Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma

Poiesz, Bernard J.; Ruscetti, Francis W.; Gazdar, Adi F.; Bunn, Paul A.; Minna, John D.; Gallo, Robert C.

doi:10.1073/pnas.77.12.7415

Cited by 4,474 publications

(2,270 citation statements)

References 27 publications

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“…5 Subsequent seroepidemiologic, morphologic, and molecular studies confirmed that HTLV-1 is the causative agent of ATLL cases that had (Diff-Quik stain, original magnification ϫ600).…”

Section: Discussionmentioning

confidence: 91%

Adult T-cell leukemia/lymphoma

Dahmoush

Hijazi

Barnes

et al. 2002

Cancer

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“…5 Subsequent seroepidemiologic, morphologic, and molecular studies confirmed that HTLV-1 is the causative agent of ATLL cases that had (Diff-Quik stain, original magnification ϫ600).…”

Section: Discussionmentioning

confidence: 91%

Adult T-cell leukemia/lymphoma

Dahmoush

Hijazi

Barnes

et al. 2002

Cancer

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“…The first description of HTLV-I came after the discovery of the human T-cell growth factor (interleukin-2; IL-2) [2], allowing long-term in vitro culture of T cells and establishment of T-cell lines from a patient with a cutaneous T-cell lymphoma (CTCL) [3]. Soon after, this virus was identified as the etiological agent of ATLL [4], and the term ''HTLV-I'' was adopted.…”

Section: Discovery and Epidemiologymentioning

confidence: 99%

Current views in HTLV-I-associated adult T-cell leukemia/lymphoma

Nicot

2005

Am. J. Hematol.

104

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Epidemiological studies have demonstrated that the relative percentage of malignant lymphoid proliferations varies widely according to geographical location and ethnic populations. HTLV-I is the etiological agent of adult T-cell leukemia/lymphoma (ATLL) and is also associated with cutaneous T-cell lymphoma (CTCL). However, a definite role of HTLV-I in mycosis fungoides (MF) and/or Sezary syndrome (SS) remains controversial. While most HTLV-I-infected individuals remain asymptomatic carriers, 1-5% will develop ATLL, an invariably fatal expansion of virus-infected CD4 + T cells. This low incidence and the long latency period preceding occurrence of the disease suggest that additional factors are involved in development of ATLL. In this review, diagnosis, clinical features, and molecular pathogenesis of HTLV-I are discussed. Am.

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“…[1][2][3] HTLV-I-mediated T-cell transformation presumably arises from multiple oncogenic processes in which the virus induces chronic T-cell proliferation, resulting in accumulation of genetic defects and dysregulated growth of infected cells. Although the mechanisms of transformation and leukemogenesis are not yet fully elucidated, the viral protein Tax is thought to play a crucial role in these processes.…”

mentioning

confidence: 99%

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Kawakami

Tomita

Matsuda

et al. 2005

Intl Journal of Cancer

142

112

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Survivin, a unique member of the inhibitor of apoptosis protein family, is overexpressed in many cancers and considered to play an important role in oncogenesis. We previously reported the survivin expression profile in ATL, a CD4-positive T-cell malignancy caused by HTLV-I. HTLV-I Tax is thought to play an important role in immortalization of T cells. We have shown also that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by deprivation of IL-2 and converted its growth from being IL-2 dependent to being IL-2 independent through the NF-kB pathway. In our study, we demonstrate that constitutive expression of survivin was associated with resistance to apoptosis after IL-2 deprivation in Tax-expressing CTLL-2 cells. Transient transfection assays showed that survivin promoter was transactivated by Tax, via the activation of NF-kB. Pharmacological NFkB inhibition resulted in suppression of survivin expression and caused apoptosis of Tax-expressing CTLL-2 cells. Our findings suggest that activated NF-kB signaling contributes directly to malignant progression of ATL by preventing apoptosis, acting through the prosurvival protein survivin. ' 2005 Wiley-Liss, Inc.

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Detection and isolation of type C retrovirus particles from fresh and cultured lymphocytes of a patient with cutaneous T-cell lymphoma

Abstract: Retrovirus particles with type C morphology were found in two T-cell lymphoblastoid cell lines, HUT 102 and CTCL-3, and in fresh peripheral blood lymphocytes obtained from a patient with a cutaneous T-cell lymphoma (mycosis fungoides).

Cited by 4,474 publications

References 27 publications

Adult T-cell leukemia/lymphoma

Adult T-cell leukemia/lymphoma

Current views in HTLV-I-associated adult T-cell leukemia/lymphoma

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

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