Publications by authors named "K Korfi"
Article Synopsis
- In follicular lymphoma (FL), doctors have trouble finding the best treatment because different patients have different types of the disease, except for one drug that helps some patients with a specific gene change.
- Researchers studied 21 patients with FL who were not getting better and were treated with two different drugs, everolimus and temsirolimus, to see how their gene changes affected treatment success.
- They found that patients who responded well to the drugs had more changes in a specific gene called CREBBP, suggesting that this gene can help predict which treatments might work better for FL patients.
Article Synopsis
- T-cell responses require two signals for effective activation: engagement of T-cell receptors (signal 1) and additional costimulatory signals (signal 2), which T-cell bispecific antibodies (TCBs) can provide by targeting specific antigens and CD3ε.
- The study introduces CD19-CD28, a bispecific CD19-targeted CD28 agonist, designed to enhance the effectiveness of glofitamab, a TCB targeting malignant B cells, by delivering the crucial costimulatory signal 2 needed for stronger T-cell responses.
- Initial results show that combining glofitamab with CD19-CD28 and the 4-1BB agonist significantly improves long
Background: Acute Myeloid leukemia is a heterogeneous disease that requires novel targeted treatment options tailored to the patients' specific microenvironment and blast phenotype.
Methods: We characterized bone marrow and/or blood samples of 37 AML patients and healthy donors by high dimensional flow cytometry and RNA sequencing using computational analysis. In addition, we performed ex vivo ADCC assays using allogeneic NK cells isolated from healthy donors and AML patient material to test the cytotoxic potential of CD25 Mab (also referred to as RG6292 and RO7296682) or isotype control antibody on regulatory T cells and CD25+ AML cells.
Despite the effectiveness of immuno-chemotherapy, 40% of patients with diffuse large B-cell lymphoma (DLBCL) experience relapse or refractory disease. Longitudinal studies have previously focused on the mutational landscape of relapse but fell short of providing a consistent relapse-specific genetic signature. In our study, we have focused attention on the changes in GEP accompanying DLBCL relapse using archival paired diagnostic/relapse specimens from 38 de novo patients with DLBCL.
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