TNFAIP3 mutation

Genetic mutations, notably in NOTCH2 and TNFAIP3 genes, have discernable negative implications on the prognosis of MZL patients. Recognizing these genetic markers can guide more personalized therapeutic interventions and inform clinical prognosis.

Together, we demonstrate variable clonal B-cell dynamics in LPL/WM patients developing DLBCL, and the occurrence of clonally unrelated DLBCL in about one-quarter of LPL/WM patients. Moreover, we identified commonly mutated genes upon DLBCL transformation, which together with preserved mutations already present in LPL characterize the mutational landscape of DLBCL occurrences in LPL/WM patients.

MYD88 L265P and to lesser extent TNFAIP3 mutations are major mutations in ABC- DLBCL and may be predictive factors for poor OS in ABC- DLBCL patients.

Detection of acquired BTK and PLCG2 mutations in ctDNA while on therapy is feasible and may herald clinical disease progression. This trial was registered at https://anzctr.org.au/ as ACTRN12619000024145.

TNFAIP3 mutation mainly occurs in adult T-ALL patients, and it was associated with adverse clinical outcomes for T-ALL patients; thus, it might be a biomarker for prognostic stratification.

A better understanding of the composition of TIME in EBV-LELCC is critical for predicting the clinical outcomes of ICB treatment.

Fig1E In support of this, SPADE clustering analysis identified three clusters including T FH , T reg and T EM cells. Conclusion We have identified three molecular clusters in IgM monoclonal gammopathies with distinct clinical, proteomic, metabolomic and immune features, suggesting a potential biologic classification that may have therapeutic implications.

An exploratory analysis of the ibrutinib-treated rrMZL study showed mutations in genes regulating NF-kB signalling pathway: TNFAIP3 ( A20 ) and MYD88 predicted response, whereas KMT2D ( MLL2 ) and CARD11 were associated with primary resistance. Conclusion Mutations in genes associated with the NFkB pathway present at baseline are predictive of response to zanubrutinib in rrMZL patients. Detection of acquired BTK and PLCy2 mutations on therapy is feasible and may herald clinical disease progression.

Our study observed comprehensive CNVs in PLELC patients which is a unique molecular feature compared with other NSCLC subtypes and EBV-positive NPC. Higher TMB level and amplifications of B2M in PLELC patients may be used as potential biomarkers to indicate better treatment responses to ICIs.

Those metabolites had intermediate levels in C3. In conclusion, we identified three molecular clusters with distinct clinical, proteomic and metabolomic features, suggesting a potential biologic classification that may have therapeutic implications.