Development of a sensitive two-site immunoradiometric assay for parathyroid hormone-related peptide: evidence for elevated levels in plasma from patients with adult T-cell leukemia/lymphoma and B-cell lymphoma

1994 ◽  
Vol 79 (5) ◽  
pp. 1322-1327 ◽  
Author(s):  
K. Ikeda
Keyword(s):  
Parathyroid Hormone ◽  
T Cell ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Immunoradiometric Assay ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Related Peptide ◽  
Parathyroid Hormone Related Peptide

Epstein-Barr virus (EBV) genome carrying monoclonal B-cell lymphoma in a patient with adult T-cell leukemia-lymphoma

1991 ◽  
Vol 15 (9) ◽  
pp. 837-846 ◽  
Author(s):  
Kensei Tobinai ◽  
Tomoko Ohtsu ◽  
Masaki Hayashi ◽  
Tomohiro Kinoshita ◽  
Yoshihiro Matsuno ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Smoldering Adult T-Cell Leukemia with B-Cell Lymphoma and Early Gastric Cancer.

1995 ◽  
Vol 34 (2) ◽  
pp. 118-121 ◽  
Author(s):  
Mayumi KODAMA ◽  
Hitoshi MATSUOKA ◽  
Koichi MAEDA ◽  
Muneou SUZUKI ◽  
Akihiko OKAYAMA ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cell ◽  
Early Gastric Cancer ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia

Epstein–Barr virus-related diffuse large B-cell lymphoma in mogamulizumab-treated adult T-cell leukemia with incomplete T-cell reconstitution

2018 ◽  
Vol 109 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Kazuharu Kamachi ◽  
Takero Shindo ◽  
Masaharu Miyahara ◽  
Kazutaka Kitaura ◽  
Michiaki Akashi ◽  
...  
Keyword(s):  
T Cell ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Epstein Barr ◽  
Large B Cell

Clinical Applications of the Genomic Landscape of Aggressive Non-Hodgkin Lymphoma

2017 ◽  
Vol 35 (9) ◽  
pp. 955-962 ◽  
Author(s):  
Andrea B. Moffitt ◽  
Sandeep S. Dave
Keyword(s):  
T Cell ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large Cell ◽  
T Cell Lymphoma ◽  
Adult T Cell Leukemia ◽  
Non Hodgkin Lymphoma ◽  
T Cell Lymphomas

In this review, we examine the genomic landscapes of lymphomas that arise from B, T, and natural killer cells. Lymphomas represent a striking spectrum of clinical behaviors. Although some lymphomas are curable with standard therapy, the majority of the affected patients succumb to their disease. Here, the genetic underpinnings of these heterogeneous entities are reviewed. We consider B-cell lymphomas, including Burkitt lymphoma, diffuse large B-cell lymphoma, Hodgkin lymphoma, and primary mediastinal B-cell lymphoma. We also examine T-cell lymphomas, including anaplastic large-cell lymphoma, angioimmunoblastic T-cell lymphoma, cutaneous T-cell lymphoma, adult T-cell leukemia/lymphoma, and other peripheral T-cell lymphomas. Together, these malignancies make up most lymphomas diagnosed around the world. Genomic technologies, including microarrays and next-generation sequencing, have enabled a better understanding of the molecular underpinnings of these cancers. We describe the broad genomics findings that characterize these lymphoma types and discuss new therapeutic opportunities that arise from these findings.

Whole-genome landscape of adult T-cell leukemia/lymphoma

Blood ◽  
2021 ◽  
Author(s):  
Yasunori Kogure ◽  
Takuro Kameda ◽  
Junji Koya ◽  
Makoto Yoshimitsu ◽  
Kisato Nosaka ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cell ◽  
B Cell Lymphoma ◽  
Genetic Alterations ◽  
Whole Genome ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Driver Genes ◽  
Adult T Cell Leukemia

Adult T-cell leukemia/lymphoma (ATL) is an aggressive neoplasm immunophenotypically resembling regulatory T cells, associated with human T-cell leukemia virus type-1. Here we performed whole-genome sequencing (WGS) of 150 ATL cases to reveal the overarching landscape of genetic alterations in ATL. We discovered frequent (33%) loss-of-function alterations preferentially targeting the CIC long isoform, which were overlooked by previous exome-centric studies of various cancer types. Long but not short isoform-specific inactivation of Cic selectively increased CD4+CD25+Foxp3+ T cells in vivo. We also found recurrent (13%) 3′-truncations of REL, which induce transcriptional upregulation and generate gain-of-function proteins. More importantly, REL truncations are also common in diffuse large B-cell lymphoma, especially in germinal center B-cell-like subtype (12%). In the non-coding genome, we identified recurrent mutations in regulatory elements, particularly splice sites, of several driver genes. In addition, we characterized the different mutational processes operative in clustered hypermutation sites within and outside immunoglobulin/T-cell receptor genes and identified the mutational enrichment at the binding sites of host and viral transcription factors suggesting their activities in ATL. By combining the analyses for coding and non-coding mutations, structural variations, and copy number alterations, we discovered 56 recurrently altered driver genes, including 11 novel ones. Finally, ATL cases were classified into two molecular groups with distinct clinical and genetic characteristics based on the driver alteration profile. Our findings not only help to improve diagnostic and therapeutic strategies in ATL, but also provide insights into T-cell biology and have implications for genome-wide cancer driver discovery.

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