Metabolic adaptations in cancers expressing isocitrate dehydrogenase mutations - Scienc... - 0 views
Metabolic management of brain cancer - 0 views
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Glutamine is a major metabolic fuel for both brain tumor cells and tumor-associated macrophages (TAMs)
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the malignant phenotype of brain tumor cells that survive radiotherapy is often greater than that of the cells from the original tumor.
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Conventional chemotherapy has faired little better than radiation therapy for the long-term management of malignant brain cancer
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Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors i... - 0 views
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The presence and activity of PR significantly affect the prognostic value of ER.
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The observed loss of PR protein expression in a subset of ER+/PR+ breast cancers, because of hypermethylation or deletion of the PR gene locus, results in the loss of ER prognostic value
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These findings emphasize the clinical value of assessing both PR and ER expression in breast cancer samples
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WOW!! study finds that progesterone through PR activity antagonizes ER protein expression by the cell. This has huge implications in breast cancer and possible prostate cancer. But then again, women don't need progesterone; only estrogen. The presence of PR correlates with improved clinicopathological outcomes. The authors do seem to get confused about progesterone and progestins. They are not one in the same.
Mitochondrial Fission Induces Glycolytic Reprogramming in Cancer-Associated Myofibrobla... - 0 views
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L-lactate functions as an onco-metabolite, stimulating mitochondrial biogenesis and OXPHOS in adjacent cancer cells, directly providing energy for tumor growth
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Oxidative stress in stromal fibroblasts then induces their metabolic conversion into cancer-associated fibroblasts. Such oxidative stress drives the onset of autophagy, mitophagy, and aerobic glycolysis in fibroblasts, resulting in the local production of high-energy mitochondrial fuels (such as L-lactate, ketone bodies, and glutamine). These recycled nutrients are then transferred to cancer cells, where they are efficiently burned via oxidative mitochondrial metabolism (OXPHOS)
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stromal L-lactate serves as a high-energy mitochondrial “fuel” for cancer cells. We have termed this new model of cancer metabolism “Two-Compartment Tumor Metabolism”, where two opposing metabolic compartments co-exist, side-by-side, with stromal glycolysis fueling OXPHOS in cancer cells
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A good discussion of what is proposed the Reverse Warburg effect. A process by which the local environment dictates tumor progression. The cancer cells release ROS primarily in the form of H2O2 and this leads to Cancer Associated Fibroblasts (CAFs) in the stroma. The altered stromal environment increases ROS further and promotes ocogenic metabolites through the classic Warburg effect. This high lactate production from the CAFs then is used by the cancer cells via classic oxidative phosphorylation. Complex, beautiful and still an the understanding is a work in progress. This study/article points to the importance of oxidative stress in some cancer development through CAFs.
Adenoid cystic carcinoma: current therapy and potential therapeutic advances based on g... - 0 views
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Cisplatin and 5-FU or CAP (cisplatin, doxorubicin, and cyclophosphamide) regimens can be used for combination chemotherapy
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patients with advanced salivary gland malignancy treated with the CAP regimen achieved partial response (PR) or stable disease (SD) rates of 67% (8 out of 12 patients)
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Agents commonly given as monotherapy for treating ACC are cisplatin, mitoxantrone, epirubicin, vinorelbine, paclitaxel, and gemcitabine. However, few of these agents have shown efficacy
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Anticancer mechanisms of cannabinoids - 0 views
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modulating key cell signalling pathways involved in the control of cancer cell proliferation and survival
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cannabinoids inhibit angiogenesis and decrease metastasis in various tumour types in laboratory animals
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Cannabis sativa L. (marijuana)
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The current state and future perspectives of cannabinoids in cancer biology - 0 views
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The activation of each of them leads to an inhibition of adenylyl cyclase via G proteins (Gi/o), which in turn activates many metabolic pathways such as mitogen‐activated protein kinase pathway (MAPK), phosphoinositide 3‐kinase pathway (PI3K), cyclooxygenase‐2 pathway (COX‐2), accumulation of ceramide, modulation of protein kinase B (Akt), and ion channels
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phytocannabinoids, endocannabinoids, and synthetic cannabinoids
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Action of THC in human organism relies on mimicking endogenous agonists of CB receptors—endocannabinoids
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