyttebroeck A, Vanhentenrijk V, Hagemeijer A, Boeckx N, Renard M, Wlodarska I, Vandenberghe P, Depaepe P, De Wolf-Peeters C: Is there a difference in childhood T-cell acute lymphoblastic leukaemia and T-cell lymphoblastic lymphoma? Leuk Lymphoma; 2007 Sep;48(9):1745-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is there a difference in childhood T-cell acute lymphoblastic leukaemia and T-cell lymphoblastic lymphoma?
  • To distinguish the similarities or differences between T-cell acute lymphoblastic leukaemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LBL), we retrospectively analyzed the clinical, immunophenotypic, cytogenetic, and molecular characteristics in 37 children diagnosed between December 1990 and December 2003.
  • The clinical presentation and cytogenetic characteristics are largely similar for T-ALL and T-LBL supporting the concept that both represent a spectrum of one single disease.
  • The differences that were found between both neoplasms, in particular in their phenotype and in their expression profile may suggest that most T-ALL derive from a T-cell progenitor of the bone marrow, while thymocytes represent the normal counterpart of T-LBL.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17786710.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
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86. Bhanushali AA, Babu S, Thangapandi VR, Pillai R, Chheda P, Das BR: Mutations in the HD and PEST domain of Notch-1 receptor in T-cell acute lymphoblastic leukemia: report of novel mutations from Indian population. Oncol Res; 2010;19(2):99-104
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  • [Title] Mutations in the HD and PEST domain of Notch-1 receptor in T-cell acute lymphoblastic leukemia: report of novel mutations from Indian population.
  • Notch-1 is a transmembrane receptor protein that directs T-cell differentiation.
  • Gain-of-function mutations in Notch-1 have been reported in more than 50% of human T-cell acute lymphoblastic leukemia (T-ALL).
  • RNA was isolated from peripheral blood/bone marrow of 15 de novo T-ALL subjects; the Notch-1 HD and PEST regions were amplified and sequenced.
  • [MeSH-major] Mutation. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

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  • (PMID = 21302811.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptor, Notch1
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87. Chai YH, Lü H, Li JQ, Lu J, Xiao PF, He YX, Shao XJ: [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia]. Zhonghua Er Ke Za Zhi; 2007 Sep;45(9):684-6
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  • [Title] [Classical and molecular cytogenetic abnormalities in 124 pediatric patients with acute lymphoblastic leukemia].
  • OBJECTIVE: In childhood acute lymphoblastic leukemia (ALL), cytogenetics plays an important role in diagnosis, allocation of treatment and prognosis.
  • The diagnosis and FAB subtypes of ALL was determined by Wright-Giemsa-stained bone marrow smears and cytochemical staining.
  • Multiplex polymerase chain reaction (Multiplex PCR) analysis was performed to detect the 29 most common leukemia translocations for routine molecular diagnostic hematopathology practice, and complement the information gained from conventional cytogenetic analysis.
  • Thirteen cases of TEL-AML1, 10 cases of rearrangement in the MLL gene, 4 cases of E2A-PBX1, 4 cases of E2A-HLF, 3 cases of BCR-ABL, 2 cases of TLS-ERG, 32 cases of HOX11 were detected by Multiplex PCR in B-lineage leukemias.
  • SIL-TAL1 had been found in 4 of 7 of T-lineage leukemias.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Cytogenetic Analysis. Karyotyping. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Transcription Factors / genetics. Child. Child, Preschool. DNA-Binding Proteins / genetics. Female. Fusion Proteins, bcr-abl / genetics. Gene Fusion / genetics. Homeodomain Proteins. Humans. Immunophenotyping / methods. Infant. Male. Myeloid-Lymphoid Leukemia Protein / genetics. Polymerase Chain Reaction. Proto-Oncogene Proteins / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 18021563.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / TEL-AML1 fusion protein; 0 / pbx1 protein, human; 135471-20-4 / TAL1 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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88. Babusikova O, Stevulova L, Fajtova M: Immunophenotyping parameters as prognostic factors in T-acute leukemia patients. Neoplasma; 2009;56(6):508-13
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  • [Title] Immunophenotyping parameters as prognostic factors in T-acute leukemia patients.
  • The main aim of this study represents the extension of our studies using multiparametric flow cytometry analysis for exact definition of membrane and intracellular (cytoplasmic and nuclear) markers of acute leukemia cells of T-phenotype.
  • The study of blasts of each patient with all available monoclonal antibodies targeted to T-cell differential antigens and against possible marker coexistence from different lineages has been performed.
  • The main aim was concerned to more proper T-ALL diagnosis and stage definition and identification of the prognostic factors and the useful markers for the follow-up of T-ALL in remission.
  • New knowledge of the T-cell maturation stages of hematopoietic cells in bone marrow and thymus has been applied, as each T-acute leukemia clone is representative of one blocked stage through maturation.
  • Patients with more favorable prognosis (i. e. those of cortical stage) could have been already differentiated at diagnosis from those, allocated to pro-T stage, with very immature phenotypes and of an unfavorable clinical course.
  • The patients were either completely unresponsive to therapy or because of persistent MRD during continuation therapy, indicated for allogeneic hematopoietic stem-cell transplant.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Differentiation, T-Lymphocyte / immunology. Biomarkers, Tumor / immunology. HLA-DR Antigens / analysis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / immunology

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  • (PMID = 19728759.001).
  • [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
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation, T-Lymphocyte; 0 / Biomarkers, Tumor; 0 / HLA-DR Antigens
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89. Tydell CC, David-Fung ES, Moore JE, Rowen L, Taghon T, Rothenberg EV: Molecular dissection of prethymic progenitor entry into the T lymphocyte developmental pathway. J Immunol; 2007 Jul 1;179(1):421-38
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  • Notch signaling activates T lineage differentiation from hemopoietic progenitors, but relatively few regulators that initiate this program have been identified, e.g., GATA3 and T cell factor-1 (TCF-1) (gene name Tcf7).
  • To identify additional regulators of T cell specification, a cDNA library from mouse Pro-T cells was screened for genes that are specifically up-regulated in intrathymic T cell precursors as compared with myeloid progenitors.
  • The few genes sharply up-regulated between multipotent progenitors and Pro-T cell stages included those encoding transcription factors Bcl11b, TCF-1 (Tcf7), and HEBalt, Notch target Deltex1, Deltex3L, Fkbp5, Eva1, and Tmem131.
  • Like GATA3 and Deltex1, Bcl11b, Fkbp5, and Eva1 were dependent on Notch/Delta signaling for induction in fetal liver precursors, but only Bcl11b and HEBalt were up-regulated between the first two stages of intrathymic T cell development (double negative 1 and double negative 2) corresponding to T lineage specification.
  • [MeSH-major] Cell Differentiation / immunology. Cell Lineage / immunology. Gene Expression Profiling. Hematopoietic Stem Cells / immunology. Lymphopoiesis / immunology. Signal Transduction / immunology. T-Lymphocyte Subsets / immunology. Thymus Gland / immunology

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  • (PMID = 17579063.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ EL773010/ EL773011/ EL773012/ EL773013/ EL773014/ EL773015/ EL773016/ EL773017/ EL773018
  • [Grant] United States / NIAID NIH HHS / AI / F32 AI 068366; United States / NIAID NIH HHS / AI / K08 AI 054699; United States / NCI NIH HHS / CA / R01 CA 90233; United States / NCI NIH HHS / CA / R01 CA 98925
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bcl11b protein, mouse; 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins; 0 / delta protein
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90. Del Prete G, Chiumiento L, Amedei A, Piazza M, D'Elios MM, Codolo G, de Bernard M, Masetti M, Bruschi F: Immunosuppression of TH2 responses in Trichinella spiralis infection by Helicobacter pylori neutrophil-activating protein. J Allergy Clin Immunol; 2008 Nov;122(5):908-913.e5
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  • The addition of anti-Toll-like receptor 2 antibody abrogated the anti-T(H)2/pro-T(H)1 activity of HP-NAP.
  • [MeSH-minor] Animals. Antigens, Bacterial / immunology. Disease Models, Animal. Down-Regulation. Eosinophilia / immunology. Female. Immunoglobulin E / immunology. Interferon-gamma / immunology. Interleukin-12 / immunology. Interleukin-4 / immunology. Interleukin-5 / immunology. Mice. Mice, Inbred BALB C. Th1 Cells / immunology

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  • (PMID = 18804852.001).
  • [ISSN] 1097-6825
  • [Journal-full-title] The Journal of allergy and clinical immunology
  • [ISO-abbreviation] J. Allergy Clin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Bacterial Proteins; 0 / Interleukin-5; 0 / neutrophil-activating protein A, Helicobacter pylori; 187348-17-0 / Interleukin-12; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
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91. Lima K, Abrahamsen TG, Foelling I, Natvig S, Ryder LP, Olaussen RW: Low thymic output in the 22q11.2 deletion syndrome measured by CCR9+CD45RA+ T cell counts and T cell receptor rearrangement excision circles. Clin Exp Immunol; 2010 Jul 1;161(1):98-107
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  • [Title] Low thymic output in the 22q11.2 deletion syndrome measured by CCR9+CD45RA+ T cell counts and T cell receptor rearrangement excision circles.
  • We measured the expression of T cell receptor rearrangement excision circles (TREC) and used flow cytometry for direct subtyping of recent thymic emigrant (RTE)-related T cells in 43 patients (aged 1-54 years; median 9 years) from all over Norway and in age-matched healthy controls.
  • TREC levels correlated well with RTE-related T cells defined by co-expression of CD3, CD45RA and CCR9 (r=0.84) as well as with the CD4+ and CD8+ T cell subtypes.
  • RTE-related T cell counts also paralleled age-related TREC reductions.
  • Apart from CD45RA- T cells, all T cell subsets were lower in patients than in controls.
  • RTE-related T cells and TREC levels also correlated well (r=0.88) in patients without an identifiable thymus.
  • [MeSH-major] Antigens, CD45 / analysis. Chromosome Deletion. Chromosome Disorders / immunology. Chromosomes, Human, Pair 22 / ultrastructure. DNA, Circular / blood. DiGeorge Syndrome / immunology. Gene Rearrangement, T-Lymphocyte. Receptors, CCR / analysis. T-Lymphocyte Subsets / pathology. Thymus Gland / pathology

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  • (PMID = 20491792.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CC chemokine receptor 9; 0 / DNA, Circular; 0 / Receptors, CCR; EC 3.1.3.48 / Antigens, CD45; EC 3.1.3.48 / PTPRC protein, human
  • [Other-IDs] NLM/ PMC2940154
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92. Zhu YM, Zhao WL, Fu JF, Shi JY, Pan Q, Hu J, Gao XD, Chen B, Li JM, Xiong SM, Gu LJ, Tang JY, Liang H, Jiang H, Xue YQ, Shen ZX, Chen Z, Chen SJ: NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis. Clin Cancer Res; 2006 May 15;12(10):3043-9
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  • [Title] NOTCH1 mutations in T-cell acute lymphoblastic leukemia: prognostic significance and implication in multifactorial leukemogenesis.
  • PURPOSE: NOTCH signaling pathway is essential in T-cell development and NOTCH1 mutations are frequently present in T-cell acute lymphoblastic leukemia (T-ALL).
  • These mutations were significantly associated with elevated WBC count at diagnosis and independently linked to short survival time.
  • CONCLUSION: NOTCH1 mutation is an important prognostic marker in T-ALL and its predictive value could be even further increased if coevaluated with other T-cell-related regulatory genes.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Receptor, Notch1 / genetics

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  • [ErratumIn] Clin Cancer Res. 2009 Feb 15;15(4):1506
  • (PMID = 16707600.001).
  • [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 / NOTCH1 protein, human; 0 / Receptor, Notch1
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93. Ryan DP, Duncan JL, Lee C, Kuchel PW, Matthews JM: Assembly of the oncogenic DNA-binding complex LMO2-Ldb1-TAL1-E12. Proteins; 2008 Mar;70(4):1461-74
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  • The nuclear proteins TAL1 (T-cell acute leukaemia protein 1) and LMO2 (LIM-only protein 2) have critical roles in haematopoietic development, but are also often aberrantly activated in T-cell acute lymphoblastic leukaemia.
  • TAL1 and LMO2 operate within multifactorial protein-DNA complexes that regulate gene expression in the developing blood cell.
  • Our data provide biophysical evidence for a mechanism, by which LMO2 and TAL1 both regulate transcription in normal blood cell development, and synergistically disrupt E2A function in T-cells to promote the onset of leukaemia.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Basic Helix-Loop-Helix Transcription Factors / metabolism. Basic Helix-Loop-Helix Transcription Factors / physiology. Blood Cells. LIM Domain Proteins. Leukemia-Lymphoma, Adult T-Cell / etiology. Metalloproteins / metabolism. Metalloproteins / physiology. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins / physiology. T-Lymphocytes. TCF Transcription Factors / metabolism. TCF Transcription Factors / physiology. Transcription Factor 7-Like 1 Protein. Transcription Factors. Transcription, Genetic

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  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17910069.001).
  • [ISSN] 1097-0134
  • [Journal-full-title] Proteins
  • [ISO-abbreviation] Proteins
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA-Binding Proteins; 0 / LDB1 protein, human; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Multiprotein Complexes; 0 / Proto-Oncogene Proteins; 0 / TCF Transcription Factors; 0 / TCF7L1 protein, human; 0 / Transcription Factor 7-Like 1 Protein; 0 / Transcription Factors; 135471-20-4 / TAL1 protein, human; 9007-49-2 / DNA
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94. Meng YS, Khoury H, Dick JE, Minden MD: Oncogenic potential of the transcription factor LYL1 in acute myeloblastic leukemia. Leukemia; 2005 Nov;19(11):1941-7
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  • [Title] Oncogenic potential of the transcription factor LYL1 in acute myeloblastic leukemia.
  • The LYL1 gene encodes a basic helix-loop-helix transcription factor involved in T-cell acute lymphoblastic leukemia.
  • Using real-time quantitative RT-PCR assay, we found that the expression of LYL1 was at higher levels in the majority cases of acute myeloblastic leukemia (AML) or myelodysplastic syndrome when compared to normal bone marrow.
  • Our study also showed that LYL1 was highly expressed in most AML cell lines and in CD34+ AML cells.
  • Both of the derivative cell lines with overexpression of LYL1 had an increased growth rate and clonogenecity.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Gene Expression Profiling. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics

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  • (PMID = 16094422.001).
  • [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 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / DNA, Complementary; 0 / DNA-Binding Proteins; 0 / LYL1 protein, human; 0 / Neoplasm Proteins; 04079A1RDZ / Cytarabine; 5688UTC01R / Tretinoin
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95. Wang Y, Becker D, Vass T, White J, Marrack P, Kappler JW: A conserved CXXC motif in CD3epsilon is critical for T cell development and TCR signaling. PLoS Biol; 2009 Dec;7(12):e1000253
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  • [Title] A conserved CXXC motif in CD3epsilon is critical for T cell development and TCR signaling.
  • Virtually all T cell development and functions depend on its antigen receptor.
  • The T cell receptor (TCR) is a multi-protein complex, comprised of a ligand binding module and a signal transmission module.
  • In the CD3epsilon mutant mice, all stages of T cell development and activation that are TCR-dependent were impaired, but not eliminated, including activation of mature naïve T cells with the MHCII presented superantigen, staphylococcal enterotoxin B, or with a strong TCR cross-linking antibody specific for either TCR-Cbeta or CD3epsilon.
  • [MeSH-major] Antigens, CD3 / chemistry. Conserved Sequence. Receptors, Antigen, T-Cell / metabolism. T-Lymphocytes / cytology

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  • (PMID = 19956738.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI018785; United States / NIAID NIH HHS / AI / AI-17134; United States / NIAID NIH HHS / AI / AI-18785; United States / NIAID NIH HHS / AI / R01 AI017134; United States / NIAID NIH HHS / AI / R37 AI018785; United States / NIAID NIH HHS / AI / R56 AI017134; United States / NIAID NIH HHS / AI / AI-22295; United States / NIAID NIH HHS / AI / R56 AI018785; United States / NIAID NIH HHS / AI / P01 AI022295
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, CD3; 0 / Cd3e protein, mouse; 0 / Enterotoxins; 0 / Receptors, Antigen, T-Cell; 39424-53-8 / enterotoxin B, staphylococcal
  • [Other-IDs] NLM/ PMC2776832
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96. Schade AE, Wlodarski MW, Maciejewski JP: Pathophysiology defined by altered signal transduction pathways: the role of JAK-STAT and PI3K signaling in leukemic large granular lymphocytes. Cell Cycle; 2006 Nov;5(22):2571-4
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  • Signal transduction pathways integrate a variety of microenvironmental cues to guide cell function by regulating gene transcription, cell cycle status, growth, and differentiation.
  • It is well established that perturbation of these processes plays a key role in hematologic malignancies including lymphomas and chronic and acute lymphocytic leukemias.
  • Altered intracellular signaling pathways have been proposed to mediate many biological properties of T cell large granular lymphocytic leukemia (T-LGL), a disorder characterized by a clonal proliferation of CD8 T cells resulting in immune-mediated cytopenias, most commonly neutropenia.
  • Since T-LGL offers a unique opportunity to study signal transduction in the pathologic clonal cytotoxic T cell (CTL) compared to normal CTL, we have investigated a potential imbalance in T-LGL pro-survival signaling to define the mechanisms underlying the semi-autonomous proliferation leading to leukemia.
  • [MeSH-major] Janus Kinases / metabolism. Leukemia, T-Cell / metabolism. Phosphatidylinositol 3-Kinases / metabolism. STAT Transcription Factors / metabolism. Signal Transduction

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  • (PMID = 17172839.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT Transcription Factors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / Janus Kinases
  • [Number-of-references] 38
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97. Meleshko A, Savitski VP, Shman TV, Aleinikova OV: Immunophenotypically heterogeneous acute T-lymphoblastic leukemia has invariable immunogenotype: analysis of two cases. J Pediatr Hematol Oncol; 2006 Jan;28(1):50-2
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  • [Title] Immunophenotypically heterogeneous acute T-lymphoblastic leukemia has invariable immunogenotype: analysis of two cases.
  • Two patients with acute T-lymphoblastic leukemia showed heterogeneous expression of some immunophenotypic cell markers.
  • Cell sorting was used to separate two CD34/CD117/TCRgammadelta and CD34/CD117/TCRgammadelta cell populations.
  • The authors assume the presence of two immunophenotypically different cell subsets in different maturation stages at diagnosis.
  • [MeSH-major] Gene Rearrangement, T-Lymphocyte / immunology. Immunophenotyping. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Adolescent. Antigens, CD34 / genetics. Antigens, CD34 / immunology. Child, Preschool. Genotype. Humans. Polymerase Chain Reaction. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / immunology. Receptors, Antigen, T-Cell, gamma-delta / genetics. Receptors, Antigen, T-Cell, gamma-delta / immunology

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  • (PMID = 16394895.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Receptors, Antigen, T-Cell, gamma-delta; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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98. Patel KJ, Latif SU, de Calaca WM: An unusual presentation of precursor T cell lymphoblastic leukemia/lymphoma with cholestatic jaundice: case report. J Hematol Oncol; 2009;2:12
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  • [Title] An unusual presentation of precursor T cell lymphoblastic leukemia/lymphoma with cholestatic jaundice: case report.
  • BACKGROUND: Cholestatic jaundice as a presenting symptom of Precursor T-lymphoblastic leukemia (T-ALL)/lymphoma (T-LBL) has never been reported in literature.
  • Similarly, precursor T-ALL/T-LBL is characteristically negative for synaptophysin.
  • We report the first case of a patient with precursor T-ALL/T-LBL who presented with cholestatic jaundice and aberrant tumor expression of synaptophysin.
  • CT guided biopsy of the mass showed malignant lymphoma with diffuse proliferation of medium sized lymphoid cells.
  • Thus, the diagnosis of precursor T-ALL/T-LBL was made and jaundice with elevated CA 19-9 were attributed to intrahepatic cholestasis.
  • It is the first case report of neoplastic precursor T cell lymphoblasts with unusual expression of synaptophysin.
  • Tissue biopsy with thorough immunohistochemistry is required to differentiate precursor T-ALL/T-LBL from thymoma and small cell carcinoma.
  • [MeSH-major] Jaundice, Obstructive / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male. Obesity / complications. Synaptophysin / metabolism

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  • (PMID = 19284608.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Synaptophysin
  • [Other-IDs] NLM/ PMC2663564
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99. Akahane K, Inukai T, Zhang X, Hirose K, Kuroda I, Goi K, Honna H, Kagami K, Nakazawa S, Endo K, Kubota T, Yagita H, Koyama-Okazaki T, Sugita K: Resistance of T-cell acute lymphoblastic leukemia to tumor necrosis factor--related apoptosis-inducing ligand-mediated apoptosis. Exp Hematol; 2010 Oct;38(10):885-95
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  • [Title] Resistance of T-cell acute lymphoblastic leukemia to tumor necrosis factor--related apoptosis-inducing ligand-mediated apoptosis.
  • OBJECTIVE: Cytotoxic ligands are involved in tumor immunity and graft-vs.-leukemia effect after allogeneic stem cell transplantation for leukemia.
  • To clarify the susceptibility of T-cell acute lymphoblastic leukemia (T-ALL) to tumor immunity, sensitivity to recombinant human soluble Fas ligand (rhsFasL) and tumor necrosis factor-related apoptosis-inducing ligand (rhsTRAIL) was determined.
  • MATERIALS AND METHODS: Sensitivity to rhsFasL and rhsTRAIL and cell surface expression of their receptors were tested in T-ALL cell lines (n = 7) and patients' samples (n = 17) and compared with those in B-precursor ALL cell lines (n = 30).
  • Expression of components of the death-inducing signaling complex and the TRAIL receptor genes (DR4/DR5), and the methylation status and promoter activity of the DR4/DR5 gene were tested in T-ALL cell lines.
  • RESULTS: T-ALL cell lines showed higher level of Fas expression and higher sensitivity to rhsFasL than did B-precursor ALL cell lines.
  • Despite comparable expression of components of death-inducing signaling complex, cell lines and patients' samples of T-ALL showed TRAIL-resistance associated with low cell surface expression of DR4/DR5.
  • Gene expression of DR4/DR5 in T-ALL cell lines was significantly lower than that in B-precursor ALL cell lines, and the methylation status of the gene promoter in T-ALL cell lines was associated with the gene expression level at least for DR4.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Fas Ligand Protein / pharmacology. TNF-Related Apoptosis-Inducing Ligand / pharmacology
  • [MeSH-minor] Antigens, CD95 / metabolism. Cell Line, Tumor. Cells, Cultured. DNA Methylation / drug effects. Dose-Response Relationship, Drug. Drug Resistance. Flow Cytometry. Gene Expression / drug effects. Humans. Immunoblotting. Jurkat Cells. Luciferases / genetics. Luciferases / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Promoter Regions, Genetic / genetics. Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright © 2010 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20670671.001).
  • [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 / Antigens, CD95; 0 / FAS protein, human; 0 / Fas Ligand Protein; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 1.13.12.- / Luciferases
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100. Gros F, Sebti Y, de Guibert S, Branger B, Bernard M, Fauchet R, Amiot L: Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages. Neoplasia; 2006 Mar;8(3):223-30
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  • [Title] Soluble HLA-G molecules increase during acute leukemia, especially in subtypes affecting monocytic and lymphoid lineages.
  • Assay of these molecules by enzyme-linked immunosorbent assay in patients suffering from another hematologic disorder (acute leukemia) highlights increased sHLA-G secretion.
  • This increased secretion seems more marked in acute leukemia subtypes affecting monocytic and lymphoid lineages such as FABM4 and FABM5, as well as both B and T acute lymphoblastic leukemia (ALL).
  • All these findings suggest that sHLA-G molecules could be a factor in tumoral escape from immune survey during acute leukemia.
  • [MeSH-major] Antigens, Neoplasm / blood. HLA Antigens / blood. Histocompatibility Antigens Class I / blood. Leukemia / blood
  • [MeSH-minor] Acute Disease. Biomarkers, Tumor / blood. Burkitt Lymphoma / blood. Burkitt Lymphoma / genetics. Burkitt Lymphoma / metabolism. Burkitt Lymphoma / pathology. Cell Line, Tumor / chemistry. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Cytokines / blood. Cytokines / pharmacology. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Leukemic / drug effects. HLA-G Antigens. Humans. Leukemia, Myeloid / blood. Leukemia, Myeloid / classification. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Leukemia, Myeloid / pathology. Leukemia-Lymphoma, Adult T-Cell / blood. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / blood. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Retrospective Studies. Solubility. Tumor Escape

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  • (PMID = 16611416.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / HLA Antigens; 0 / HLA-G Antigens; 0 / Histocompatibility Antigens Class I
  • [Other-IDs] NLM/ PMC1578523
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