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Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling
TLDR
It is shown that there is diversity in gene expression among the tumours of DLBCL patients, apparently reflecting the variation in tumour proliferation rate, host response and differentiation state of the tumour.
Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray.
TLDR
In summary, immunostains can be used to determine the GCB and non-GCB subtypes of DLBCL and predict survival similar to the cDNA microarray.
Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma
TLDR
Findings establish chronic active BCR signalling as a new pathogenetic mechanism in ABC DLBCL, suggesting several therapeutic strategies.
Stromal gene signatures in large-B-cell lymphomas.
TLDR
Survival after treatment of diffuse large-B-cell lymphoma is influenced by differences in immune cells, fibrosis, and angiogenesis in the tumor microenvironment, and a multivariate model created from three gene-expression signatures predicted survival both in patients who received CHOP and patients who receive R-CHOP.
Oncogenically active MYD88 mutations in human lymphoma
TLDR
The dependence of ABC DLBCLs on MYD88, an adaptor protein that mediates toll and interleukin (IL)-1 receptor signalling, is described and the development of inhibitors of IRAK4 kinase and other components of this pathway for the treatment of tumours bearing oncogenic MyD88 mutations are supported.
The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma.
TLDR
DNA microarrays can be used to formulate a molecular predictor of survival after chemotherapy for diffuse large-B-cell lymphoma and this gene-based predictor and the international prognostic index were independent prognostic indicators.
Constitutive Nuclear Factor κB Activity Is Required for Survival of Activated B Cell–like Diffuse Large B Cell Lymphoma Cells
TLDR
Findings establish the NF-κB pathway as a new molecular target for drug development in the most clinically intractable subtype of DLBCL and demonstrate that the twoDLBCL subtypes defined by gene expression profiling utilize distinct pathogenetic mechanisms.
Targeting B cell receptor signaling with ibrutinib in diffuse large B cell lymphoma
TLDR
The selective development of ibrutinib for the treatment of ABC DLBCL is supported, with the highest number of responses occurred in ABC tumors that lacked BCR mutations, suggesting that oncogenic BCR signaling in ABC does not require B CR mutations and might be initiated by non-genetic mechanisms.
Control of inflammation, cytokine expression, and germinal center formation by BCL-6.
TLDR
Dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6-deficient mice and participate in lymphoid malignancies.
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