Integrated molecular analysis of adult T cell leukemia/lymphoma

Kataoka, Keisuke; Nagata, Yasunobu; Kitanaka, Akira; Shiraishi, Yuichi; Shimamura, Teppei; Yasunaga, Jun Ichirou; Totoki, Yasushi; Chiba, Kenichi; Sato‐Otsubo, Aiko; Nagae, Genta; Ishii, Ryohei; Muto, Satsuki; Kotani, Shunsuke; Watatani, Yosaku; Takeda, June; Sanada, Masashi; Tanaka, Hiroko; Suzuki, Hiromichi; Sato, Yusuke; Shiozawa, Yusuke; Yoshizato, Tetsuichi; Yoshida, Kenichi; Makishima, Hideki; Iwanaga, Masako; Ma, Guangyong; Nosaka, Kisato; Hishizawa, Masakatsu; Itonaga, Hidehiro; Imaizumi, Yoshitaka; Munakata, Wataru; Ogasawara, Haruhiko; Sato, Toshitaka; Sasai, Ken; Muramoto, Koji; Penova, Marina; Kawaguchi, Takahisa; Nakamura, Hiromi; Hama, Natsuko; Shide, Kotaro; Kubuki, Yoko; Hidaka, Tomonori; Kameda, Takuro; Nakamaki, Tsuyoshi; Ishiyama, Ken; Miyawaki, Shuichi; Yoon, Sung Soo; Tobinai, Kensei; Miyazaki, Yasushi; Takaori‐Kondo, Akifumi; Matsuda, Fumihiko; Takeuchi, Kengo; Nureki, Osamu; Aburatani, Hiroyuki; Watanabe, Toshiki; Shibata, Tatsuhiro; Matsuoka, Masao; Miyano, Satoru; Shimoda, Kazuya; Ogawa, Seishi

doi:10.1038/ng.3415

Cited by 661 publications

(1,044 citation statements)

References 60 publications

(62 reference statements)

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“…-further develop whole-genome sequencing to identify hostassociated driver mutations in all conditions, as recently performed for ATL (Kataoka et al, 2015); -correlate the emergence of driver mutations with disease onset; -develop assays allowing early prediction of differential disease development and the identification of progression.…”

Section: Identify Biomarkers To Predict Disease Progressionmentioning

confidence: 99%

“…-genes promoting viral replication and persistence (Tax and HBZ) (Matsuoka and Jeang, 2007); -modes of viral entry and replication (infectious and mitotic cycles) (Ghez et al, 2010;Boxus et al, 2012;Gillet et al, 2011Gillet et al, , 2013Sibon et al, 2006); -genomic and epigenetic mechanisms leading to ATL (oncogenic stress, driver mutations) (Kataoka et al, 2015;Yamagishi et al, 2012); -the role of the immune response in the control of infection (Asquith and Bangham, 2008); -the pathogenic potential of HTLV-2, -3 and -4 (Calattini et al, 2006).…”

Section: Perform Basic Research To Unravel Mechanisms Of Viral Persismentioning

confidence: 99%

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Reducing the global burden of HTLV-1 infection: An agenda for research and action

et al. 2017

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a b s t r a c tEven though an estimated 10e20 million people worldwide are infected with the oncogenic retrovirus, human T-lymphotropic virus type 1 (HTLV-1), its epidemiology is poorly understood, and little effort has been made to reduce its prevalence. In response to this situation, the Global Virus Network launched a taskforce in 2014 to develop new methods of prevention and treatment of HTLV-1 infection and promote basic research. HTLV-1 is the etiological agent of two life-threatening diseases, adult T-cell leukemia and HTLV-associated myelopathy/tropical spastic paraparesis, for which no effective therapy is currently available. Although the modes of transmission of HTLV-1 resemble those of the more familiar HIV-1, routine diagnostic methods are generally unavailable to support the prevention of new infections. In * Corresponding author. Molecular and Cellular Epigenetics, Interdisciplinary Cluster for Applied Genoproteomics (GIGA) of University of Liege (ULg), B34, 1 Avenue de l'Hôpital, 4000, Sart-Tilman, Liege, Belgium.E-mail address: luc.willems@ulg.ac.be (L. Willems). Contents lists available at ScienceDirect Antiviral Researchj o u rn a l h o m e p a g e : w w w . e l s e v i e r . c o m / l o c a t e / a n t iv i r a l the present article, the Taskforce proposes a series of actions to expand epidemiological studies; increase research on mechanisms of HTLV-1 persistence, replication and pathogenesis; discover effective treatments; and develop prophylactic and therapeutic vaccines.

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Section: Identify Biomarkers To Predict Disease Progressionmentioning

confidence: 99%

Section: Perform Basic Research To Unravel Mechanisms Of Viral Persismentioning

confidence: 99%

Reducing the global burden of HTLV-1 infection: An agenda for research and action

et al. 2017

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“…High-throughput methodologies were used to identify the cell of origin and to characterize commonly altered pathways in PTCL [51,59–67]. These efforts were successful in defining characteristic gene expression profiles for AITL, ALK + ALCL, ATLL, and PTCL-NOS, identifying recurrent mutations and recognizing specific subtypes, which can now help to support correct diagnosis and classification of patients to distinct disease subgroups with different prognoses [46,59,60,62,63].…”

Section: Targets In Ptcl and Driver Mutationsmentioning

confidence: 99%

Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas

Orlova

Wingelhofer

Neubauer

et al. 2017

Expert Opinion on Therapeutic Targets

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Introduction: Hematopoietic neoplasms are often driven by gain-of-function mutations of the JAK-STAT pathway together with mutations in chromatin remodeling and DNA damage control pathways. The interconnection between the JAK-STAT pathway, epigenetic regulation or DNA damage control is still poorly understood in cancer cell biology. Areas covered: Here, we focus on a broader description of mutational insights into myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas, since sequencing efforts have identified similar combinations of driver mutations in these diseases covering different lineages. We summarize how these pathways might be interconnected in normal or cancer cells, which have lost differentiation capacity and drive oncogene transcription. Expert opinion: Due to similarities in driver mutations including epigenetic enzymes, JAK-STAT pathway activation and mutated checkpoint control through TP53, we hypothesize that similar therapeutic approaches could be of benefit in these diseases. We give an overview of how driver mutations in these malignancies contribute to hematopoietic cancer initiation or progression, and how these pathways can be targeted with currently available tools.

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“…We previously proposed that stimulation of the TCR/CD3 complex, represented by a low density of the CD3 antigen, is a unique feature of ATL/ATLL cells . A recent integrated molecular study of the ATL/ATLL genome also showed frequent alteration of TCR-nuclear factor κB signaling, which may suggest stimulation of ATL/ATLL cells through the TCR (Kataoka et al 2015). Gal-9 shows apoptotic activity toward tumor cells or T cells (Fujihara et al 2013), and it should be studied whether Gal-9 has an apoptotic effect on fresh ATL/ATLL cells.…”

Section: Discussionmentioning

confidence: 99%

Galectin-9 as a Predictive Marker for the Onset of Immune-Related Adverse Effects Associated with Anti-CCR4 MoAb Therapy in Patients with Adult T Cell Leukemia

Mohammed

Chagan-Yasutan

Ashino

et al. 2017

Tohoku J. Exp. Med.

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Adult T-cell leukemia/lymphoma (ATL/ATLL) is one of the most malignant lymphomas with poor prognosis. ATL/ATLL cells express CC chemokine receptor 4, and mogamulizumab (anti-CCR4 monoclonal antibody) exhibits strong cytotoxicity for ATL/ATLL cells. We analyzed plasma samples of 6 patients with ATL/ATLL treated with chemotherapy followed by mogamulizumab therapy (mogatherapy) for changes in the levels of biomarkers in relation to immune-related adverse effects. As treatment is often associated with skin eruptions, we investigated the profiles of inflammatory cytokines, including galectin-9 (Gal-9), which becomes increased in various infectious diseases and allergic patients. Gal-9, soluble interleukin (IL)-2 receptor, tumor necrosis factor-α, and IL-10 levels were increased before chemotherapy, and Gal-9 levels were associated with the sIL-2 receptor, which reflects tumor burden. Inflammatory levels decreased after chemotherapy. After mogatherapy, 5 of 6 patients attained complete remission (CR), whereas 1 patient showed no response (NR) and died. Among 5 patients with CR, the biomarkers remained low during mogatherapy, except for a 3-5-fold increment in Gal-9 (associated with skin eruptions). A skin biopsy showed infiltration by inflammatory cells and Gal-9 synthesis in areas with CD8 cell infiltration. In the patient with NR, increased levels of Gal-9 and the aforementioned biomarkers were noted 3 days after mogatherapy, followed by opportunistic infections resembling immune reconstitution inflammatory syndrome. Therefore, an increased Gal-9 plasma level in ATL/ATLL indicates tumor burden and reflects immune activation by mogatherapy. These findings may indicate that an increase in the Gal-9 level, a novel immune checkpoint molecule, can reflect immune-related adverse effects of various biotherapies.

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Integrated molecular analysis of adult T cell leukemia/lymphoma

Cited by 661 publications

References 60 publications

Reducing the global burden of HTLV-1 infection: An agenda for research and action

Reducing the global burden of HTLV-1 infection: An agenda for research and action

Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas

Galectin-9 as a Predictive Marker for the Onset of Immune-Related Adverse Effects Associated with Anti-CCR4 MoAb Therapy in Patients with Adult T Cell Leukemia

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