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Aardbeien tegen kanker*
De bioactieve stof fisetine (vooral voorkomend in aardbeien) blijkt volgens nieuwe studies kankercellen te kunnen doden. Uit een Chinese studie blijkt dat hoe dat gaat met borstkankercellen. Andere studies laten dit zien bij prostaatkanker en blaaskanker. Fisetine is in staat om kankercellen al in een vroeg stadium te doden door in te grijpen op het aangeboren immuunsysteem.
Fisetin Demonstrates Potent Anti-Cancer Properties
Fisetin is a unique polyphenol flavonoid found in many plants and fruits, especially strawberries and mangoes. Standardized fisetin extracts are available as a dietary supplement and have demonstrated a high level of neuro-protection and support for memory, as I documented in a previous article, Fisetin for Neuro-Protection. An impressive array of new studies shows that fisetin has strong anti-cancer activity.
Helping cancer cells die faster, while protecting non-cancer cells, is turning out to be the forte of many nutrients. Fisetin has now demonstrated this property against human breast cancer cells. It demonstrated the ability to help membranes of cancer cells rupture, interfere with how cancer cells make energy, along with activating various gene-related death signals. At the same time, none of these cell death properties take place in healthy cells. The researchers concluded that, “These data allow us to propose that fisetin appears as a new potential anticancer agent which can be applied to develop a clinical protocol of human breast cancers.”
I often explain that TNFa (tumor necrosis factor alpha) is involved with inflammation that is adverse. However, as the name implies, this inflammatory messenger was first discovered and named based on its ability to knock out cancer. TNFa activation in the right amount and at the right time does just that. However, in situations of poor health such as obesity, which is invariably associated with higher levels of TNFa, the TNFa loses its ability to kill cancer. You might say “TNFa resistance” is like insulin resistance, meaning that too much of something at the wrong time is like crying wolf and your body simply tunes it out. Researchers have found that TNFa transitions into a new molecule called Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), which is required to activate the cancer-killing activity of TNFa and that the success of cancer cells to escape TRAIL is typical in tumor growth. A new study with prostate cancer cells shows that fisetin restores the ability of TRAIL to kill prostate cancer cells, leading the researchers to state, “Our data indicate the usefulness of fisetin in prostate cancer chemoprevention through enhancement of TRAIL-mediated apoptosis.”
P53 is a gene-signal that suppresses tumors. Its activity is typically lacking in cancer patients. NF-kappaB is the core inflammatory gene signal, which is typically too active in any type of cancer situation. Researchers working with bladder cancer cells have shown that fisetin helps boost p53 while helping to suppress NF-kappaB, two very helpful general mechanisms that would help guard against cancer.
It is a common theme of any cancer that various healthy gene-signaling pathways have been hijacked and perverted to aid the survival of the cancer. In a another prostate cancer example, this one involving the type of prostate cancer cells that are not treatable with androgen-suppressing therapy, it was found that fisetin could reclaim an important gene pathway, thus overcoming the hijacking and thereby assisting in the death of prostate cancer cells. The University of Wisconsin researchers said, “These results suggest that fisetin could be a useful chemotherapeutic agent in treatment of hormone refractory prostate cancer.”
University of Wisconsin researchers have also shown that fisetin used similar mechanisms to help kill lung cancer cells. And they have shown that fisetin, once again interrupting cancer gene-signaling, is able to help kill melanoma cancer cells. They state, “Our data suggest that fisetin can be developed as an effective agent against melanoma because of its potential inhibitory effect on β-catenin/Mitf signaling.”
True enough, these are all cell studies. However, they lay a solid foundation for the intake of a nutrient to assist in prevention of cancer and to be potentially used along with appropriate therapy in the treatment of cancer. While no human dose is currently documented for this purpose at this time, it sure doesn’t hurt to have fisetin on your nutrient support team. 

Int J Oncol. 2012 Feb;40(2):469-78. doi: 10.3892/ijo.2011.1203. 
Dietary flavonoid fisetin targets caspase-3-deficient human breast cancer MCF-7 cells by induction of caspase-7-associated apoptosis and inhibition of autophagy.
Yang PM, Tseng HH, Peng CW, Chen WS, Chiu SJ.
Source
Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan, ROC.
Abstract
The outcome of producing apoptotic defects in cancer cells is the primary obstacle that limits the therapeutic efficacy of anticancer agents, and hence the development of novel agents targeting novel non-canonical cell death pathways has become an imperative mission for clinical research. Fisetin (3,3',4',7-tetrahydroxyflavone) is a naturally occurring flavonoid commonly found in fruits and vegetables. In this study, we investigated the potential anticancer effects of fisetin on breast cancer cells. The result showed fisetin induced higher cytotoxicity in human breast cancer MCF-7 than in MDA-MB-231 cells otherwise it did not exert any detectable cytotoxicity in non-tumorigenic MCF-10A cells. We found fisetin can trigger a novel form of atypical apoptosis in caspase-3-deficient MCF-7 cells, which was characterized by several apoptotic features, including plasma membrane rupture, mitochondrial depolarization, activation of caspase-7, -8 and -9, and PARP cleavage; however, neither DNA fragmentation and phosphotidylserine (PS) externalization was observed. Although p53 was also activated by fisetin, the fisetin-induced apoptosis was not rescued by the p53 inhibitor pifithrin-α. In contrast, the fisetin-induced apoptosis was abrogated by pan-caspase inhibitor z-VAD-fmk. Furthermore, inhibition of autophagy by fisetin was shown as additional route to prompt anticancer activity in MCF-7 cells. These data allow us to propose that fisetin appears as a new potential anticancer agent which can be applied to develop a clinical protocol of human breast cancers. (Januari 2012)