Publications by authors named "Christine Klement"
Article Synopsis
- Natural killer (NK) cells are vital for fighting metastasis, but disseminated tumor cells (DTCs) in the lungs release prostaglandin E2 (PGE), which leads to NK cell dysfunction.
- This dysfunction is triggered by PGE binding to specific receptors (EP2 and EP4), altering NK cell gene expression and reducing the production of important anti-metastatic signals.
- Targeting the PGE-EP2/EP4 pathway may provide a new therapeutic strategy to enhance NK cell activity against metastatic tumors in distant organs.
The PDCD1-encoded immune checkpoint receptor PD-1 is a key tumor suppressor in T cells that is recurrently inactivated in T cell non-Hodgkin lymphomas (T-NHLs). The highest frequencies of PDCD1 deletions are detected in advanced disease, predicting inferior prognosis. However, the tumor-suppressive mechanisms of PD-1 signaling remain unknown.
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- Scientists studied how changes in gene regulation, which are not directly about the genes themselves, affect cancer in mice.
- They found that small variations in gene activity can play a big role in how tumors develop and grow.
- Their research helped identify certain non-coding regions linked to cancer and showed how these changes can lead to serious tumors in specific types of cells.
Article Synopsis
- SNAIL is a crucial transcriptional regulator that plays significant roles in embryonic development and cancer, specifically through its influence on epithelial-to-mesenchymal transition (EMT).
- Research indicates that SNAIL has oncogenic functions independent of EMT, exhibiting varied effects depending on the tissue and genetic context, such as either protecting against or promoting tumor growth in different types of cancer.
- The findings reveal that SNAIL's oncogenic effects do not involve typical mechanisms like E-cadherin downregulation, but instead facilitate cancer progression by bypassing cellular senescence and affecting cell cycle regulation through inactivation of the Retinoblastoma (RB) protein.
Unlabelled: The mortality of patients with pancreatic ductal adenocarcinoma (PDAC) is strongly associated with metastasis, a multistep process that is incompletely understood in this disease. Although genetic drivers of PDAC metastasis have not been defined, transcriptional and epigenetic rewiring can contribute to the metastatic process. The epigenetic eraser histone deacetylase 2 (HDAC2) has been connected to less differentiated PDAC, but the function of HDAC2 in PDAC has not been comprehensively evaluated.
View Article and Find Full Text PDFThe lymphoid-myeloid transdifferentiation potentials of members of the C/EBP family (C/EBPα, β, δ, and ε) were compared in v-Abl-immortalized primary B cells. Conversion of B cells to macrophages was readily induced by the ectopic expression of any C/EBP, and enhanced by endogenous C/EBPα and β activation. High transgene expression of C/EBPβ or C/EBPε, but not of C/EBPα or C/EBPδ, also induced the formation of granulocytes.
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