I posted a number of threads over the last 6 months that show cancer's appetite for fat and how inhibiting fatty acid oxidation or transport into the cell can have dramatic therapeutic results even for highly lethal malignancies like pancreatic cancer.
Triple-Negative Breast Cancers Depend On Fat As Fuel
Cancer Cells Addicted To Fat And Use Fat Oxidation For Survival
Achilles Heel Of Cancer Found - Its Addiction To Fat
Dietary Fat And Its Oxidation Drives Cancer Metastasis
Cancer Addiction To Fat Confirmed; Niacinamide As Possible Treatment
Niacinamide Can Cure Liver (and Maybe Pancreatic) Cancer
Now this new study shows that even inhibiting just lipolysis (hello, again, niacinamide) is enough to kill the cancer stem cells, which are responsible for metastasis. Perhaps just as importantly, it shows that the cancer metabolism is akin to hibernation - i.e. the organism relies on fat to satisfy its energetic needs. Inhibiting this supply of fat quickly kills the cancer stem cells, or wakes up the animal from sleep (in the case of hibernation).
The lipolysis pathway sustains normal and transformed stem cells in adult <i>Drosophila</i>
Eliminating cancer stem cells: an interview with CCR’s Steven Hou | Center for Cancer Research
"...Cancer stem cells, or CSCs, are usually localized to a storage niche surrounded by a dense cellular environment, which may make them less accessible to the sugar and amino acid nutrition from the body’s circulatory system. Most normal cells rely on sugar and amino acids for their energy supply with lipolysis (fat) playing only a minor role in their survival. Our results show that CSCs are metabolically unique. Like hibernating animals, they mainly rely on lipid reserves for their energy supply, and blocking a process called COPI/Arf1-mediated lipolysis can starve them to death. We also discovered that CSC-like stem cells were more sensitive than normal stem cells to Arf1 inhibition. So we think that by selectively blocking lipolysis, we may be able to kill CSCs without severe side effects. Further, targeting the COPI/Arf1 complex or the lipolysis pathway appear to be novel approaches for eliminating CSCs."
Can Behenic Acid (C22:0) Levels be a Prognostic Factor in Glial Tumors? - PubMed - NCBI
"...BACKGROUND: Inhibition of fatty acid synthase leads to apoptosis in cancers, which leads to high levels of fatty acid synthesis. This indicates that cancer cells depend on fatty acid in order to survive. In this study, we investigated whether or not there was a relationship between the glial tumor grade and free fatty acid level of tumor tissue."
Triple-Negative Breast Cancers Depend On Fat As Fuel
Cancer Cells Addicted To Fat And Use Fat Oxidation For Survival
Achilles Heel Of Cancer Found - Its Addiction To Fat
Dietary Fat And Its Oxidation Drives Cancer Metastasis
Cancer Addiction To Fat Confirmed; Niacinamide As Possible Treatment
Niacinamide Can Cure Liver (and Maybe Pancreatic) Cancer
Now this new study shows that even inhibiting just lipolysis (hello, again, niacinamide) is enough to kill the cancer stem cells, which are responsible for metastasis. Perhaps just as importantly, it shows that the cancer metabolism is akin to hibernation - i.e. the organism relies on fat to satisfy its energetic needs. Inhibiting this supply of fat quickly kills the cancer stem cells, or wakes up the animal from sleep (in the case of hibernation).
The lipolysis pathway sustains normal and transformed stem cells in adult <i>Drosophila</i>
Eliminating cancer stem cells: an interview with CCR’s Steven Hou | Center for Cancer Research
"...Cancer stem cells, or CSCs, are usually localized to a storage niche surrounded by a dense cellular environment, which may make them less accessible to the sugar and amino acid nutrition from the body’s circulatory system. Most normal cells rely on sugar and amino acids for their energy supply with lipolysis (fat) playing only a minor role in their survival. Our results show that CSCs are metabolically unique. Like hibernating animals, they mainly rely on lipid reserves for their energy supply, and blocking a process called COPI/Arf1-mediated lipolysis can starve them to death. We also discovered that CSC-like stem cells were more sensitive than normal stem cells to Arf1 inhibition. So we think that by selectively blocking lipolysis, we may be able to kill CSCs without severe side effects. Further, targeting the COPI/Arf1 complex or the lipolysis pathway appear to be novel approaches for eliminating CSCs."
Can Behenic Acid (C22:0) Levels be a Prognostic Factor in Glial Tumors? - PubMed - NCBI
"...BACKGROUND: Inhibition of fatty acid synthase leads to apoptosis in cancers, which leads to high levels of fatty acid synthesis. This indicates that cancer cells depend on fatty acid in order to survive. In this study, we investigated whether or not there was a relationship between the glial tumor grade and free fatty acid level of tumor tissue."
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