About: Advances in understanding of angioimmunoblastic T-cell lymphoma

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Advances in understanding of angioimmunoblastic T-cell lymphoma
Creator	Chiba, Shigeru Sakata-Yanagimoto, Mamiko
Source	PMC
abstract	It has been nearly half a century since angioimmunoblastic T-cell lymphoma (AITL) was characterized in the early 1970’s. Our understanding of the disease has dramatically changed due to multiple discoveries and insights. One of the key features of AITL is aberrant immune activity. Although AITL is now understood to be a neoplastic disease, pathologists appreciated that it was an inflammatory condition. The more we understand AITL at cellular and genetic levels, the more we view it as both a neoplastic and an inflammatory disease. Here, we review recent progress in our understanding of AITL, focusing on as yet unsolved questions.
has issue date	2020-07-23(xsd:dateTime)
bibo:doi	10.1038/s41375-020-0990-y
has license	cc-by
sha1sum (hex)	c4fbcbef6923fe4dccd88f625068dbd94d6c898f
schema:url	https://doi.org/10.1038/s41375-020-0990-y
resource representing a document's title	Advances in understanding of angioimmunoblastic T-cell lymphoma
has PubMed Central identifier	PMC7376827
schema:publication	Leukemia
resource representing a document's body	covid:c4fbcbef6923fe4dccd88f625068dbd94d6c898f#body_text
is schema:about of	named entity 'neoplastic' named entity 'insights' named entity 'HALF' named entity 'NEOPLASTIC DISEASE' named entity 'PROGRESS' named entity 'Here' named entity 'changed' named entity 'cellular' named entity 'pathologists' named entity 'inflammatory condition' named entity 'neoplastic disease' named entity 'FDCs' named entity 'chronic myelomonocytic leukemia' named entity 'dysplastic' named entity 'cell differentiation' named entity 'IDH2' named entity 'PDL1' named entity 'Tfh' named entity 'Tfh' named entity 'FDCs' named entity 'Rhoa' named entity 'macrophages' named entity 'SRBC' named entity 'FDC' named entity 'RHOA' named entity 'RHOA' named entity 'TET2' named entity 'germinal center' named entity 'tumor cells' named entity 'Tet2' named entity 'abnormal cells' named entity 'PTCL-NOS' named entity 'T-cell' named entity 'CD4' named entity 'prognosis' named entity 'Bcl6' named entity 'Tfh' named entity 'VAV1' named entity 'neoplastic' named entity 'mantle cell lymphoma' named entity 'antigens' named entity 'ICOS' named entity 'PTCL-NOS' named entity 'Tfh' named entity 'ISH' named entity '5-fC' named entity 'gene' named entity 'cell migration' named entity 'mutated gene' named entity 'transgenic mice' named entity 'BCL6' named entity 'tumor' named entity 'TCR' named entity 'Tfh' named entity 'TET2' named entity 'aerobic glycolysis' named entity 'IDH1' named entity 'PTCL-NOS' named entity 'DNMT3A' named entity 'deficient mice' named entity 'hyperplasia' named entity 'clinical trial' named entity 'somatic' named entity 'immunostaining' named entity 'tumor cells' named entity 'Tfh' named entity 'AML' named entity 'checkpoint inhibition' named entity 'hyperplastic' named entity 'RHOA' named entity 'NOTCH signaling' named entity 'cells differentiate' named entity 'phenotypically' named entity 'TET2' named entity 'lymphocytes' named entity 'transcription factor' named entity 'Tfh' named entity 'VAV1' named entity 'downregulation' named entity 'CD4 +' named entity 'interact' named entity 'RHOA'

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