People who have Cancer report that their symptoms have decreased after taking an Nrf2 activator.  Following the testimonials are current research articles that report new information about the cause of Cancer and how Nrf2 activators can be effective in treating it at the cellular level where it starts.

Nancy Levitt:  "The most profound thing that happened to me is that I struggled and suffered with skin cancer for years. That was due to being a sun worshipper with a light complexion and being in tanning booths for years and being in the sun for years. I had suffered major skin damage. I have had several surgeries removing skin cancer. In fact my entire top lip was cut off due to skin cancer. Over the years I've also had a total of ten different surgeries of basal cell carcinoma and squamous cell carcinoma spots removed from my chest.   Then two more spots appeared on my forehead that my doctor said needed to be removed and one more spot on my leg. I wanted to wait to have this surgery done because number one, obviously it's expensive, and it causes different scars and such, and then you have to have other treatments to remove that. I started taking Protandim and TrueScience. After six weeks of using Protandim and TrueScience the two spots on my forehead completely disappeared, and the spot on my leg completely disappeared as well. So my symptoms of skin cancer are totally gone. It's been a miraculous thing for me.", search "Protandim"
Dorothy Ensign:  "I am a five time Cancer Survivor. One of the real pleasures after taking Protandim for a year is the number of other medications I no longer need. I've cut my allergy medicine especially, a great deal. I'd say two-thirds of the things I was supposed to take before, I'm no longer taking after talking with my physicians and having their approval. One month after taking Protandim I had my annual physical, and my internist found my blood work outstanding. Especially in the area of cholesterol. Apparently it was very much improved from prior times. All of the other blood work was in perfect balance, so I appreciate it so much having physical proof that my good health was returning. It gave me my energy and stamina back.

"Within two months of being on it, at the oncologist's, the doctor said I looked so good that he was not going to go on with the chemo medicines that he was giving me, and that he would see me in six months. The next physician I saw was my eye doctor. She said, you don't need to change your glasses this time. Your eyes are holding so well. So it was the first time in a long time that I didn't have to have a new prescription., search "Protandim"
Bonnie Aksterowicz: “I’ve definitely noticed that my hip does not hurt, and my skin cancer has healed super fast. My doctor was impressed. He said that he thought that he would have to take a 2nd layer off when I went to my follow up last week and I told him about Cellgevity!”

Jim Kemp: Enjoying good health for his first 47 years, the past 10 years have not been kind to Jim Kemp of Castle Rock, CO.  He has endured 37 different surgeries (2 from different auto accidents); had cancer three times (prostate, colon, thyroid); suffered from fibromyalgia and kidney stones; had issues with the pituitary, pancreas, gall bladder, and esophagus; and dealt with NASH (non-alcoholic steatohepatitis, a fatty liver condition).  He has been subjected to numerous medications, narcotic pain killers, chemotherapy, and radiation.  2009 was particularly unkind, with 5 of those 37 surgeries and 8 hospitalizations occurring within a 9 month stretch.  

When not in the hospital, Jim’s daily routine for five years (2004-2009), has started at 5:00 a.m., when he would arise to take 7 medications.  Then he would go back to bed for a while, getting up later to take a hot bath for 40 minutes to relieve the muscle and joint pain and stiffness.  The balance of the day was spent coordinating the ingestion of food and additional medications—some with food, some before food, and some after food, and maneuvering around the house attached to an oxygen bottle and cannula.  At bedtime, Jim would be so revved up from the meds that he would have to take sleeping pills to get to sleep.

 Prior to starting two tablets per day of Protandim on January 10, 2010, Jim traveled to Utah to say his goodbye’s to his family, and met with his attorney to finalize his will and estate issues, as he was preparing to die.  Swallowing 25 meds each day, stooped over, jaundiced, walking with a cane, attached to an oxygen bottle 24/7, and skin turning gray, Jim didn’t hold out much hope.  However, after taking Protandim for 2 months, Jim reports that there is:

 No cane required for walking, and no being stooped over

No oxygen required for breathing

No need for narcotic pain killers (and there were no withdrawal symptoms from discontinuing them!  An occasional Tylenol does the job now.)

No gray skin tones (and his hair color is starting to come back)

No liver spots on the back of his hands

No jaundice

No $380 per month in co-pays for medications (now $25 per month)

Only 7 pills required as of now, down from the 25 he was taking before (including a reduction in Lyrica from 300 mg daily down to 75 mg every 4th day)

Normal liver enzymes for the first time in 8 years

Normal blood work for the first time in 9 years

 He also reports that he now sleeps better, has more energy, and states that “I feel better than I have in years!”

 Jim’s wife, Beverly, and his two adult children rejoice in having their husband and father back again.  And Jim has returned full-time to his technical support position with Sprint Nextel.


Oncotarget. 2016 Jun 15. doi: 10.18632/oncotarget.10078. [Epub ahead of print]
Simvastatin induces heme oxygenase-1 via NF-E2-related factor 2 (Nrf2) activation through ERK and PI3K/Akt pathway in colon cancer.

Statin has been known not only as their cholesterol-lowering action but also on their pleiotropic effects including anti-inflammatory and anti-oxidant as well as anti-cancer effect. Nrf2 (NF-E2-related factor 2) is a transcription factor to activate cellular antioxidant response to oxidative stress. There are little known whether statins affect activation of Nrf2 and Nrf2signaling pathway in colon cancer cells. We investigated whether simvastatin stimulates the expression of Nrf2 and nuclear translocation of Nrf2 and which signal pathway is involved in the expression of Nrf2 and antioxidant enzymes. We investigated the effect of simvastatin on the expression of Nrf2 and nuclear translocation of Nrf2 in two human colon cancer cell lines, HT-29 and HCT 116 through cell proliferation assay, Western blotting and immunocytochemical analysis. We evaluated which signal pathway such as ERK or PI3K pathway affect Nrf2 activation and whether simvastatin induces antioxidant enzymes (heme oxygenase-1 (HO-1), NAD(P)H: quinine oxidoreductase 1 (NQO1), γ-glutamate-cysteine ligase catalytic subunit (GCLC)). We demonstrated simvastatin-induced dose-dependent up-regulation of Nrf2 expression and stimulated Nrf2 nuclear translocation in colon cancer cells. We also demonstrated that simvastatin-induced anti-oxidant enzymes (HO-1, NQO1, and GCLC) in HT-29 and HCT 116 cells. PI3K/Akt inhibitor (LY294002) and ERK inhibitor (PD98059) suppressed simvastatin-induced Nrf2 and HO-1 expression in both HT-29 and HCT 116 cells. This study shows that simvastatin induces the activation and nuclear translocation of Nrf2 and the expression of various anti-oxidant enzymes via ERK and PI3K/Akt pathway in colon cancer cells.

PMID: 27323826
[INTERPRETATION:   Simvastatin activates Nrf2, which causes anti-swelling, anti-oxidant, and anti-cancer effects.  This study specifically shows that Nrf2 activation works with colon cancer too.]


Sci Rep. 2016 May 24;6:26585. doi: 10.1038/srep26585.
An inhibitor of the Keap1-Nrf2 protein-protein interaction protects NCM460 colonic cells and alleviates experimental colitis.

Ulcerative colitis (UC) is a chronic relapsing-remitting form of inflammatory bowel disease (IBD) that increases the risk of colorectal cancer, the third most common malignancy in humans. Oxidative stress is a risk factor for the development of UC. The Keap1-Nrf2-ARE pathway is one of the most important defensive mechanisms against oxidative and/or electrophilic stresses. In this study, we identified CPUY192018 as a potent small-molecule inhibitor of the Keap1-Nrf2 PPI, investigated the cyto-protective effects of CPUY192018 on the NCM460 colonic cells and evaluated whether treatment with the inhibitor of the Keap1-Nrf2 PPI exerts protection on an established experimental model of UC induced by dextran sodium sulfate (DSS). Our study clearly demonstrated that CPUY192018 had a cytoprotective effect against DSS in both NCM460 cells and mouse colon via the activation of Nrf2 signaling. These results suggested that activation of Nrf2 by directly inhibiting the Keap1-Nrf2 PPI may be beneficial as a treatment for UC.

PMID: 27215610
[INTERPRETATION:   Activation of Nrf2 may be a good treatment for colorectal cancer.  This is because it reduces the oxidative stress that is at the beginning of ulcerative colitis (a form of intestinal inflammation), which in turn leads people to get the cancer.]


Zhonghua Liu Xing Bing Xue Za Zhi. 2016 Aug 10;37(8):1175-82. doi: 10.3760/cma.j.issn.0254-6450.2016.08.024.
[Research progress on free radicals in human body].
Free radicals are the intermediates of metabolism, widely exist in the human bodies. Under normal circumstances, the free radicals play an important role in the metabolic process on human body, cell signal pathway, gene regulation, induction of cell proliferation and apoptosis, so as to maintain the normal growth and development of human body and to inhibit the growth of bacteria, virus and cancer. However, when organic lesion occurs affected by external factors or when equilibrium of the free radicals is tipped in the human body, the free radicals will respond integratedly with lipids, protein or nucleic acid which may jeopardize the health of human bodies. This paper summarizes the research progress of the free radicals conducted in recent years, in relations to the perspective of the types, origins, test methods of the free radicals and their relationship with human's health. In addition, the possible mechanisms of environmental pollutants (such as polycyclic aromatic hydrocarbons) mediating oxidative stress and free radicals scavenging in the body were also summarized.
PMID: 27539355
[INTERPRETATION:  Free radicals (oxidants) are important to inhibit bad things in the body, but when there are too many free radicals, they are harmful to health.]


Toxicol Appl Pharmacol. 2015 Feb 10. pii: S0041-008X(15)00054-X. doi: 10.1016/j.taap.2015.02.003. [Epub ahead of print]

Blackberry extract inhibits UVB-induced oxidative damage and inflammation through MAP kinases and NF-κB signalling pathways in SKH-1 mice skin.

Extensive exposure of solar ultraviolet-B (UVB) radiation to skin induces oxidative stress and inflammation that play a crucial role in the induction of skin cancer. Photochemoprevention with natural products represents a simple but very effective strategy for the management of cutaneous neoplasia. In this study, we investigated whether blackberry extract (BBE) reduces chronic inflammatory responses induced by UVB irradiation in SKH-1 hairless mice skin. Mice were exposed to UVB radiation (100mJ/cm2) on alternate days for 10weeks, and BBE (10% and 20%) was applied topically a day before UVB exposure. Our results show that BBE suppressed UVB-induced hyperplasia and reduced infiltration of inflammatory cells in the SKH-1 hairless mice skin. BBE treatment reduced glutathione (GSH) depletion, lipid peroxidation (LPO), and myeloperoxidase (MPO) in mouse skin by chronic UVB exposure. BBE significantly decreased the level of pro-inflammatory cytokines IL-6 and TNF-α in UVB-exposed skin. Likewise, UVB-induced inflammatory responses were diminished by BBE as observed by a remarkable reduction in the levels of phosphorylated MAP Kinases, Erk1/2, p38, JNK1/2 and MKK4. Furthermore, BBE also reduced inflammatory mediators such as cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and inducible nitric oxide synthase (iNOS) levels in UVB-exposed skin. Treatment with BBE inhibited UVB-induced nuclear translocation of NF-κB and degradation of IκBα in mouse skin. Immunohistochemistry analysis revealed that topical application of BBE inhibited the expression of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodG), cyclobutane pyrimidine dimers (CPD), proliferating cell nuclear antigen (PCNA), and cyclin D1 in UVB-exposed skin. Collectively, these data indicates that BBE protects from UVB-induced oxidative damage and inflammation by modulating MAP kinase and NF-κB signaling pathways.

Copyright © 2015. Published by Elsevier Inc.

PMID:  25680589  [PubMed - as supplied by publisher]

 [INTERPRETATION:  Skin cancer is caused by oxidative stress (cell damage) and inflammation from too much sun exposure.  Blackberry extract ensures more glutathione (a body-made antioxidant) that reduces the cell damage and inflammation.]


EMBO Mol Med. 2015 Feb 13. pii: e201404181. doi: 10.15252/emmm.201404181. [Epub ahead of print]

STAMP2 increases oxidative stress and is critical for prostate cancer.

The six transmembrane protein of prostate 2 (STAMP2) is an androgen-regulated gene whose mRNA expression is increased in prostate cancer (PCa). Here, we show that STAMP2 protein expression is increased in human PCa compared with benign prostate that is also correlated with tumor grade and treatment response. We also show that STAMP2 significantly increased reactive oxygen species (ROS) in PCa cells through its iron reductase activity which also depleted NADPH levels. Knockdown of STAMP2 expression in PCa cells inhibited proliferation, colony formation, and anchorage-independent growth, and significantly increased apoptosis. Furthermore, STAMP2 effects were, at least in part, mediated by activating transcription factor 4 (ATF4), whose expression is regulated by ROS. Consistent with in vitro findings, silencing STAMP2 significantly inhibited PCa xenograft growth in mice. Finally, therapeutic silencing of STAMP2 by systemically administered nanoliposomal siRNA profoundly inhibited tumor growth in two established preclinical PCa models in mice. These data suggest that STAMP2 is required for PCa progression and thus may serve as a novel therapeutic target.

© 2015 The Authors. Published under the terms of the CC BY 4.0 license.

PMID: 25680860  [PubMed - as supplied by publisher]

[INTERPRETATION:  STAMP2 increases oxidants (ROS) in prostate cancer.  Reducing the oxidants (ROS) stops cancer growth and kills the cancer cells, and is a new therapy.]