[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 165759
1. Matutes E: Adult T-cell leukaemia/lymphoma. J Clin Pathol; 2007 Dec;60(12):1373-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a mature T-cell neoplasm of post-thymic lymphocytes aetiologically linked to the human T-cell lymphotropic virus, HTLV-I, and with a distinct geographical distribution.
  • The disease manifests with leukaemia in greater than two thirds of patients, while the remaining patients have a lymphomatous form.
  • According to the disease manifestations, various forms which differ in clinical course and prognosis have been recognised: acute, chronic, smouldering and lymphoma.
  • Organomegaly, skin involvement, circulating atypical lymphocytes ("flower" cells) with a CD4+ CD25+ phenotype and hypercalcaemia are the most common disease features.
  • The diagnosis should be based on a constellation of clinical features and laboratory investigations.
  • The latter comprise: lymphocyte morphology, immunophenotype, histology of the tissues affected in the pure lymphoma forms and serology or DNA analysis for HTLV-I.
  • The differential diagnosis of ATLL includes other mature T-cell neoplasms such as T-cell prolymphocytic leukaemia (T-PLL), Sézary syndrome (SS), peripheral T-cell lymphomas and occasionally healthy carriers of the virus or Hodgkin disease.
  • The clinical course is aggressive with a median survival of less than 12 months in the acute and lymphoma forms.
  • Despite major advances in understanding the pathogenesis of the disease, management of these patients remains a challenge for clinicians as they do not respond or achieve only transient responses to therapies used in high-grade lymphomas.
  • The use of antiretroviral agents such as zidovudine in combination with interferon-alpha, with or without concomitant chemotherapy, has shown activity in this disease with improvement in survival and response rate.
  • Consolidation with high dose therapy and autologous or allogeneic stem-cell transplantation should be considered in young patients.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Biomarkers, Tumor / blood. Diagnosis, Differential. Drug Therapy, Combination. Humans. Immunophenotyping. Prognosis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1985 Oct 1;56(7):1688-90 [2992744.001]
  • [Cites] Int J Cancer. 1985 Jan 15;35(1):65-72 [2578441.001]
  • [Cites] Lancet. 1987 Jul 11;2(8550):94-5 [2885585.001]
  • [Cites] Blood. 1987 Nov;70(5):1554-64 [2889485.001]
  • [Cites] Blood. 1988 Apr;71(4):1027-32 [2895676.001]
  • [Cites] Lancet. 1990 Oct 20;336(8721):987-90 [1977015.001]
  • [Cites] Lancet. 1991 Jan 12;337(8733):76-7 [1670727.001]
  • [Cites] Cancer. 1991 Mar 15;67(6):1622-8 [2001551.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1701-12 [8400227.001]
  • [Cites] Lancet. 1994 Jan 22;343(8891):213-6 [7904671.001]
  • [Cites] Leukemia. 1994 Nov;8(11):1834-7 [7967729.001]
  • [Cites] J Clin Oncol. 1994 Dec;12(12):2588-93 [7989933.001]
  • [Cites] Leukemia. 1995 Apr;9(4):594-7 [7723390.001]
  • [Cites] Leukemia. 1995 Apr;9(4):598-604 [7723391.001]
  • [Cites] Br J Haematol. 1995 Mar;89(3):615-9 [7734362.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1744-8 [7760890.001]
  • [Cites] N Engl J Med. 1995 Jun 29;332(26):1749-51 [7760891.001]
  • [Cites] Leuk Lymphoma. 1995 May;17(5-6):459-64 [7549838.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4063-75 [7492762.001]
  • [Cites] Br J Haematol. 1998 Jun;101(4):703-11 [9674744.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Br J Haematol. 2005 Aug;130(4):511-5 [16098064.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3380-2 [16076875.001]
  • [Cites] Leuk Res. 2006 Jan;30(1):103-5 [15979704.001]
  • [Cites] Leuk Lymphoma. 1999 Nov;35(5-6):637-40 [10609805.001]
  • [Cites] Bone Marrow Transplant. 2006 Jan;37(1):41-4 [16247419.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] J Clin Pathol. 2007 Dec;60(12):1392-6 [18042695.001]
  • [Cites] Bone Marrow Transplant. 2001 Jan;27(1):15-20 [11244433.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Br J Haematol. 2001 Jun;113(3):779-84 [11380470.001]
  • [Cites] Hematol J. 2002;3(6):276-82 [12522449.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):304-9 [12542491.001]
  • [Cites] Am J Hematol. 2004 Jun;76(2):187-9 [15164389.001]
  • [Cites] Leuk Res. 1985;9(11):1353-9 [2867255.001]
  • (PMID = 18042693.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / Biomarkers, Tumor
  • [Number-of-references] 42
  • [Other-IDs] NLM/ PMC2095573
  •  go-up   go-down


2. Naresh KN, Marks AJ: Peripheral blood and bone marrow morphology in adult T-cell leukaemia/lymphoma. Am J Hematol; 2010 Jul;85(7):518
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peripheral blood and bone marrow morphology in adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology

  • Genetic Alliance. consumer health - Peripheral T-cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20575019.001).
  • [ISSN] 1096-8652
  • [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
  •  go-up   go-down


3. Shanmugam H, Eow GI, Nadarajan VS: A case report of adult T-cell leukaemia/lymphoma. Malays J Pathol; 2009 Jun;31(1):63-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case report of adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a rare T lymphoproliferative disorder which is aetiologically linked with human T-cell lymphotropic virus type-1 (HTLV-1).
  • HTLV-1 is endemic in Japan, Caribbean and Africa.
  • The highest incidence of ATLL is in Japan although sporadic cases have been reported elsewhere in the world.
  • We describe a case of ATLL with an unusual presentation which we believe is the first reported case of ATLL in Malaysia based on our literature search.
  • A 51-year-old Indian lady was referred to University Malaya Medical Centre for an incidental finding of lymphocytosis while being investigated for pallor and giddiness.
  • Clinical examination revealed bilateral shotty cervical lymph nodes with no hepato-splenomegaly or skin lesions.
  • Immunophenotyping of the bone marrow mononuclear cells showed CD3+, CD4+, CD5+, CD7- and CD25+ which is characteristic of ATLL phenotype.
  • HTLV-1 infection was confirmed by the presence of HTLV-1 proviral DNA in the tumor cells using conventional Polymerase Chain Reaction (PCR) and real-time PCR.
  • Here, we discuss the pathogenesis and characteristics of ATLL as well as the detection of HTLV-1 by real time PCR.
  • [MeSH-major] Leukemia, T-Cell / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Antigens, CD / metabolism. Bone Marrow Cells / pathology. Bone Marrow Cells / virology. DNA, Viral / analysis. Female. Flow Cytometry. HTLV-I Infections / complications. HTLV-I Infections / pathology. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / isolation & purification. Humans. Immunophenotyping. L-Lactate Dehydrogenase / blood. Leukocytosis / etiology. Leukocytosis / pathology. Lymph Nodes / metabolism. Lymph Nodes / pathology. Lymph Nodes / virology. Middle Aged. Monocytes / pathology. Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19694316.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / DNA, Viral; EC 1.1.1.27 / L-Lactate Dehydrogenase
  •  go-up   go-down


Advertisement
4. Osborne GE, Pagliuca A, Ho A, du Vivier AW: Novel treatment of Sézary-like syndrome due to adult T-cell leukaemia/lymphoma with daclizumab (humanized anti-interleukin-2 receptor alpha antibody). Br J Dermatol; 2006 Sep;155(3):617-20
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel treatment of Sézary-like syndrome due to adult T-cell leukaemia/lymphoma with daclizumab (humanized anti-interleukin-2 receptor alpha antibody).
  • We describe a patient with erythrodermic adult T-cell leukaemia/lymphoma resistant to multiple systemic therapies who, on the commencement of daclizumab, a humanized anti-interleukin-2 receptor antibody, developed a rapid and sustained complete response with resolution of previously debilitating erythroderma, suggesting significant activity of this agent in this disease process.

  • Genetic Alliance. consumer health - Sezary syndrome.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16911291.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Immunoglobulin G; 0 / Immunosuppressive Agents; CUJ2MVI71Y / daclizumab
  •  go-up   go-down


5. Liu TY, Chen CY, Tien HF, Lin CW: Loss of CD7, independent of galectin-3 expression, implies a worse prognosis in adult T-cell leukaemia/lymphoma. Histopathology; 2009 Jan;54(2):214-20
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of CD7, independent of galectin-3 expression, implies a worse prognosis in adult T-cell leukaemia/lymphoma.
  • AIMS: Loss of CD7 is characteristic of adult T-cell lymphoma/leukaemia (ATLL).
  • Galectin-3 (Gal-3) is strongly induced in cultured human T lymphotropic virus-1-infected T lymphocytes, and may cause apoptosis through interaction with CD7.
  • The aim was to investigate the clinical relevance of the Gal-3-CD7 pathway in ATLL.
  • METHODS AND RESULTS: Immunohistochemistry for Gal-3 and CD7 was performed on 22 cases of ATLL in the leukaemic phase.
  • We found that the lymphoma cells were not necessarily Gal-3+, but Gal-3+ stromal cells could always be found.
  • CONCLUSIONS: These data suggest that, by down-regulating CD7, ATLL cells could have escaped Gal-3-induced apoptosis to run a more aggressive clinical course.
  • [MeSH-major] Antigens, CD7 / metabolism. Galectin 3 / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology
  • [MeSH-minor] Adult. Aged. Apoptosis. Cells, Cultured. Chromosome Aberrations. Down-Regulation. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19207946.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD7; 0 / Galectin 3
  •  go-up   go-down


6. Chandesris MO, Ghez D, Besson C, Suarez F, Delarue R, Rubio MT, Bazarbachi A, Varet B, Hermine O: Complete remission of a relapsing adult T cell leukaemia following treatment of a secondary acute promyelocytic leukaemia: towards a reappraisal of arsenic trioxide and all-transretinoic acid? BMJ Case Rep; 2009;2009

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remission of a relapsing adult T cell leukaemia following treatment of a secondary acute promyelocytic leukaemia: towards a reappraisal of arsenic trioxide and all-transretinoic acid?
  • Despite improvements in therapeutic options, human T cell lymphotropic virus type 1 (HTLV-1)-related adult T cell leukaemia/lymphoma (ATLL) has a dismal prognosis.
  • The present report concerns the case of a multirelapsing ATLL that reached a complete remission following the treatment of a secondary acute promyelocytic leukaemia with cytarabine, anthracyclin, all-transretinoic acid and arsenic trioxide.
  • This unexpected result with a multitreated/chemorefractory disease led us to reconsider the potential therapeutic benefits of arsenic trioxide, which has demonstrated efficacy against ATLL cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Haematologica. 2007 May;92(5):719-20 [17488707.001]
  • [Cites] Antiviral Res. 2006 Jul;70(3):132-9 [16540180.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2849-55 [11023521.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] Hematol J. 2002;3(6):276-82 [12522449.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4576-82 [12560223.001]
  • [Cites] J Clin Oncol. 2003 Jun 15;21(12):2326-34 [12805334.001]
  • [Cites] J Infect Dis. 2003 Aug 1;188(3):424-7 [12870124.001]
  • [Cites] Haematologica. 2007 Jun;92(6):753-62 [17550847.001]
  • [Cites] Cell Death Differ. 2005 Aug;12 Suppl 1:871-7 [15846376.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1010-7 [15843825.001]
  • [Cites] Hematol J. 2004;5(2):130-4 [15048063.001]
  • [Cites] Blood. 1999 Jan 1;93(1):278-83 [9864171.001]
  • [Cites] Leuk Lymphoma. 2005 Mar;46(3):347-55 [15621824.001]
  • [Cites] Lancet Oncol. 2004 Nov;5(11):664-72 [15522654.001]
  • (PMID = 21829417.001).
  • [ISSN] 1757-790X
  • [Journal-full-title] BMJ case reports
  • [ISO-abbreviation] BMJ Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3030139
  •  go-up   go-down


7. Lyell V, Khatamzas E, Allain T: Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report. J Med Case Rep; 2007;1:56
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Severe hypercalcaemia and lymphoma in an HTLV-1 positive Jamaican woman: a case report.
  • Human T cell lymphotrophic virus type-1 infection is endemic in the Afro-Caribbean community in Britain, with carriage rates of about 3%.
  • Although there is a long latency, carriers have a 1-5% chance of developing adult T cell leukaemia/lymphoma, a condition frequently complicated by marked and refractory hypercalcaemia, and with a poor prognosis.
  • We present the case of an elderly Jamaican woman with severe hypercalcaemia and a raised PTHrP who was found to have lymphoma and was positive for HTLV-1.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Endocrinol Metab. 1999 Oct;84(10):3545-50 [10522993.001]
  • [Cites] BMJ. 2000 Mar 4;320(7235):611-2 [10698878.001]
  • [Cites] Endocr Relat Cancer. 2003 Sep;10(3):403-7 [14503917.001]
  • [Cites] Clin Lymphoma. 2004 Jun;5(1):29-36 [15245605.001]
  • [Cites] Am J Med Sci. 1995 Jun;309(6):312-4 [7771500.001]
  • [Cites] Am J Hematol. 2005 Mar;78(3):232-9 [15726602.001]
  • [Cites] Cancer Res. 2005 Jun 1;65(11):4467-70 [15930259.001]
  • [Cites] Endocr Relat Cancer. 2005 Sep;12(3):549-83 [16172192.001]
  • [Cites] J Natl Med Assoc. 1995 Oct;87(10):746-8 [7473848.001]
  • [Cites] Anticancer Res. 2004 Sep-Oct;24(5A):2665-73 [15517871.001]
  • (PMID = 17651486.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1950877
  •  go-up   go-down


8. Taylor G: Molecular aspects of HTLV-I infection and adult T-cell leukaemia/lymphoma. J Clin Pathol; 2007 Dec;60(12):1392-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular aspects of HTLV-I infection and adult T-cell leukaemia/lymphoma.
  • Human T-cell lymphotropic virus-I (HTLV-I) is the cause of adult T-cell leukaemia/lymphoma.
  • Tax transactivates a large and apparently ever expanding list of human genes through transcriptional factors.
  • Elucidating not only the pathways but also the timing of action of HTLV proteins is important for understanding the pathogenesis and development of new treatments.
  • [MeSH-major] HTLV-I Infections / complications. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Adult. Apoptosis. Cell Cycle / genetics. Cell Transformation, Neoplastic. Cell Transformation, Viral. Gene Products, tax / physiology. Genomic Instability. Humans. Transcription Factors / physiology. Viral Regulatory and Accessory Proteins / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1757-64 [11080823.001]
  • [Cites] J Biol Chem. 2000 Nov 17;275(46):35926-31 [10931836.001]
  • [Cites] Virology. 2001 Jan 5;279(1):38-46 [11145887.001]
  • [Cites] J Immunol. 2001 Feb 1;166(3):1723-9 [11160217.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • [Cites] J Virol. 1992 Mar;66(3):1294-302 [1738191.001]
  • [Cites] J Virol. 1992 Jul;66(7):4570-5 [1351105.001]
  • [Cites] J Biol Chem. 1992 Aug 15;267(23):16288-91 [1644814.001]
  • [Cites] J Virol. 1992 Oct;66(10):6191-3 [1527856.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1701-12 [8400227.001]
  • [Cites] Oncogene. 1993 Nov;8(11):3029-36 [8414503.001]
  • [Cites] J Virol. 1993 Dec;67(12):7001-7 [8230424.001]
  • [Cites] Cell. 1993 Nov 19;75(4):805-16 [8242751.001]
  • [Cites] Oncogene. 1993 Dec;8(12):3189-97 [7504230.001]
  • [Cites] Cell. 1994 Mar 25;76(6):1013-23 [8137420.001]
  • [Cites] J Virol. 1994 May;68(5):3374-9 [8151796.001]
  • [Cites] J Biol Chem. 1994 May 27;269(21):14946-50 [8195127.001]
  • [Cites] J Immunol. 2002 Sep 15;169(6):3120-30 [12218129.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Oncogene. 2003 Jun 12;22(24):3734-41 [12802280.001]
  • [Cites] J Virol. 2003 Oct;77(20):11027-39 [14512551.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] J Gen Virol. 2003 Dec;84(Pt 12):3203-14 [14645902.001]
  • [Cites] J Virol. 2004 Apr;78(8):3837-45 [15047799.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6629-34 [15100416.001]
  • [Cites] J Virol. 2004 Jun;78(12):6081-90 [15163701.001]
  • [Cites] J Virol. 2004 Oct;78(20):11077-83 [15452228.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2523-31 [15226182.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Princess Takamatsu Symp. 1982;12:285-94 [6984702.001]
  • [Cites] Science. 1988 Sep 23;241(4873):1652-5 [2843985.001]
  • [Cites] Blood. 1988 Nov;72(5):1805-16 [2846094.001]
  • [Cites] J Virol. 1989 Aug;63(8):3220-6 [2501514.001]
  • [Cites] Int J Cancer. 1990 Feb 15;45(2):237-43 [2303290.001]
  • [Cites] Science. 1990 Mar 2;247(4946):1082-4 [2309119.001]
  • [Cites] J Exp Med. 1990 Jul 1;172(1):121-9 [2358774.001]
  • [Cites] J Exp Med. 1990 Sep 1;172(3):759-65 [2388034.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] Gene. 2007 Jan 15;386(1-2):191-201 [17071021.001]
  • [Cites] J Biol Chem. 2007 Feb 9;282(6):4185-92 [17145747.001]
  • [Cites] Oncogene. 1995 Jan 19;10(2):269-77 [7838527.001]
  • [Cites] AIDS Res Hum Retroviruses. 1994 Oct;10(10):1259-68 [7531462.001]
  • [Cites] Virus Genes. 1995 Jan;9(2):161-70 [7732661.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4063-75 [7492762.001]
  • [Cites] EMBO J. 1996 Jul 15;15(14):3744-50 [8670878.001]
  • [Cites] Virology. 1997 Apr 28;231(1):135-40 [9143312.001]
  • [Cites] Oncogene. 1997 May 15;14(19):2265-72 [9178902.001]
  • [Cites] J Gen Virol. 1997 Dec;78 ( Pt 12):3277-85 [9400978.001]
  • [Cites] J Virol. 1998 Jan;72(1):633-40 [9420268.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] J Virol. 1998 May;72(5):4458-62 [9557741.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3620-32 [9584203.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23):14119-29 [9603911.001]
  • [Cites] Blood. 1998 Jun 15;91(12):4701-7 [9616168.001]
  • [Cites] J Biol Chem. 1998 Aug 28;273(35):22382-8 [9712859.001]
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3993-4000 [9731513.001]
  • [Cites] Oncogene. 2005 Jan 20;24(4):525-40 [15580311.001]
  • [Cites] J Virol. 2005 Aug;79(15):9449-57 [16014908.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5976-85 [16155604.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):720-5 [16407133.001]
  • [Cites] J Biol Chem. 2006 Mar 31;281(13):8927-38 [16436385.001]
  • [Cites] Nat Med. 2006 Apr;12(4):466-72 [16550188.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Virus Genes. 2001 Jun;22(3):279-87 [11450946.001]
  • [Cites] Blood. 2001 Aug 1;98(3):823-9 [11468184.001]
  • [Cites] J Virol. 2001 Oct;75(20):9885-95 [11559821.001]
  • [Cites] Virus Genes. 2001;23(2):123-35 [11724264.001]
  • [Cites] J Biol Chem. 2002 Feb 15;277(7):5187-93 [11729202.001]
  • [Cites] J Virol. 2002 Apr;76(7):3493-501 [11884573.001]
  • [Cites] J Virol. 2002 Apr;76(8):4022-33 [11907241.001]
  • [Cites] J Biomed Sci. 2002 Jul-Aug;9(4):292-8 [12145525.001]
  • [Cites] Retrovirology. 2007;4:14 [17306025.001]
  • [Cites] J Virol. 2007 Jun;81(11):5714-23 [17344291.001]
  • [Cites] J Virol. 2007 Jun;81(11):6089-98 [17376895.001]
  • [Cites] Leukemia. 2007 Aug;21(8):1752-62 [17554373.001]
  • [Cites] Retrovirology. 2007;4:49 [17634129.001]
  • [Cites] J Virol. 2007 Sep;81(17):9088-99 [17582004.001]
  • [Cites] J Clin Pathol. 2007 Dec;60(12):1373-7 [18042693.001]
  • [Cites] J Virol. 1999 Dec;73(12):9917-27 [10559304.001]
  • [Cites] Oncogene. 1999 Oct 28;18(44):5967-72 [10557085.001]
  • [Cites] J Gen Virol. 1999 Dec;80 ( Pt 12):3073-81 [10567637.001]
  • [Cites] J Virol. 2000 Feb;74(3):1094-100 [10627519.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):319-24 [10652420.001]
  • [Cites] J Virol. 2000 May;74(9):3933-40 [10756004.001]
  • [Cites] Oncogene. 2000 Apr 27;19(18):2240-8 [10822374.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2849-55 [11023521.001]
  • [Cites] J Virol. 2000 Dec;74(23):11270-7 [11070026.001]
  • (PMID = 18042695.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / Transcription Factors; 0 / Viral Regulatory and Accessory Proteins; 0 / tax protein, Human T-lymphotrophic virus 1
  • [Number-of-references] 91
  • [Other-IDs] NLM/ PMC2095577
  •  go-up   go-down


9. Chiou CC, Wang PN, Yang LC, Kuo TT, Hong HS: Disseminated xanthogranulomas associated with adult T-cell leukaemia/lymphoma: a case report and review the association of haematologic malignancies. J Eur Acad Dermatol Venereol; 2007 Apr;21(4):532-5
MedlinePlus Health Information. consumer health - Skin Conditions.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disseminated xanthogranulomas associated with adult T-cell leukaemia/lymphoma: a case report and review the association of haematologic malignancies.
  • Xanthogranuloma (XG) is rarely observed in adults and has been reported to be associated with chronic myelogenous leukaemia (CML) and/or neurofibromatosis type 1 (NF1).
  • A 68-year-old woman with adult T-cell leukaemia/lymphoma (ATLL) gradually developed disseminated XGs over the 3 years since disease onset.
  • The lesions of XGs persisted despite chemotherapy with prednisolone and chlorambucil for her ATLL.
  • This is the first report of disseminated XGs associated with ATLL.
  • [MeSH-major] Granuloma / etiology. Leukemia-Lymphoma, Adult T-Cell / complications. Skin Diseases / etiology. Xanthomatosis / etiology
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Follow-Up Studies. Giant Cells / pathology. Histiocytes / pathology. Humans. Lymphocytes / pathology. Skin / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17373983.001).
  • [ISSN] 0926-9959
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 23
  •  go-up   go-down


10. Shimauchi T, Hirokawa Y, Tokura Y: Purpuric adult T-cell leukaemia/lymphoma: expansion of unusual CD4/CD8 double-negative malignant T cells expressing CCR4 but bearing the cytotoxic molecule granzyme B. Br J Dermatol; 2005 Feb;152(2):350-2

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Purpuric adult T-cell leukaemia/lymphoma: expansion of unusual CD4/CD8 double-negative malignant T cells expressing CCR4 but bearing the cytotoxic molecule granzyme B.
  • A 78-year-old Japanese woman with adult T-cell leukaemia/lymphoma (ATL) presented with an unusual purpuric and erythematous eruption on the face and trunk.
  • In a purpuric lesion, extravasation of erythrocytes was associated with an infiltrate of these cytotoxic tumour cells.
  • Our case suggests phenotypical and functional heterogeneity of tumour cells in ATL, which may be closely related to the clinical appearance of the skin eruption.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Purpura / immunology. Receptors, Chemokine / metabolism. Serine Endopeptidases / metabolism. T-Lymphocyte Subsets / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15727651.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD8; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 0 / Receptors, Chemokine; EC 3.4.21.- / GZMB protein, human; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Serine Endopeptidases
  •  go-up   go-down


11. Martyn-Simmons CL, Holden CA: Adult T-cell leukaemia/lymphoma masquerading as a hair dye allergy. Br J Dermatol; 2006 Jan;154(1):196-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukaemia/lymphoma masquerading as a hair dye allergy.
  • [MeSH-major] Dermatitis, Contact / diagnosis. Hair Dyes / adverse effects. Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16403124.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hair Dyes
  •  go-up   go-down


12. Takeuchi S, Matsushita M, Tsukasaki K, Takeuchi N, Tomonaga M, Komatsu N, Ikezoe T, Uehara Y, Koeffler HP: P53 codon 72 polymorphism is associated with disease progression in adult T-cell leukaemia/lymphoma. Br J Haematol; 2005 Nov;131(4):552-3
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P53 codon 72 polymorphism is associated with disease progression in adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Genes, p53. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Codon. Disease Progression. Humans. Polymorphism, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16281948.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Codon
  •  go-up   go-down


13. Senba-Nakata K, Hatano Y, Ishikawa K, Ishikawa T, Otani Y, Takeuchi Y, Katagiri K, Okamoto O, Fujiwara S: Etretinate combined with low-dose prednisolone for an aged patient with adult T-cell leukaemia/lymphoma. Clin Exp Dermatol; 2010 Jun;35(4):e153-4
Hazardous Substances Data Bank. ETRETINATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Etretinate combined with low-dose prednisolone for an aged patient with adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy

  • Hazardous Substances Data Bank. PREDNISOLONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19925487.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 65M2UDR9AG / Etretinate; 9PHQ9Y1OLM / Prednisolone
  •  go-up   go-down


14. Roncador G, Garcia JF, Garcia JF, Maestre L, Lucas E, Menarguez J, Ohshima K, Nakamura S, Banham AH, Piris MA: FOXP3, a selective marker for a subset of adult T-cell leukaemia/lymphoma. Leukemia; 2005 Dec;19(12):2247-53

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FOXP3, a selective marker for a subset of adult T-cell leukaemia/lymphoma.
  • FOXP3 is a forkhead transcription factor family member, implicated in T-cell regulation, activation and differentiation.
  • In this study, FOXP3 protein expression has been analysed using a new anti-FOXP3 monoclonal antibody in 172 paraffin-embedded lymphoma samples.
  • FOXP3 expression in tumour cells was confined to adult T-cell leukaemia/lymphoma (ATLL) cases (17/25, 68%), with some variability in the intensity of the staining and the proportion of positive cells.
  • No other lymphoma types studied exhibited FOXP3 expression in the malignant population.
  • The selective expression of FOXP3 by tumour cells in ATLL makes this antibody a potentially useful diagnostic tool.
  • [MeSH-major] Forkhead Transcription Factors / analysis. Leukemia-Lymphoma, Adult T-Cell / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16193085.001).
  • [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 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors
  •  go-up   go-down


15. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • METHODS: Retrospective review of all patients files diagnosed with T-ALL from 1989 until now with data collection including; sex, age, white cell count (WBCs), CNS disease, type of protocol used, length of survival, overall survival, cause of death (toxic, disease).
  • Median WBCs 50,000/Cmm (range: 1.500-619,000/Cmm) and positive CNS at diagnosis 10/52 (20%).
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Using augmented therapy based on CCG1961 was associated with better outcome.
  • Further risk and response stratification in addition to intensification of therapy for T-cell ALL in our center may prove to be beneficial.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Nakase K, Hara M, Kozuka T, Tanimoto K, Nawa Y: Bone marrow transplantation from unrelated donors for patients with adult T-cell leukaemia/lymphoma. Bone Marrow Transplant; 2006 Jan;37(1):41-4
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow transplantation from unrelated donors for patients with adult T-cell leukaemia/lymphoma.
  • Adult T-cell leukaemia/lymphoma (ATLL) is a highly aggressive haematological malignancy.
  • More than 40 cases of ATLL treated by allogeneic bone marrow transplantation (BMT) from sibling donors have been reported, while there have been only a few cases of unrelated BMT for treatment of this disease.
  • We began performing allogeneic BMT from unrelated donors in 1999 to improve the outcome of ATLL patients with no suitable sibling donors.
  • Eight ATLL patients underwent unrelated BMT; five received the conventional conditioning regimen consisting of cyclophosphamide and total body irradiation, while three received a reduced-intensity preparative regimen.
  • Two patients died due to encephalopathy of unknown aetiology on days 10 and 35, and one patient died due to progression of ATLL 25 months after BMT.
  • Five patients are currently alive and disease-free at a median of 20 months after BMT.
  • Proviral human T-lymphotropic virus type-I (HTLV-I) DNA load in peripheral blood mononuclear cells (PBMCs) was assessed in four cases before and after BMT.
  • HTLV-I proviral DNA load was reduced significantly after transplantation.
  • Unrelated BMT is feasible for treatment of ATLL.
  • Further studies in a larger number of cases are required to determine the optimal conditioning regimen and stem cell source.
  • [MeSH-major] Bone Marrow Transplantation. Leukemia-Lymphoma, Adult T-Cell / therapy. Living Donors. Transplantation Conditioning
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Histocompatibility Testing. Humans. Male. Middle Aged. Myeloablative Agonists / administration & dosage. Retrospective Studies. Transplantation, Homologous. Whole-Body Irradiation / methods


17. Lee WJ, Park GH, Kang SM, Lee MW, Choi JH, Moon KC, Koh JK: Adult T-cell leukaemia/lymphoma presenting as a contact dermatitis-like localized patch. J Eur Acad Dermatol Venereol; 2009 Jul;23(7):847-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adult T-cell leukaemia/lymphoma presenting as a contact dermatitis-like localized patch.
  • [MeSH-major] Dermatitis, Contact / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Immunophenotyping. Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19207648.001).
  • [ISSN] 1468-3083
  • [Journal-full-title] Journal of the European Academy of Dermatology and Venereology : JEADV
  • [ISO-abbreviation] J Eur Acad Dermatol Venereol
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Netherlands
  •  go-up   go-down


18. Ishitsuka K, Ikeda S, Utsunomiya A, Saburi Y, Uozumi K, Tsukasaki K, Etou K, Muta K, Ohno Y, Kinosita K, Tamura K: Smouldering adult T-cell leukaemia/lymphoma: a follow-up study in Kyushu. Br J Haematol; 2008 Nov;143(3):442-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Smouldering adult T-cell leukaemia/lymphoma: a follow-up study in Kyushu.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Disease Progression. Female. Follow-Up Studies. Humans. Male. Middle Aged. Prognosis. Skin Neoplasms / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18759766.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  •  go-up   go-down


19. Hiraoka N, Yokote T, Nakayama-Ichiyama S, Takayama A, Iwaki K, Kobayashi K, Oka S, Miyoshi T, Akioka T, Takubo T, Tsuji M, Hanafusa T: High fever and shock induced by interferon-γ and interleukin-6 produced by adult T-cell leukaemia/lymphoma cells. Leuk Res; 2010 Nov;34(11):e290-1
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High fever and shock induced by interferon-γ and interleukin-6 produced by adult T-cell leukaemia/lymphoma cells.
  • [MeSH-major] Fever / etiology. Interferon-gamma / secretion. Interleukin-6 / secretion. Leukemia-Lymphoma, Adult T-Cell / metabolism. Shock / etiology

  • MedlinePlus Health Information. consumer health - Fever.
  • MedlinePlus Health Information. consumer health - Shock.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20650530.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


20. Takeuchi S, Hofmann WK, Tsukasaki K, Takeuchi N, Ikezoe T, Matsushita M, Uehara Y, Phillip Koeffler H: Loss of H19 imprinting in adult T-cell leukaemia/lymphoma. Br J Haematol; 2007 May;137(4):380-1

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of H19 imprinting in adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Genes, Tumor Suppressor. Leukemia-Lymphoma, Adult T-Cell / genetics. RNA, Untranslated
  • [MeSH-minor] Adult. Gene Deletion. Genomic Imprinting. Humans. RNA, Long Noncoding

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17408396.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / H19 long non-coding RNA; 0 / RNA, Long Noncoding; 0 / RNA, Untranslated
  •  go-up   go-down


21. Mukhopadhyay A, Gupta P, Mukhopadhyay S, Dey S, Basak J, Pandey R: Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country. J Clin Oncol; 2009 May 20;27(15_suppl):10046

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Result of adolescent acute lymphoblastic leukemia protocol (MCP 841) from a developing country.
  • : 10046 Background: Acute Lymphatic Leukemia is a curable disease in the range of 80 - 90% in developed countries by aggressive protocol like BFM, St. Judes' but result is much less in adolescence age group (60-70%).
  • Fever 48 (64.0%), lymphadenopathy 35 (46.7%), and haepatosplenomegaly 28 (37.3%) were the major clinical presentation.
  • In a follow-up period of 24 - 88 months (with an average of 54 months) the disease-free survival ( DFS) was 42 (56%) patients with an overall survival of 46 (61.34%) patients.
  • The major cause of the mortality was infection 18% (24.0% patients) followed progressive disease 9 (12.0%) and hemorrhage 2 (2.7%).
  • CONCLUSIONS: The data of acute lymphatic leukemia in adolescent is not satisfactory as compared to other pediatric patients.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962472.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


22. Suga M, Yamaguchi M, Ichimiya M, Yoshikawa Y, Hamamoto Y, Muto M: A rare case of the cutaneous form of adult T-cell leukaemia/lymphoma: assessment of remission by PCR for clonal T-cell receptor gamma gene rearrangements in an electron beam-irradiated cutaneous lesion. Clin Exp Dermatol; 2005 Jan;30(1):40-2
Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A rare case of the cutaneous form of adult T-cell leukaemia/lymphoma: assessment of remission by PCR for clonal T-cell receptor gamma gene rearrangements in an electron beam-irradiated cutaneous lesion.
  • Adult T-cell leukaemia/lymphoma is a lymphoproliferative disorder aetiologically associated with human T-cell lymphotropic virus type I infection.
  • A cutaneous lesion often develops in the disease, and in rare cases, is even the only manifestation.
  • Here we report a rare case of 'cutaneous' adult T-cell leukaemia/lymphoma with neither atypical cells in the peripheral blood nor lymph node involvement.
  • To evaluate whether or not there were residual lymphoma cells in the skin, we performed PCR to detect clonal T cell receptor gamma gene rearrangements.
  • The findings suggest that this procedure is useful for the evaluation of therapeutic effects and the early detection of lymphoma recurrence.
  • [MeSH-major] Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, T-Cell, Cutaneous / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15663501.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


23. Inozume T, Matsue H, Furuhashi M, Nakamura Y, Mitsui H, Ando N, Mitzutani M, Miyahara A, Kawamura T, Shibagaki N, Tsukamoto K, Shimada S: Successful use of etretinate for long-term management of a patient with cutaneous-type adult T-cell leukaemia/lymphoma. Br J Dermatol; 2005 Dec;153(6):1239-41
Hazardous Substances Data Bank. ETRETINATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful use of etretinate for long-term management of a patient with cutaneous-type adult T-cell leukaemia/lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Etretinate / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Skin Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16307674.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 65M2UDR9AG / Etretinate
  •  go-up   go-down


24. Yano H, Ishida T, Imada K, Sakai T, Ishii T, Inagaki A, Iida S, Uchiyama T, Ueda R: Augmentation of antitumour activity of defucosylated chimeric anti-CCR4 monoclonal antibody in SCID mouse model of adult T-cell leukaemia/lymphoma using G-CSF. Br J Haematol; 2008 Mar;140(5):586-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Augmentation of antitumour activity of defucosylated chimeric anti-CCR4 monoclonal antibody in SCID mouse model of adult T-cell leukaemia/lymphoma using G-CSF.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / therapy. Receptors, CCR4 / immunology
  • [MeSH-minor] Adult. Animals. Antineoplastic Agents / therapeutic use. Disease Models, Animal. Granulocyte Colony-Stimulating Factor / therapeutic use. Humans. Mice. Mice, SCID

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3625-34 [14506150.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2127-33 [15026353.001]
  • [Cites] J Exp Med. 2004 Jun 21;199(12):1659-69 [15210744.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Leukemia. 2006 Dec;20(12):2162-8 [17039235.001]
  • [Cites] Clin Cancer Res. 2004 Nov 15;10(22):7529-39 [15569983.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Nat Rev Immunol. 2006 May;6(5):343-57 [16622479.001]
  • [Cites] Cancer Sci. 2006 Nov;97(11):1139-46 [16952304.001]
  • [Cites] Jpn J Cancer Res. 1996 Sep;87(9):887-92 [8878449.001]
  • (PMID = 18205860.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / CCR4 protein, human; 0 / Receptors, CCR4; 134088-74-7 / nartograstim; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Other-IDs] NLM/ PMC2268953
  •  go-up   go-down


25. Verdonck K, González E, Van Dooren S, Vandamme AM, Vanham G, Gotuzzo E: Human T-lymphotropic virus 1: recent knowledge about an ancient infection. Lancet Infect Dis; 2007 Apr;7(4):266-81
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-lymphotropic virus 1: recent knowledge about an ancient infection.
  • Human T-lymphotropic virus 1 (HTLV-1) has infected human beings for thousands of years, but knowledge about the infection and its pathogenesis is only recently emerging.
  • The virus can be transmitted from mother to child, through sexual contact, and through contaminated blood products.
  • Although the majority of HTLV-1 carriers remain asymptomatic, the virus is associated with severe diseases that can be subdivided into three categories: neoplastic diseases (adult T-cell leukaemia/lymphoma), inflammatory syndromes (HTLV-1-associated myelopathy/tropical spastic paraparesis and uveitis among others), and opportunistic infections (including Strongyloides stercoralis hyperinfection and others).
  • The understanding of the interaction between virus and host response has improved markedly, but there are still no clear surrogate markers for prognosis and there are few treatment options.
  • [MeSH-major] HTLV-I Infections. Human T-lymphotropic virus 1
  • [MeSH-minor] Disease Transmission, Infectious. Genome, Viral. Global Health. Humans. Infectious Disease Transmission, Vertical. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / virology. Paraparesis, Tropical Spastic / diagnosis. Paraparesis, Tropical Spastic / epidemiology. Paraparesis, Tropical Spastic / virology. Prevalence. Proviruses / physiology. Strongyloidiasis / etiology. T-Lymphocytes / virology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17376384.001).
  • [ISSN] 1473-3099
  • [Journal-full-title] The Lancet. Infectious diseases
  • [ISO-abbreviation] Lancet Infect Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 179
  •  go-up   go-down


26. Sargent JT, Smith OP: Haematological emergencies managing hypercalcaemia in adults and children with haematological disorders. Br J Haematol; 2010 May;149(4):465-77

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hypercalcaemia is a common metabolic complication of malignant disease often requiring emergency intervention.
  • Although it is more frequently associated with solid tumours, malignancy-associated hypercalcaemia (MAH) is seen in a significant number of patients with blood diseases.
  • Its association with myeloma and adult T-cell leukaemia/lymphoma is well recognized but the incidence of hypercalcaemia in other haematological neoplasms, affecting adults and children, is less clearly defined.
  • Haematologists need to be familiar with the clinical manifestations of, the differential diagnosis to be considered and the most effective management strategies that are currently available for MAH.
  • [MeSH-minor] Adult. Bone Density Conservation Agents / therapeutic use. Child. Diphosphonates / therapeutic use. Fluid Therapy / methods. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20377591.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates
  • [Number-of-references] 96
  •  go-up   go-down


27. Tseliou PM, Spanakis N, Spiliotakara A, Markogiannakis A, Legakis NJ, Tsakris A: Prevalence of infection by HTLV-I/II among pregnant women and high-risk groups in the Peloponnese peninsula, Greece. Int J STD AIDS; 2006 Aug;17(8):543-6
MedlinePlus Health Information. consumer health - Infections and Pregnancy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prevalence of infection by HTLV-I/II among pregnant women and high-risk groups in the Peloponnese peninsula, Greece.
  • Although screening for human T-cell lymphotropic virus types I and II (HTLV-I/II) antibodies in volunteer blood donors has been systematic in Greece since 1995, the epidemiology and the determinants of HTLV-I/II infection are not well defined among population groups.
  • During 1997-2005, the prevalence of HTLV-I/II infection was investigated in a sample of 2016 pregnant women, 102 multitransfused haematologic and oncologic patients, 93 thalassaemic patients and 57 intravenous drug users originating from four geographic areas of Pelopennese peninsula, Greece.
  • One recipient of HTLV-I infected blood and the relatives of a woman died from adult T-cell leukaemia/lymphoma (ATTL) related to HTLV-I have also been tested.
  • The subjects were initially screened by an enzyme immunoassay whereas Western blot, INNO-LIA HTLV, polymerase chain reaction and nucleotide sequencing confirmed the infection.
  • One thalassaemic patient had proved HTLV-I infection giving an overall prevalence of 11 per 1000.
  • In the recipient of the infected blood and in two of the five relatives of the woman died from ATTL, HTLV-I infection was also detected.
  • In none of the pregnant women, multitransfused patients and intravenous drug users HTLV-I/II infection was confirmed.
  • These data suggest that HTLV-I is present in Greece among populations at high-risk.
  • However, they would not support the need for HTLV-I/II antenatal screening in Greece.
  • [MeSH-major] Human T-lymphotropic virus 1. Human T-lymphotropic virus 2. Leukemia, T-Cell / epidemiology. Leukemia-Lymphoma, Adult T-Cell / epidemiology. Pregnancy Complications, Infectious / epidemiology. Pregnancy Complications, Infectious / virology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16925902.001).
  • [ISSN] 0956-4624
  • [Journal-full-title] International journal of STD & AIDS
  • [ISO-abbreviation] Int J STD AIDS
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


28. Salcedo-Cifuentes M, Cabrera J, Cuesta-Astroz Y, Carrasca E, Eizuru Y, Domínguez MC, Sánchez A, García-Vallejo F: [Clonal expansion and genomic characterization of the human T-cell lymphotropic virus type I during the integration process in adult T-cell leukemia/lymphoma]. Biomedica; 2009 Jun;29(2):218-31

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clonal expansion and genomic characterization of the human T-cell lymphotropic virus type I during the integration process in adult T-cell leukemia/lymphoma].
  • [Transliterated title] Expansión clónica y caracterización genómica del proceso de integración del virus linfotrópico humano tipo I en la leucemia/linfoma de células T en adultos.
  • INTRODUCTION: Although the integration of human T-cell lymphotropic virus type I into the T-cells is not a random process, the mechanistic details are not understood.
  • OBJECTIVES: The characteristics of the flanking host chromatin were evaluated at the integration sites in adult T-cell leukaemia/lymphoma (ATLL) patients infected with the virus.
  • MATERIALS AND METHODS: From seven leukemic Colombian patients positive for the human T-cell lymphotropic virus type I (HTLV-I), lymphocyte DNA samples were extracted and amplified by inverse polymerase chain reaction (IPCR).
  • Clonal expansion and human genome nucleotide composition in an extension of 50 bp was determined.
  • To establish the characteristics of the human genome flanking provirus, 61 IPCR sequences from Colombian and Japanese ATLL patients, were analyzed in silico to obtain insights about the genomic structure, functions and nature of associated chromatin.
  • RESULTS: The clonal expansion of cell clones was predominantly oligoclonal.
  • Fifty percent of the proviral integrations were associated with chromosomes of A and B groups.
  • Viral DNA integration tended to favor exons of genes that replicated early, controlled the cell cycle, or were involved in signal transduction.
  • CONCLUSIONS: The results indicated that HTLV-I integration was preferentially directed towards genomic environments with high C:G content, and toward genes that replicate early, regulate cell cycle or involved with signal transduction.
  • [MeSH-major] Genome, Viral. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / virology. Proviruses / genetics. T-Lymphocytes / virology. Virus Integration / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Composition. Cell Transformation, Viral / genetics. Child. Child, Preschool. Clone Cells / virology. DNA Replication / genetics. DNA, Neoplasm / genetics. DNA, Viral / genetics. Female. Genes, cdc. Genes, pX. Humans. Male. Middle Aged. Sequence Alignment. Sequence Analysis, DNA. Sequence Homology, Nucleic Acid. Signal Transduction / genetics. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20128347.001).
  • [ISSN] 0120-4157
  • [Journal-full-title] Biomédica : revista del Instituto Nacional de Salud
  • [ISO-abbreviation] Biomedica
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Colombia
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / DNA, Viral
  •  go-up   go-down


29. Schlaf G, Altermann WW, Rothhoff A, Seliger B: Soluble CD30 serum level--an adequate marker for allograft rejection of solid organs? Histol Histopathol; 2007 11;22(11):1269-79
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The CD30 molecule, a 120 kDa cell surface glycoprotein, is a member of the tumor necrosis factor receptor (TNF-R) superfamily and was originally identified on the surface of Reed-Sternberg cells and anaplastic large cell lymphomas in Hodgkin's disease patients.
  • Low serum levels of soluble CD30 were found in healthy humans, whereas increased sCD30 serum concentrations were detected under pathophysiological situations such as systemic lupus erythematosus, rheumatoid arthritis, certain viral infections and adult T cell leukaemia/lymphoma.
  • In addition, it has recently been suggested that pre- or post-transplant levels of sCD30 represent a biomarker for graft rejection associated with an impaired outcome for transplanted patients.
  • We here review (i) the current knowledge of the clinical significance of sCD30 serum levels for solid organ transplantations and (ii) our own novel data regarding inter- and intra-individual variations as well as time-dependent alterations of sCD30 levels in patients. (iii) Based on this information the implementation of sCD30 as predictive pre-transplant or post-transplant parameter for solid organ transplantation is critically discussed.
  • [MeSH-major] Antigens, CD30 / blood. Biomarkers / blood. Graft Rejection / blood. Graft Rejection / diagnosis. Monitoring, Immunologic / methods. Organ Transplantation

  • MedlinePlus Health Information. consumer health - Organ Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17647199.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / Biomarkers
  • [Number-of-references] 76
  •  go-up   go-down


30. Duval A, Rivet J, Moulonguet I, Cassar O, Agbalika F, Wallach D, Gessain A, Petit A: Atypical presentation of adult T-cell leukaemia/lymphoma due to HTLV-1: prurigo nodularis lasting twelve years followed by an acute micropapular eruption. Acta Derm Venereol; 2010 May;90(3):287-90
Hazardous Substances Data Bank. ZIDOVUDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atypical presentation of adult T-cell leukaemia/lymphoma due to HTLV-1: prurigo nodularis lasting twelve years followed by an acute micropapular eruption.
  • Human T-cell lymphotropic virus type 1 (HTLV-1) causes adult T-cell leukaemia/lymphoma.
  • HTLV-1 is not considered to be a cause of prurigo nodularis.
  • A 52-year-old black man, from the French West Indies, who had had prurigo nodularis for 12 years, presented with a distinct micropapular eruption with the typical pathological picture of epidermotropic T-cell lymphoma.
  • Based on HTLV-1-positive serology and monoclonal integration of HTLV-1 we diagnosed smouldering adult T-cell leukaemia/lymphoma.
  • Re-examination of previous skin biopsies revealed that the disease had been evolving for 12 years.
  • Treatment with alpha-interferon, 3 x 106 units three times a week, associated with zidovudine, 1 g daily, resulted in complete remission within 4 months.
  • When investigating a prurigo nodularis, we therefore recommend: (i) performing HTLV-1 serology if the patient comes from an endemic area;.
  • (ii) if positive, performing CD25 staining and looking for a HTLV-1 clonal integration; and (iii) if positive, using a treatment targeting HTLV-1.
  • [MeSH-major] Anemia, Refractory, with Excess of Blasts / virology. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Prurigo / virology. Skin / virology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antiviral Agents / therapeutic use. Biopsy. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / virology. Humans. Interferon-alpha / therapeutic use. Interleukin-2 Receptor alpha Subunit / analysis. Male. Middle Aged. Recombinant Proteins. Time Factors. Treatment Outcome. Zidovudine / therapeutic use

  • Genetic Alliance. consumer health - Prurigo nodularis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20526548.001).
  • [ISSN] 1651-2057
  • [Journal-full-title] Acta dermato-venereologica
  • [ISO-abbreviation] Acta Derm. Venereol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / IL2RA protein, human; 0 / Interferon-alpha; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Recombinant Proteins; 4B9XT59T7S / Zidovudine; 76543-88-9 / interferon alfa-2a
  •  go-up   go-down


31. Nascimento MC, Primo J, Bittencourt A, Siqueira I, de Fátima Oliveira M, Meyer R, Schriefer A, Santos SB, Carvalho EM: Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis. Clin Exp Immunol; 2009 Jun;156(3):455-62
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Infective dermatitis has similar immunological features to human T lymphotropic virus-type 1-associated myelopathy/tropical spastic paraparesis.
  • Human T lymphotropic virus-type 1 (HTLV-1) is the causal agent of the HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), adult T cell leukaemia/lymphoma and infective dermatitis associated with HTLV-1 (IDH).
  • Over-production of proinflammatory cytokines and an increase in HTLV-1 proviral load are features of HAM/TSP, but the immunological basis of IDH has not been established.
  • In this study we determined the immune response in patients with IDH measuring interleukin (IL)-4, IL-5, IL-10, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha levels as well as the HTLV-1 proviral load.
  • HTLV-1 carriers and patients with HAM/TSP served as controls.
  • TNF-alpha and IFN-gamma levels were higher in IDH than in HTLV-1 carriers.
  • There was a tendency for higher IL-4 mRNA expression and immunoglobulin E (IgE) levels in IDH than in HTLV-1 carriers, but the difference did not reach statistical significance.
  • The HTLV-1 proviral load was significantly higher in IDH patients than in HTLV-1 carriers.
  • IDH is characterized by an exaggerated Th1 immune response and high HTLV-1 proviral load.

  • Genetic Alliance. consumer health - Spastic paraparesis.
  • Genetic Alliance. consumer health - Tropical spastic paraparesis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Infect Dis. 2001 Jan 15;183(2):197-205 [11120926.001]
  • [Cites] J Exp Med. 2007 Feb 19;204(2):285-97 [17283207.001]
  • [Cites] J Acquir Immune Defic Syndr. 2001 May 1;27(1):1-6 [11404513.001]
  • [Cites] Am J Trop Med Hyg. 2001 Aug;65(2):87-9 [11508396.001]
  • [Cites] J Neurovirol. 2001 Jun;7(3):228-34 [11517397.001]
  • [Cites] Ann Neurol. 2001 Dec;50(6):807-12 [11761481.001]
  • [Cites] J Virol Methods. 2002 Apr;102(1-2):37-51 [11879691.001]
  • [Cites] Dermatol Nurs. 2003 Aug;Suppl:6-9 [14520891.001]
  • [Cites] Ann Dermatol Venereol. 2004 Feb;131(2):191-3 [15026748.001]
  • [Cites] BMC Infect Dis. 2004 Mar 2;4:7 [15070424.001]
  • [Cites] Br J Dermatol. 2004 May;150(5):958-65 [15149509.001]
  • [Cites] J Infect Dis. 2004 Nov 15;190(10):1797-803 [15499536.001]
  • [Cites] Br J Dermatol. 1967 Apr;79(4):229-36 [6024739.001]
  • [Cites] Br J Dermatol. 1974 May;90(5):525-30 [4601016.001]
  • [Cites] Neurology. 1983 Nov;33(11):1444-52 [6685237.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Ann Neurol. 1990 Feb;27(2):149-56 [2317010.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5218-22 [2367534.001]
  • [Cites] J Acquir Immune Defic Syndr. 1990;3(12):1199-200 [2243322.001]
  • [Cites] Ann Neurol. 1991 Feb;29(2):194-201 [2012389.001]
  • [Cites] Lancet. 1991 Dec 21-28;338(8782-8783):1593-4 [1683991.001]
  • [Cites] Br J Rheumatol. 1992 May;31(5):293-8 [1581770.001]
  • [Cites] J Neuropathol Exp Neurol. 1994 Jan;53(1):72-7 [8301322.001]
  • [Cites] Lancet. 1995 Sep 9;346(8976):710 [7658857.001]
  • [Cites] J Clin Invest. 1995 Nov;96(5):2339-47 [7593621.001]
  • [Cites] Neurology. 1996 Apr;46(4):1016-21 [8780082.001]
  • [Cites] Transfusion. 1997 Feb;37(2):242-3 [9051104.001]
  • [Cites] J Immunol. 1997 Aug 15;159(4):2018-25 [9257869.001]
  • [Cites] Arch Dermatol. 1998 Apr;134(4):439-44 [9554295.001]
  • [Cites] Arch Dermatol. 1998 Apr;134(4):487-8 [9554302.001]
  • [Cites] J Invest Dermatol. 1999 Feb;112(2):171-6 [9989792.001]
  • [Cites] J Neurovirol. 1998 Dec;4(6):586-93 [10065900.001]
  • [Cites] J Immunol. 1999 Jul 1;163(1):466-75 [10384150.001]
  • [Cites] Eur J Dermatol. 2005 Jan-Feb;15(1):26-30 [15701589.001]
  • [Cites] Clin Infect Dis. 2005 Jun 1;40(11):e90-6 [15889351.001]
  • [Cites] Clin Infect Dis. 2005 Aug 15;41(4):535-41 [16028164.001]
  • [Cites] Clin Exp Immunol. 2006 Aug;145(2):296-301 [16879249.001]
  • [Cites] Clin Infect Dis. 2006 Nov 15;43(10):1257-63 [17051489.001]
  • [Cites] Neuroimmunomodulation. 2006;13(3):145-51 [17119343.001]
  • [Cites] J Immunol. 2001 Feb 15;166(4):2602-9 [11160322.001]
  • (PMID = 19438598.001).
  • [ISSN] 1365-2249
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] ENG
  • [Grant] United States / FIC NIH HHS / TW / D43 TW007127; United States / FIC NIH HHS / TW / TW007127-05; United States / FIC NIH HHS / TW / D43 TW007127-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 207137-56-2 / Interleukin-4; 37341-29-0 / Immunoglobulin E; 82115-62-6 / Interferon-gamma
  • [Other-IDs] NLM/ PMC2691974
  •  go-up   go-down


32. Beltran BE, Morales D, Quiñones P, Salas R, Castillo J: Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of prognostic factors in patients with adult T-cell leukemia/lymphoma.
  • : 8575 Background: Adult T-cell leukemia/lymphoma (ATLL) is associated with human T-cell lymphotropic virus type-I (HTLV-1) described in Southern Japan, Europe, Caribbean and South America.
  • Risk-stratification tools for ATLL have not been adequately evaluated.
  • This study attempts to define prognostic factors for patients with ATLL.
  • Diagnosis was based on clinical history and histological findings consistent with ATLL and either positive HTLV-1 serology or evidence of HTLV-1 integration.
  • Clinical types were acute (n=45), lymphomatous (n=43), cutaneous (n=10), smoldering (n=3) and chronic (n=1).
  • Median OS for acute, lymphomatous, smoldering and cutaneous subtype were 2, 11, 17 and 39 months, respectively (log-rank 28.5, p<0.00001).
  • In the univariate analysis, presence of B symptoms, ECOG performance status 2, clinical stage II or higher, elevated LDH level and bone marrow (BM) involvement were independent factors for survival with p<0.05.
  • The prognostic index for T-cell lymphoma (PIT) score was determined in 80 patients; 20 (25%), 17 (21%), 33 (41%) and 10 (13%) patients had scores of 0-1, 2, 3 and 4, respectively.
  • CONCLUSIONS: This retrospective series represents the largest Latin-American experience on ATLL, which is a heterogeneous disease with distinct clinical features and outcomes.
  • The IPI ant PIT scores, used for risk-stratification of aggressive B-cell and peripheral T-cell lymphomas, respectively, appear as good prognostic indicators for ATLL as well.
  • Further research is needed to better risk-stratify this unique lymphoma.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962272.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


33. Hasegawa H, Yamada Y, Harasawa H, Tsuji T, Murata K, Sugahara K, Tsuruda K, Ikeda S, Imaizumi Y, Tomonaga M, Masuda M, Takasu N, Kamihira S: Sensitivity of adult T-cell leukaemia lymphoma cells to tumour necrosis factor-related apoptosis-inducing ligand. Br J Haematol; 2005 Jan;128(2):253-65
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sensitivity of adult T-cell leukaemia lymphoma cells to tumour necrosis factor-related apoptosis-inducing ligand.
  • Adult T-cell leukaemia lymphoma (ATLL) is a neoplasm of T-lymphocyte origin aetiologically associated with human T-lymphotropic virus type 1 (HTLV-I), and is resistant to standard anti-cancer therapy.
  • We thus characterized the sensitivity of ATLL cells to TRAIL in this study.
  • Although most primary ATLL cells and cell lines expressed TRAIL death receptors on their surface, they showed only restricted sensitivity to TRAIL.
  • Among the 10 ATLL cell lines examined, one was sensitive, but two had insufficient death-receptor expression, two had an unknown resistant mechanism with abrogation of the death signal upstream of caspase-8, and the remaining five showed attenuation of the signal in both extrinsic and intrinsic pathways by X-linked inhibitor of apoptosis and Bcl-2/Bcl-xL respectively.
  • Furthermore, the level of HTLV-I tax expression was significantly correlated to TRAIL resistance.
  • Interestingly, ATLL cells themselves expressed TRAIL on the cell surface.
  • Constitutive production of TRAIL may offer resistance, thus allowing the development of TRAIL-resistant ATLL cells.
  • Consequently, the resistant mechanism in ATLL cells against TRAIL was assigned to multiple factors and was not explained by a definitive single agent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Membrane Glycoproteins / therapeutic use. Tumor Necrosis Factor-alpha / therapeutic use

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15638862.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


34. Yamaguchi T, Ohshima K, Karube K, Tutiya T, Kawano R, Suefuji H, Shimizu A, Nakayama J, Suzumiya J, Moroi Y, Urabe K, Furue M, Koga T, Kikuchi M: Clinicopathological features of cutaneous lesions of adult T-cell leukaemia/ lymphoma. Br J Dermatol; 2005 Jan;152(1):76-81
Genetic Alliance. consumer health - Cutaneous T-Cell Lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathological features of cutaneous lesions of adult T-cell leukaemia/ lymphoma.
  • BACKGROUND: Adult T-cell leukaemia/lymphoma (ATLL) is a human malignancy associated with human T-cell leukaemia virus type I (HTLV-I).
  • ATLL frequently involves the skin.
  • OBJECTIVES: To correlate the clinicopathological features and prognosis in patients with ATLL and cutaneous lesions.
  • METHODS: We examined the HTLV-I proviral state and the clinicopathological features of the cutaneous lesions in 80 patients with serum anti-ATL antibody, to clarify the correlation between macroscopic/histopathological findings and prognosis.
  • Southern blot analysis was performed in all cases to detect monoclonal HTLV-I proviral DNA integration.
  • RESULTS: The cutaneous lesions of 46 patients were positive for proviral DNA integration.
  • Histopathologically, the prognosis was poorer in patients with nodular or diffuse infiltration of medium-sized to large lymphoma cells, compared with those with perivascular infiltration of small to medium-sized lymphoma cells.
  • CONCLUSIONS: Our results show a close correlation between clinicopathological features of HTLV-I-associated cutaneous lesions and prognosis.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemic Infiltration. Skin / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA, Viral / analysis. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Prognosis. Proviruses / isolation & purification. Survival Analysis. Virus Integration

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15656804.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
  •  go-up   go-down


35. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • In addition, we identified deletions and associated mutations in the WT1 tumor suppressor gene in 2 of 9 samples.
  • Subsequent analysis showed WT1 mutations in 28 of 211 (13.2%) of pediatric and 10 of 85 (11.7%) of adult T-ALL cases.
  • Survival analysis demonstrated that WT1 mutations do not confer adverse prognosis in pediatric and adult T-ALL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6010-4 [1321431.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Hum Mol Genet. 1993 Mar;2(3):259-64 [8388765.001]
  • [Cites] Blood. 1994 May 15;83(10):2922-30 [8180387.001]
  • [Cites] Hum Mol Genet. 1995 Mar;4(3):351-8 [7795587.001]
  • [Cites] Blood. 1996 Mar 15;87(6):2171-9 [8630376.001]
  • [Cites] Hum Mutat. 1997;9(3):209-25 [9090524.001]
  • [Cites] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110.001]
  • [Cites] Eur J Haematol. 1997 May;58(5):346-9 [9222290.001]
  • [Cites] Blood. 1998 Apr 15;91(8):2961-8 [9531607.001]
  • [Cites] Kidney Int. 1998 Jun;53(6):1512-8 [9607183.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Pediatr Blood Cancer. 2006 Jan;46(1):18-25 [15929133.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Leukemia. 2007 Mar;21(3):550-1; author reply 552 [17205055.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]
  • [Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]
  • [Cites] Leukemia. 2007 Jun;21(6):1258-66 [17443227.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9006-12 [17909001.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):83-93 [18094723.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] Leukemia. 2008 Apr;22(4):762-70 [18185524.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Blood. 2008 May 1;111(9):4668-80 [18299449.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Science. 2008 Nov 28;322(5906):1377-80 [19039135.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Genome Biol. 2001;2(8):RESEARCH0032 [11532216.001]
  • [Cites] Leukemia. 2001 Oct;15(10):1495-504 [11587205.001]
  • [Cites] J Pediatr Hematol Oncol. 2001 Oct;23(7):416-9 [11878574.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128.001]
  • [Cites] Nat Genet. 2004 Oct;36(10):1084-9 [15361874.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Clin Nephrol. 1985 Dec;24(6):269-78 [3000666.001]
  • [Cites] Genomics. 1989 Nov;5(4):685-93 [2556343.001]
  • [Cites] Cell. 1990 Jun 29;61(7):1257-69 [2163761.001]
  • [Cites] FEBS Lett. 1993 Feb 8;317(1-2):39-43 [8381368.001]
  • (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 / R01 CA120196-03; 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 Kingdom / Medical Research Council / / MC/ U137686861; United States / NCI NIH HHS / CA / CA02111; United Kingdom / Medical Research Council / / G0500389; United States / NCI NIH HHS / CA / CA120196-03; 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
  • [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
  •  go-up   go-down


36. Clappier E, Cuccuini W, Kalota A, Crinquette A, Cayuela JM, Dik WA, Langerak AW, Montpellier B, Nadel B, Walrafen P, Delattre O, Aurias A, Leblanc T, Dombret H, Gewirtz AM, Baruchel A, Sigaux F, Soulier J: The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children. Blood; 2007 Aug 15;110(4):1251-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young children.
  • The C-Myb transcription factor is essential for hematopoiesis, including in the T-cell lineage.
  • The C-Myb locus is a common site of retroviral insertional mutagenesis, however no recurrent genomic involvement has been reported in human malignancies.
  • Here, we identified 2 types of genomic alterations involving the C-MYB locus at 6q23 in human T-cell acute leukemia (T-ALL).
  • Expression analysis, including allele-specific approaches, showed stronger C-MYB expression in the MYB-rearranged cases compared with other T-ALLs, and a dramatically skewed C-MYB allele expression in the TCRB-MYB cases, which suggests that a translocation-driven deregulated expression may overcome a cellular attempt to down-regulate C-MYB.
  • Strikingly, profiling of the T-ALLs by clinical, genomic, and large-scale gene expression analyses shows that the TCRB-MYB translocation defines a new T-ALL subtype associated with a very young age for T-cell leukemia (median, 2.2 years) and with a proliferation/mitosis expression signature.
  • By contrast, the MYB(dup) alteration was associated with the previously defined T-ALL subtypes.
  • [MeSH-major] Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Proto-Oncogene Proteins c-myb / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Base Sequence. Child. Child, Preschool. Female. Gene Dosage. Gene Expression Profiling. Genome, Human. Humans. Infant. Male. Middle Aged. Molecular Sequence Data. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Sequence Homology, Nucleic Acid

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17452517.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA101859
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myb
  •  go-up   go-down


37. Ferrando AA: The role of NOTCH1 signaling in T-ALL. Hematology Am Soc Hematol Educ Program; 2009;:353-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The identification of activating mutations in NOTCH1 in over 50% of T-cell acute lymphoblastic leukemias (T-ALL) has generated major interest in the elucidation of the mechanisms of transformation downstream of oncogenic NOTCH and in the targeting of the NOTCH signaling pathway in this disease.
  • Small molecule gamma-secretase inhibitors (GSIs) block NOTCH1 signaling in T-ALL lymphoblasts, yet the clinical development of GSIs has been held back by the development of gastrointestinal toxicity and their weak antileukemic effects against human T-ALL.
  • This review focuses on the molecular basis of NOTCH1-induced transformation, the mechanisms of action of oncogenic NOTCH1 and clinical significance of NOTCH1 mutations in T-ALL.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Immunol. 2005 Sep;6(9):881-8 [16056227.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7159-68 [16103066.001]
  • [Cites] EMBO J. 2006 Jan 11;25(1):129-38 [16319921.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Haematologica. 2006 Sep;91(9):1212-21 [16956820.001]
  • [Cites] Mol Cell Biol. 2006 Nov;26(21):8022-31 [16954387.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 28;103(48):18261-6 [17114293.001]
  • [Cites] Nat Immunol. 2007 May;8(5):451-6 [17440450.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] Exp Cell Res. 2007 Aug 15;313(14):3141-52 [17560996.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):6964-9 [18056171.001]
  • [Cites] Blood. 2008 Jan 1;111(1):376-8 [17901244.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] EMBO Rep. 2008 Apr;9(4):377-83 [18274550.001]
  • [Cites] Haematologica. 2008 Apr;93(4):533-42 [18322257.001]
  • [Cites] Blood. 2008 Aug 1;112(3):733-40 [18411416.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Oncogene. 2008 Oct 2;27(44):5833-44 [18560356.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 6;106(1):244-9 [19118200.001]
  • [Cites] Nat Med. 2009 Jan;15(1):50-8 [19098907.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1730-40 [18984862.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1689-98 [19001083.001]
  • [Cites] Cancer Res. 2009 Apr 1;69(7):3060-8 [19318552.001]
  • [Cites] J Exp Med. 2009 Apr 13;206(4):779-91 [19349467.001]
  • [Cites] Blood. 2009 Apr 23;113(17):3918-24 [19109228.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4381-90 [19075186.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6172-81 [19246562.001]
  • [Cites] Br J Haematol. 2009 Apr;145(2):198-206 [19245433.001]
  • [Cites] J Clin Oncol. 2009 Sep 10;27(26):4352-6 [19635999.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2937-44 [14583609.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cell Cycle. 2005 Oct;4(10):1356-9 [16131838.001]
  • (PMID = 20008221.001).
  • [ISSN] 1520-4383
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA120196-03; United States / NCI NIH HHS / CA / CA129382-02; United States / NCI NIH HHS / CA / R01 CA129382; United States / NCI NIH HHS / CA / CA120196-03; 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 / R01 CA129382-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Number-of-references] 40
  • [Other-IDs] NLM/ NIHMS168983; NLM/ PMC2847371
  •  go-up   go-down


38. Dik WA, Brahim W, Braun C, Asnafi V, Dastugue N, Bernard OA, van Dongen JJ, Langerak AW, Macintyre EA, Delabesse E: CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Leukemia; 2005 Nov;19(11):1948-57
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(10;11)(p13;q14-21) is found in T-ALL and acute myeloid leukemia and fuses CALM (Clathrin-Assembly protein-like Lymphoid-Myeloid leukaemia gene) to AF10.
  • Microarray results were validated by quantitative RT-PCR on an independent group of T-ALL and compared to mixed lineage leukemia-translocated acute leukemias (MLL-t AL).
  • The overexpression of HOXA genes was associated with overexpression of its cofactor MEIS1 in CALM-AF10+ T-ALL, reaching levels of expression similar to those observed in MLL-t AL.
  • We propose to define a HOXA+ leukemia group composed of at least MLL-t, CALM-AF10 and HOXA-t AL, which may benefit from adapted management.
  • [MeSH-major] Homeodomain Proteins / biosynthesis. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / physiopathology. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis. Proto-Oncogene Proteins / biosynthesis. Repressor Proteins / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Cell Proliferation. Cell Transformation, Neoplastic. Child. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Polycomb Repressive Complex 1. Reverse Transcriptase Polymerase Chain Reaction. Transcription, Genetic. Up-Regulation

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16107895.001).
  • [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 / AF10-CALM fusion protein, human; 0 / BMI1 protein, human; 0 / Homeodomain Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 157907-48-7 / HoxA protein; EC 6.3.2.19 / Polycomb Repressive Complex 1
  •  go-up   go-down


39. Van Vlierberghe P, Homminga I, Zuurbier L, Gladdines-Buijs J, van Wering ER, Horstmann M, Beverloo HB, Pieters R, Meijerink JP: Cooperative genetic defects in TLX3 rearranged pediatric T-ALL. Leukemia; 2008 Apr;22(4):762-70
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder, in which multiple genetic abnormalities cooperate in the malignant transformation of thymocytes.
  • Array-CGH analysis revealed five recurrent genomic deletions in TLX3 rearranged T-ALL, including del(1)(p36.31), del(5)(q35), del(13)(q14.3), del(16)(q22.1) and del(19)(p13.2).
  • From these, the cryptic deletion, del(5)(q35), was exclusively identified in about 25% of TLX3 rearranged T-ALL cases.
  • [MeSH-major] Chromosome Aberrations. Homeodomain Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Sequence Deletion
  • [MeSH-minor] Cell Cycle Proteins / genetics. Child. DNA Mutational Analysis. F-Box Proteins / genetics. Gene Dosage. Gene Rearrangement. Genome, Human. Humans. In Situ Hybridization, Fluorescence. Ubiquitin-Protein Ligases / genetics. WT1 Proteins / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18185524.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Homeodomain Proteins; 0 / TLX3 protein, human; 0 / WT1 Proteins; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


40. O'Neil J, Calvo J, McKenna K, Krishnamoorthy V, Aster JC, Bassing CH, Alt FW, Kelliher M, Look AT: Activating Notch1 mutations in mouse models of T-ALL. Blood; 2006 Jan 15;107(2):781-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent studies have demonstrated that most patients with T-cell acute lymphocytic leukemia (T-ALL) have activating mutations in NOTCH1.
  • We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.
  • Cell lines derived from these tumors undergo G(0)/G(1) arrest and apoptosis when treated with a gamma-secretase inhibitor.
  • In addition, we found activating Notch1 mutations in 31% of thymic lymphomas that occur in mice deficient for various combinations of the H2AX, Tp53, and Rag2 genes.
  • Thus, Notch1 mutations are often acquired as a part of the molecular pathogenesis of T-ALLs that develop in mice with known predisposing genetic alterations.
  • [MeSH-major] Disease Models, Animal. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma / genetics. Mutation / genetics. Receptor, Notch1 / genetics. Thymus Neoplasms / genetics

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Thymus Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Oncogene. 2006 May 18;25(21):3023-31 [16407836.001]
  • [Cites] Immunity. 2000 Jul;13(1):73-84 [10933396.001]
  • [Cites] Blood. 2000 Sep 1;96(5):1906-13 [10961893.001]
  • [Cites] J Virol. 2000 Oct;74(20):9786-91 [11000255.001]
  • [Cites] Semin Hematol. 2000 Oct;37(4):381-95 [11071360.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1211-8 [11222362.001]
  • [Cites] Science. 2002 May 3;296(5569):922-7 [11934988.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8173-8 [12034884.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):75-87 [12086890.001]
  • [Cites] Cell. 2003 Aug 8;114(3):359-70 [12914700.001]
  • [Cites] Cell. 2003 Aug 8;114(3):371-83 [12914701.001]
  • [Cites] Blood. 2003 Oct 1;102(7):2593-6 [12816868.001]
  • [Cites] Semin Hematol. 2003 Oct;40(4):274-80 [14582078.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1909-11 [14604958.001]
  • [Cites] Lancet. 2004 Feb 14;363(9408):535-6 [14975618.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):587-96 [15193261.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1992 Mar 6;68(5):855-67 [1547487.001]
  • [Cites] Cell. 1996 Apr 5;85(1):27-37 [8620534.001]
  • [Cites] EMBO J. 1996 Oct 1;15(19):5160-6 [8895560.001]
  • [Cites] Oncogene. 1998 Jan 29;16(4):517-22 [9484841.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Blood. 2000 Jun 1;95(11):3310-22 [10828010.001]
  • (PMID = 16166587.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [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 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / H2AX protein, mouse; 0 / Histones; 0 / NOTCH1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Rag2 protein, mouse; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; 0 / Tumor Suppressor Protein p53; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human; EC 3.4.23.46 / Bace1 protein, mouse
  • [Other-IDs] NLM/ PMC1895623
  •  go-up   go-down


41. Nonaka M, Uota S, Saitoh Y, Takahashi M, Sugimoto H, Amet T, Arai A, Miura O, Yamamoto N, Yamaoka S: Role for protein geranylgeranylation in adult T-cell leukemia cell survival. Exp Cell Res; 2009 Jan 15;315(2):141-50
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role for protein geranylgeranylation in adult T-cell leukemia cell survival.
  • Adult T-cell leukemia (ATL) is a fatal lymphoproliferative disease that develops in human T-cell leukemia virus type I (HTLV-I)-infected individuals.
  • Despite the accumulating knowledge of the molecular biology of HTLV-I-infected cells, effective therapeutic strategies remain to be established.
  • Here, we report that statins hinder the survival of ATL cells and induce apoptotic cell death.
  • Inhibition of protein geranylgeranylation is responsible for these effects, since simultaneous treatment with isoprenoid precursors, geranylgeranyl pyrophosphate or farnesyl pyrophosphate, but not a cholesterol precursor squalene, restored the viability of ATL cells.
  • Simvastatin inhibited geranylgeranylation of small GTPases Rab5B and Rac1 in ATL cells, and a geranylgeranyl transferase inhibitor GGTI-298 reduced ATL cell viability more efficiently than a farnesyl transferase inhibitor FTI-277.
  • These results not only unveil an important role for protein geranylgeranylation in ATL cell survival, but also implicate therapeutic potentials of statins in the treatment of ATL.
  • [MeSH-minor] Adult. Benzamides / pharmacology. Caspase 3 / metabolism. Cell Line, Tumor. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cell Survival / drug effects. Cell Survival / physiology. Enzyme Inhibitors / pharmacology. Humans. Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology. I-kappa B Proteins / metabolism. Leukemia-Lymphoma, Adult T-Cell / metabolism. Leukemia-Lymphoma, Adult T-Cell / pathology. Methionine / analogs & derivatives. Methionine / pharmacology. NF-kappa B / metabolism. Phosphorylation / drug effects. Polyisoprenyl Phosphates / pharmacology. Sesquiterpenes / pharmacology. rab5 GTP-Binding Proteins / metabolism. rac1 GTP-Binding Protein / metabolism

  • Hazardous Substances Data Bank. (L)-Methionine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18992741.001).
  • [ISSN] 1090-2422
  • [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 / Benzamides; 0 / Enzyme Inhibitors; 0 / FTI 277; 0 / GGTI 298; 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Polyisoprenyl Phosphates; 0 / RAC1 protein, human; 0 / Sesquiterpenes; 139874-52-5 / NF-kappaB inhibitor alpha; 6699-20-3 / geranylgeranyl pyrophosphate; 79W6B01D07 / farnesyl pyrophosphate; AE28F7PNPL / Methionine; EC 3.4.22.- / Caspase 3; EC 3.6.5.2 / rab5 GTP-Binding Proteins; EC 3.6.5.2 / rac1 GTP-Binding Protein
  •  go-up   go-down


42. Mahieux R, Gessain A: [New human retroviruses: HTLV-3 and HTLV-4]. Med Trop (Mars); 2005 Nov;65(6):525-8
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [New human retroviruses: HTLV-3 and HTLV-4].
  • [Transliterated title] Les nouveaux rétrovirus humains HTLV-3 et HTLV-4.
  • Human T cell leukemia/lymphoma virus Type 1 and 2 (HTLV-1 and HTLV-2), together with their simian counterparts (STLV-1, STLV-2 and STLV-3), belong to the Primate T lymphotropic viruses group (PTLV).
  • HTLV-1 infects 15 to 20 million people worldwide, while STLV-1 is endemic in a number of simian species living in the Old World.
  • Due to the high percentage of homologies between HTLV-1 and STLV-1 strains, it has now been widely accepted that most HTLV-1 subtypes arose from interspecies transmission between monkeys and humans.
  • On the opposite, there is no close human homolog of the two STLV-2 strains that have been discovered in African bonobos chimpanzees.
  • These results suggest that the interspecies transmission that lead to the present day HTLV-2 must have occurred in a distant past.
  • STLV-3 viruses are very divergent, both from HTLV-1 and from HTLV-2.
  • Recently, two laboratories independently reported the discovery of the human homolog (HTLV-3) of STLV-3 in two inhabitants from south Cameroon whose sera exhibited HTLV indeterminate serologies.
  • Together with STLV-3, these two viruses belong therefore to the PTLV-3 group.
  • In addition, a fourth HTLV type (HTLV-4) was also discovered in the same geographical area.
  • Current studies are aimed at determining the molecular characterization of these viruses.
  • In particular, the possible oncogenic properties of their viral transactivator Tax is being investigated, as well as their modes of transmission and their possible association with human diseases.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16555510.001).
  • [ISSN] 0025-682X
  • [Journal-full-title] Médecine tropicale : revue du Corps de santé colonial
  • [ISO-abbreviation] Med Trop (Mars)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 23
  •  go-up   go-down


43. Sertöz R, Turhan A, Bozkurt H, Samlıoğlu P, Değirmenci A, Aydınok Y, Erensoy S: [Investigation of anti-HTLV I/II seroprevalence in healthy blood donors in Izmir region, Turkey]. Mikrobiyol Bul; 2010 Oct;44(4):579-84
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Investigation of anti-HTLV I/II seroprevalence in healthy blood donors in Izmir region, Turkey].
  • [Transliterated title] İzmir bölgesinde sağlıklı kan vericilerinde anti-HTLV-I/II seroprevalansının araştırılması
  • Almost 10-20 million people in the world are thought to be infected by human deltaretroviruses, namely human T-cell lymphotropic virus (HTLV) type I and II, recently.
  • HTLV-I is endemic in southwestern Japan, the Caribbean and sub-Saharan Africa, whereas HTLV-II is more prevalent in intravenous drug addicts, and in American indian populations, endemically.
  • HTLV-I is mainly responsible for adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), however, HTLVII is not clearly associated with a known clinical disease.
  • Both viruses may be transmitted by sexual contact, parenteral route, whole blood transfusion and breast-feeding.
  • In most of the countries [USA, Canada, South America, Caribbean, Japan, Taiwan and some Europe countries (France, UK, Ireland, Sweden, Denmark, The Netherlands, Portugal, Romania, Greece)] routine screening of anti-HTLV-I/II in blood donors is mandatory, however, there is no such practice in Turkey since seroepidemiologic data on HTLVI/II infections is insufficient.
  • In this study, the seroprevalence of HTLV-I/II in healthy blood donors admitted to the blood bank of Ege University Medical Faculty Hospital, Izmir (located at Aegean region), was investigated to support data on the decision making process on routine screening of anti-HTLV-I/II in blood centers.
  • Serum samples from 10.000 healthy blood donors (mean age: 32.6 years; 87.8% were male), who succeeded the donor history questionnaire, were included to the study, and HTLV-I/II antibodies were screened by a commercial enzyme immunoassay (ELISA) (Murex HTLVI-II, Murex Diagnostics, UK) method.
  • Serum samples which were yielded reactive and borderline results were retested by ELISA, and repeated reactive/borderline results were then confirmed by HTLV-I/II confirmation test (INNO-LIA HTLV-I/II, Innogenetics, Belgium).
  • According to our data HTLV-I/II infections are not endemic in Izmir region, and anti-HTLV-I/II screening of blood donors is not required in our blood center currently.
  • Thus, even its prevalence is very low, much more comprehensive and multi-centered studies are necessary for making the decision of integrating HTLV-I/II in routine blood bank screening tests in Turkey.
  • [MeSH-major] Blood Donors / statistics & numerical data. HTLV-I Antibodies / blood. HTLV-I Infections / epidemiology. HTLV-II Antibodies / blood. HTLV-II Infections / epidemiology
  • [MeSH-minor] Adult. Enzyme-Linked Immunosorbent Assay. Female. Humans. Male. Mandatory Testing. Seroepidemiologic Studies. Turkey / epidemiology

  • MedlinePlus Health Information. consumer health - Blood Transfusion and Donation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21063970.001).
  • [ISSN] 0374-9096
  • [Journal-full-title] Mikrobiyoloji bülteni
  • [ISO-abbreviation] Mikrobiyol Bul
  • [Language] tur
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Turkey
  • [Chemical-registry-number] 0 / HTLV-I Antibodies; 0 / HTLV-II Antibodies
  •  go-up   go-down


44. Demarest RM, Ratti F, Capobianco AJ: It's T-ALL about Notch. Oncogene; 2008 Sep 1;27(38):5082-91
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL.
  • Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease.
  • In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Neoplasm Proteins / physiology. Receptors, Notch / physiology. T-Lymphocytes / pathology
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Cycle / physiology. F-Box Proteins / physiology. Gene Expression Regulation, Leukemic. Genes, Tumor Suppressor. Humans. Ikaros Transcription Factor / genetics. Ikaros Transcription Factor / physiology. Ligands. Mice. Mice, Transgenic. Oncogenes. PTEN Phosphohydrolase / deficiency. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / physiology. Signal Transduction / physiology. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18758476.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA09171
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / F-Box Proteins; 0 / Fbxw7 protein, mouse; 0 / IKZF1 protein, human; 0 / Ligands; 0 / Neoplasm Proteins; 0 / Receptors, Notch; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 148971-36-2 / Ikaros Transcription Factor; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Number-of-references] 84
  •  go-up   go-down


45. Dik WA, Nadel B, Przybylski GK, Asnafi V, Grabarczyk P, Navarro JM, Verhaaf B, Schmidt CA, Macintyre EA, van Dongen JJ, Langerak AW: Different chromosomal breakpoints impact the level of LMO2 expression in T-ALL. Blood; 2007 Jul 1;110(1):388-92

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The t(11;14)(p13;q11) is presumed to arise from an erroneous T-cell receptor delta TCRD V(D)J recombination and to result in LMO2 activation.
  • We performed combined in vivo, ex vivo, and in silico analyses on 9 new t(11;14)(p13;q11)-positive T-cell acute lymphoblastic leukemia (T-ALL) as well as normal thymocytes.
  • [MeSH-major] Chromosome Breakage. DNA-Binding Proteins / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Metalloproteins / genetics
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Genes, T-Cell Receptor delta. Humans. LIM Domain Proteins. Proto-Oncogene Proteins / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17360939.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
  •  go-up   go-down


46. Harashima N, Tanosaki R, Shimizu Y, Kurihara K, Masuda T, Okamura J, Kannagi M: Identification of two new HLA-A*1101-restricted tax epitopes recognized by cytotoxic T lymphocytes in an adult T-cell leukemia patient after hematopoietic stem cell transplantation. J Virol; 2005 Aug;79(15):10088-92
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of two new HLA-A*1101-restricted tax epitopes recognized by cytotoxic T lymphocytes in an adult T-cell leukemia patient after hematopoietic stem cell transplantation.
  • We previously reported that Tax-specific CD8(+) cytotoxic T lymphocytes (CTLs), directed to single epitopes restricted by HLA-A2 or A24, expanded in vitro and in vivo in peripheral blood mononuclear cells (PBMC) from some adult T-cell leukemia (ATL) patients after but not before allogeneic hematopoietic stem cell transplantation (HSCT).
  • Here, we demonstrated similar Tax-specific CTL expansion in PBMC from another post-HSCT ATL patient without HLA-A2 or A24, whose CTLs equally recognized two newly identified epitopes, Tax88-96 and Tax272-280, restricted by HLA-A11, suggesting that these immunodominant Tax epitopes are present in the ATL patient in vivo.
  • [MeSH-major] Epitopes / immunology. Gene Products, tax / immunology. HLA-A Antigens / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Leukemia-Lymphoma, Adult T-Cell / therapy. Stem Cell Transplantation. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Amino Acid Sequence. Coculture Techniques. Human T-lymphotropic virus 1 / immunology. Humans. Leukocytes, Mononuclear. Male. Middle Aged. Molecular Sequence Data. Peptides / genetics. T-Cell Antigen Receptor Specificity. Transplantation, Homologous

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunogenetics. 1999 Nov;50(3-4):201-12 [10602880.001]
  • [Cites] Immunol Today. 1996 Jun;17(6):261-6 [8962628.001]
  • [Cites] Bone Marrow Transplant. 2001 Jan;27(1):15-20 [11244433.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] Br J Haematol. 2003 Jan;120(2):304-9 [12542491.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] Trends Microbiol. 2004 Jul;12(7):346-52 [15223062.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] J Immunol. 1980 Mar;124(3):1045-9 [6244347.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] J Immunol. 1999 Feb 1;162(3):1765-71 [9973440.001]
  • [Cites] J Immunol. 1999 Nov 1;163(9):4994-5004 [10528204.001]
  • [Cites] J Clin Oncol. 1988 Jan;6(1):128-41 [2891797.001]
  • [Cites] Nature. 1990 Nov 15;348(6298):245-8 [2146511.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] J Virol. 1992 May;66(5):2928-33 [1373197.001]
  • [Cites] Virology. 1992 Jun;188(2):628-36 [1374983.001]
  • [Cites] J Immunol. 1992 Jul 1;149(1):214-21 [1607654.001]
  • [Cites] J Exp Med. 1993 Jun 1;177(6):1567-73 [8496677.001]
  • [Cites] J Immunol. 1993 Oct 1;151(7):3874-83 [7690819.001]
  • [Cites] J Immunol. 1994 Jan 1;152(1):163-75 [8254189.001]
  • [Cites] J Immunol. 1994 Apr 15;152(8):3913-24 [8144960.001]
  • [Cites] N Engl J Med. 1996 Feb 1;334(5):281-5 [8532022.001]
  • [Cites] J Virol. 2000 Oct;74(20):9610-6 [11000233.001]
  • (PMID = 16014972.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Epitopes; 0 / Gene Products, tax; 0 / HLA-A Antigens; 0 / Peptides
  • [Other-IDs] NLM/ PMC1181560
  •  go-up   go-down


47. Kurihara K, Harashima N, Hanabuchi S, Masuda M, Utsunomiya A, Tanosaki R, Tomonaga M, Ohashi T, Hasegawa A, Masuda T, Okamura J, Tanaka Y, Kannagi M: Potential immunogenicity of adult T cell leukemia cells in vivo. Int J Cancer; 2005 Mar 20;114(2):257-67
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potential immunogenicity of adult T cell leukemia cells in vivo.
  • Experimental vaccines targeting human T cell leukemia virus type-I (HTLV-I) Tax have been demonstrated in a rat model of HTLV-I-induced lymphomas.
  • However, the scarcity of HTLV-I-expression and the presence of defective HTLV-I-proviruses in adult T cell leukemia (ATL) cells have raised controversy about the therapeutic potential of HTLV-I-targeted immunotherapy in humans.
  • We investigated the expression of HTLV-I antigens in fresh ATL cells by using both in vitro and in vivo assays.
  • In flow cytometric analysis, we found that 3 of 5 acute-type and six of fifteen chronic-type ATL patients tested showed significant induction of HTLV-I Tax and Gag in their ATL cells in a 1-day culture.
  • Concomitantly with HTLV-I-expression, these ATL cells expressed co-stimulatory molecules such as CD80, CD86 and OX40, and showed elevated levels of antigenicity against allogeneic T cells and HTLV-I Tax-specific cytotoxic T-lymphocytes (CTL).
  • Representative CTL epitopes restricted by HLA-A2 or A24 were conserved in 4 of 5 acute-type ATL patients tested.
  • Furthermore, spleen T cells from rats, which had been subcutaneously inoculated with formalin-fixed uncultured ATL cells, exhibited a strong interferon gamma-producing helper T cell responses specific for HTLV-I Tax-expressing cells.
  • Our study indicated that ATL cells from about half the patients tested readily express HTLV-I antigens including Tax in vitro, and that ATL cells express sufficient amounts of Tax or Tax-induced antigens to evoke specific T cell responses in vivo.
  • [MeSH-major] Human T-lymphotropic virus 1 / isolation & purification
  • [MeSH-minor] Adult. Aged. Animals. Base Sequence. DNA Primers. Female. Humans. Japan. Leukemia, Prolymphocytic, T-Cell / pathology. Leukemia, Prolymphocytic, T-Cell / virology. Leukemia-Lymphoma, Adult T-Cell / pathology. Leukemia-Lymphoma, Adult T-Cell / virology. Male. Middle Aged. Polymerase Chain Reaction. Rats. Rats, Inbred F344. Reference Values. Transplantation, Heterologous / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551352.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers
  •  go-up   go-down


48. Sugita K, Shimauchi T, Tokura Y: Chronic actinic dermatitis associated with adult T-cell leukemia. J Am Acad Dermatol; 2005 Feb;52(2 Suppl 1):38-40
Genetic Alliance. consumer health - Leukemia, T-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic actinic dermatitis associated with adult T-cell leukemia.
  • We describe a patient with chronic actinic dermatitis that occurred with the progress of adult T-cell leukemia.
  • Immunohistochemically, CD8 + T cells, but not CD4 + cells, predominantly infiltrated the lichenoid lesional skin, indicating that the eruption was induced by reactive, normal CD8 + T cells but not adult T-cell leukemia cells.
  • Our patient suggests that chronic actinic dermatitis may occur in association with the advanced human T-lymphotrophic virus-I infectious disorder.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / complications. Photosensitivity Disorders / etiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15692511.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCR4 protein, human; 0 / Cytokines; 0 / Receptors, CCR4; 0 / Receptors, Chemokine
  •  go-up   go-down


49. Shahnaz S, Reich D, Arévalo-Valencia D, Kucinska S, Tulczynska J, Fleischman J: HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia. J Gen Intern Med; 2007 Mar;22(3):420-3
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-1-associated adult T cell leukemia lymphoma presenting as granulomatous pneumocystis jiroveci pneumonia (PJP) and hypercalcemia.
  • BACKGROUND: Since the initial description of human T cell lymphotropic virus (HTLV-1), clusters of this infection have been detected globally.
  • Unlike HIV infection, most patients infected with HTLV-1 remain asymptomatic throughout their lifetime.
  • CASE REPORT: We report the case of a 39-year-old Afro-Caribbean man with HTLV-1 infection presenting as hypercalcemia and granulomatous pneumocystis jiroveci pneumonia.
  • HTLV-1-associated adult T cell leukemia lymphoma (ATLL) was diagnosed in this patient by bone marrow and lymph node biopsy.
  • This is believed to be the first description of this type of reaction to pneumocystis jiroveci in a HTLV-1-infected ATLL patient.
  • [MeSH-major] HTLV-I Infections / diagnosis. Hypercalcemia / diagnosis. Leukemia-Lymphoma, Adult T-Cell / diagnosis. Pneumocystis jirovecii. Pneumonia, Pneumocystis / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Female. Humans

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leuk Lymphoma. 1994 Aug;14(5-6):395-400 [7812198.001]
  • [Cites] Leuk Lymphoma. 1994 Feb;12(5-6):471-6 [8180610.001]
  • [Cites] Clin Infect Dis. 1996 Jun;22(6):1111-2 [8783726.001]
  • [Cites] J Clin Invest. 1996 Oct 1;98(7):1544-9 [8833902.001]
  • [Cites] Leukemia. 1997 Mar;11(3):453-4 [9067590.001]
  • [Cites] Int J Hematol. 1997 Oct;66(3):257-78 [9401272.001]
  • [Cites] Aust N Z J Med. 1999 Feb;29(1):102-3 [10200829.001]
  • [Cites] Intern Med. 1999 Feb;38(2):83-5 [10225661.001]
  • [Cites] Semin Neurol. 2005 Sep;25(3):315-27 [16170744.001]
  • [Cites] Eur Respir J. 2000 Jan;15(1):213-6 [10678649.001]
  • [Cites] Leuk Lymphoma. 2001 Apr;41(3-4):435-8 [11378559.001]
  • [Cites] Am J Kidney Dis. 2002 Feb;39(2):E8 [11840399.001]
  • [Cites] Thorax. 2002 May;57(5):435-7 [11978921.001]
  • [Cites] J R Soc Med. 2003 Mar;96(3):126-7 [12612113.001]
  • [Cites] Am J Clin Pathol. 1975 Mar;63(3):384-90 [1090147.001]
  • [Cites] J Clin Invest. 1986 Aug;78(2):592-6 [3016032.001]
  • [Cites] Cancer Res. 1989 Jul 15;49(14):3849-52 [2544261.001]
  • [Cites] Semin Diagn Pathol. 1989 Aug;6(3):273-86 [2678337.001]
  • [Cites] Arch Pathol Lab Med. 1989 Nov;113(11):1281-4 [2684091.001]
  • [Cites] J Exp Med. 1990 Sep 1;172(3):759-65 [2388034.001]
  • [Cites] Br J Cancer. 1991 Oct;64(4):745-8 [1911223.001]
  • [Cites] Br J Haematol. 1991 Nov;79(3):428-37 [1751370.001]
  • [Cites] J La State Med Soc. 1992 Jan;144(1):35-8 [1538186.001]
  • [Cites] J Biol Chem. 1993 Jan 15;268(2):1174-9 [8380405.001]
  • [Cites] Blood. 1993 Feb 15;81(4):1017-24 [8427983.001]
  • [Cites] Endocrinology. 1993 Jun;132(6):2551-6 [8099324.001]
  • [Cites] J Biol Chem. 1993 Aug 5;268(22):16730-6 [8393873.001]
  • [Cites] Clin Infect Dis. 1995 Oct;21(4):1014-6 [8645790.001]
  • (PMID = 17356979.001).
  • [ISSN] 1525-1497
  • [Journal-full-title] Journal of general internal medicine
  • [ISO-abbreviation] J Gen Intern Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1824742
  •  go-up   go-down


50. Hernandez CP, Morrow K, Lopez-Barcons LA, Zabaleta J, Sierra R, Velasco C, Cole J, Rodriguez PC: Pegylated arginase I: a potential therapeutic approach in T-ALL. Blood; 2010 Jun 24;115(25):5214-21
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Adult patients with acute lymphoblastic T cell leukemia (T-ALL) have a very poor prognosis and few effective therapeutic options.
  • In addition, treatment of malignant T-cell lines with peg-Arg I significantly impaired their proliferation, which correlated with a decreased progression into the cell cycle, followed by the induction of apoptosis.
  • The results suggest the potential benefit of L-Arginine depletion by peg-Arg I in the treatment of T-cell malignancies.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2007 Feb 15;109(4):1568-73 [17023580.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):309-17 [17210712.001]
  • [Cites] Cancer Res. 2009 Feb 15;69(4):1553-60 [19201693.001]
  • [Cites] Blood. 2009 Feb 19;113(8):1689-98 [19001083.001]
  • [Cites] Cancer Lett. 2009 May 8;277(1):91-100 [19138817.001]
  • [Cites] Nat Rev Mol Cell Biol. 2009 Jun;10(6):430-6 [19461665.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1215-24 [10914545.001]
  • [Cites] Trends Genet. 2000 Oct;16(10):469-73 [11050335.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1986-94 [11877270.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4843-8 [12655043.001]
  • [Cites] Trends Immunol. 2003 Jun;24(6):302-6 [12810105.001]
  • [Cites] J Immunol. 2003 Aug 1;171(3):1232-9 [12874210.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):451-61 [14706337.001]
  • [Cites] Cell Death Differ. 2004 Apr;11(4):381-9 [14685163.001]
  • [Cites] Curr Opin Clin Nutr Metab Care. 2004 Jan;7(1):45-51 [15090903.001]
  • [Cites] J Clin Oncol. 2004 May 15;22(10):1815-22 [15143074.001]
  • [Cites] Cancer Res. 2004 Aug 15;64(16):5839-49 [15313928.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5335-41 [15328169.001]
  • [Cites] J Nutr. 2004 Oct;134(10 Suppl):2760S-2764S; discussion 2765S-2767S [15465781.001]
  • [Cites] J Clin Oncol. 2004 Oct 15;22(20):4075-86 [15353542.001]
  • [Cites] Cancer Res. 1979 Oct;39(10):3893-6 [383278.001]
  • [Cites] Leuk Res. 1992;16(5):475-83 [1625473.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 6;93(3):1065-70 [8577715.001]
  • [Cites] Semin Oncol. 1997 Feb;24(1):70-82 [9045306.001]
  • [Cites] N Engl J Med. 1998 Aug 27;339(9):605-15 [9718381.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Apr;6(4):318-27 [15803138.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3044-8 [15833831.001]
  • [Cites] Cell Immunol. 2004 Nov-Dec;232(1-2):21-31 [15922712.001]
  • [Cites] Nat Rev Immunol. 2005 Aug;5(8):641-54 [16056256.001]
  • [Cites] J Exp Med. 2005 Oct 3;202(7):931-9 [16186186.001]
  • [Cites] J Clin Oncol. 2005 Oct 20;23(30):7660-8 [16234528.001]
  • [Cites] Cell. 2006 Jun 16;125(6):1111-24 [16777601.001]
  • [Cites] Cell Cycle. 2007 Nov 15;6(22):2768-72 [17986863.001]
  • (PMID = 20407034.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20RR021970; United States / NCRR NIH HHS / RR / P20 RR021970; United States / NCI NIH HHS / CA / R01 CA082689; United States / NIGMS NIH HHS / GM / P20 GM103501; United States / NCI NIH HHS / CA / R01 CA107974
  • [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 / CCND3 protein, human; 0 / Cyclin D3; 04079A1RDZ / Cytarabine; 30IQX730WE / Polyethylene Glycols; 94ZLA3W45F / Arginine; EC 3.5.3.1 / Arginase
  • [Other-IDs] NLM/ PMC2892956
  •  go-up   go-down


51. Eguchi-Ishimae M, Eguchi M, Kempski H, Greaves M: NOTCH1 mutation can be an early, prenatal genetic event in T-ALL. Blood; 2008 Jan 1;111(1):376-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • NOTCH1 mutations are common in T-lineage acute lymphoblastic leukemia (T-ALL).
  • Twin studies and retrospective screening of neonatal blood spots provide evidence that fusion genes and other chromosomal abnormalities associated with pediatric leukemias can originate prenatally.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17901244.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
  •  go-up   go-down


52. Dohnal AM, Inthal A, Felzmann T, Glatt S, Sommergruber W, Mann G, Gadner H, Panzer-Grümayer ER: Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL. Int J Cancer; 2006 Dec 15;119(12):2870-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated antigenic isoforms induce a specific immune response in children with T-ALL.
  • The potential immunogenicity of acute lymphoblastic leukemia of the T cell (T-ALL), a small subgroup of childhood leukemia with increased risk for treatment failure and early relapse, was addressed by serological identification of leukemia-derived antigens by recombinant expression cloning (SEREX).
  • Further characterization of the 4 novel isoforms revealed that 3 (HECTD1Delta, CX-ORF-15Delta and hCAP-EDelta) had restricted mRNA expression in more than 70% of T-ALLs (n = 22) and that specific antibodies against these isoforms were detected in up to 30% of patients (n = 16), with the highest frequency for HECTD1Delta.
  • The latter protein was present at high abundance in T-ALLs but not in normal hematopoietic tissues.
  • Given that the leukemia-associated antigens detected in this study have an intracellular localization, the generation of immune effector responses most likely requires antigen presentation.
  • To test this assumption, dendritic cells were loaded with HECTD1Delta protein and used for T cell stimulation.
  • A specific T cell response was induced in vitro in all 3 healthy donors studied, including a former T-ALL patient.
  • [MeSH-major] Antigens, Neoplasm / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Adolescent. Adult. Antibodies / blood. Antibodies / immunology. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / metabolism. Child. Child, Preschool. Cloning, Molecular / methods. DNA, Complementary / chemistry. DNA, Complementary / genetics. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation, Neoplastic. Humans. Infant. Interferon-gamma / biosynthesis. Jurkat Cells. Male. Protein Isoforms / genetics. Protein Isoforms / immunology. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Sequence Analysis, DNA

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17016825.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antigens, Neoplasm; 0 / DNA, Complementary; 0 / Protein Isoforms; 0 / RNA, Messenger; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


53. Burmeister T, Gökbuget N, Reinhardt R, Rieder H, Hoelzer D, Schwartz S: NUP214-ABL1 in adult T-ALL: the GMALL study group experience. Blood; 2006 Nov 15;108(10):3556-9
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NUP214-ABL1 in adult T-ALL: the GMALL study group experience.
  • The NUP214-ABL1 fusion gene in T-cell acute lymphoblastic leukemia (T-ALL) has recently been identified as a possible target for imatinib and related tyrosine kinase inhibitors, but exact data regarding the prognostic impact and frequency of the several putative NUP214-ABL1 mRNA transcripts are still missing.
  • We investigated 279 adult patients with T-ALL treated within the framework of the GMALL 5/93 and 6/99 therapy trials for NUP214-ABL1 by using a novel multiplex real-time, quantitative polymerase chain reaction (PCR).
  • Eleven (3.9%) patients were NUP214-ABL1 positive, and 5 different transcripts were observed; 8 patients had a thymic immunophenotype, 1 had an early T-cell immunophenotype, and 2 had a mature T-cell immunophenotype.
  • NUP214-ABL1-positive and -negative patients did not differ significantly in their major clinical features.
  • In contrast to previous reports suggesting an adverse clinical course for NUP214-ABL1-positive patients, no significant difference in overall survival was observed.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Nuclear Pore Complex Proteins / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-abl / genetics
  • [MeSH-minor] Adolescent. Adult. Benzamides. Female. Humans. Imatinib Mesylate. Immunophenotyping. Male. Piperazines / therapeutic use. Polymerase Chain Reaction. Prognosis. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / therapeutic use. RNA, Messenger / analysis. Survival Rate

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16873673.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / NUP214 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / RNA, Messenger; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins c-abl
  •  go-up   go-down


54. Yamasaki M, Fujita S, Ishiyama E, Mukai A, Madhyastha H, Sakakibara Y, Suiko M, Hatakeyama K, Nemoto T, Morishita K, Kataoka H, Tsubouchi H, Nishiyama K: Soy-derived isoflavones inhibit the growth of adult T-cell leukemia cells in vitro and in vivo. Cancer Sci; 2007 Nov;98(11):1740-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Soy-derived isoflavones inhibit the growth of adult T-cell leukemia cells in vitro and in vivo.
  • Adult T-cell leukemia occurs in human T-lymphotropic virus type I-infected individuals and is endemic to the south-western area of Kyushu in Japan.
  • In this communication, we examined the effect of soy isoflavones on the growth of adult T-cell leukemia cells in vitro and in vivo.
  • Among the isoflavones studied, genistein had the highest growth-inhibitory effect; however, genistein did not exert an apparent growth-inhibitory effect on Jurkat and Molt-4 cells, which were non-adult T-cell leukemia cells.
  • The in vivo studies demonstrated that soy-derived isoflavones significantly inhibit ED-40515 cell growth and infiltration into various organs in non-obese diabetic severe combined-immunodeficiency common gamma-chain knockout mice.
  • Taken together, it is evident that soy isoflavones might serve as a promising compound for the treatment of adult T-cell leukemia.
  • [MeSH-major] Isoflavones / pharmacology. Isoflavones / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Soybeans
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Genistein / pharmacology. Humans. Jurkat Cells. Mice. Mice, Knockout. Mice, SCID. Transplantation, Heterologous

  • Hazardous Substances Data Bank. GENISTEIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17727682.001).
  • [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 / Isoflavones; 6287WC5J2L / daidzein; 92M5F28TVF / glycitein; DH2M523P0H / Genistein
  •  go-up   go-down


55. Sanda T, Asamitsu K, Ogura H, Iida S, Utsunomiya A, Ueda R, Okamoto T: Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor. Leukemia; 2006 Apr;20(4):590-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of cell death in adult T-cell leukemia cells by a novel IkappaB kinase inhibitor.
  • NF-kappaB is constitutively activated in adult T-cell leukemia (ATL) and is considered responsible for cell growth and prevention of cell death.
  • In this study, we demonstrate that NF-kappaB is constitutively activated in various HTLV-1-infected T-cell lines and ATL-derived cell lines irrespectively of Tax expression as evidenced by the phosphorylation of IkappaBalpha and p65 subunit of NF-kappaB, activation of NF-kappaB DNA binding, and upregulation of various target genes including bcl-xL, bcl-2, XIAP, c-IAP1, survivin, cyclinD1, ICAM-1 and VCAM-1.
  • The effects of a novel IkappaB kinase (IKK) inhibitor, 2-amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-piperidin-4-yl nicotinonitrile (ACHP), were examined on cell growth of these cell lines and fresh ATL leukemic cells.
  • We found that ACHP could inhibit the phosphorylation of IkappaBalpha and p65, as well as NF-kappaB DNA-binding, associated with downregulation of the NF-kappaB target genes and induce cell growth arrest and apoptosis in these cells.
  • When Tax-active and Tax-inactive cell lines were compared, ACHP could preferentially inhibit cell growth of Tax-active cells.
  • Moreover, ACHP exhibited strong apoptosis-inducing activity in fresh ATL cells.
  • These findings indicate that ACHP and its derivatives are effective in inducing ATL cell death and thus feasible candidates for the treatment of ATL.
  • [MeSH-major] Enzyme Inhibitors / pharmacology. I-kappa B Kinase / antagonists & inhibitors. Leukemia-Lymphoma, Adult T-Cell / metabolism. Nicotinic Acids / pharmacology. Nitriles / pharmacology. T-Lymphocytes / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Binding Sites. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. DNA / metabolism. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Enzyme Activation / genetics. Enzyme Activation / physiology. Gene Expression Regulation, Enzymologic / drug effects. Human T-lymphotropic virus 1 / metabolism. Humans. In Vitro Techniques. Phosphorylation. Protein Subunits / antagonists & inhibitors. Protein Subunits / genetics. Protein Subunits / metabolism. Structure-Activity Relationship. Transcription Factor RelA / antagonists & inhibitors. Transcription Factor RelA / genetics. Transcription Factor RelA / metabolism

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16453001.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 2-amino-6-(2-(cyclopropylmethoxy)-6-hydroxyphenyl)-4-piperidin-4-yl nicotinonitrile; 0 / Enzyme Inhibitors; 0 / Nicotinic Acids; 0 / Nitriles; 0 / Protein Subunits; 0 / Transcription Factor RelA; 9007-49-2 / DNA; EC 2.7.11.10 / I-kappa B Kinase
  •  go-up   go-down


56. Marçais A, Jeannet R, Hernandez L, Soulier J, Sigaux F, Chan S, Kastner P: Genetic inactivation of Ikaros is a rare event in human T-ALL. Leuk Res; 2010 Apr;34(4):426-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic inactivation of Ikaros is a rare event in human T-ALL.
  • The Ikaros (Ikzf1) gene, encoding a transcription regulator, is a major tumor suppressor in B-cell acute lymphoblastic leukemia (B-ALL).
  • In the mouse, however, loss of Ikaros is primarily associated with T-ALL development.
  • Whether Ikaros is also implicated in human T-ALL remains unclear.
  • We studied Ikaros in 25 human T-ALL samples from diverse molecular subtypes at the mRNA, protein, sequence and genomic copy number level.
  • Thus, inactivation of Ikaros by deletion or mutation is rare in human T-ALL.
  • [MeSH-major] Gene Silencing. Ikaros Transcription Factor / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Child. Child, Preschool. Cohort Studies. Comparative Genomic Hybridization. Gene Deletion. Gene Expression Regulation, Leukemic. Humans. Infant. Jurkat Cells. Middle Aged. Mutation / physiology. Protein Isoforms / genetics. Young Adult

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • [CommentIn] Leuk Res. 2010 Apr;34(4):416-7 [19892402.001]
  • (PMID = 19796813.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / IKZF1 protein, human; 0 / Protein Isoforms; 148971-36-2 / Ikaros Transcription Factor
  •  go-up   go-down


57. Braun C, Duffau P, Mahon FX, Rosier E, Leguay T, Etienne G, Michaud M: [Acute pancreatitis due to hypercalcemia revealing adult T-cell leukemia]. Rev Med Interne; 2007 Feb;28(2):116-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acute pancreatitis due to hypercalcemia revealing adult T-cell leukemia].
  • [Transliterated title] Une pancréatite aiguë révélant une leucémie/lymphome T de l'adulte.
  • INTRODUCTION: Hypercalcemia frequently occurs in the course of Adult T-cell leukemia/lymphoma (ATLL).
  • We report the first case of acute pancreatitis revealing ATLL.
  • EXEGESIS: A 41-year-old woman, without medical history, presented with acute pancreatitis.
  • Biochemical tests showed severe hypercalcemia and the peripheral white blood cell count revealed an atypical lymphocytosis.
  • ATLL was diagnosed by immunophenotypic and morphological analysis of circulating lymphocytes, bone marrow and lymphatic node biopsy.
  • CONCLUSION: In spite of the high prevalence of hypercalcemia in ATLL, acute pancreatitis revealing this pathology is an exceptional condition.

  • Genetic Alliance. consumer health - Pancreatitis.
  • MedlinePlus Health Information. consumer health - Pancreatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17157965.001).
  • [ISSN] 0248-8663
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


58. Baba M, Okamoto M, Hamasaki T, Horai S, Wang X, Ito Y, Suda Y, Arima N: Highly enhanced expression of CD70 on human T-lymphotropic virus type 1-carrying T-cell lines and adult T-cell leukemia cells. J Virol; 2008 Apr;82(8):3843-52
Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Highly enhanced expression of CD70 on human T-lymphotropic virus type 1-carrying T-cell lines and adult T-cell leukemia cells.
  • Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia (ATL).
  • In Japan, the number of HTLV-1 carriers is estimated to be 1.2 million and more than 700 cases of ATL have been diagnosed every year.
  • Considering the poor prognosis and lack of curative therapy of ATL, it seems mandatory to establish an effective strategy for the treatment of ATL.
  • In this study, we attempted to identify the cell surface molecules that will become suitable targets of antibodies for anti-ATL therapy.
  • The expression levels of approximately 40,000 host genes of three human T-cell lines carrying HTLV-1 genomes were analyzed by oligonucleotide microarray and compared with the expression levels of the genes in an HTLV-1-negative T-cell line.
  • The HTLV-1-carrying T-cell lines used for experiments had totally different expression patterns of viral genome.
  • Among the genes evaluated, the expression levels of 108 genes were found to be enhanced more than 10-fold in all of the T-cell lines examined and 11 of the 108 genes were considered to generate the proteins expressed on the cell surface.
  • In particular, the CD70 gene was upregulated more than 1,000-fold and the enhanced expression of the CD70 molecule was confirmed by laser flow cytometry for various HTLV-1-carrying T-cell lines and primary CD4(+) T cells isolated from acute-type ATL patients.
  • Since CD70 expression is strictly restricted in normal tissues, such as highly activated T and B cells, CD70 appears to be a potential target for effective antibody therapy against ATL.
  • [MeSH-major] Antigens, CD70 / biosynthesis. Human T-lymphotropic virus 1 / immunology. T-Lymphocytes / chemistry. T-Lymphocytes / virology. Up-Regulation
  • [MeSH-minor] Antigens, Surface / biosynthesis. Cell Line, Tumor. Flow Cytometry. Gene Expression Profiling. Gene Expression Regulation, Viral. Humans. Japan. Leukemia-Lymphoma, Adult T-Cell / virology. Oligonucleotide Array Sequence Analysis. Viral Proteins / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Opin Immunol. 2005 Jun;17(3):275-81 [15886117.001]
  • [Cites] J Urol. 2005 Jun;173(6):2150-3 [15879877.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5428-38 [15958592.001]
  • [Cites] Retrovirology. 2004;1:39 [15560845.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Eur J Cancer. 2005 Aug;41(12):1794-801 [16043348.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6047-57 [16155611.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):6058-68 [16155612.001]
  • [Cites] Cancer Metastasis Rev. 2005 Dec;24(4):487-99 [16408158.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2328-37 [16489038.001]
  • [Cites] Eur J Haematol Suppl. 2007 Jan;(67):5-14 [17206982.001]
  • [Cites] Blood. 2007 Feb 1;109(3):1185-92 [17038522.001]
  • [Cites] Oncogene. 2007 Feb 22;26(8):1245-55 [16909099.001]
  • [Cites] Blood. 2000 Jul 1;96(1):275-81 [10891462.001]
  • [Cites] AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1695-700 [11080812.001]
  • [Cites] Virus Genes. 2001 Jun;22(3):279-87 [11450946.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1150-9 [11493464.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4484-96 [11494144.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2592-9 [11980654.001]
  • [Cites] Mol Pharmacol. 2002 Jun;61(6):1359-65 [12021397.001]
  • [Cites] Cancer Res. 2002 Jun 15;62(12):3562-71 [12068005.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):304-11 [14686487.001]
  • [Cites] Lancet Oncol. 2004 May;5(5):292-302 [15120666.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5978-88 [15199151.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Nature. 1981 Dec 24;294(5843):770-1 [6275274.001]
  • [Cites] Virology. 1983 Aug;129(1):51-64 [6412453.001]
  • [Cites] EMBO J. 1984 Jun;3(6):1339-43 [6086318.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Jpn J Cancer Res. 1990 Mar;81(3):225-31 [2161813.001]
  • [Cites] J Virol. 1991 Dec;65(12):6892-9 [1719236.001]
  • [Cites] Br J Haematol. 1991 Oct;79(2):263-70 [1958484.001]
  • [Cites] Blood. 1994 Jan 15;83(2):435-45 [7506951.001]
  • [Cites] J Virol. 1996 May;70(5):3258-63 [8627808.001]
  • [Cites] Oncogene. 1996 Apr 18;12(8):1645-52 [8622884.001]
  • [Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996;13 Suppl 1:S69-75 [8797707.001]
  • [Cites] J Histochem Cytochem. 1997 Apr;45(4):515-25 [9111230.001]
  • [Cites] J Immunol. 1998 Sep 15;161(6):3087-95 [9743375.001]
  • [Cites] Oncogene. 1999 Feb 11;18(6):1341-9 [10022816.001]
  • [Cites] Clin Immunol. 1999 Nov;93(2):114-23 [10527687.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1204-13 [15471956.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):129-38 [15671537.001]
  • [Cites] AIDS Res Hum Retroviruses. 2005 Apr;21(4):273-84 [15943569.001]
  • (PMID = 18256142.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD70; 0 / Antigens, Surface; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC2292990
  •  go-up   go-down


59. Bellon M, Lepelletier Y, Hermine O, Nicot C: Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia. Blood; 2009 May 14;113(20):4914-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulation of microRNA involved in hematopoiesis and the immune response in HTLV-I adult T-cell leukemia.
  • Human T-cell leukemia virus type-I (HTLV-I) is the etiologic agent of adult T-cell leukemia (ATL), an aggressive lymphoproliferative disease.
  • MicroRNAs (miRNAs) are differentially expressed during hematopoiesis and lineage commitment of hematopoietic stem cell progenitors (HSCPs).
  • Here, we report aberrant expression of hematopoietic-specific miR-223, miR-181a, miR-150, miR-142.3p, and miR-155 in HTLV-I-infected cells in vitro and uncultured ex vivo ATL cells.
  • Our results suggest that HTLV-I-infected cells have an unbalanced expression of miRNA that favors T-cell differentiation.
  • Strikingly, our data also revealed significant differences between ex vivo ATL tumor cells and in vitro HTLV-I cell lines.
  • Specifically, miR-150 and miR-223 were up-regulated in ATL patients but consistently down-regulated in HTLV-I cell lines, suggesting that ATL cells and in vitro-established cells are derived from distinct cellular populations.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 2005 Nov;79(22):14069-78 [16254341.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1021-9 [16569765.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12481-6 [16885212.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1931-6 [16990772.001]
  • [Cites] Genes Dev. 2007 Mar 1;21(5):578-89 [17344418.001]
  • [Cites] Cell. 2007 Apr 6;129(1):147-61 [17382377.001]
  • [Cites] Science. 2007 Apr 27;316(5824):608-11 [17463290.001]
  • [Cites] Cell. 2007 Oct 5;131(1):146-59 [17923094.001]
  • [Cites] Nat Med. 2008 Apr;14(4):429-36 [18376405.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]
  • [Cites] Dev Cell. 2008 Jun;14(6):815-6 [18539110.001]
  • [Cites] Nat Immunol. 2008 Aug;9(8):839-45 [18645592.001]
  • [Cites] J Exp Med. 2008 Sep 1;205(9):1983-91 [18725525.001]
  • [Cites] Oncogene. 2000 Oct 12;19(43):4954-60 [11042682.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Oncogene. 1989 Jun;4(6):671-6 [2660069.001]
  • [Cites] Haematologia (Budap). 1994;26(1):1-9 [7959369.001]
  • [Cites] J Virol. 1996 Jun;70(6):4038-44 [8648741.001]
  • [Cites] Semin Immunol. 2005 Apr;17(2):155-65 [15737576.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):311-21 [15803157.001]
  • [Cites] J Clin Invest. 2005 May;115(5):1361-8 [15864353.001]
  • [Cites] Cell. 2005 Dec 2;123(5):819-31 [16325577.001]
  • (PMID = 19246560.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106258; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / R01CA106258; United States / NCI NIH HHS / CA / R01CA115398
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  • [Other-IDs] NLM/ PMC2686141
  •  go-up   go-down


60. Beltrán B, Palomino E, Quiñones P, Morales D, Cotrina E: [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature]. Rev Gastroenterol Peru; 2010 Apr-Jun;30(2):153-7
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gastric adult T cell leukemia/lymphoma: report of four cases and review of literature].
  • [Transliterated title] Leucemia/linfoma T del adulto gástrico: reporte de cuatro casos y revisión de la literatura.
  • Adult T-cell leukemia/lymphoma (ATLL) is an aggressive disease associated with human T-cell lymphotropic virus type-I (HTLV-I) with heterogeneous clinical presentation and outcomes.
  • We describe clinical and endoscopic findings of cases and review literature.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell. Stomach Neoplasms
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Etoposide / administration & dosage. Fatal Outcome. Female. Human T-lymphotropic virus 1 / isolation & purification. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Prednisone / administration & dosage. Prevalence. Stomach Ulcer / etiology. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Gastric Lymphoma.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20644608.001).
  • [ISSN] 1609-722X
  • [Journal-full-title] Revista de gastroenterología del Perú : órgano oficial de la Sociedad de Gastroenterología del Perú
  • [ISO-abbreviation] Rev Gastroenterol Peru
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Peru
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VB0R961HZT / Prednisone; CHOEP protocol; CHOP protocol
  •  go-up   go-down


61. Satou Y, Yasunaga J, Yoshida M, Matsuoka M: HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells. Proc Natl Acad Sci U S A; 2006 Jan 17;103(3):720-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HTLV-I basic leucine zipper factor gene mRNA supports proliferation of adult T cell leukemia cells.
  • Human T cell leukemia virus type I (HTLV-I) causes adult T cell leukemia (ATL) in 2-5% of carriers after a long latent period.
  • An HTLV-I encoded protein, Tax, induces proliferation and inhibits apoptosis, resulting in clonal proliferation of infected cells.
  • However, tax gene expression in ATL cells is disrupted by several mechanisms, including genetic changes in the tax gene and DNA methylation/deletion of the 5' long terminal repeat (LTR).
  • Because Tax is the major target of cytotoxic T-lymphocytes in vivo, loss of Tax expression should enable ATL cells to escape the host immune system.
  • The 5' LTR of HTLV-I is frequently hypermethylated or deleted in ATL cells, whereas the 3' LTR remains unmethylated and intact, suggesting the involvement of the 3' LTR in leukemogenesis.
  • Here we show that a gene encoded by the minus strand of the HTLV-I proviral genome, HTLV-I basic leucine zipper factor (HBZ), is transcribed from 3'-LTR in all ATL cells.
  • Suppression of HBZ gene transcription by short interfering RNA inhibits proliferation of ATL cells.
  • In addition, HBZ gene expression promotes proliferation of a human T cell line.
  • Analyses of T cell lines transfected with mutated HBZ genes showed that HBZ promotes T cell proliferation in its RNA form, whereas HBZ protein suppresses Tax-mediated viral transcription through the 5' LTR.
  • The growth-promoting activity of HBZ RNA likely plays an important role in oncogenesis by HTLV-I.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / genetics. Cell Proliferation. Human T-lymphotropic virus 1 / genetics. Leucine Zippers / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Leukemia-Lymphoma, Adult T-Cell / pathology. RNA, Messenger / physiology. Viral Proteins / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Cell Line, Transformed. Gene Expression Regulation, Neoplastic. Humans. Mice. Mice, Transgenic. Molecular Sequence Data

  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2003 Nov 1;63(21):7062-7 [14612496.001]
  • [Cites] Blood. 2001 Feb 15;97(4):987-93 [11159527.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Hum Mol Genet. 2001 Apr;10(7):699-703 [11257102.001]
  • [Cites] Oncogene. 2001 Apr 19;20(17):2055-67 [11360190.001]
  • [Cites] J Virol. 2002 Sep;76(18):9389-97 [12186921.001]
  • [Cites] Immunol Rev. 2002 Jul;185:236-65 [12190935.001]
  • [Cites] J Virol. 2002 Dec;76(24):12813-22 [12438606.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3406-15 [12824337.001]
  • [Cites] Gene Ther. 2003 Aug;10(17):1446-57 [12900759.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):280-96 [14686485.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):297-303 [14686486.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2753-60 [14656887.001]
  • [Cites] Science. 2004 Apr 30;304(5671):734-6 [15118162.001]
  • [Cites] Nat Rev Genet. 2004 Jul;5(7):522-31 [15211354.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5332-7 [15289339.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] Blood. 1987 Oct;70(4):1069-72 [3115332.001]
  • [Cites] J Virol. 1989 Aug;63(8):3234-9 [2545901.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Sep 15;163(2):1006-13 [2476979.001]
  • [Cites] J Virol. 1991 Aug;65(8):4525-8 [2072462.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4243-9 [7492783.001]
  • [Cites] Cell. 1996 May 17;85(4):457-9 [8653779.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3065-73 [8874205.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4862-7 [9354450.001]
  • [Cites] J Exp Med. 1998 May 4;187(9):1439-49 [9565636.001]
  • [Cites] Oncogene. 1998 Jul 9;17(1):77-82 [9671316.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8858-63 [9671769.001]
  • [Cites] Cell Growth Differ. 1998 Aug;9(8):585-93 [9716176.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4137-43 [10435595.001]
  • [Cites] Immunity. 2005 May;22(5):607-19 [15894278.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):682-6 [15931223.001]
  • [Cites] Retrovirology. 2004;1:44 [15601474.001]
  • [Cites] Retrovirology. 2005;2:27 [15854229.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] Retrovirology. 2005;2:64 [16242045.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [ErratumIn] Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8906
  • (PMID = 16407133.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ273132
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Messenger; 0 / Viral Proteins
  • [Other-IDs] NLM/ PMC1334651
  •  go-up   go-down


62. Yamaguchi T, Maeda Y, Ueda S, Hijikata Y, Morita Y, Miyatake JI, Matsuda M, Kanamaru A: Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia. Leukemia; 2005 Jun;19(6):1010-7
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dichotomy of all-trans retinoic acid inducing signals for adult T-cell leukemia.
  • We previously reported that all-trans retinoic acid (ATRA) inhibits growth in human T-cell leukemia virus type 1 (HTLV-1)-positive T-cell lines and fresh cells from patients with adult T-cell leukemia.
  • In the present study, we observed that NF-kappaB transcriptional activity as well as cell growth decreased significantly in HTLV-1-positive T-cell lines in the presence of ATRA.
  • Furthermore, we observed that ATRA reduced HTLV-1 proviral DNA, HTLV-1 genes (gag, tax, or pol mRNA) using the real-time quantitative polymerase chain reaction.
  • SIL-2R was reduced by ATRA in both protein level (culture supernantant) and mRNA level in HTLV-1-positive T-cell lines.
  • Interestingly, ATRA significantly inhibited RT activity similar to azidothimidine (AZT) in HTLV-1-positive T-cell lines.
  • Moreover, AZT inhibited proviral DNA but not NF-kappaB transcriptional activity, and sIL-2R on HTLV-1; however, ATRA inhibited of NF-kappaB, proviral DNA and sIL-2R on HTLV-1.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Leukemia, T-Cell / drug therapy. Leukemia, T-Cell / metabolism. Signal Transduction / drug effects. Tretinoin / pharmacology
  • [MeSH-minor] Adult. Cell Division / drug effects. Deltaretrovirus Infections / drug therapy. Deltaretrovirus Infections / metabolism. Deltaretrovirus Infections / physiopathology. Gene Expression Regulation, Leukemic / drug effects. Gene Expression Regulation, Viral / drug effects. Gene Products, gag / genetics. Gene Products, pol / genetics. Genes, pX / genetics. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / growth & development. Humans. In Vitro Techniques. Jurkat Cells. NF-kappa B / metabolism. Proviruses / genetics. Receptors, Interleukin-2 / metabolism. Solubility. Transcriptional Activation / drug effects. Viral Load

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15843825.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Gene Products, gag; 0 / Gene Products, pol; 0 / NF-kappa B; 0 / Receptors, Interleukin-2; 5688UTC01R / Tretinoin
  •  go-up   go-down


63. Miura H, Maeda M, Yamamoto N, Yamaoka S: Distinct IkappaB kinase regulation in adult T cell leukemia and HTLV-I-transformed cells. Exp Cell Res; 2005 Aug 1;308(1):29-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct IkappaB kinase regulation in adult T cell leukemia and HTLV-I-transformed cells.
  • We have recently shown constitutive IkappaB kinase (IKK) activation and aberrant p52 expression in adult T cell leukemia (ATL) cells that do not express human T cell leukemia virus type I (HTLV-I) Tax, but the mechanism of IKK activation in these cells has remained unknown.
  • Here, we demonstrate distinct regulation of IKK activity in ATL and HTLV-I-transformed T cells in response to protein synthesis inhibition or arsenite treatment.
  • Protein synthesis inhibition for 4 h by cycloheximide (CHX) barely affects IKK activity in Tax-positive HTLV-I-transformed cells, while it diminishes IKK activity in Tax-negative ATL cells.
  • Treatment of ATL cells with a proteasome inhibitor MG132 prior to protein synthesis inhibition reverses the inhibitory effect of CHX, and MG132 alone greatly enhances IKK activity.
  • In addition, treatment of HTLV-I-transformed cells with arsenite for 1 h results in down-regulation of IKK activity without affecting Tax expression, while 8 h of arsenite treatment does not impair IKK activity in ATL cells.
  • These results indicate that a labile protein sensitive to proteasome-dependent degradation governs IKK activation in ATL cells, and suggest a molecular mechanism of IKK activation in ATL cells distinct from that in HTLV-I-transformed T cells.
  • [MeSH-major] Cell Transformation, Viral / physiology. Leukemia-Lymphoma, Adult T-Cell / metabolism. Protein-Serine-Threonine Kinases / metabolism
  • [MeSH-minor] Arsenites / pharmacology. Cell Line, Transformed. Cell Line, Tumor. Cycloheximide / antagonists & inhibitors. Cycloheximide / pharmacology. Enzyme Inhibitors / pharmacology. Human T-lymphotropic virus 1 / physiology. Humans. I-kappa B Kinase. Leupeptins / pharmacology. Proteasome Endopeptidase Complex / metabolism. Protein Synthesis Inhibitors / pharmacology. T-Lymphocytes / drug effects. T-Lymphocytes / metabolism

  • Hazardous Substances Data Bank. CYCLOHEXIMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878527.001).
  • [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 / Arsenites; 0 / Enzyme Inhibitors; 0 / Leupeptins; 0 / Protein Synthesis Inhibitors; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 98600C0908 / Cycloheximide; EC 2.7.1.- / IKBKE protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / CHUK protein, human; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex; N5509X556J / arsenite
  •  go-up   go-down


64. 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

  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


65. Estes DA, Lovato DM, Khawaja HM, Winter SS, Larson RS: Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples. Br J Haematol; 2007 Oct;139(1):20-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic alterations determine chemotherapy resistance in childhood T-ALL: modelling in stage-specific cell lines and correlation with diagnostic patient samples.
  • Acquired drug resistance eventually leads to treatment failure in T-cell acute lymphoblastic leukaemia (T-ALL).
  • Immunophenotypic and cytogenetic heterogeneities within T-ALL influence susceptibility to cytotoxic therapy, and little is known about the mechanisms of drug resistance at specific stages of T-cell ontogeny.
  • We developed tolerance to therapeutic concentrations of daunorubicin (DNR) and L-asparaginase (L-asp) in Jurkat (CD1a(-), sCD3(+)) and Sup T1 (CD1a(+), sCD3(-)) cell lines, having respective 'mature' and 'cortical' stages of developmental arrest.
  • Microarray analysis identified upregulation of asparagine synthetase (ASNS) and argininosuccinate synthase 1 (ASS1) to cell lines with acquired resistance to L-asp, and in the case of DNR, upregulation of ATP-binding cassette B1 (ABCB1).
  • This study expands the pool of available drug resistant cell lines having cortical and mature stages of developmental arrest, introduces three new drug resistant T-ALL cell lines, and identifies gene interactions leading to L-asp and DNR resistance.
  • [MeSH-major] Cell Line, Tumor. Drug Resistance, Neoplasm / genetics. Gene Expression Regulation, Leukemic. Genes, MDR. Leukemia-Lymphoma, Adult T-Cell / genetics

  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17854304.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R01 CA114589; United States / NCI NIH HHS / CA / U10 CA98543-03-14305
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / P-Glycoprotein; 0 / RNA, Small Interfering; 5J49Q6B70F / Vincristine; 9PHQ9Y1OLM / Prednisolone; EC 3.5.1.1 / Asparaginase; EC 6.3.1.1 / Aspartate-Ammonia Ligase; EC 6.3.4.5 / Argininosuccinate Synthase; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down


66. Maeda Y, Yamaguchi T, Hijikata Y, Tanaka M, Hirase C, Takai S, Morita Y, Sano T, Miyatake J, Tatsumi Y, Kanamaru A: Clinical efficacy of all-trans retinoic acid for treating adult T cell leukemia. J Cancer Res Clin Oncol; 2008 Jun;134(6):673-7
Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical efficacy of all-trans retinoic acid for treating adult T cell leukemia.
  • PURPOSE: We previously reported that all-trans retinoic acid (ATRA) inhibited growth in human T-cell leukemia virus type I (HTLV-I)-positive T-cell lines and in fresh cells from patients with adult T cell leukemia (ATL).
  • Here, we confirmed the clinical effects of ATRA in 20 patients with ATL.
  • MATERIALS AND METHODS: The 20 patients (n = 20) with a median age of 56 (range 35-73) years who were diagnosed with ATL received ATRA orally.
  • RESULTS: The efficacy of treatment was as follows: no complete response (CR), a partial response (PR) in 40% of the patients, no change (NC) in 45% of the patients, and a progressive disease (PD) in 15% of the patients.
  • In seven acute-type ATL patients, a PR was achieved in two (28.5%), NC was observed in two (28.5%), and a PD was observed in three (42.8%).
  • In three lymphoma-type ATL patients, a PR (100%) was achieved.
  • Among four chronic-type ATL patients, a PR was achieved in one (25%) and NC was observed in the remaining three (75%).
  • In six smoldering-type ATL patients, a PR was achieved in two (33.3%) and NC was observed in four (66.6%).
  • CONCLUSION: These results indicated that ATRA might be a useful agent for the safe treatment of ATL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tretinoin / therapeutic use
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18008086.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  •  go-up   go-down


67. Nomura K, Utsunomiya A, Furushou H, Tara M, Hazeki M, Tokunaga M, Uozumi K, Hanada S, Yashiki S, Tajima K, Sonoda S: A family predisposition to adult T-cell leukemia. J Clin Exp Hematop; 2006 Nov;46(2):67-71

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A family predisposition to adult T-cell leukemia.
  • We report here the rare case of a family predisposed to adult T-cell leukemia (ATL).
  • Six of seven siblings developed ATL with ages of onset of 77, 48, 60, 64, 72, and 62 years old.
  • Although virological tests for human T-lymphotropic virus type 1 were unavailable for two of the six patients, all were diagnosed with ATL based on their clinical, hematological, and histopathological features.
  • Two of the six patients were tested for HLA haplotypes using fresh blood samples, and both were carriers of the HLA-A*26 allele known in the southern Japanese population to be susceptible to ATL.
  • This series of genetic traits may help explain the familial predisposition to ATL.
  • [MeSH-major] Genetic Predisposition to Disease. HLA-A Antigens / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics
  • [MeSH-minor] Aged. Female. HTLV-I Infections / complications. Human T-lymphotropic virus 1. Humans. Male. Middle Aged. Pedigree

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17142956.001).
  • [ISSN] 1346-4280
  • [Journal-full-title] Journal of clinical and experimental hematopathology : JCEH
  • [ISO-abbreviation] J Clin Exp Hematop
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / HLA-A Antigens
  •  go-up   go-down


68. Malan R, Berini CA, Eirin ME, Delfino CM, Pedrozo W, Krupp R, García Plichta A, Biglione MM: [Seroprevalence of HTLV-1/2 in blood donors from Misiones Province]. Medicina (B Aires); 2010;70(1):71-4
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Seroprevalence of HTLV-1/2 in blood donors from Misiones Province].
  • [Transliterated title] Seroprevalencia de HTLV-1/2 en donantes de sangre de la Provincia de Misiones.
  • Human T-cell Lymphotropic viruses type 1 (HTLV-1), the first human oncoretrovirus to be discovered, is the etiologic agent of Adult T-cell Leukemia (ATL) and HTLV-1 Associated Mielopathy or Tropical Spastic Paraparesis (HAM/TSP).
  • It is endemic worldwide, including the North of Argentina where both associated diseases have also been detected.
  • No etiologic role has been described for HTLV-2, although it has been associated with HAM/TSP-like neurologic syndromes.
  • The aim of this study was to estimate the seroprevalence of HTLV-1/2 in a blood donor population from Misiones province.
  • HTLV-1/2 screening was performed with ELISA and particle agglutination, and reactive samples were confirmed by Western Blot.
  • Out of the 5 positive samples, one was an HTLV, three HTLV-1 and one HTLV-2.
  • This study demonstrates the presence of HTLV-1/2 in a population of Misiones with a prevalence rate similar to those reported among blood donors from non-endemic areas.
  • [MeSH-major] Blood Donors / statistics & numerical data. HTLV-I Infections / epidemiology. HTLV-II Infections / epidemiology
  • [MeSH-minor] Adult. Argentina / epidemiology. Enzyme-Linked Immunosorbent Assay. Female. Human T-lymphotropic virus 1 / isolation & purification. Human T-lymphotropic virus 2 / isolation & purification. Humans. Male. Seroepidemiologic Studies

  • MedlinePlus Health Information. consumer health - Blood Transfusion and Donation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20228028.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Argentina
  •  go-up   go-down


69. Sakashita A, Ashizawa K, Minami K, Fukuda T, Fukuda M, Abe K, Hayashi T, Uetani M: Localized ground glass opacities with multiple pulmonary small cysts in adult T-cell leukemia or lymphoma: an "alloy wheel" appearance. J Thorac Imaging; 2009 Nov;24(4):321-4
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Localized ground glass opacities with multiple pulmonary small cysts in adult T-cell leukemia or lymphoma: an "alloy wheel" appearance.
  • We herein report a case of adult T-cell leukemia or lymphoma showing multiple lung cysts within a localized ground glass opacity (GGO) on computed tomography scan.
  • [MeSH-major] Cysts / radiography. Leukemia-Lymphoma, Adult T-Cell / radiography. Lung Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19935228.001).
  • [ISSN] 1536-0237
  • [Journal-full-title] Journal of thoracic imaging
  • [ISO-abbreviation] J Thorac Imaging
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


70. Ashworth TD, Pear WS, Chiang MY, Blacklow SC, Mastio J, Xu L, Kelliher M, Kastner P, Chan S, Aster JC: Deletion-based mechanisms of Notch1 activation in T-ALL: key roles for RAG recombinase and a conserved internal translational start site in Notch1. Blood; 2010 Dec 16;116(25):5455-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Point mutations that trigger ligand-independent proteolysis of the Notch1 ectodomain occur frequently in human T-cell acute lymphoblastic leukemia (T-ALL) but are rare in murine T-ALL, suggesting that other mechanisms account for Notch1 activation in murine tumors.
  • Here we show that most murine T-ALLs harbor Notch1 deletions that fall into 2 types, both leading to ligand-independent Notch1 activation.
  • Type 1 deletions remove exon 1 and the proximal promoter, appear to be RAG-mediated, and are associated with mRNA transcripts that initiate from 3' regions of Notch1.
  • Type 2 deletions remove sequences between exon 1 and exons 26 to 28 of Notch1, appear to be RAG-independent, and are associated with transcripts in which exon 1 is spliced out of frame to 3' Notch1 exons.
  • Thus, like human T-ALL, murine T-ALL is often associated with acquired mutations that cause ligand-independent Notch1 activation.
  • [MeSH-major] Homeodomain Proteins / physiology. Peptide Chain Initiation, Translational / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology

  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 2002 Jun 28;109(7):811-21 [12110179.001]
  • [Cites] Radiat Res. 2002 Mar;157(3):331-40 [11839096.001]
  • [Cites] Nat Immunol. 2003 Feb;4(2):168-74 [12514733.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):551-64 [12842084.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1257-68 [12807718.001]
  • [Cites] Science. 2003 Aug 22;301(5636):1096-9 [12934008.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1683-8 [8643690.001]
  • [Cites] Genes Dev. 1996 Aug 1;10(15):1930-44 [8756350.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3780-92 [9808572.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):8882-90 [15604248.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):221-6 [16015321.001]
  • [Cites] Cell. 2005 Aug 12;122(3):435-47 [16096062.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3898-906 [16118316.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Blood. 2006 Jan 15;107(2):781-5 [16166587.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2540-3 [16282337.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Mol Cell Biol. 2000 Oct;20(20):7505-15 [11003647.001]
  • [Cites] Mol Cell. 2000 Oct;6(4):939-45 [11090631.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Nat Struct Mol Biol. 2007 Apr;14(4):295-300 [17401372.001]
  • [Cites] Nature. 2007 Jun 21;447(7147):966-71 [17515920.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Oncogene. 2008 Jan 10;27(3):404-8 [17621273.001]
  • [Cites] J Biol Chem. 2008 Mar 21;283(12):8046-54 [18182388.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Immunity. 2009 Jan 16;30(1):67-79 [19110448.001]
  • [Cites] Mutat Res. 2009 Jan 15;660(1-2):22-32 [19000702.001]
  • [Cites] Cell. 2009 Apr 17;137(2):216-33 [19379690.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4381-90 [19075186.001]
  • [Cites] J Biol Chem. 2009 May 8;284(19):13013-22 [19254953.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6172-81 [19246562.001]
  • [Cites] Genes Dev. 2009 Jul 15;23(14):1665-76 [19605688.001]
  • [Cites] Mol Cell Biol. 2009 Nov;29(21):5679-95 [19704010.001]
  • [Cites] Nature. 2009 Nov 12;462(7270):182-8 [19907488.001]
  • [Cites] J Neurosci. 2010 Feb 3;30(5):1648-56 [20130175.001]
  • [Cites] PLoS One. 2010;5(2):e9094 [20161710.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):5106-11 [20194733.001]
  • [Cites] Cell. 2010 Apr 30;141(3):419-31 [20398922.001]
  • [Cites] Blood. 2010 Dec 16;116(25):5443-54 [20829372.001]
  • [CommentIn] Blood. 2010 Dec 16;116(25):5436-8 [21163932.001]
  • (PMID = 20852131.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Notch1 protein, mouse; 0 / RNA, Messenger; 0 / Receptor, Notch1; 0 / Zfpn1a1 protein, mouse; 128559-51-3 / RAG-1 protein; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3031398
  •  go-up   go-down


71. Ikezoe T, Nishioka C, Bandobashi K, Yang Y, Kuwayama Y, Adachi Y, Takeuchi T, Koeffler HP, Taguchi H: Longitudinal inhibition of PI3K/Akt/mTOR signaling by LY294002 and rapamycin induces growth arrest of adult T-cell leukemia cells. Leuk Res; 2007 May;31(5):673-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Longitudinal inhibition of PI3K/Akt/mTOR signaling by LY294002 and rapamycin induces growth arrest of adult T-cell leukemia cells.
  • This study found that phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling was activated in human T-cell lymphotropic virus type I (HTLV-1)-infected leukemia cells.
  • Rapamycin (1-100 nM, 48h), the inhibitor of mTOR and its analog RAD001 (1-100 nM, 48 h)-induced growth inhibition and G0/G1 cell cycle arrest of these cells in association with de-phosphorylation of p70S6K and 4E-BP-1, although IC50 was not achieved.
  • Blockade of Akt signaling by the PI3K inhibitor LY294002 (1-20 microM, 48 h) also resulted in the growth inhibition and G0/G1 cell cycle arrest of HTLV-1-infected cells, with IC50 ranging from 5 to 20muM, and it caused de-phosphorylation of p70S6K and 4E-BP-1.
  • Of note, when rapamycin was combined with LY294002, rapamycin-induced phosphorylation of Akt was blocked, and the ability of rapamycin to induce growth arrest of HTLV-1-infected T-cells and suppress the p-p70S6K and p-4E-BP-1 proteins was potentiated.
  • Moreover, both LY294002 and rapamycin down-regulated the levels of c-Myc and cyclin D1 proteins in these cells, and their combination further decreased levels of these cell cycle-regulating proteins.
  • Taken together, longitudinal inhibition of PI3K/Akt/mTOR signaling represents a promising treatment strategy for individuals with adult T-cell leukemia.
  • [MeSH-major] Chromones / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein Kinases. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Sirolimus / pharmacology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Cell Cycle / drug effects. Cyclin D. Cyclins / metabolism. Enzyme Inhibitors / pharmacology. Human T-lymphotropic virus 1. Humans. Immunosuppressive Agents / pharmacology. Phosphoproteins / metabolism. Phosphorylation / drug effects. Proto-Oncogene Proteins c-myc / metabolism. Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction / drug effects. T-Lymphocytes / metabolism. T-Lymphocytes / virology. TOR Serine-Threonine Kinases. Tumor Cells, Cultured

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17007924.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Chromones; 0 / Cyclin D; 0 / Cyclins; 0 / EIF4EBP1 protein, human; 0 / Enzyme Inhibitors; 0 / Immunosuppressive Agents; 0 / MYC protein, human; 0 / Morpholines; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins c-myc; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


72. Matsubar Y, Hori T, Morita R, Sakaguchi S, Uchiyama T: Delineation of immunoregulatory properties of adult T-cell leukemia cells. Int J Hematol; 2006 Jul;84(1):63-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Delineation of immunoregulatory properties of adult T-cell leukemia cells.
  • We characterized leukemic cells from 20 adult T-cell leukemia (ATL) cases and 7 ATL-derived cell lines in terms of Foxp3 messenger RNA (mRNA) expression, cytokine production, cell surface markers associated with regulatory T-cells (Treg), and in vitro immunoregulatory activity and compared the results with those of cells from 3 T-cell-type chronic lymphocytic leukemia (T-CLL) patients and normal CD4+ T-cells.
  • Real-time polymerase chain reaction analysis showed that cells from 10 ATL cases, 1 T-CLL case, and 1 ATL cell line had higher Foxp3 mRNA levels than CD4+ T-cells.
  • In 5 ATL cases, Foxp3 levels were comparable to those of CD4+CD25+ T-cells.
  • Flow cytometric analysis revealed that CTLA-4 expression correlated with Foxp3 mRNA level in ATL cells.
  • The cells of all ATL cases examined produced no interleukin 2 or interferon gamma after iono-mycin and phorbolmyristate acetate stimulation.
  • An in vitro inhibition assay showed that the proliferation of normal CD4+CD25- T-cells stimulated with anti-CD3 monoclonal antibody and autologous dendritic cells was significantly suppressed by coculture with Foxp3-high ATL cells.
  • These results indicate that Foxp3 expression is variable in ATL cases and that Foxp3-high ATL cells, which resemble Treg phenotypically as well as functionally, may be involved in immune suppression in ATL.
  • [MeSH-major] Gene Expression Regulation, Leukemic / immunology. Immune Tolerance. Leukemia-Lymphoma, Adult T-Cell / immunology
  • [MeSH-minor] Aged. Cell Line, Tumor. Coculture Techniques. Female. Humans. Male. Middle Aged. T-Lymphocytes, Regulatory / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16867905.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


73. Okudaira T, Tomita M, Uchihara JN, Matsuda T, Ishikawa C, Kawakami H, Masuda M, Tanaka Y, Ohshiro K, Takasu N, Mori N: NIK-333 inhibits growth of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells in association with blockade of nuclear factor-kappaB signal pathway. Mol Cancer Ther; 2006 Mar;5(3):704-12
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NIK-333 inhibits growth of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells in association with blockade of nuclear factor-kappaB signal pathway.
  • Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type I (HTLV-I) and remains incurable.
  • NIK-333, a novel synthetic retinoid, prevents the recurrence of human hepatoma after surgical resection of primary tumors.
  • We explored the effects of NIK-333 on HTLV-I-infected T-cell lines and ATL cells.
  • NIK-333 inhibited cell proliferation, induced G1 arrest, and resulted in massive apoptosis in all tested HTLV-I-infected T-cell lines and ATL cells, whereas little effect was observed on normal peripheral blood mononuclear cells.
  • Further analysis showed that NIK-333 inactivated nuclear factor-kappaB in HTLV-I-infected T-cell lines.
  • In animal studies, treatment with NIK-333 (100 mg/kg given orally every other day) produced partial inhibition of growth of tumors of a HTLV-I-infected T-cell line transplanted s.c. in severe combined immunodeficient mice.
  • Our results indicate that NIK-333 is a potentially useful therapeutic agent for patients with ATL.
  • [MeSH-major] HTLV-I Infections / drug therapy. Human T-lymphotropic virus 1. Leukemia, T-Cell / drug therapy. Leukemia-Lymphoma, Adult T-Cell / drug therapy. NF-kappa B / antagonists & inhibitors. Retinoids / therapeutic use
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Transformed. Cell Line, Tumor. Cyclin D1 / metabolism. Cyclin D2. Cyclins / metabolism. Down-Regulation. Female. Humans. Inhibitor of Apoptosis Proteins / metabolism. Mice. Mice, Inbred Strains. Signal Transduction. T-Lymphocytes / virology. X-Linked Inhibitor of Apoptosis Protein / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16546985.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Inhibitor of Apoptosis Proteins; 0 / NF-kappa B; 0 / Retinoids; 0 / X-Linked Inhibitor of Apoptosis Protein; 11ALM7A4RV / (2E,4E,6E,10E)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid; 136601-57-5 / Cyclin D1
  •  go-up   go-down


74. Przybylski GK, Dik WA, Wanzeck J, Grabarczyk P, Majunke S, Martin-Subero JI, Siebert R, Dölken G, Ludwig WD, Verhaaf B, van Dongen JJ, Schmidt CA, Langerak AW: Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL. Leukemia; 2005 Feb;19(2):201-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Disruption of the BCL11B gene through inv(14)(q11.2q32.31) results in the expression of BCL11B-TRDC fusion transcripts and is associated with the absence of wild-type BCL11B transcripts in T-ALL.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with chromosomal aberrations characterized by juxtaposition of proto-oncogenes to T-cell receptor gene loci (TCR), resulting in the deregulated transcription of these proto-oncogenes.
  • The TRDV1-BCL11B joining region was 1344 bp long and contained fragments derived from 20q11.22, 3p21.33 and from 11p12, indicating the complex character of this aberration.
  • Screening of 37 other T-ALLs revealed one additional case with expression of the BCL11B-TRDC fusion transcript.
  • As BCL11B appears to play a key role in T-cell differentiation, BCL11B disruption and disturbed expression may contribute to the development of T-cell malignancies in man.
  • [MeSH-major] Chromosomes, Human, Pair 11. Chromosomes, Human, Pair 14. Leukemia-Lymphoma, Adult T-Cell / genetics. Translocation, Genetic

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15668700.001).
  • [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 / BCL11B protein, human; 0 / DNA-Binding Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


75. Jeannet R, Mastio J, Macias-Garcia A, Oravecz A, Ashworth T, Geimer Le Lay AS, Jost B, Le Gras S, Ghysdael J, Gridley T, Honjo T, Radtke F, Aster JC, Chan S, Kastner P: Oncogenic activation of the Notch1 gene by deletion of its promoter in Ikaros-deficient T-ALL. Blood; 2010 Dec 16;116(25):5443-54
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The Notch pathway is frequently activated in T-cell acute lymphoblastic leukemias (T-ALLs).
  • Of the Notch receptors, Notch1 is a recurrent target of gain-of-function mutations and Notch3 is expressed in all T-ALLs, but it is currently unclear how these receptors contribute to T-cell transformation in vivo.
  • While deletion of Notch3 has little effect, T cell-specific deletion of floxed Notch1 promoter/exon 1 sequences significantly accelerates leukemogenesis.
  • Further, spontaneous deletion of 5' Notch1 sequences occurs in approximately 75% of Ikaros-deficient T-ALLs.
  • [MeSH-major] Ikaros Transcription Factor / physiology. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Promoter Regions, Genetic / genetics. Receptor, Notch1 / genetics. Transcriptional Activation / physiology
  • [MeSH-minor] Animals. Blotting, Northern. Blotting, Western. Cell Transformation, Neoplastic. DNA Primers / chemistry. DNA Primers / genetics. Flow Cytometry. Gene Expression Regulation, Neoplastic. Immunoglobulin J Recombination Signal Sequence-Binding Protein / physiology. Mice. Mice, Knockout. Mutation / genetics. RNA, Messenger / genetics. Receptors, Notch / physiology. Reverse Transcriptase Polymerase Chain Reaction. Sequence Deletion. Survival Rate

  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell. 2005 Dec 22;20(6):971-8 [16364921.001]
  • [Cites] Mol Cell Biol. 2000 Jun;20(11):3831-42 [10805726.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3891-9 [10845925.001]
  • [Cites] EMBO J. 2000 Jul 3;19(13):3337-48 [10880446.001]
  • [Cites] Immunity. 2000 Jul;13(1):73-84 [10933396.001]
  • [Cites] Nat Immunol. 2001 Mar;2(3):235-41 [11224523.001]
  • [Cites] Genes Dev. 2002 Feb 1;16(3):295-300 [11825871.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3788-93 [11891328.001]
  • [Cites] Int Immunol. 2002 Jun;14(6):637-45 [12039915.001]
  • [Cites] Immunity. 2002 Jun;16(6):869-79 [12121668.001]
  • [Cites] Carcinogenesis. 2003 Jul;24(7):1257-68 [12807718.001]
  • [Cites] Science. 2003 Aug 22;301(5636):1096-9 [12934008.001]
  • [Cites] Genesis. 2003 Nov;37(3):139-43 [14595837.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(2):757-64 [14701747.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4936-41 [15044701.001]
  • [Cites] Immunity. 2004 May;20(5):611-22 [15142529.001]
  • [Cites] Semin Cancer Biol. 2004 Oct;14(5):329-40 [15288258.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2283-91 [8642337.001]
  • [Cites] Mol Cell Biol. 1997 Nov;17(11):6265-73 [9343387.001]
  • [Cites] Immunity. 1999 Mar;10(3):345-55 [10204490.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Cell. 2005 Nov 18;123(4):581-92 [16286007.001]
  • [Cites] Cell. 2005 Nov 18;123(4):593-605 [16286008.001]
  • [Cites] Mol Cell Biol. 2006 Jan;26(1):209-20 [16354692.001]
  • [Cites] Mol Cell. 2007 Jan 12;25(1):31-42 [17218269.001]
  • [Cites] EMBO J. 2007 Mar 21;26(6):1670-80 [17332745.001]
  • [Cites] J Biol Chem. 2007 Oct 12;282(41):30227-38 [17681952.001]
  • [Cites] Lancet. 2008 Mar 22;371(9617):1030-43 [18358930.001]
  • [Cites] J Biol Chem. 2008 Apr 18;283(16):10476-84 [18287091.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Mol Cell Biol. 2008 Dec;28(24):7465-75 [18852286.001]
  • [Cites] Genes Dev. 2009 Jul 15;23(14):1665-76 [19605688.001]
  • [Cites] Bioinformatics. 2009 Aug 1;25(15):1952-8 [19505939.001]
  • [Cites] Leuk Res. 2010 Apr;34(4):426-9 [19796813.001]
  • [Cites] Blood. 2010 Dec 16;116(25):5455-64 [20852131.001]
  • [CommentIn] Blood. 2010 Dec 16;116(25):5436-8 [21163932.001]
  • (PMID = 20829372.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD034883
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Immunoglobulin J Recombination Signal Sequence-Binding Protein; 0 / Notch1 protein, mouse; 0 / Notch3 protein, mouse; 0 / RNA, Messenger; 0 / Rbpj protein, mouse; 0 / Receptor, Notch1; 0 / Receptors, Notch; 0 / Zfpn1a1 protein, mouse; 148971-36-2 / Ikaros Transcription Factor
  • [Other-IDs] NLM/ PMC3100247
  •  go-up   go-down


76. Kannagi M: Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia. Int J Hematol; 2007 Aug;86(2):113-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunologic control of human T-cell leukemia virus type I and adult T-cell leukemia.
  • Host T-cell responses to human T-cell leukemia virus type I (HTLV-I) control the expansion of HTLV-I-infected cells and are determinants of the equilibrium proviral load in vivo.
  • Insufficient T-cell responses are regarded as an immunologic risk factor for adult T-cell leukemia (ATL) because they allow increased proviral loads, which represent an epidemiologic risk factor for ATL.
  • ATL cells from approximately half of ATL cases retain the ability to express HTLV-I Tax, a major target antigen of HTLV-I-specific cytotoxic T-lymphocytes (CTL), whereas Tax-specific CTL in ATL patients are inactive.
  • Tax-specific CTL responses are strongly activated after hematopoietic stem cell transplantation in some ATL patients in long-term remission, indicating that HTLV-I Tax is expressed in vivo rather than being silent, and that the donor-derived T-cell system can recognize it.
  • These findings strongly suggest that reactivation of Tax-specific CTL by vaccines may be promising for prophylaxis of ATL in the high-risk group of HTLV-I carriers and for therapy of ATL in patients whose tumor cells are capable of expressing Tax.
  • [MeSH-major] Human T-lymphotropic virus 1 / immunology. Immunity. Leukemia-Lymphoma, Adult T-Cell / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17875523.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 39
  •  go-up   go-down


77. 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
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • Genetic Alliance. consumer health - Histiocytosis.
  • Genetic Alliance. consumer health - Langerhans cell histiocytosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


78. Indraccolo S, Minuzzo S, Masiero M, Amadori A: Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)? Cell Cycle; 2010 Jan 1;9(1):80-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ligand-driven activation of the notch pathway in T-ALL and solid tumors: why Not(ch)?
  • The Notch pathway is an evolutionally conserved cell-cell interaction signalling system involved in several key aspects of cell life, ranging from differentiation and proliferation to apoptosis.
  • The clearest example of oncogenic Notch signalling is observed in T acute lymphoblastic leukemia (T-ALL), an aggressive neoplasm of immature T-cells, due to genetic alterations leading to ligand-independent increased Notch1 receptor signalling.
  • In solid tumors, however, extrinsic regulation through canonical cell-cell interactions appears to drive activation of the pathway.
  • [MeSH-major] Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Receptors, Notch / metabolism
  • [MeSH-minor] Animals. Humans. Intracellular Signaling Peptides and Proteins. Leukemia / metabolism. Membrane Proteins / metabolism. Models, Biological. Neovascularization, Pathologic / metabolism. Signal Transduction / genetics. Signal Transduction / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20016278.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / delta protein
  •  go-up   go-down


79. Yamasaki M, Mukai A, Ohba M, Mine Y, Sakakibara Y, Suiko M, Morishita K, Nishiyama K: Genistein induced apoptotic cell death in adult T-cell leukemia cells through estrogen receptors. Biosci Biotechnol Biochem; 2010;74(10):2113-5
Hazardous Substances Data Bank. ESTRADIOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genistein induced apoptotic cell death in adult T-cell leukemia cells through estrogen receptors.
  • Adult T-cell leukemia (ATL) occurs in human T-lymphotropic virus type I-infected individuals and is endemic to the southwestern area of Kyushu in Japan.
  • Here, we found that nM levels of genistein and 17β-estradiol had cytotoxic effects on ATL cells and activated caspase-3.
  • In addition, G protein-coupled estrogen receptor agonist G-1 also had a cytotoxic effect on ATL cells.
  • This is the first report suggesting that estrogen receptors are a molecular target for ATL therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Genistein / pharmacology. Leukemia-Lymphoma, Adult T-Cell / pathology. Receptors, Estrogen / metabolism
  • [MeSH-minor] Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Estradiol / analogs & derivatives. Estradiol / pharmacology. Humans

  • Hazardous Substances Data Bank. FULVESTRANT .
  • Hazardous Substances Data Bank. GENISTEIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20944417.001).
  • [ISSN] 1347-6947
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Estrogen; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; DH2M523P0H / Genistein; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


80. Watters KM, Dean J, Gautier V, Hall WW, Sheehy N: Tax 1-independent induction of vascular endothelial growth factor in adult T-cell leukemia caused by human T-cell leukemia virus type 1. J Virol; 2010 May;84(10):5222-8
Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tax 1-independent induction of vascular endothelial growth factor in adult T-cell leukemia caused by human T-cell leukemia virus type 1.
  • Adult T-cell leukemia (ATL) is caused by human T-cell leukemia virus type 1 (HTLV-1).
  • Elevated expression of vascular endothelial growth factor (VEGF) in ATL patients is associated with leukemic cell invasion and infiltration in different organs.
  • The regulatory protein Tax 1 encoded by HTLV-1 plays a pivotal role in T-cell transformation by deregulating the function and expression of several cellular factors.
  • We showed that VEGF was secreted by HTLV-1-transformed and nontransformed cells, irrespective of Tax 1 expression.
  • Overall our data indicate that, contrary to a previous report, Tax 1 downregulates VEGF expression and suggest there are Tax 1-independent mechanisms of VEGF activation in ATL.
  • [MeSH-major] Cell Adhesion Molecules, Neuronal / physiology. Down-Regulation. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / virology. Up-Regulation. Vascular Endothelial Growth Factor A / biosynthesis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8136-45 [10567539.001]
  • [Cites] Mol Cell Biol. 2009 May;29(10):2483-8 [19273606.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2719-26 [11555584.001]
  • [Cites] Anticancer Res. 2001 Jul-Aug;21(4A):2281-6 [11724283.001]
  • [Cites] Semin Oncol. 2001 Dec;28(6):560-4 [11740809.001]
  • [Cites] Am J Physiol Cell Physiol. 2002 Mar;282(3):C578-87 [11832343.001]
  • [Cites] Blood. 2002 May 1;99(9):3383-9 [11964307.001]
  • [Cites] Cancer Chemother Pharmacol. 2002 Dec;50(6):479-89 [12451475.001]
  • [Cites] J Infect Dis. 2003 Apr 1;187(7):1116-25 [12660926.001]
  • [Cites] Neoplasia. 2004 May-Jun;6(3):266-78 [15153339.001]
  • [Cites] Nucleic Acids Res. 2004;32(9):2829-37 [15155851.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Oct;15(5):297-324 [15450248.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048.001]
  • [Cites] Cancer Res. 1985 Sep;45(9 Suppl):4644s-4645s [2861896.001]
  • [Cites] Lancet. 1985 Aug 24;2(8452):407-10 [2863442.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5389-93 [3037548.001]
  • [Cites] Oncogene. 1987;1(3):285-9 [2838779.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11445-9 [1763059.001]
  • [Cites] J Exp Med. 1992 Nov 1;176(5):1375-9 [1402682.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):610-4 [8421695.001]
  • [Cites] J Immunol. 1994 Apr 15;152(8):4149-56 [7511670.001]
  • [Cites] J Biol Chem. 1995 Jan 6;270(1):308-12 [7814392.001]
  • [Cites] Nature. 1995 Jul 6;376(6535):66-70 [7596436.001]
  • [Cites] J Biol Chem. 1996 Jan 12;271(2):736-41 [8557680.001]
  • [Cites] J Biol Chem. 1996 Nov 8;271(45):28220-8 [8910439.001]
  • [Cites] Am J Pathol. 1997 Mar;150(3):815-21 [9060819.001]
  • [Cites] Oncogene. 1997 Aug 7;15(6):669-76 [9264407.001]
  • [Cites] Mol Cell Biol. 1997 Sep;17(9):5629-39 [9271438.001]
  • [Cites] J Biol Chem. 1997 Oct 24;272(43):27411-21 [9341193.001]
  • [Cites] Int J Clin Lab Res. 1998;28(1):55-68 [9594364.001]
  • [Cites] Nature. 1998 Jul 30;394(6692):485-90 [9697772.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Leukemia. 1999 Oct;13(10):1634-5 [10516769.001]
  • [Cites] Oncogene. 2005 Sep 5;24(39):5952-64 [16155602.001]
  • [Cites] Retrovirology. 2006;3:20 [16551350.001]
  • [Cites] RNA Biol. 2005 Jan;2(1):11-3 [17132932.001]
  • [Cites] J Virol. 2007 Feb;81(4):1690-700 [17121800.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):270-80 [17384582.001]
  • [Cites] Biomed Pharmacother. 2007 May;61(4):201-8 [17391906.001]
  • [Cites] Recent Prog Horm Res. 2000;55:15-35; discussion 35-6 [11036931.001]
  • (PMID = 20237090.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CNTN2 protein, human; 0 / Cell Adhesion Molecules, Neuronal; 0 / Contactin 2; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 9007-49-2 / DNA
  • [Other-IDs] NLM/ PMC2863836
  •  go-up   go-down


81. Yasunaga J, Matsuoka M: Human T-cell leukemia virus type I induces adult T-cell leukemia: from clinical aspects to molecular mechanisms. Cancer Control; 2007 Apr;14(2):133-40
SciCrunch. KEGG: Data: Disease Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia virus type I induces adult T-cell leukemia: from clinical aspects to molecular mechanisms.
  • BACKGROUND: Human T-cell leukemia virus type I (HTLV-I) is a causative virus of adult T-cell leukemia (ATL), HTLV-I-associated myelopathy/tropical spastic paraparesis, and HTLV-I-associated uveitis.
  • ATL is a neoplastic disease of CD4-positive T lymphocytes that is characterized by pleomorphic tumor cells with hypersegmented nuclei, termed "flower cells."
  • METHODS: The authors reviewed the virological, clinical, and immunological features of HTLV-I and ATL and summarized recent findings on the oncogenic mechanisms of ATL and therapeutic advances.
  • RESULTS: Multiple factors, such as viral genes, genetic and epigenetic alterations, and the host immune system, may be implicated in the leukemogenesis of ATL.
  • The prognosis of aggressive-type ATL remains poor, regardless of intensive chemotherapy.
  • Effectiveness of allogeneic stem cell transplantation for ATL has been recently reported.
  • CONCLUSIONS: Although the precise mechanism of leukemogenesis of ATL remains unclear, recent progress provides important clues in oncogenesis by HTLV-I.
  • [MeSH-major] CD4-Positive T-Lymphocytes / virology. Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell / virology
  • [MeSH-minor] Adult. Anti-Retroviral Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Gene Expression Regulation, Viral. Genes, pX. Humans. NF-kappa B / antagonists & inhibitors. Viral Proteins / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17387298.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Retroviral Agents; 0 / Antibodies, Monoclonal; 0 / NF-kappa B; 0 / Viral Proteins
  • [Number-of-references] 79
  •  go-up   go-down


82. Nagasaki A, Taira N, Tomoyose T, Miyagi T, Nakachi S, Shinzato O, Hasegawa H, Takasu N: [Development of acute type, CD 8 positive adult T-cell leukemia in a carrier of hepatitis B virus--possible therapeutic effect of lamivudine combined with chemotherapy]. Gan To Kagaku Ryoho; 2006 May;33(5):683-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Development of acute type, CD 8 positive adult T-cell leukemia in a carrier of hepatitis B virus--possible therapeutic effect of lamivudine combined with chemotherapy].
  • Cases of adult T-cell leukemia (ATL) with aberrant phenotypes have a very poor prognosis.
  • We report the development of acute type, CD 8 positive ATL in a carrier of hepatitis B virus (HBV).
  • He was positive for anti-HTLV-1 antibody and HBV surface antigen.
  • Cytological examination of ascitis revealed numerous atypical lymphoid cells,which were positive for CD 2, CD 5, CD 8, and CD 25.
  • Monoclonal integration of HTLV-1 provirus was detected by Southern blot analysis on DNA extracted from lymphoid cells.
  • A diagnosis of acute type, CD 8 positive ATL was made.
  • He maintained clinical remission during a follow-up of 13 months and then relapsed.
  • It is possible that lamivudine combined with chemotherapy may have had a therapeutic effect on ATL in this case.
  • [MeSH-major] Anti-HIV Agents / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. CD8-Positive T-Lymphocytes / immunology. Carrier State / immunology. Hepatitis B / immunology. Lamivudine / administration & dosage. Leukemia-Lymphoma, Adult T-Cell / drug therapy
  • [MeSH-minor] Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Drug Administration Schedule. Etoposide / administration & dosage. HTLV-I Antibodies / immunology. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Nitrosourea Compounds / administration & dosage. Pentostatin / administration & dosage. Prednisone / administration & dosage. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Hepatitis B.
  • MedlinePlus Health Information. consumer health - HIV/AIDS Medicines.
  • Hazardous Substances Data Bank. LAMIVUDINE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. PENTOSTATIN .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16685173.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / HTLV-I Antibodies; 0 / Nitrosourea Compounds; 2T8Q726O95 / Lamivudine; 395575MZO7 / Pentostatin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7673326042 / irinotecan; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; RYH2T97J77 / ranimustine; VB0R961HZT / Prednisone; XT3Z54Z28A / Camptothecin; CHOP protocol
  •  go-up   go-down


83. Fujiwara H, Ozaki A, Yoshimitsu M, Hamada H, Masamoto I, Matsushita K, Yasukawa M, Tei C: Allogeneic stem cell transplantation for refractory adult T-cell leukemia using a non-T-cell-depleted HLA-incompatible family donor graft, with reference to the grown-up child donor to parent recipient setting: report of a pilot study. Int J Hematol; 2008 Apr;87(3):319-26
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Allogeneic stem cell transplantation for refractory adult T-cell leukemia using a non-T-cell-depleted HLA-incompatible family donor graft, with reference to the grown-up child donor to parent recipient setting: report of a pilot study.
  • To increase the availability of alternative stem-cell donors for patients with adult T-cell leukemia (ATL), we examined the feasibility of HLA-incompatible family transplantation, especially from a grown-up child (donor) to a parent (recipient).
  • Since January 2004, seven patients with advanced-phase ATL (three males and four females, median age 59 years), for whom a timely HLA-compatible donor was unavailable, were enrolled.
  • All patients received allografts from their HLA-incompatible sons with reduced-intensity conditioning stem cell transplantation (RIST).
  • Combined graft-versus-host disease (GVHD) prophylaxis involved cyclosporine A or tacrolimus, mycophenolate mofetil or corticosteroid, and short-term methotrexate.
  • Only one patient had grade-IV acute-GVHD, but this was resolved.
  • Four patients died, with causes of death being relapse (n = 2), transplantation-associated microangiopathy (n = 1), and septicemia (n = 1).
  • Three are currently alive: two are in complete remission and one has stable disease.
  • Despite a high rate of relapse, RIST using an allograft from an HLA-incompatible grown-up child donor may be feasible for patients with advanced-phase ATL, and may prolong survival.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, T-Cell / therapy. Lymphocyte Transfusion. Transplantation Conditioning

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18288565.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


84. Asnafi V, Buzyn A, Le Noir S, Baleydier F, Simon A, Beldjord K, Reman O, Witz F, Fagot T, Tavernier E, Turlure P, Leguay T, Huguet F, Vernant JP, Daniel F, Béné MC, Ifrah N, Thomas X, Dombret H, Macintyre E: NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study. Blood; 2009 Apr 23;113(17):3918-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NOTCH1/FBXW7 mutation identifies a large subgroup with favorable outcome in adult T-cell acute lymphoblastic leukemia (T-ALL): a Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL) study.
  • Many somatic genetic abnormalities have been identified in T-cell acute lymphoblastic leukemia (T-ALL) but each individual abnormality accounts for a small proportion of cases; therapeutic stratification consequently still relies on classical clinical markers.
  • We screened 141 adult diagnostic T-ALL samples from patients treated on either the Lymphoblastic Acute Leukemia in Adults (LALA)-94 (n = 87) or the GRAALL-2003 (n = 54) trials.
  • [MeSH-major] Cell Cycle Proteins / genetics. F-Box Proteins / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / classification. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor, Notch1 / genetics. Ubiquitin-Protein Ligases / genetics
  • [MeSH-minor] Adult. Genotype. Humans. Mutation / genetics. Phenotype. Prognosis. Societies, Medical. Survival Rate. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19109228.001).
  • [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 / Cell Cycle Proteins; 0 / F-Box Proteins; 0 / Receptor, Notch1; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  •  go-up   go-down


85. Pancewicz J, Taylor JM, Datta A, Baydoun HH, Waldmann TA, Hermine O, Nicot C: Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia. Proc Natl Acad Sci U S A; 2010 Sep 21;107(38):16619-24
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1-associated adult T-cell leukemia.
  • Human T-cell leukemia virus type 1 (HTLV-I) is the etiological agent of adult T-cell leukemia (ATL).
  • The disease has a dismal prognosis and is invariably fatal.
  • In this study, we report a high frequency of constitutively activated Notch in ATL patients.
  • We found activating mutations in Notch in more than 30% of ATL patients.
  • These activating mutations are phenotypically different from those previously reported in T-ALL leukemias and may represent polymorphisms for activated Notch in human cancers.
  • Compared with the exclusive activating frameshift mutations in the proline, glutamic acid, serine, and threonine (PEST) domain in T-ALLs, those in ATLs have, in addition, single-substitution mutations in this domain leading to reduced CDC4/Fbw7-mediated degradation and stabilization of the intracellular cleaved form of Notch1 (ICN1).
  • Finally, we demonstrated that inhibition of Notch signaling by γ-secretase inhibitors reduced tumor cell proliferation and tumor formation in ATL-engrafted mice.
  • These data suggest that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for therapeutic intervention in ATL patients.

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Cell Cycle. 2005 Oct;4(10):1356-9 [16131838.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Blood. 2007 Jul 1;110(1):278-86 [17363738.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1813-24 [17646409.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2205-11 [17657714.001]
  • [Cites] Nat Med. 2007 Oct;13(10):1203-10 [17873882.001]
  • [Cites] Oncogene. 2007 Oct 15;26(47):6838-49 [17934490.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):83-93 [18094723.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2220-9 [18039953.001]
  • [Cites] Nat Rev Immunol. 2008 May;8(5):380-90 [18421304.001]
  • [Cites] Oncogene. 2008 Sep 1;27(38):5148-67 [18758484.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3181-94 [18677410.001]
  • [Cites] Nat Med. 2009 Jan;15(1):50-8 [19098907.001]
  • [Cites] J Clin Oncol. 2009 Jan 20;27(3):453-9 [19064971.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6172-81 [19246562.001]
  • [Cites] Nat Genet. 2000 Dec;26(4):484-9 [11101851.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34371-8 [11425854.001]
  • [Cites] Cancer Biol Ther. 2002 Jul-Aug;1(4):337-41 [12432242.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] Blood. 2004 Sep 15;104(6):1696-702 [15187027.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9265-73 [15485896.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131.001]
  • [Cites] J Exp Med. 1985 Dec 1;162(6):2169-74 [2866223.001]
  • [Cites] Science. 1995 Jul 7;269(5220):79-81 [7604283.001]
  • [Cites] Nature. 1995 Sep 28;377(6547):355-8 [7566092.001]
  • [Cites] Science. 1999 Apr 30;284(5415):770-6 [10221902.001]
  • [Cites] Oncogene. 2005 Sep 22;24(42):6333-44 [15940249.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3043-9 [16707600.001]
  • (PMID = 20823234.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA106258; United States / NCI NIH HHS / CA / R01 CA115398; United States / NCI NIH HHS / CA / CA106258; United States / NCI NIH HHS / CA / CA115398
  • [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 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / F-Box Proteins; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 6.3.2.19 / FBXW7 protein, human; EC 6.3.2.19 / Ubiquitin-Protein Ligases
  • [Other-IDs] NLM/ PMC2944748
  •  go-up   go-down


86. Duc Dodon M, Mesnard JM, Barbeau B: [Adult T-cell leukemia induced by HTLV-1: before and after HBZ]. Med Sci (Paris); 2010 Apr;26(4):391-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adult T-cell leukemia induced by HTLV-1: before and after HBZ].
  • [Transliterated title] Leucémies T induites par HTLV-1 : y a-t-il un avant et un après HBZ ?
  • Adult T-cell leukemia (ATL) is an often fatal leukemia of CD4+ T lymphocytes associated with a complex retrovirus, human T-cell leukemia virus type 1 (HTLV-1).
  • In 2002, we described the characterization of a novel viral protein that we have termed HBZ for HTLV-1 bZIP factor.
  • This viral factor is encoded on the antisense strand of HTLV-1 proviral DNA, demonstrating the existence of antisense transcription from a promoter located in the 3' LTR.
  • [MeSH-major] Basic-Leucine Zipper Transcription Factors / physiology. Cell Transformation, Viral / genetics. Gene Expression Regulation, Viral. Human T-lymphotropic virus 1 / physiology. Leukemia-Lymphoma, Adult T-Cell / virology. Viral Proteins / physiology
  • [MeSH-minor] Activating Transcription Factors / metabolism. Animals. Cell Division. Cyclic AMP Response Element-Binding Protein / metabolism. Gene Products, tax / metabolism. Genes, pX. Humans. Leucine Zippers / genetics. Leucine Zippers / physiology. Models, Genetic. Promoter Regions, Genetic / genetics. Proviruses / genetics. RNA, Small Interfering / pharmacology. Rabbits. Terminal Repeat Sequences / genetics. Transcription, Genetic / drug effects. Transcription, Genetic / genetics. p300-CBP Transcription Factors / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20412744.001).
  • [ISSN] 0767-0974
  • [Journal-full-title] Médecine sciences : M/S
  • [ISO-abbreviation] Med Sci (Paris)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Activating Transcription Factors; 0 / Basic-Leucine Zipper Transcription Factors; 0 / CREB1 protein, human; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Gene Products, tax; 0 / HBZ protein, human T-cell leukemia virus type I; 0 / RNA, Small Interfering; 0 / Viral Proteins; 0 / tax protein, Human T-lymphotrophic virus 1; EC 2.3.1.48 / p300-CBP Transcription Factors
  • [Number-of-references] 31
  •  go-up   go-down


87. Kawahara M, Hori T, Matsubara Y, Okawa K, Uchiyama T: Cyclin-dependent kinaselike 5 is a novel target of immunotherapy in adult T-cell leukemia. J Immunother; 2007 Jul-Aug;30(5):499-505
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclin-dependent kinaselike 5 is a novel target of immunotherapy in adult T-cell leukemia.
  • In the present study, we attempted a comprehensive analysis of human leukocyte antigen (HLA) class I-bound peptides presented on adult T-cell leukemia (ATL) cells by the latest technology of mass spectrometry combined with reversed phase liquid chromatography (LC/MS) to identify novel tumor-associated antigens.
  • Then, we narrowed down the candidate peptides according to the differential expression of their source proteins between ATL cells and normal CD4 T cells.
  • Among these candidates, we focused on cyclin-dependent kinaselike 5 (CDKL5) because it was highly expressed in several ATL cell lines and some ATL clinical samples but not in normal CD4 T cells.
  • To examine its immunogenicity, we stimulated CD8 T cells from an HLA-B62 healthy donor several times with autologous monocyte-derived dendritic cells loaded with HLA-B*62-restricted CDKL5 peptide1012-1021 QVNQAALLTY that we identified.
  • CDKL5-stimulated bulk CD8 T cells exerted higher cytotoxicity against CDKL5 peptide-loaded autologous Epstein Barr virus-transformed B cell line (LCL) than against unloaded LCL.
  • Furthermore these T cells had strong cytotoxic activity against HLA-B*62-positive CDKL5-positive but not HLA-B*62-negative CDKL5-positive ATL cells.
  • These results demonstrate that CDKL5 is a novel tumor (leukemia) antigen in ATL and that the HLA-B*62-restricted CDKL5 peptide can be used for cytotoxic T-lymphocyte-mediated immunotherapy.
  • Identification of tumor-associated antigens by LC/MS is an eligible and efficient method suitable for future taylor-made immunotherapy of hematologic malignancies.
  • [MeSH-major] Antigens, Neoplasm / immunology. Histocompatibility Antigens Class I / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Peptides / analysis. Protein-Serine-Threonine Kinases / immunology
  • [MeSH-minor] B-Lymphocytes. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. CD8-Positive T-Lymphocytes / immunology. Cell Line. Cell Line, Transformed. Cell Line, Tumor. Chromatography, Liquid. Cytotoxicity, Immunologic. Dendritic Cells / immunology. HLA-B Antigens / immunology. Herpesvirus 4, Human. Humans. Immunotherapy. Mass Spectrometry. Oligopeptides / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17589290.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA-B Antigens; 0 / Histocompatibility Antigens Class I; 0 / Oligopeptides; 0 / Peptides; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.22 / CDKL5 protein, human
  •  go-up   go-down


88. Nakamura M, Hamasaki T, Tokitou M, Baba M, Hashimoto Y, Aoyama H: Discovery of tetrahydrotetramethylnaphthalene analogs as adult T-cell leukemia cell-selective proliferation inhibitors in a small chemical library constructed based on multi-template hypothesis. Bioorg Med Chem; 2009 Jul 1;17(13):4740-6
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Discovery of tetrahydrotetramethylnaphthalene analogs as adult T-cell leukemia cell-selective proliferation inhibitors in a small chemical library constructed based on multi-template hypothesis.
  • Adult T cell leukemia (ATL), caused by infection of human T-lymphotropic virus type 1 (HTLV-1), has a poor prognosis and curative therapy is unavailable, so it is important to find or design superior lead compounds for the drug treatment of ATL.
  • We used our micro-reversed fragment-based drug design hypothesis and multi-template hypothesis to extract the tetrahydrotetramethylnaphthalene (TMN) skeleton from tamibarotene, a useful medicament for the treatment of acute promyelocytic leukemia (APL).
  • Structural development of TMN yielded highly ATL cell-selective growth inhibitors, including 2-acetyl-3-hydroxy-5,6,7,8-tetrahydro-5,5,8,8-tetramethylnaphthalene (6).
  • Structure-activity relationship analysis suggests the existence of a specific target molecule for ATL cell-selective inhibition of proliferation through G2 arrest.
  • [MeSH-major] Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Leukemia-Lymphoma, Adult T-Cell / drug therapy. Tetrahydronaphthalenes / chemistry. Tetrahydronaphthalenes / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Drug Design. Human T-lymphotropic virus 1 / isolation & purification. Humans. Models, Molecular. Molecular Structure. Retinoids. Small Molecule Libraries. Structure-Activity Relationship. T-Lymphocytes / cytology. T-Lymphocytes / virology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19443225.001).
  • [ISSN] 1464-3391
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Retinoids; 0 / Small Molecule Libraries; 0 / Tetrahydronaphthalenes
  •  go-up   go-down


89. Takizawa J, Aoki S, Kurasaki T, Higashimura M, Honma K, Kitajima T, Momoi A, Takahashi H, Nakamura N, Furukawa T, Aizawa Y: Successful treatment of adult T-cell leukemia with unrelated cord blood transplantation. Am J Hematol; 2007 Dec;82(12):1113-5
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful treatment of adult T-cell leukemia with unrelated cord blood transplantation.
  • This study reports the first well-documented case of adult T-cell leukemia (ATL) successfully treated with unrelated cord blood transplantation (UCBT).
  • A 49-year-old woman was diagnosed with acute-type of ATL.
  • Chemotherapy induced complete remission, but the human T-cell leukemia virus type 1 (HTLV-1) proviral load was detected in mononuclear cells of her peripheral blood.
  • She remains in remission 30 months after UCBT and the HTLV-1 proviral load has fallen to undetectable levels.
  • This result suggests that UCBT should be a therapeutic option for ATL patients who do not have suitable donors and those who urgently require treatment.
  • [MeSH-major] Cord Blood Stem Cell Transplantation / methods. Leukemia-Lymphoma, Adult T-Cell / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17696205.001).
  • [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 / HLA Antigens
  •  go-up   go-down


90. Calzavara E, Chiaramonte R, Cesana D, Basile A, Sherbet GV, Comi P: Reciprocal regulation of Notch and PI3K/Akt signalling in T-ALL cells in vitro. J Cell Biochem; 2008 Apr 1;103(5):1405-12
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our analyses indicate that the PI3K/Akt pathway is constitutively active in the four T-ALL cell lines tested.
  • PTEN expression was not detected in 3/4 cell lines tested, suggesting the loss of PTEN-mediated Akt activation.
  • We analysed the relationship between Notch-1 and the PI3K/Akt signalling and show that inhibition of the Akt pathway changes Notch expression; Notch-1 protein decreased in all the cell lines upon treatment with the inhibitor.
  • [MeSH-major] Phosphatidylinositol 3-Kinases / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / metabolism. Signal Transduction
  • [MeSH-minor] Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Leukemic / drug effects. Humans. Jurkat Cells. PTEN Phosphohydrolase / metabolism. bcl-2-Associated X Protein / metabolism. ras Proteins / antagonists & inhibitors. ras Proteins / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2007 Wiley-Liss, Inc.
  • (PMID = 17849443.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 0 / bcl-2-Associated X Protein; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


91. Gu L, Zhou C, Liu H, Gao J, Li Q, Mu D, Ma Z: Rapamycin sensitizes T-ALL cells to dexamethasone-induced apoptosis. J Exp Clin Cancer Res; 2010;29:150
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Glucocorticoid (GC) resistance is frequently seen in acute lymphoblastic leukemia of T-cell lineage (T-ALL).
  • METHODS: Cell proliferation was detected by 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) assay.
  • Fluorescence-activated cell sorting (FACS) analysis was used to analyze apoptosis and cell cycles.
  • Western blot analysis was performed to test the expression of the downstream effector proteins of mammalian target of rapamycin (mTOR), the cell cycle regulatory proteins, and apoptosis associated proteins.
  • Cell cycle arrest was associated with modulation of G1-S phase regulators.
  • CONCLUSION: Our data suggests that rapamycin can effectively reverse GC resistance in T-ALL and this effect is achieved by inducing cell cycles arrested at G0/G1 phase and activating the intrinsic apoptotic program.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Dexamethasone / pharmacology. Drug Resistance, Neoplasm / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Sirolimus / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Separation. Drug Synergism. Flow Cytometry. Humans

  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2008 Jan;22(1):124-31 [17928886.001]
  • [Cites] Cancer Cell. 2007 Jul;12(1):9-22 [17613433.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2091-6 [18685609.001]
  • [Cites] J Clin Oncol. 2009 May 1;27(13):2278-87 [19332717.001]
  • [Cites] Br J Haematol. 2009 Jun;145(5):569-80 [19344392.001]
  • [Cites] Pediatr Blood Cancer. 2009 Dec;53(6):984-91 [19621425.001]
  • [Cites] Semin Oncol. 2009 Dec;36 Suppl 3:S3-S17 [19963098.001]
  • [Cites] Leukemia. 2010 Feb;24(2):265-84 [20010625.001]
  • [Cites] Clin Cancer Res. 2001 Aug;7(8):2168-81 [11489790.001]
  • [Cites] Clin Cancer Res. 2002 Jun;8(6):1681-94 [12060604.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3138-47 [15070696.001]
  • [Cites] Ann Hematol. 2004;83 Suppl 1:S121-3 [15124702.001]
  • [Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 2):4270s-4275s [15217973.001]
  • [Cites] J Leukoc Biol. 2004 Jul;76(1):7-14 [15075361.001]
  • [Cites] Cell Death Differ. 2004 Jul;11 Suppl 1:S65-72 [15017388.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1926-45 [15314020.001]
  • [Cites] J Antibiot (Tokyo). 1975 Oct;28(10):721-6 [1102508.001]
  • [Cites] Leuk Lymphoma. 1994 Apr;13(3-4):187-201 [8049644.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):525-37 [15728109.001]
  • [Cites] Blood. 2005 Jul 1;106(1):274-86 [15774621.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1801-7 [15886325.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2305-13 [16489035.001]
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6589-97 [16818631.001]
  • [Cites] Ann N Y Acad Sci. 2006 Jun;1069:1-9 [16855130.001]
  • [Cites] Blood. 2006 Aug 1;108(3):1045-9 [16574952.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):331-42 [17010674.001]
  • [Cites] Am J Pathol. 2006 Dec;169(6):2171-80 [17148679.001]
  • [Cites] Cancer Treat Rev. 2007 Feb;33(1):78-84 [17161912.001]
  • [Cites] Curr Opin Hematol. 2008 Mar;15(2):88-94 [18300753.001]
  • (PMID = 21083937.001).
  • [ISSN] 1756-9966
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7S5I7G3JQL / Dexamethasone; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC2998469
  •  go-up   go-down


92. Matsuoka M: Human T-cell leukemia virus type I (HTLV-I) infection and the onset of adult T-cell leukemia (ATL). Retrovirology; 2005;2:27

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Human T-cell leukemia virus type I (HTLV-I) infection and the onset of adult T-cell leukemia (ATL).
  • The clinical entity of adult T-cell leukemia (ATL) was established around 1977, and human T-cell leukemia virus type 1 (HTLV-I) was subsequently identified in 1980.
  • In the 25 years since the discovery of HTLV-I, HTLV-I infection and its associated diseases have been extensively studied, and many of their aspects have been clarified.
  • However, the detailed mechanism of leukemogenesis remains unsolved yet, and the prognosis of ATL patients still poor because of its resistance to chemotherapy and immunodeficiency.
  • In this review, I highlight the recent progress and remaining enigmas in HTLV-I infection and its associated diseases, especially ATL.
  • [MeSH-major] Human T-lymphotropic virus 1 / pathogenicity. Leukemia-Lymphoma, Adult T-Cell
  • [MeSH-minor] Adult. Female. Humans. Infant, Newborn. Virus Replication

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2004 Oct 15;279(42):43998-4004 [15308664.001]
  • [Cites] Blood. 1977 Sep;50(3):481-92 [301762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654.001]
  • [Cites] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725.001]
  • [Cites] Oncogene. 1999 Jun 24;18(25):3766-72 [10391685.001]
  • [Cites] Oncogene. 1999 Jul 15;18(28):4137-43 [10435595.001]
  • [Cites] J Virol. 1999 Oct;73(10):7981-7 [10482545.001]
  • [Cites] J Obstet Gynaecol Res. 2004 Dec;30(6):436-8 [15566458.001]
  • [Cites] Clin Cancer Res. 2004 Nov 15;10(22):7529-39 [15569983.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):63-8 [15623561.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1204-13 [15471956.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):419-30 [15543232.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):1001-10 [15592508.001]
  • [Cites] Blood. 2005 May 15;105(10):4143-5 [15665110.001]
  • [Cites] Int J Cancer. 2005 Jul 20;115(6):967-74 [15729715.001]
  • [Cites] J Virol. 2005 Jul;79(14):9346-50 [15994832.001]
  • [Cites] Retrovirology. 2004;1:20 [15310405.001]
  • [Cites] Retrovirology. 2005;2:17 [15743526.001]
  • [Cites] Retrovirology. 2005;2:16 [15743528.001]
  • [Cites] J Exp Med. 1999 Dec 20;190(12):1741-54 [10601350.001]
  • [Cites] Blood. 2000 Jan 1;95(1):30-8 [10607681.001]
  • [Cites] J Emerg Med. 2000 Jan;18(1):109-19 [10645850.001]
  • [Cites] Int J Cancer. 2000 Feb 1;85(3):319-24 [10652420.001]
  • [Cites] Annu Rev Genet. 1999;33:29-55 [10690403.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):1043-8 [10706122.001]
  • [Cites] Oncogene. 2000 Mar 16;19(12):1491-9 [10734308.001]
  • [Cites] Mol Cell Biol. 2000 May;20(10):3377-86 [10779327.001]
  • [Cites] Blood. 2000 Jul 1;96(1):275-81 [10891462.001]
  • [Cites] Immunity. 2000 Nov;13(5):657-64 [11114378.001]
  • [Cites] Blood. 2001 Feb 15;97(4):987-93 [11159527.001]
  • [Cites] Annu Rev Immunol. 2001;19:475-96 [11244044.001]
  • [Cites] Bone Marrow Transplant. 2001 Jan;27(1):15-20 [11244433.001]
  • [Cites] Blood. 2001 Apr 1;97(7):2137-44 [11264182.001]
  • [Cites] Mol Biol Evol. 2001 Apr;18(4):661-71 [11264418.001]
  • [Cites] Int J Cancer. 2001 Mar 15;91(6):869-75 [11275994.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3770-4 [11325850.001]
  • [Cites] Blood. 2001 May 15;97(10):3177-83 [11342446.001]
  • [Cites] Br J Haematol. 2001 May;113(2):375-82 [11380402.001]
  • [Cites] Proc Biol Sci. 2001 Jun 22;268(1473):1215-21 [11410146.001]
  • [Cites] Blood. 2001 Aug 15;98(4):1200-8 [11493471.001]
  • [Cites] Oncogene. 2001 Jul 27;20(33):4484-96 [11494144.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 5;93(23):1775-83 [11734593.001]
  • [Cites] Blood. 2002 Jan 15;99(2):634-40 [11781248.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1505-11 [11861261.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):1083-6 [11861386.001]
  • [Cites] J Virol. 2002 Mar;76(6):2648-53 [11861831.001]
  • [Cites] J Infect Dis. 2002 Mar 1;185(5):691-5 [11865428.001]
  • [Cites] Clin Infect Dis. 2002 Jun 15;34(12):1551-7 [12032888.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1481-93 [1540956.001]
  • [Cites] Blood. 1992 Dec 15;80(12):3205-16 [1361372.001]
  • [Cites] Cancer. 1993 Aug 1;72(3):735-40 [8101469.001]
  • [Cites] Virology. 1993 Sep;196(1):25-33 [8356797.001]
  • [Cites] Blood. 1993 Sep 15;82(6):1701-12 [8400227.001]
  • [Cites] Int J Cancer. 1994 Feb 1;56(3):337-40 [8314320.001]
  • [Cites] Leukemia. 1995 Apr;9(4):598-604 [7723391.001]
  • [Cites] Blood. 1995 May 15;85(10):2699-704 [7742529.001]
  • [Cites] Blood. 1995 Sep 1;86(5):1924-30 [7655021.001]
  • [Cites] Blood. 1995 Dec 1;86(11):4063-75 [7492762.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1828-34 [12176906.001]
  • [Cites] J Virol. 2002 Sep;76(18):9389-97 [12186921.001]
  • [Cites] J Biol Chem. 2002 Sep 13;277(37):33766-75 [12097320.001]
  • [Cites] J Infect Dis. 2002 Oct 1;186(7):932-9 [12232833.001]
  • [Cites] Cancer Causes Control. 2002 Sep;13(7):657-63 [12296513.001]
  • [Cites] Science. 2003 Mar 14;299(5613):1713-6 [12589003.001]
  • [Cites] Immunol Rev. 2003 Jun;193:58-69 [12752671.001]
  • [Cites] Blood. 2003 Jul 1;102(1):284-8 [12649132.001]
  • [Cites] Oncogene. 2003 Aug 11;22(33):5131-40 [12910250.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43620-7 [12937177.001]
  • [Cites] Transpl Int. 1992;5 Suppl 1:S450-3 [14621843.001]
  • [Cites] Cell. 2003 Nov 14;115(4):449-59 [14622599.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):280-96 [14686485.001]
  • [Cites] Int J Hematol. 2003 Nov;78(4):297-303 [14686486.001]
  • [Cites] J Biol Chem. 2004 Jan 2;279(1):495-508 [14530271.001]
  • [Cites] Cancer. 1984 Jul 1;54(1):131-4 [6609759.001]
  • [Cites] Lancet. 1984 May 26;1(8387):1183-4 [6144909.001]
  • [Cites] Vox Sang. 1984;46(5):245-53 [6328765.001]
  • [Cites] Cancer. 1985 Jan 1;55(1):181-5 [2981140.001]
  • [Cites] Cancer. 1985 Oct 1;56(7):1688-90 [2992744.001]
  • [Cites] Lancet. 1986 May 3;1(8488):1031-2 [2871307.001]
  • [Cites] Cancer. 1987 Mar 15;59(6):1187-91 [2880656.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3653-7 [3035544.001]
  • [Cites] Cancer Res. 1989 Jul 15;49(14):3849-52 [2544261.001]
  • [Cites] Jpn J Ophthalmol. 1989;33(4):472-81 [2576286.001]
  • [Cites] J Exp Med. 1990 Sep 1;172(3):759-65 [2388034.001]
  • [Cites] Lancet. 1990 Dec 1;336(8727):1345-7 [1978165.001]
  • [Cites] Int Immunol. 1991 Aug;3(8):761-7 [1911545.001]
  • [Cites] Leuk Res. 1991;15(9):837-46 [1656151.001]
  • [Cites] Blood. 1992 Jan 15;79(2):477-80 [1730092.001]
  • [Cites] EMBO J. 1996 Feb 15;15(4):873-87 [8631308.001]
  • [Cites] Jpn J Cancer Res. 1996 Mar;87(3):227-31 [8613423.001]
  • [Cites] EMBO J. 1996 Apr 1;15(7):1607-14 [8612584.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2185-95 [8642328.001]
  • [Cites] Br J Haematol. 1996 Sep;94(4):713-5 [8826899.001]
  • [Cites] Blood. 1996 Oct 15;88(8):3065-73 [8874205.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4862-7 [9354450.001]
  • [Cites] J Biol Chem. 1998 Mar 20;273(12):6698-703 [9506967.001]
  • [Cites] Cell. 1998 Apr 3;93(1):81-91 [9546394.001]
  • [Cites] Blood. 1998 May 15;91(10):3935-42 [9573032.001]
  • [Cites] Mol Cell Biol. 1998 Jul;18(7):3744-51 [9632757.001]
  • [Cites] Oncogene. 1998 Jul 9;17(1):77-82 [9671316.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3557-61 [9808547.001]
  • [Cites] Nat Med. 1999 Jan;5(1):11-2 [9883827.001]
  • [Cites] Nature. 1999 Feb 4;397(6718):436-41 [9989410.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3848-53 [10097126.001]
  • [Cites] J Exp Med. 1999 Apr 5;189(7):1063-71 [10190897.001]
  • [Cites] Int J Cancer. 1999 Jun 11;81(6):859-64 [10362130.001]
  • [Cites] Cancer Res. 2004 Jan 1;64(1):391-9 [14729650.001]
  • [Cites] Nat Med. 2004 Feb;10(2):197-201 [14730358.001]
  • [Cites] Virology. 2004 Jan 5;318(1):327-36 [14972558.001]
  • [Cites] Int J Cancer. 2004 Apr 20;109(4):559-67 [14991578.001]
  • [Cites] Mol Biol Evol. 2004 Mar;21(3):603-11 [14739252.001]
  • [Cites] Blood. 2004 Apr 1;103(7):2753-60 [14656887.001]
  • [Cites] Int J Cancer. 2004 Jul 1;110(4):621-5 [15122598.001]
  • [Cites] Br J Haematol. 2004 Jul;126(1):81-4 [15198736.001]
  • [Cites] Trends Microbiol. 2004 Jul;12(7):346-52 [15223062.001]
  • [Cites] Blood. 2004 Aug 1;104(3):802-9 [15090453.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1357-63 [15190257.001]
  • [Cites] J Biol Chem. 2004 Jul 30;279(31):31991-4 [15090550.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6002-9 [15342380.001]
  • [Cites] J Infect Dis. 2004 Oct 1;190(7):1275-8 [15346338.001]
  • [Cites] J Immunol. 2004 Oct 15;173(8):5121-9 [15470056.001]
  • (PMID = 15854229.001).
  • [ISSN] 1742-4690
  • [Journal-full-title] Retrovirology
  • [ISO-abbreviation] Retrovirology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 129
  • [Other-IDs] NLM/ PMC1131926
  •  go-up   go-down


93. Sulis ML, Williams O, Palomero T, Tosello V, Pallikuppam S, Real PJ, Barnes K, Zuurbier L, Meijerink JP, Ferrando AA: NOTCH1 extracellular juxtamembrane expansion mutations in T-ALL. Blood; 2008 Aug 1;112(3):733-40
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Heterodimerization domain (HD) mutations in NOTCH1 induce ligand-independent activation of the receptor and contribute to the pathogenesis of one-third of human T-cell lymphoblastic leukemias (T-ALLs).
  • Here we report a novel class of activating mutations in NOTCH1 leading to aberrant activation of NOTCH1 signaling in T-cell lymphoblasts.
  • Notably, structure-function analysis of leukemia-derived and synthetic JME mutants demonstrated that the aberrant activation of NOTCH1 signaling is dependent on the number of residues introduced in the extracellular juxtamembrane region of the receptor and not on the specific amino acid sequence of these insertions.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Opin Immunol. 2000 Apr;12(2):166-72 [10712939.001]
  • [Cites] Annu Rev Pathol. 2008;3:587-613 [18039126.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):197-206 [10882062.001]
  • [Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]
  • [Cites] Immunity. 2001 Mar;14(3):253-64 [11290335.001]
  • [Cites] J Exp Med. 2001 Oct 1;194(7):991-1002 [11581320.001]
  • [Cites] Immunity. 2002 Jun;16(6):869-79 [12121668.001]
  • [Cites] J Immunol. 2002 Aug 15;169(4):1817-21 [12165504.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):203-5 [12676578.001]
  • [Cites] Semin Immunol. 2003 Apr;15(2):69-79 [12681943.001]
  • [Cites] J Exp Med. 2004 Aug 16;200(4):469-79 [15314075.001]
  • [Cites] Science. 2004 Oct 8;306(5694):269-71 [15472075.001]
  • [Cites] Cell. 1991 Aug 23;66(4):649-61 [1831692.001]
  • [Cites] Cell. 1996 Nov 1;87(3):483-92 [8898201.001]
  • [Cites] Cell. 1997 Mar 21;88(6):833-43 [9118226.001]
  • [Cites] Development. 1997 Dec;124(23):4759-67 [9428412.001]
  • [Cites] Genes Dev. 1998 Jun 15;12(12):1751-62 [9637676.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8108-12 [9653148.001]
  • [Cites] Science. 1999 Jan 1;283(5398):91-4 [9872749.001]
  • [Cites] Nature. 1999 Apr 8;398(6727):522-5 [10206646.001]
  • [Cites] Immunity. 1999 May;10(5):547-58 [10367900.001]
  • [Cites] Immunity. 1999 Sep;11(3):299-308 [10514008.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):314-22 [15665828.001]
  • [Cites] Cell. 2005 Aug 12;122(3):435-47 [16096062.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):347-59 [16612405.001]
  • [Cites] Mol Cell Biol. 2006 Jun;26(12):4642-51 [16738328.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1279-87 [16688224.001]
  • [Cites] Blood. 2006 Aug 15;108(4):1151-7 [16614245.001]
  • [Cites] Nat Struct Mol Biol. 2007 Apr;14(4):295-300 [17401372.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1825-35 [17646408.001]
  • [Cites] Nucleic Acids Res. 2008 Jan;36(Database issue):D25-30 [18073190.001]
  • [CommentIn] Blood. 2008 Aug 1;112(3):457-8 [18650457.001]
  • (PMID = 18411416.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA120196-03; United States / NCI NIH HHS / CA / R01 CA120196; United States / NCI NIH HHS / CA / CA120196; 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 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2481531
  •  go-up   go-down


94. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
MedlinePlus Health Information. consumer health - Neurofibromatosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.
  • Neurofibromatosis type 1 (NF1) is an autosomal dominant genetic disorder caused by mutations in the NF1 gene.
  • Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).
  • In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.
  • However, our patients lacked clinical NF1 symptoms.
  • Mutation analysis in 4 of these del(17)(q11.2)-positive patients revealed that mutations in the remaining NF1 allele were present in 3 patients, confirming its role as a tumor-suppressor gene in cancer.
  • NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

  • Genetic Alliance. consumer health - Neurofibromatosis.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18172006.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger
  •  go-up   go-down


95. Kubuki Y, Suzuki M, Sasaki H, Toyama T, Yamashita K, Maeda K, Ido A, Matsuoka H, Okayama A, Nakanishi T, Tsubouchi H: Telomerase activity and telomere length as prognostic factors of adult T-cell leukemia. Leuk Lymphoma; 2005 Mar;46(3):393-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase activity and telomere length as prognostic factors of adult T-cell leukemia.
  • In this study, clinical data and disease outcomes were analyzed in conjunction with the telomerase activity (TA) and telomere length (TL) of peripheral blood mononuclear cells.
  • The study was carried out in 22 patients with adult T-cell leukemia (ATL) (7 chronic and 15 acute types) and in 13 asymptomatic human T-lymphotropic virus type 1 (HTLV-1) carriers.
  • The mean values of TA in acute and chronic type patients were 13.8 and 1.6 total product generated (TPG) units, respectively, as determined by telomeric repeat amplification assays.
  • The mean TA values in HTLV-1 carriers and healthy volunteers were 1.8 and 0.7 TPG, respectively.
  • The mean TA value in acute type patients was significantly higher than in the three other subject groups.
  • The mean TL values in patients with acute and chronic types were 5.39 and 4.38 Kb, respectively, while the mean TL values in HTLV-1 carriers and healthy volunteers were 7.69 and 7.06 Kb, respectively.
  • The mean TL values in all ATL patients and in non-ATL subjects were 5.2 and 7.3 Kb, respectively.
  • Neither TA nor TL of ATL cells showed any significant association with the number of ATL cells, serum soluble interleukin-2 receptor, or serum lactate dehydrogenase in the peripheral blood of acute type patients.
  • This suggests that the levels of TA and TL did not reflect the ATL tumor load.
  • The median survival period of acute ATL patients with high TA and shortened TL was 0.47 years, however, which was significantly shorter than that of acute ATL patients with low TA and normal TL (4.21 years) (p < 0.002).
  • These data suggest that high TA and shortened TL were associated with poorer prognosis, and that TA and TL may be novel markers for the prognosis of ATL patients.
  • [MeSH-major] HTLV-I Infections / enzymology. Leukemia-Lymphoma, Adult T-Cell / enzymology. Telomerase / metabolism. Telomere / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Leukocytes, Mononuclear / chemistry. Leukocytes, Mononuclear / enzymology. Male. Middle Aged. Prognosis. Prospective Studies. Restriction Mapping. Serologic Tests. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15621829.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.7.49 / Telomerase
  •  go-up   go-down


96. Xu SN, Chen JP: [Research advance on the pathogenesis of T-ALL induced by notch 1 activating mutations]. Zhongguo Shi Yan Xue Ye Xue Za Zhi; 2010 Feb;18(1):242-5
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • T-cell acute lymphoblastic leukemia (T-ALL) is the hematological malignancy of bone marrow characterized by the rapid proliferation and subsequent accumulation of immature T lymphocyte and mainly occurs in children and adolescents.
  • This review briefly discusses the four main subtypes of Notch 1 activating mutations, also focuses on how these mutations change the normal signaling pathways and genes expression during their participation in the pathogenesis of T-ALL, and how these insights will promote the development of newly targeting therapies for patients with this aggressive form of leukemia.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20137156.001).
  • [ISSN] 1009-2137
  • [Journal-full-title] Zhongguo shi yan xue ye xue za zhi
  • [ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Receptor, Notch1
  •  go-up   go-down


97. Kozako T, Arima N, Toji S, Masamoto I, Akimoto M, Hamada H, Che XF, Fujiwara H, Matsushita K, Tokunaga M, Haraguchi K, Uozumi K, Suzuki S, Takezaki T, Sonoda S: Reduced frequency, diversity, and function of human T cell leukemia virus type 1-specific CD8+ T cell in adult T cell leukemia patients. J Immunol; 2006 Oct 15;177(8):5718-26
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced frequency, diversity, and function of human T cell leukemia virus type 1-specific CD8+ T cell in adult T cell leukemia patients.
  • Human T cell lymphotropic virus type 1 (HTLV-1)-specific CTL are thought to be immune effectors that reduce the risk of adult T cell leukemia (ATL).
  • However, in vivo conditions of anti-HTLV-1 CTL before and after ATL development have yet to be determined.
  • To characterize anti-HTLV-1 CTL in asymptomatic HTLV-1 carriers (AC) and ATL patients, we analyzed the frequency and diversity of HTLV-1-specific CD8+ T cells in PBMC of 35 AC and 32 ATL patients using 16 distinct epitopes of HTLV-1 Tax or Env/HLA tetramers along with intracellular cytolytic effector molecules (IFN-gamma, perforin, and granzyme B).
  • Overall frequency of subjects possessing Tax-specific CD8+ T cells was significantly lower in ATL than AC (53 vs 90%; p = 0.001), whereas the difference in Env-specific CD8+ T cells was not statistically significant.
  • In contrast, ATL recognized only Tax11-19 with HLA-A*0201 and Tax301-309 with HLA-A*2402 at frequencies of 30 and 55%.
  • There were also significant differences in percentage of cells binding Tax11-19/HLA-A*0201 and Tax301-309/HLA-A*2402 tetramers between AC and ATL.
  • Anti-HTLV-1 Tax CD8+ T cells in AC and ATL produced IFN-gamma in response to Tax.
  • In contrast, perforin and granzyme B expression in anti-HTLV-1 CD8+ T cells of ATL was significant lower than that of AC.
  • These results suggest that decreased frequency, diversity, and function of anti-HTLV-1 Tax CD8+ T cell clones may be one of the risks of ATL development.
  • [MeSH-major] CD8-Positive T-Lymphocytes / immunology. Human T-lymphotropic virus 1 / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. T-Cell Antigen Receptor Specificity
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Clone Cells. Female. Gene Products, tax / immunology. HLA Antigens / immunology. Humans. Interferon-gamma / biosynthesis. Male. Middle Aged. T-Lymphocytes, Cytotoxic / immunology

  • Genetic Alliance. consumer health - Human T-cell leukemia virus type 1.
  • Immune Epitope Database and Analysis Resource. gene/protein/disease-specific - Related Immune Epitope Information .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17015761.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gene Products, tax; 0 / HLA Antigens; 82115-62-6 / Interferon-gamma
  •  go-up   go-down


98. Rüdiger T, Zettl A, Adam P, Bonzheim I, Geissinger E, Müller-Hermelink HK: [Peripheral NK/T-cell lymphoma]. Pathologe; 2007 Feb;28(1):55-8
SciCrunch. The Antibody Registry: Reagent: Antibodies .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Peripheral NK/T-cell lymphoma].
  • [Transliterated title] Periphere NK/T-Zell-Lymphome.
  • Peripheral T-cell lymphomas comprise 8% of the malignant lymphomas in Germany.
  • Such localizations are typical for the respective disease and form the basis for the classification of extranodal peripheral T-cell lymphoma.
  • Extranodal NK/T-cell lymphomas of the nasal type are characterized by an angiocentric growth pattern and large confluent areas of necrosis.
  • In addition, there is a clonal infection by Epstein-Barr virus in the T-lymphocytes.
  • In the differential diagnosis, B-cell lymphomas are more frequent at all localizations than T- or NK-cell lymphomas.
  • [MeSH-major] Killer Cells, Natural / pathology. Lymphoma, T-Cell / pathology. T-Lymphocytes / immunology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunophenotyping. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / pathology

  • Genetic Alliance. consumer health - Peripheral T-cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17195040.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


99. Guo D, Ye J, Dai J, Li L, Chen F, Ma D, Ji C: Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines. Leuk Res; 2009 May;33(5):678-85
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Notch-1 regulates Akt signaling pathway and the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 in T-ALL cell lines.
  • Gain-of-function mutations in Notch-1 are common in T-cell lymphoblastic leukemia (T-ALL), making this receptor a promising target for drugs such as gamma-secretase inhibitors (GSIs).
  • However, GSIs seem to be active in only a small fraction of T-ALL cell lines with constitutive Notch-1 activity and the downstream response of Notch signaling is only partially understood.
  • To further investigate the molecular mechanisms underlying proliferation suppression and apoptosis and explore effective downstream target genes, we used RNA interference (RNAi) technology to down-regulate the expression of Notch-1 in GSIs-resistant T-ALL cell lines.
  • Results showed that down-regulation of Notch-1 by transfection of a small interfering RNA (siRNA) could cause SupT1 cells proliferation inhibition by inducing G(0)/G(1) cell cycle arrest and apoptosis.
  • The proliferation inhibitory and apoptotic effects resulting from down-regulation of Notch-1 may be mediated through regulating the expression of cell cycle regulatory proteins cyclin D1, CDK2 and p21 and the activity of Akt signaling.
  • Taken together, cell cycle regulatory proteins and Akt signaling may be attractive targets in T-ALL.
  • [MeSH-major] CDC2 Protein Kinase / genetics. Cyclin D1 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogene Proteins c-akt / metabolism. Receptor, Notch1 / physiology. Signal Transduction / physiology
  • [MeSH-minor] Apoptosis. Base Sequence. Cell Cycle. Cell Line, Tumor. Cell Proliferation. Down-Regulation / physiology. Humans. Mutation. RNA Interference. RNA, Small Interfering. Reverse Transcriptase Polymerase Chain Reaction

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19091404.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / NOTCH1 protein, human; 0 / RNA, Small Interfering; 0 / Receptor, Notch1; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / CDC2 Protein Kinase
  •  go-up   go-down


100. Liu S, Breit S, Danckwardt S, Muckenthaler MU, Kulozik AE: Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines. Ann Hematol; 2009 Jul;88(7):613-21
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Downregulation of Notch signaling by gamma-secretase inhibition can abrogate chemotherapy-induced apoptosis in T-ALL cell lines.
  • Activation of Notch1 signaling plays an important role in the pathogenesis of precursor T-cell lymphoblastic leukemia (T-ALL).
  • In this study, we analyzed the response of four T-ALL cell lines to compound E, a potent gamma-secretase inhibitor, and to the combination of compound E with vincristine, daunorubicin, L-asparaginase (L-ASP), and dexamethasone (DEX).
  • We identified two distinct types of responses: In type 1 cell lines, represented by TALL1 and HSB2, GSI-induced apoptosis followed cell cycle arrest and enhanced the induction of apoptosis caused by DEX and L-ASP.
  • In type 2 cell lines, represented by CEM and Jurkat J6, GSI caused neither cell cycle block nor cell death.
  • In conclusion, the data presented here caution against clinical use of a combination treatment of GSI and chemotherapy in T-ALL.
  • [MeSH-major] Amyloid Precursor Protein Secretases / physiology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / pathology. Receptor, Notch1 / antagonists & inhibitors
  • [MeSH-minor] Asparaginase / pharmacology. Benzodiazepinones / pharmacology. Cell Line, Tumor. Daunorubicin / pharmacology. Dexamethasone / pharmacology. Down-Regulation. Humans. Signal Transduction. Vincristine / pharmacology

  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19057901.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 2-(((3,5-difluorophenyl)acetyl)amino)-N-(1-methyl-2-oxo-5-phenyl-2,3-dihydro-1H-1,4-benzodiazepin-3-yl)propanamide; 0 / Benzodiazepinones; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.5.1.1 / Asparaginase; ZS7284E0ZP / Daunorubicin
  •  go-up   go-down






Advertisement