Nerea Martinez

TL;DR: Functional studies demonstrated that PLCG1 mutants elicited increased downstream signaling toward NFAT activation, and inhibition of this pathway resulted in reduced CTCL cell proliferation and cell viability, suggesting increased proliferative and survival mechanisms in C TCL may partially depend on the acquisition of somatic mutations in PLCg1 and other genes that are essential for normal T-cell differentiation.

TL;DR: MCL seems to combine a disease-specific signature and different sets of genes of which the expression is associated with key clinical, molecular, and immunophenotypical events, which yields a gene-expression based survival predictor.

TL;DR: Examination of expression profiling and tissue microarray studies of 209 and 323 non‐Hodgkin's lymphomas respectively, including the most frequent sub‐types of NHL, showed that NF‐κB activation is a common phenomenon in NHL, resulting in the expression of distinct sets of NF-κB target genes, depending on the cell context.

TL;DR: Characterizing this tumor more comprehensively, and of identifying new diagnostic and prognostic markers, cDNA microarray expression profiling and tissue microarray immunohistochemical studies in a relatively large series of 44 SMZLs revealed a largely homogenous signature, implying the existence of a single molecular entity.

TL;DR: Nonrandom usage of IgV(H) segments suggests that specific antigens may play a pathogenically relevant role in the genesis or progression of subsets of MCL cases and may help in distinguishing a significant group of M CL long-term survivors.