Publications by authors named "R N Rys"
Article Synopsis
- * The review explores how neutrophils can survive in the tumor microenvironment (TME) and emphasizes that simply stopping neutrophil influx isn't enough, as these cells can evade treatment.
- * It suggests that targeting and eliminating long-lived neutrophils could improve the effectiveness of cancer therapies beyond conventional methods.
Article Synopsis
- Venous thromboembolism is linked to endothelial cell activation, inflammation, and the release of extracellular RNA (eRNA), with TLR3 potentially serving as the receptor for eRNA in this process.
- Experiments involving mice with and without TLR3 showed that eRNA influenced thrombus size and formation, with treatments affecting signaling pathways and neutrophil recruitment.
- Overall, the study highlights the role of TLR3 and eRNA in promoting venous thromboembolism, indicating their potential as therapeutic targets for managing this condition.
We report the case of a patient who was referred to our institution with a diagnosis of CD4+ small/medium-sized pleomorphic lymphoma. At the time, the patient showed a plethora of lesions mainly localizing to the legs; thus, we undertook studies to investigate the lineage and immunophenotype of the neoplastic clone. Immunohistochemistry (IHC) showed marked CD4 and CD8 positivity.
View Article and Find Full Text PDFThe treatment of patients with relapsed or refractory lymphoid neoplasms represents a significant clinical challenge. Here, we identify the pro-survival BCL-2 protein family member MCL-1 as a resistance factor for the BCL-2 inhibitor venetoclax in non-Hodgkin lymphoma (NHL) cell lines and primary NHL samples. Mechanistically, we show that the antibody-drug conjugate polatuzumab vedotin promotes MCL-1 degradation via the ubiquitin/proteasome system.
View Article and Find Full Text PDFBackground: Acute myeloid leukemia (AML) is an aggressive hematological cancer resulting from uncontrolled proliferation of differentiation-blocked myeloid cells. Seventy percent of AML patients are currently not cured with available treatments, highlighting the need of novel therapeutic strategies. A promising target in AML is the mammalian target of rapamycin complex 1 (mTORC1).
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