Gene expression profiling (GEP) defined molecular signatures for AITL and delineated biological and prognostic subgroups within PTCL-NOS (PTCL-GATA3 and PTCL-TBX21).
MRI-derived measures of liver and spleen stiffness as well as laboratory-based APRI and FIB-4 scores are highly associated with imaging findings of portal hypertension in children and young adults with AILD and thus might be useful for predicting portal hypertension impending onset and directing personalized patient management.
Reexamination and immunohistochemical staining of the previously biopsied lymph node specimen revealed the same clonal population of T cells positive for CD3, CD4, CD10, and programmed cell death protein 1 (PD-1) that was present in the skin and confirmed a diagnosis of AITL.
Reexamination and immunohistochemical staining of the previously biopsied lymph node specimen revealed the same clonal population of T cells positive for CD3, CD4, CD10, and programmed cell death protein 1 (PD-1) that was present in the skin and confirmed a diagnosis of AITL.
Somatic driver mutations have been found in TET2, IDH2, DNMT3A, RHOA, FYN, PLCG1, and CD28, whereas germline susceptibility to AITL has to our knowledge not been studied.
These results suggest that a combination of immunohistochemistry and AS-PCR or NGS should be considered for the identification of IDH2 mutations in AITL in a routine setting.
Immunological biomarker analysis showed elevated levels of inflammatory cytokines (IL-1β, IFN-γ, TNF-α, IL-8) and immunoglobulin A in the saliva of patients with AILD.
ALRN-6924 induced a complete remission in a patient with TP53-wild-type angioimmunoblastic T-cell lymphoma, demonstrating the potential for rapid translation of discoveries from subtype-specific preclinical models.
RhoA G17V mice crossed with <i>Tet2</i><sup>fl/fl</sup>; Vav-Cre<sup>+</sup> mice, which delete <i>Tet2</i> throughout the hematopoietic compartment, developed T-cell lymphomas that retained histologic and immunophenotypic features of AITL and had transcriptional signatures enriched for mechanistic target of rapamycin (mTOR)-associated genes.
We studied a series of 98 n-PTCL samples (comprising 57 AITL and 41 PTCL-NOS) with five T<sub>FH</sub> antibodies (CD10, BCL-6, PD-1, CXCL13, ICOS), looked for mutations in five of the genes most frequently mutated in AITL (<i>TET2</i>, <i>DNMT3A, IDH2, RHOA</i> and <i>PLCG1</i>) using the Next-Generation-Sequencing Ion Torrent platform, and measured the correlations of these characteristics with morphology and clinical features.
We studied a series of 98 n-PTCL samples (comprising 57 AITL and 41 PTCL-NOS) with five T<sub>FH</sub> antibodies (CD10, BCL-6, PD-1, CXCL13, ICOS), looked for mutations in five of the genes most frequently mutated in AITL (<i>TET2</i>, <i>DNMT3A, IDH2, RHOA</i> and <i>PLCG1</i>) using the Next-Generation-Sequencing Ion Torrent platform, and measured the correlations of these characteristics with morphology and clinical features.
We studied a series of 98 n-PTCL samples (comprising 57 AITL and 41 PTCL-NOS) with five T<sub>FH</sub> antibodies (CD10, BCL-6, PD-1, CXCL13, ICOS), looked for mutations in five of the genes most frequently mutated in AITL (<i>TET2</i>, <i>DNMT3A, IDH2, RHOA</i> and <i>PLCG1</i>) using the Next-Generation-Sequencing Ion Torrent platform, and measured the correlations of these characteristics with morphology and clinical features.
We studied a series of 98 n-PTCL samples (comprising 57 AITL and 41 PTCL-NOS) with five T<sub>FH</sub> antibodies (CD10, BCL-6, PD-1, CXCL13, ICOS), looked for mutations in five of the genes most frequently mutated in AITL (<i>TET2</i>, <i>DNMT3A, IDH2, RHOA</i> and <i>PLCG1</i>) using the Next-Generation-Sequencing Ion Torrent platform, and measured the correlations of these characteristics with morphology and clinical features.
We measured the percentage positivity of the T<sub>FH</sub> markers, BCL6 and PD1, in AITL CD4-positive cells to be approximately 26% and 45%, with 12% coexpressing both markers.
In total, 97 patients with AITL (n=37), PTCL-NOS (n=40), ALK-negative ALCL (n=11), or ALK-positive ALCL (n=9) were treated with CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone).
In total, 97 patients with AITL (n=37), PTCL-NOS (n=40), ALK-negative ALCL (n=11), or ALK-positive ALCL (n=9) were treated with CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone).
We measured serum levels of IL-5, IL-10, IL-12, and interferon-gamma (IFN-γ) at diagnosis in AITL and other common subtypes of nodal T-cell lymphoma including peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS), ALK-negative anaplastic large cell lymphoma (ALCL) or ALK-positive ALCL between September 2008 and December 2014.