Bibliografías temáticas / Human t-cell leukemia viru

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Literatura académica sobre el tema "Human t-cell leukemia viru"

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Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "Human t-cell leukemia viru"

1

Norris, Philip J., Dale F. Hirschkorn, Deborah A. DeVita, Tzong-Hae Lee y Edward L. Murphy. "Human T cell leukemia virus type 1 infection drives spontaneous proliferation of natural killer cells". Virulence 1, n.º 1 (enero de 2010): 19–28. http://dx.doi.org/10.4161/viru.1.1.9868.

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Sohn, CC, DW Blayney, JL Misset, G. Mathe, G. Flandrin, EM Moran, FC Jensen, CD Winberg y H. Rappaport. "Leukopenic chronic T cell leukemia mimicking hairy cell leukemia: association with human retroviruses". Blood 67, n.º 4 (1 de abril de 1986): 949–56. http://dx.doi.org/10.1182/blood.v67.4.949.949.

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Abstract We report two cases of a T cell lymphoproliferative disease not previously described, with cytologic and clinical features similar to those associated with Galton's “prolymphocytic” leukemia (PL). Our patients, like those with Galton's PL, had massive splenomegaly and minimal or absent hepatomegaly and lymphadenopathy. In contrast, however, our patients had leukopenia, as well as low percentages of leukemic cells in the peripheral blood and in the bone marrow. In splenic imprints, the nuclear chromatin pattern of most of the leukemic cells was intermediate between those of mature lymphocytes and those of lymphoblasts, and the nuclei contained single, centrally located, conspicuous nucleoli. In sections of the spleen, the leukemic cells diffusely infiltrated the red pulp in a pattern strikingly similar to that of hairy cell leukemia; however, when the leukemic cells were studied cytochemically, the cytoplasmic acid phosphatase positivity was punctate and tartrate-sensitive. The leukemic cells were sheep erythrocyte rosette-positive and expressed T cell-associated antigens. Initially, both patients responded well to therapeutic splenectomy. One patient received combination chemotherapy after splenectomy and is alive and well 24 months after diagnosis. The other patient was in complete clinical remission for one year after splenectomy and received chemotherapy at relapse. He died, however, 23 months after splenectomy, with disseminated disease. IgG antibody titers against human T lymphotropic virus type I (HTLV-I) were detected in one patient and against HTLV-II in the other. The leukemia in these patients represents a distinct clinicopathologic entity within the spectrum of peripheral T cell lymphoproliferative diseases that includes Galton's PL of T cell derivation, T cell chronic lymphocytic leukemia, T cell hairy cell leukemia, and adult T cell leukemia/lymphoma.
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3

Sohn, CC, DW Blayney, JL Misset, G. Mathe, G. Flandrin, EM Moran, FC Jensen, CD Winberg y H. Rappaport. "Leukopenic chronic T cell leukemia mimicking hairy cell leukemia: association with human retroviruses". Blood 67, n.º 4 (1 de abril de 1986): 949–56. http://dx.doi.org/10.1182/blood.v67.4.949.bloodjournal674949.

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We report two cases of a T cell lymphoproliferative disease not previously described, with cytologic and clinical features similar to those associated with Galton's “prolymphocytic” leukemia (PL). Our patients, like those with Galton's PL, had massive splenomegaly and minimal or absent hepatomegaly and lymphadenopathy. In contrast, however, our patients had leukopenia, as well as low percentages of leukemic cells in the peripheral blood and in the bone marrow. In splenic imprints, the nuclear chromatin pattern of most of the leukemic cells was intermediate between those of mature lymphocytes and those of lymphoblasts, and the nuclei contained single, centrally located, conspicuous nucleoli. In sections of the spleen, the leukemic cells diffusely infiltrated the red pulp in a pattern strikingly similar to that of hairy cell leukemia; however, when the leukemic cells were studied cytochemically, the cytoplasmic acid phosphatase positivity was punctate and tartrate-sensitive. The leukemic cells were sheep erythrocyte rosette-positive and expressed T cell-associated antigens. Initially, both patients responded well to therapeutic splenectomy. One patient received combination chemotherapy after splenectomy and is alive and well 24 months after diagnosis. The other patient was in complete clinical remission for one year after splenectomy and received chemotherapy at relapse. He died, however, 23 months after splenectomy, with disseminated disease. IgG antibody titers against human T lymphotropic virus type I (HTLV-I) were detected in one patient and against HTLV-II in the other. The leukemia in these patients represents a distinct clinicopathologic entity within the spectrum of peripheral T cell lymphoproliferative diseases that includes Galton's PL of T cell derivation, T cell chronic lymphocytic leukemia, T cell hairy cell leukemia, and adult T cell leukemia/lymphoma.
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Matsuoka, Masao. "Human T-cell leukemia virus type I and adult T-cell leukemia". Oncogene 22, n.º 33 (agosto de 2003): 5131–40. http://dx.doi.org/10.1038/sj.onc.1206551.

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Hori, T., T. Uchiyama, M. Tsudo, H. Umadome, H. Ohno, S. Fukuhara, K. Kita y H. Uchino. "Establishment of an interleukin 2-dependent human T cell line from a patient with T cell chronic lymphocytic leukemia who is not infected with human T cell leukemia/lymphoma virus". Blood 70, n.º 4 (1 de octubre de 1987): 1069–72. http://dx.doi.org/10.1182/blood.v70.4.1069.1069.

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Abstract We established an interleukin 2 (IL-2)-dependent human T cell line, Kit 225, from a patient with T cell chronic lymphocytic leukemia (T-CLL) with OKT3+, -T4+, -T8- phenotype. Southern blot analysis showed that Kit 225 is not infected with human T cell leukemia/lymphoma virus (HTLV) type I or II, and is probably derived from the major clone in the fresh leukemic cells. Kit 225 cells express a large amount of IL 2 receptors constitutively and their growth is absolutely dependent on IL 2. No other stimuli, such as lectins or antigens, are required for maintaining the responsiveness to IL 2. As abnormal IL 2 receptor expression was also seen originally in the fresh leukemic cells, the establishment of this cell line with IL 2 suggests that IL 2-mediated T cell proliferation is involved in the leukemogenesis of some cases of HTLV-negative T-CLL.
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6

Hori, T., T. Uchiyama, M. Tsudo, H. Umadome, H. Ohno, S. Fukuhara, K. Kita y H. Uchino. "Establishment of an interleukin 2-dependent human T cell line from a patient with T cell chronic lymphocytic leukemia who is not infected with human T cell leukemia/lymphoma virus". Blood 70, n.º 4 (1 de octubre de 1987): 1069–72. http://dx.doi.org/10.1182/blood.v70.4.1069.bloodjournal7041069.

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We established an interleukin 2 (IL-2)-dependent human T cell line, Kit 225, from a patient with T cell chronic lymphocytic leukemia (T-CLL) with OKT3+, -T4+, -T8- phenotype. Southern blot analysis showed that Kit 225 is not infected with human T cell leukemia/lymphoma virus (HTLV) type I or II, and is probably derived from the major clone in the fresh leukemic cells. Kit 225 cells express a large amount of IL 2 receptors constitutively and their growth is absolutely dependent on IL 2. No other stimuli, such as lectins or antigens, are required for maintaining the responsiveness to IL 2. As abnormal IL 2 receptor expression was also seen originally in the fresh leukemic cells, the establishment of this cell line with IL 2 suggests that IL 2-mediated T cell proliferation is involved in the leukemogenesis of some cases of HTLV-negative T-CLL.
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7

Valtieri, M., D. Santoli, D. Caracciolo, B. L. Kreider, S. W. Altmann, D. J. Tweardy, I. Gemperlein, F. Mavilio, B. Lange y G. Rovera. "Establishment and characterization of an undifferentiated human T leukemia cell line which requires granulocyte-macrophage colony stimulatory factor for growth." Journal of Immunology 138, n.º 11 (1 de junio de 1987): 4042–50. http://dx.doi.org/10.4049/jimmunol.138.11.4042.

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Abstract A human leukemia cell line (TALL-101) was established from the bone marrow of a patient with an undifferentiated acute T cell leukemia using the conditioned medium (CM) of the human T cell leukemia virus (HTLV) II-transformed human cell line J-LB1. Immunofluorescence analysis on the original leukemic cells indicated the presence of T cell markers (Leu-1, Tdt, and T11); however, the established TALL-101 cell line expressed only antigens commonly present on progenitor cells, thymocytes, and myelomonocytic cells, but not on mature T cells. A high percentage of TALL-101 cells displayed the Tac antigen which was down-regulated upon incubation in the presence of recombinant human (rH) interleukin 2 (IL 2). Interferon (IFN)-gamma induced the appearance of class II histocompatibility leukocyte antigens (HLA) and of a T cell marker (3A1), and enhanced the expression of transferrin receptors on these cells. Further evidence for a T cell lineage of the TALL-101 cell line was provided by both chromosomic and genotypic analysis showing a translocation in chromosome 14 typical of T cell leukemias, and a rearrangement of the T-beta receptor locus. The growth-promoting activity in the J-LB1-CM was identified as granulocyte-macrophage colony stimulatory factor (GM-CSF), a growth factor which stimulates proliferation of normal myelomonocytic cells and other progenitor cells, but not known to have an effect on T cells. Dose response curves of [3H]thymidine incorporation and growth indicated that TALL-101 cells were sensitive to very low concentrations of rHGM-CSF, 5 ng/ml inducing maximal proliferation in chemically defined medium. The TALL-101 cell line is strictly GM-CSF-dependent for growth: upon depletion of GM-CSF from the culture medium, the cells stop proliferating immediately and die within 1 to 2 wk. The overall data, showing that GM-CSF is able to support the growth of a highly undifferentiated T cell leukemia, strongly suggests that this factor might have similar growth promoting effects on other immature T cell leukemias, and possibly, on normal T cell progenitors.
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Nitta, Takayuki, Masayuki Kanai, Eiji Sugihara, Masakazu Tanaka, Binlian Sun, Toshiro Nagasawa, Shunro Sonoda, Hideyuki Saya y Masanao Miwa. "Centrosome amplification in adult T-cell leukemia and human T-cell leukemia virus type 1 Tax-induced human T cells". Cancer Science 97, n.º 9 (septiembre de 2006): 836–41. http://dx.doi.org/10.1111/j.1349-7006.2006.00254.x.

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Oliveira, Pedro Dantas, Lourdes Farre y Achiléa Lisboa Bittencourt. "Adult T-cell leukemia/lymphoma". Revista da Associação Médica Brasileira 62, n.º 7 (octubre de 2016): 691–700. http://dx.doi.org/10.1590/1806-9282.62.07.691.

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Summary Adult T-cell leukemia/lymphoma (ATL) is a malignancy of mature CD4+ T-cells caused by human T-cell lymphotropic virus type 1 (HTLV-1). Twenty million people are believed to be infected throughout the world, mostly in Japan, Africa, the Caribbean, and South America, particularly in Brazil and Peru. ATL affects about 5% of infected individuals and is classified in the following clinical forms: acute, lymphoma, primary cutaneous tumoral, chronic (favorable and unfavorable), and smoldering (leukemic and non-leukemic). Although it is considered an aggressive disease, there are cases with a long progression. We emphasize the importance of clinical classification as an indispensable element for evaluating prognosis and appropriate therapeutic approach. Since several cases have been published in Brazil and this disease is still poorly known, we decided to make a review paper for dissemination of clinical, hematological and pathological aspects, diagnosis, and therapy. The best way to reduce the occurrence of ATL would be halting the transmission of the virus through breastfeeding.
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Mori, Naoki, Youichi Nunokawa, Yasuaki Yamada, Shuichi Ikeda, Masao Tomonaga y Naoki Yamamoto. "Expression of Human Inducible Nitric Oxide Synthase Gene in T-Cell Lines Infected With Human T-Cell Leukemia Virus Type-I and Primary Adult T-Cell Leukemia Cells". Blood 94, n.º 8 (15 de octubre de 1999): 2862–70. http://dx.doi.org/10.1182/blood.v94.8.2862.420k24_2862_2870.

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We examined the expression of messenger RNA (mRNA) of the human inducible nitric oxide synthase (hiNOS) gene in a panel of human T-cell lines. Reverse transcriptase-polymerase chain reaction showed that human T-cell leukemia virus type-I (HTLV-I)–infected T-cell lines (MT-1, SLB-1, and C5/MJ) expressed mRNA for the hiNOS, but TL-Om1 or uninfected Jurkat, H9, and CCRF-CEM did not. The MT-1, SLB-1, and C5/MJ cell lines are infected with HTLV-I and express the viral transactivator Tax, whereas TL-Om1 cells, although derived from adult T-cell leukemia (ATL) leukemic cells, do not express Tax. There was, thus, a correlation between Tax and hiNOS mRNA expression. The transcriptional regulatory region of the hiNOS gene was activated by Tax in Jurkat, in which endogenous hiNOS is induced by Tax. Deletion analysis showed that the region of hiNOS encompassing nucleotides −159 to −111 contained the minimum Tax-responsive elements. Mutations in the NF-κB element at position −115 and −106 bp in the hiNOS promoter were still activated by Tax, and a Tax mutant defective for activation of the NF-κB pathway retained the ability to activate the hiNOS promoter. In addition, overexpression of the dominant-negative mutants of IκB and I κBβ failed to reduce Tax-induced activation of hiNOS gene. Furthermore, hiNOS mRNA was detected in leukemic cells from ATL patients. Our results show that the hiNOS promoter contains a minimum Tax-responsive element located between nucleotides −159 and −111, and imply that the expression of the hiNOS gene is involved in the pathogenesis of HTLV-I–associated diseases.
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Tesis sobre el tema "Human t-cell leukemia viru"

1

Sasada, Amane. "APOBEC3G targets human T-cell leukemia virus type 1". Kyoto University, 2006. http://hdl.handle.net/2433/143870.

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Ruggero, Katia. "Role of microRNAs in T-cell activation and transformation by human T-cell Leukemia virus type 1". Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422191.

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Human T-Lymphotropic virus type 1 (HTLV-1) is the causative agent of two distinct pathologies, adult T-cell leukemia/lymphoma (ATLL), an aggressive malignancy of mature CD4+ T-cells, and tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM), a demyelinating neurodegenerative disease. Despite intense study, many aspects of HTLV-1 replication, persistence and pathogenesis remain to be understood. The work described in the present thesis was aimed at defining the role of microRNAs (miRNAs) in HTLV-1 infection and ATLL pathogenesis. We generated small RNA libraries from normal CD4+ cells (resting and stimulated) and two T-cell lines chronically infected with HTLV-1 (MT-2 and C91PL). Libraries were analyzed by 454 mass sequencing and data were processed through a series of computational steps to identify known and candidate new miRNAs for each library. Comparison of frequencies of known miRNAs in the different libraries led to the identification of 14 downregulated miRNAs and 4 upregulated species in infected cell lines vs. resting CD4+ cells, while 21 miRNAs were differentially expressed (16 downregulated, 5 upregulated) in stimulated compared to resting CD4+ cells. We validated the expression of some new miRNA candidates identified by bioinformatic analysis of the libraries through end point and quantitative RT-PCR. Two sequences mapped to the HTLV-1 genome, suggesting that the virus may produce its own miRNAs under certain conditions. We examined the profiles of known miRNA expression in ATLL cells and normal resting and activated T CD4+ lymphocytes using microarrays. On the basis of miRNA expression, cluster analysis of ATLL samples and CD4+ controls showed that the resting controls were highly related to each other, while the tumor samples exhibited some heterogeneity. Statistical analysis revealed 6 upregulated and 21 downregulated miRNAs in ATLL cells compared to CD4+ T-cell controls. Several of the differentially expressed miRNAs identified in the libraries and by microarray analysis were validated by real time RT-PCR. Since miRNA-mRNA interactions often result in degradation of the target mRNA, integration of results from target prediction programs with expression profiles for miRNAs and mRNAs can aid in identifying genuine mRNA targets. This approach was applied to miRNA and mRNA microarray data obtained for our ATLL and resting CD4+ samples. Potential targets for 12 miRNAs differentially expressed in ATLL cells were identified by integrating miRNA and mRNA expression profiles. Functional enrichment analysis of predicted targets revealed the presence of several genes belonging to the cAMP signalling pathway, which is known to be activated upon HTLV-1 transformation. We also investigated the role of miR-34a, consistently upregulated in ATLL samples and HTLV-1 infected cells lines. Knockdown of miR-34a in infected cell lines determined an increased in cell death, suggesting that miR-34a could play an important role in the expansion of HTLV-1 infected cells and thereby in ATLL development.
Il virus T-linfotropico umano di tipo 1 (HTLV-1) è l’agente eziologico della leucemia/linfoma a cellule T dell’adulto (ATLL, adult T-cell leukemia/lymphoma) e della paraparesi spastica tropicale/mielopatia associata ad HTLV (TSP/HAM, Tropical spastic paraparesis/HTLV-associated myelopathy), una patologia degenerativa del sistema nervoso centrale. Recenti evidenze suggeriscono che i microRNA (miRNA) contribuiscano a questo processo di trasformazione mediata da HTLV-1. Le ricerche condotte nel corso del mio dottorato sono state mirate ad approfondire il ruolo dei microRNA (miRNA) nell’infezione di cellule T da parte di HTLV-1 e nella patogenesi dell’ATLL. Sono state realizzate librerie di cDNA di piccoli RNA, a partire da linfociti T CD4+ normali (resting e attivati) e da due linee cellulari cronicamente infettate con HTLV-1 (C91PL e MT-2). Le librerie sono state analizzate attraverso il sequenziamento di massa 454 e l’analisi bioinformatica delle sequenze ottenute ha permesso l’identificazione dei miRNA noti e nuovi miRNA candidati presenti in ciascuna libreria. Il confronto delle frequenze dei miRNA noti nelle diverse librerie ha evidenziato la presenza di 14 e 4 miRNA rispettivamente downregolati e upregolati nelle linee cellulari infettare rispetto ai linofociti T CD4+ resting, mentre 21 miRNA sono risultati differenzialmente espressi in linfociti T CD4+ stimolati in confronto ai linfociti T CD4+ resting (16 downregolati, 5 upregolati). L’espressione di diversi nuovi miRNA, individuati dall’analisi bioinformatica delle librerie, è stata validata attraverso RT-PCR end-point o RT-PCR quantitativa. Inoltre la nostra analisi ha rivelato nelle librerie da cellule infettate 2 sequenze che mappano in regioni trascritte del genoma di HTLV-1 e che potrebbero rappresentare dei miRNA virali. Attraverso l’impiego di microarray il profilo di espressione dei miRNA noti è stato analizzato in pazienti ATLL e in linfociti T CD4+ resting e stimolati. In base ai profili di espressione di miRNA ottenuti i campioni sono stati raggruppati in cluster che indicano una forte similitudine all’interno dei campioni di linfocititi T CD4+ resting, mentre i campioni di ATLL hanno profili di espressione di miRNA più eterogenei. L’analisi statistica ha evidenziato 21 miRNA downregolati e 6 upregolati nei pazienti ATLL vs linfociti T CD4+ resting. Diversi miRNA differenzialmente espressi identificati attraverso l’analisi delle librerie e dei microarray sono stati validati tramite RT-PCR quantitativa. Dal momento che l’interazione miRNA-mRNA spesso comporta la degradazione del messaggero bersaglio, l’analisi integrata dei risultati dei programmi di predizione di bersagli con i profili di espressione di miRNA e geni può aiutare nell’identificazione di target. Abbiamo applicato questo approccio ai dati di espressione di miRNA e geni ottenuti per i nostri campioni di ATLL e linfociti T CD4+ resting. Dall’integrazione dei profili di espressione di miRNA e mRNA sono stati identificati i target putativi per 12 miRNA differenzialmente espressi nei pazienti ATLL. L’arricchimento funzionale dei geni bersaglio predetti ha evidenziato la presenza di diversi geni coinvolti nella via di segnale di cAMP, noto per essere presente ad alti livelli in cellule trasformate da HTLV-1. Infine abbiamo indagato il significato funzionale di miR-34a, che risulta essere consistentemente upregolato in pazienti ATLL e linee cellulari infettate. Il silenziamento di miR-34a in linee cellulari infettate determina un aumento della morte cellulare, suggerendo che la deregolazione di questo miRNA possa svolgere un ruolo importante nell’espansione della popolazione di cellule infettate da HTLV-1 e quindi nello sviluppo dell’ATLL.
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Furuta, Rie. "Human T-cell leukemia virus type 1 infects multiple lineage hematopoietic cells in vivo". Kyoto University, 2018. http://hdl.handle.net/2433/232110.

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Younis, Ihab H. "Molecular analysis of human t-cell leukemia virus regulatory and accessory proteins". The Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=osu1123168747.

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Li, Min. "Kinetic analysis of Human T-cell leukemia virus type 1 gene expression". The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1228156327.

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Miura, Michi. "Characterization of simian T-cell leukemia virus type 1 in naturally infected Japanese macaques as a model of HTLV-1 infection". Kyoto University, 2014. http://hdl.handle.net/2433/188641.

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Yamamoto, Brenda Michiyo. "Molecular Analysis of Human T-cell Leukemia Virus Type 2 Accessory Protein p28". The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1241708950.

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Doueiri, Rami. "CHARACTERIZATION OF THE HUMAN T-CELL LEUKEMIA VIRUS TYPE-2 P28 ACCESSORY PROTEIN". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1343453789.

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Newbound, Garret C. "Transcriptional control of human t-cell leukemia virus type-1 in primary lymphocytes /". The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487948440826361.

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Anderson, Matthew David. "Studies with the human t-cell leukemia virus tax and rex positive trans-regulatory proteins". Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1083092375.

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Thesis (Ph. D.)--Ohio State University, 2004.
Title from first page of PDF file. Document formatted into pages; contains xv, 129 p.; also includes graphics Includes bibliographical references (p. 105-129). Available online via OhioLINK's ETD Center
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Libros sobre el tema "Human t-cell leukemia viru"

1

Vogt, Peter K., ed. Human T-Cell Leukemia Virus. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70113-9.

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1932-, Vogt P. K., ed. Human T-cell leukemia virus. Berlin: Springer, 1985.

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Essex, Myron. Selected abstracts on viral etiology of human cancer.: Human T-cell leukemia viruses. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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Kenton, Charlotte. Human T-cell leukemia/lymphoma virus (HTLV), January 1982 through September 1984, 234 citations. [Bethesda, Md.]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1985.

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Symposium, Takamatsu no Miya Hi Gan Kenkyū Kikin International. Retroviruses in human lymphoma/leukemia: Proceedings of the 15th International Symposium of the Princess Takamatsu Cancer Research Fund, Tokyo, 1984. Tokyo: Japan Scientific Societies Press, 1985.

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C, Román Gustavo, Vernant Jean-Claude, Osame Mitsuhiro, Texas Tech University. Dept. of Neurology., Meynard Hospital. Dept. of Neurology. y International Symposium on HTLV-I and the Nervous System (1968 : Meynard Hospital., eds. HTLV-I and the nervous system: Proceedings of an international meeting organized by the Departments of Neurology of Texas Tech University and La Meynard Hospital, held in Fort-de-France, Martinique, French Antilles, April 15-16, 1988. New York: Liss, 1989.

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Jean, Otter y American Association of Blood Banks., eds. Current status of HTLV-III testing. Arlington, Va: American Association of Blood Banks, 1986.

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E, Menitove Jay, Kolins Jerry, American Association of Blood Banks. Committee on Technical/Scientific Workshops. y AIDS Technical Workshop (1986 : San Francisco, Calif.), eds. AIDS. Arlington, Va: American Association of Blood Banks, 1986.

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Vogt, Peter K. Human T-Cell Leukemia Virus. Brand: Springer, 2011.

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Vogt, P. K. Human T-Cell Leukemia Virus. Springer London, Limited, 2012.

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Capítulos de libros sobre el tema "Human t-cell leukemia viru"

1

Levy, Jay A. y Edward L. Murphy. "Human T-Cell Leukemia Virus". En Encyclopedia of Cancer, 1757–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2859.

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Fujisawa, Jun-ichi. "Human T-Cell Leukemia Virus Type 1 (HTLV-1)". En Adult T-cell Leukemia/Lymphoma, 3–31. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56523-9_2.

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Miura, Kiyonori y Hideaki Masuzaki. "Prevention of Human T-Cell Leukemia Virus Type 1 (HTLV-1) Mother-to-Child Transmission". En Adult T-cell Leukemia/Lymphoma, 157–69. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56523-9_13.

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Chan, Chi-Ping, Kin-Hang Kok y Dong-Yan Jin. "Human T-Cell Leukemia Virus Type 1 Infection and Adult T-Cell Leukemia". En Advances in Experimental Medicine and Biology, 147–66. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-5765-6_9.

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Gallo, R. C., M. G. Sarngadharan, M. Popovic, J. Schupbach, P. Markham, S. Z. Salahuddin, G. Shaw, F. Wong-Staal y M. S. Reitz. "The Human T-Cell Leukemia Virus Family, Adult T Cell Leukemia, and AIDS". En Modern Trends in Human Leukemia VI New Results in Clinical and Biological Research Including Pediatric Oncology, 317–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70385-0_67.

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Kamoi, Koju y Manabu Mochizuki. "Human T-Cell Leukemia Virus Type 1". En Emerging Infectious Uveitis, 143–48. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-23416-8_15.

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Schüpbach, Jörg. "Human T-Cell Leukemia Virus Type I". En Current Topics in Microbiology and Immunology, 12–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75195-0_3.

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Schüpbach, Jörg. "Human T-Cell Leukemia Virus Type II". En Current Topics in Microbiology and Immunology, 18–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75195-0_4.

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Yoshida, Mitsuaki, Seisuke Hattori y Motoharu Seiki. "Molecular Biology of Human T-Cell Leukemia Virus Associated with Adult T-Cell Leukemia". En Current Topics in Microbiology and Immunology, 157–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70113-9_11.

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Yasunaga, Junichiro y Kuan-Teh Jeang. "Human T-Cell Leukemia Virus Type 1, Cellular Transformation, and Adult T-Cell Leukemia". En National Institute of Allergy and Infectious Diseases, NIH, 41–49. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-512-5_5.

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Actas de conferencias sobre el tema "Human t-cell leukemia viru"

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Ren, Tong, Wen Dong, Yoshinori Takahashi, Di Xiang, Yunsheng Yuan, Xin Liu, Thomas P. Loughran, Shao-Cong Sun, Hong-Gang Wang y Hua Cheng. "Abstract LB-66: Oncogenic properties of tax protein from human T cell leukemia virus type 2". En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-66.

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Bandeira, Larissa Melo, Ana Rita Motta-Castro, Marco Puga, Silvia Uehara, João Domingos, Grazielli Rezende, Gabriela Alves Cesar y Tayana Tanaka. "Human T-cell leukemia virus type 1 infection among Japanese immigrants and their descendants living in Southeast Brazil: a call for preventive and control responses". En XIII Congresso da Sociedade Brasileira de DST - IX Congresso Brasileiro de AIDS - IV Congresso Latino Americano de IST/HIV/AIDS. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/dst-2177-8264-202133p012.

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Introduction: Human T-cell leukemia virus type 1 (HTLV-1) has worldwide distribution and is considered endemic in southwestern Japan. HTLV-1 infection has been associated with adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) besides other diseases. Objective: This cross-sectional study aimed to investigate the prevalence, risk factors, and molecular characterization of HTLV-1, among the world´s largest population of Japanese immigrants and their descendants outside Japan, in São Paulo, Southeast Brazil, as well as to analyze the phylogenetic relationship among isolates of HTLV-1. Methods: From July to December 2017, 2,139 individuals from five Japanese associations were interviewed and submitted to blood collection. All serum samples were first tested for the presence of anti-HTLV-1/2 antibodies by ELISA and then peripheral blood from individuals with positive serological results were analyzed for the presence of HTLV-1 5ʹLTR proviral DNA. Partial sequencing of the 5ʹLTR region of HTLV-1 proviral DNA was performed by Sanger. Results: The prevalence of HTLV-1 infection was 5.1% (95% CI 4.2-6.0). In the multiple logistic regression model, HTLV-1 infection was associated with age 45 years, female sex, first- and second-generation Japanese immigrants, and having sexual partners with a history of blood transfusion. The phylogenetic analysis revealed that all HTLV-1 were classified as Cosmopolitan (1a) subtype. Of them, 47.8% were classified as Transcontinental (A) subgroup and 52.2% as belonging to the Japanese (B) subgroup. Although most HTLV-1-infected patients were asymptomatic (97.3%), the blurred vision was associated with HTLV-1 infection. Conclusion: The high prevalence of HTLV-1 infection found in this study population and especially the intrafamily and interfamily HTLV-1 transmission presents an urgent need for preventive and control responses of this infection in Brazil.
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Makoto, Ishihara, Natsumi Araya, Tomoo Sato, Atae Utsunomiya, Yoshihisa Yamano, Yusuke Nakamura, Hidewaki Nakagawa y Koji Ueda. "Abstract 4803: Quantitative proteome profiling of CD4+CD25+CCR4+ T-cells to identify potential therapeutic targets for adult T-cell leukemia (ATL) and Human T-lymphotropic virus type-1 associated myelopathy (HAM)". En Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4803.

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Umekita, K., S. Miyauchi, K. Kubo, A. Kawano, K. Iwao, M. Komura, M. Matsuda et al. "AB0021 Human T cell leukemia virus type 1 (HTLV-1) exacerbates rheumatoid arthritis; exosomes and IFN-GAMMA derived from HTLV-1 infected cells enhance the inflammatory response of rheumatoid arthritis synovial fibroblasts via pattern recognition receptor, RIG-I". En Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2036.

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Ma, Wenxue, Alejandro Gutierrez, Qinghai Peng, Daniel Goff, Christina Wu, Alice Shih, Angela Court et al. "Abstract 4313: Mouse model of human T-cell acute lymphoblastic leukemia stem cells". En Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4313.

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Chu, Ching-Yu, Szu-Yuan Chen, Fu-Yu Chueh, Mei-Ling Cheng y Chao-Lan Yu. "Abstract 2564: Integrated transcriptomic, proteomic, and metabolomic analyses of human and mouse T cell leukemia". En Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2564.

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Chueh, Fu-Yu, Shahrooz Vahedi, Fu-Shin Chueh y Chao-Lan Yu. "Abstract 2702: Therapeutic potentials of STAT5 inhibitors in overcoming bortezomib resistance in human T-cell leukemia". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2702.

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Lovell, Gillian, Clare Szybut, Kalpana Patel, Hinnah Campwala, Nicola Bevan, Dan Appledorn, Tim James Dale y Derek John Trezise. "Abstract 2648: CD47 antibody-induced engulfment of human T-cell leukemia cells by bone marrow-derived macrophages". En Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2648.

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Amorós, Mariana, M. Florencia Cayrol, M. Celeste Díaz Flaque, Luciana Gutiérrez, Osvaldo Podhjacer, Leandro Cerchietti, Graciela Cremaschi y Marcela F. Bolontrade. "Abstract 97: Establishment of a new in vivo model for human T-cell lymphoblastic leukemia (T-ALL) suitable for evaluation of the tumor stromal component". En Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-97.

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Bhavsar, Preeya, Mugahed Hamza, Sepideh Mehravaran, Qin He, Steven Tyring, Peter Rady, Bhuvaneswari Krishnan, Gustavo Rivero, Daniel N. Cohen y Iberia Romina Sosa. "Abstract 4898: The contribution of human papilloma virus infection to cutaneous squamous cell carcinoma in patients with chronic lymphocytic leukemia". En Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4898.

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