Exact(4)
In summary, these experiments demonstrate that a RANK-mediated signaling network can drive PCa tumor growth in the mouse skeleton.
Thus, our data and previous studies reveal that promoter hypermethylation of SLIT2 and SLIT3 regions drive PCa progression and downregulation of miR-218 in PCa cells.
Understanding the factors that drive PCa towards increased cell proliferation is crucial for the development of new therapies that can prevent and/or inhibit the initiation and/or progression of PCa.
Despite a growing number of studies, the mechanisms leading to these phenotypes are still poorly defined, even though understanding the factors that drive PCa to apoptosis resistance is vital for the development of new therapies for advanced PCa.
Similar(55)
Therefore, identifying cellular components and molecular mechanisms that drive aggressive PCa at early stage is critical for disease prognosis and therapeutic intervention.
As androgens regulate secretion and development of the normal prostate and drive prostate cancer (PCa) growth, they may affect UPR pathways.
Strategies to reduce prostate-specific antigen (PSA)–driven prostate cancer (PCa) overdiagnosis and overtreatment seem to be necessary.
Specifically, we hypothesize that the simultaneous presence of PCE and PCI that is, product configuration ambidexterity (PCA)—drives superior firm responsiveness and, indirectly firm sales and operating margin.
In summary, we describe here a novel genetically engineered mouse model of invasive PCA driven by MAPK activation via inducible BRAF mutation under an androgen-insensitive promoter.
The instant Gardos channel-mediated response observed upon membrane deformation under the patch pipette (Figures 1 and 2A), suggests that calcium entering the cell via PCa, driven by the steep inward Ca2+ gradient, induces a new pump-leak balance with [Ca2+]i high enough to elicit maximal activation of the Gardos channels.
The similarity of reactive stroma in primary and bone metastatic site could drive the coevolution of PCa toward an osteotropic phenotype stimulating the expression of the cytokines CXCL1 and CXCL16 [ 55].
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