Publications by authors named "T Bonnefoix"
Background: MYC-driven lymphomas are a subset of B-cell lymphomas characterized by genetic alterations that dysregulate the expression of the MYC oncogene. When overexpressed, typically through chromosomal translocations, amplifications, or other mechanisms, MYC can drive uncontrolled cell growth and contribute to cancer development. MYC-driven lymphomas are described as aggressive entities which require intensive treatment approaches and can be associated with poor prognosis.
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- R-CHOP immuno-chemotherapy is effective for treating diffuse large B-cell lymphoma (DLBCL), but a significant percentage (30-40%) of patients either don't respond or relapse.
- Researchers have identified the protein CYCLON as a key factor linked to disease progression and treatment resistance in DLBCL, establishing it as a potential predictor of poor outcomes.
- The study also highlights the interaction between CYCLON and NPM1, suggesting that their co-expression and specific locations within the cell could provide insights for developing more tailored treatment strategies for high-risk DLBCL patients.
Article Synopsis
- Diffuse large B-cell lymphoma (DLBCL) is a diverse cancer type treated primarily with the R-CHOP immuno-chemotherapy regimen, but about 30% of patients do not respond or experience a relapse.
- This study examined the expression of biomarkers like c-MYC, p53, and others in a cohort of 94 DLBCL patients to understand their correlation with patient outcomes and tumor characteristics.
- Results showed that p53 overexpression was linked to poorer outcomes, while the “starry-sky” tissue pattern indicated better survival in certain high-risk DLBCL patients, suggesting that these biomarkers can help inform prognosis and treatment strategies.
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and highly aggressive leukemia for which knowledge on disease mechanisms and effective therapies are currently lacking. Only a handful of recurring genetic mutations have been identified and none is specific to BPDCN. In this study, through molecular cloning in an index case that presented a balanced t(3;5)(q21;q31) and molecular cytogenetic analyses in a further 46 cases, we identify monoallelic deletion of NR3C1 (5q31), encoding the glucocorticoid receptor (GCR), in 13 of 47 (28%) BPDCN patients.
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