30 research outputs found
Predictive value of VEGF gene polymorphisms for metastatic colorectal cancer patients receiving first-line treatment including fluorouracil, irinotecan, and bevacizumab
The aim of this study is to evaluate the influence of germline vascular endothelial growth factor (VEGF) gene polymorphisms (VGPs) on the efficacy of the anti-VEGF antibody bevacizumab (Bev) in metastatic colorectal cancer (MCRC) patients
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PTHrP produced by myeloma plasma cells regulates their survival and pro-osteoclast activity for bone disease progression.
To promote their survival and progression in the skeleton, osteotropic malignancies of breast, lung, and prostate produce parathyroid
hormoneârelated protein (PTHrP), which induces hypercalcemia. PTHrP serum elevations have also been described in multiple
myeloma (MM), although their role is not well defined. When we investigated MM cells from patients and cell lines, we found that
PTHrP and its receptor (PTHâR1) are highly expressed, and that PTHrP is secreted both as a fullâlength molecule and as small subunits.
Among these subunits, the midâregion, including the nuclear localization sequence (NLS), exerted a proliferative effect because it was
accumulated in nuclei of MM cells surviving in starvation conditions. This was confirmed by increased transcription of several genes
enrolled in proliferation and apoptosis control. PTHrP was also found to stimulate PTHâR1 inMMcells. PTHâR1âs selective activation by
the fullâlength PTHrP molecule or the NH2âterminal fragment resulted in a significant increase of intracellular Ca2ĂŸ influx, cyclic
adenosine monophosphate (cAMP) content, and expression of receptor activator of NFâkB ligand (RANKL) and monocyte
chemoattractant proteinâ1 (MCPâ1). Our data definitely clarify the role of PTHrP in MM. The PTHrP peptide is functionally secreted by
malignant plasma cells and contributes to MM tumor biology and progression, both by intracrine maintenance of cell proliferation in
stress conditions and by autocrine or paracrine stimulation of PTHâR1, which in turn reinforces the production of osteoclastogenic
factors
A novel K-ras mutation in colorectal cancer. A case report and literature review
Activating mutations in the K-ras oncogene mainly occur in codons 12 and 13 and may be predictive of response to drugs directly linked to the K-ras signaling pathway, such as panitumumab and cetuximab