Human T-cell leukemia virus type 1 (HTLV-1) and leukemic transformation: viral infectivity, Tax, HBZ and therapy

Matsuoka, Masao; Jeang, Kuan‐Teh

doi:10.1038/onc.2010.537

Cited by 238 publications

(248 citation statements)

References 162 publications

(172 reference statements)

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“…The maintenance phase follows, with low immunogenicity and clonal expansion of infected cells mainly driven by HBZ. 6,16,19 This is consistent with the observation that Tax expression is depleted and HBZ is persistently detectable in ATLL. 6,16,19 HTLV-1 can infect different cell types, including T cells, B cells, fibroblasts, dendritic cells, and macrophages.…”

Section: Clinical Findingssupporting

confidence: 77%

“…6,16,19 This is consistent with the observation that Tax expression is depleted and HBZ is persistently detectable in ATLL. 6,16,19 HTLV-1 can infect different cell types, including T cells, B cells, fibroblasts, dendritic cells, and macrophages. However, regulatory T cells expressing CD25 and transcription factor forkhead box P3 (FOXP3) are considered to be the cell type that transforms to ATLL.…”

Section: Clinical Findingssupporting

confidence: 77%

“…2 Whether HTLV-1 integrates into CD4 þ T cells or hematopoietic progenitor stem cells in infants is not currently well established. 3,16 However, recent studies show that hematopoietic progenitor stem cells play a major part in the initiation of tumorigenesis and also serve as a viral reservoir. The latter function helps HTLV-1 evade the host immune response and ultimately results in long survival and latency.…”

Section: Clinical Findingsmentioning

confidence: 99%

“…Two HTLV-1 transactivator x (Tax) protein and HTLV-1 basic leucine zipper factor (HBZ), appear to play a central role. 6,[16][17][18][19] Tax protein is a transactivator of viral RNA and also has a profound role in immortalization through multiple mechanisms. 6,17 HTLV infection is considered to be a 2-phase process.…”

Section: Clinical Findingsmentioning

confidence: 99%

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Adult T-Cell Leukemia/Lymphoma

Qayyum

Choi

2014

Archives of Pathology &Amp; Laboratory Medicine

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Adult T-cell leukemia/lymphoma is a rare mature CD4+ T-cell neoplasm caused by the retrovirus human T-lymphotrophic virus type 1. At present there are approximately 20 million people infected globally with this virus, and most of these individuals belong to the endemic areas in southern Japan, Africa, the Caribbean basin, and Latin America. In the United States, it is usually seen in immigrants from these endemic regions. Adult T-cell leukemia/lymphoma predominantly affects the adult population and is rare in children. Adult T-cell leukemia/lymphoma has 4 subtypes: acute, lymphomatous, chronic, and smoldering. Clinically, the first 2 variants are classified as aggressive, and the latter two are classified as indolent. Given the rare occurrence and diagnostic challenges associated with adult T-cell leukemia/lymphoma, this review will highlight its salient features to aid in recognition of this entity and perform a comprehensive diagnostic workup.

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Section: Clinical Findingssupporting

confidence: 77%

Section: Clinical Findingssupporting

confidence: 77%

Section: Clinical Findingsmentioning

confidence: 99%

Section: Clinical Findingsmentioning

confidence: 99%

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Adult T-Cell Leukemia/Lymphoma

Qayyum

Choi

2014

Archives of Pathology &Amp; Laboratory Medicine

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“…Other cancer-associated viruses, HTLV-1 [14], KSHV [15], and MCV [16][17], have been reviewed elsewhere [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Immunotherapy against cancer-related viruses

2016

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Approximately 12% of all cancers worldwide are associated with viral infections. To date, eight viruses have been shown to contribute to the development of human cancers, including Epstein-Barr virus (EBV), Hepatitis B and C viruses, and Human papilloma virus, among others. These DNA and RNA viruses produce oncogenic effects through distinct mechanisms. First, viruses may induce sustained disorders of host cell growth and survival through the genes they express, or may induce DNA damage response in host cells, which in turn increases host genome instability. Second, they may induce chronic inflammation and secondary tissue damage favoring the development of oncogenic processes in host cells. Viruses like HIV can create a more permissive environment for cancer development through immune inhibition, but we will focus on the previous two mechanisms in this review. Unlike traditional cancer therapies that cannot distinguish infected cells from non-infected cells, immunotherapies are uniquely equipped to target virus-associated malignancies. The targeting and functioning mechanisms associated with the immune response can be exploited to prevent viral infections by vaccination, and can also be used to treat infection before cancer establishment. Successes in using the immune system to eradicate established malignancy by selective recognition of virus-associated tumor cells are currently being reported. For example, numerous clinical trials of adoptive transfer of ex vivo generated virus-specific T cells have shown benefit even for established tumors in patients with EBV-associated malignancies. Additional studies in other virus-associated tumors have also been initiated and in this review we describe the current status of immunotherapy for virus-associated malignancies and discuss future prospects.

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Angiotensin II type 1 receptor blocker telmisartan induces apoptosis and autophagy in adult T‐cell leukemia cells

et al. 2016

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Adult T‐cell leukemia/lymphoma ( ATL ), an aggressive T‐cell malignancy that develops after long‐term infection with human T‐cell leukemia virus ( HTLV ‐1), requires new treatments. Drug repositioning, reuse of a drug previously approved for the treatment of another condition to treat ATL , offers the possibility of reduced time and risk. Among clinically available angiotensin II receptor blockers, telmisartan is well known for its unique ability to activate peroxisome proliferator‐activated receptor‐γ, which plays various roles in lipid metabolism, cellular differentiation, and apoptosis. Here, telmisartan reduced cell viability and enhanced apoptotic cells via caspase activation in ex vivo peripheral blood monocytes from asymptomatic HTLV ‐1 carriers ( AC s) or via caspase‐independent cell death in acute‐type ATL , which has a poor prognosis. Telmisartan also induced significant growth inhibition and apoptosis in leukemia cell lines via caspase activation, whereas other angiotensin II receptor blockers did not induce cell death. Interestingly, telmisartan increased the LC 3‐ II ‐enriched protein fraction, indicating autophagosome accumulation and autophagy. Thus, telmisartan simultaneously caused caspase activation and autophagy. A hypertension medication with antiproliferation effects on primary and leukemia cells is intriguing. Patients with an early diagnosis of ATL are generally monitored until the disease progresses; thus, suppression of progression from AC and indolent ATL to acute ATL is important. Our results suggest that telmisartan is highly effective against primary cells and leukemia cell lines in caspase‐dependent and ‐independent manners, and its clinical use may suppress acute transformation and improve prognosis of patients with this mortal disease. This is the first report demonstrating a cell growth‐inhibitory effect of telmisartan in fresh peripheral blood mononuclear cells from leukemia patients.

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Human T-cell leukemia virus type 1 (HTLV-1) and leukemic transformation: viral infectivity, Tax, HBZ and therapy

Cited by 238 publications

References 162 publications

Adult T-Cell Leukemia/Lymphoma

Adult T-Cell Leukemia/Lymphoma

Immunotherapy against cancer-related viruses

Angiotensin II type 1 receptor blocker telmisartan induces apoptosis and autophagy in adult T‐cell leukemia cells

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