In this episode of Conners Clinic Live, Dr Kevin Conners goes into detail regarding mTOR and KRAS pathways and discusses how cancer cell growth and genetics are related.

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Cancer Cell Growth and Genetics: What You Should Know! | Conners Clinic Live

Transcript

Dr. Conners
Hello everybody. This is Dr. Kevin Conners and on today’s Conners Clinc Live, I want to talk about growth pathways in cancer. Specifically, the mTOR the KRAS pathways.

I’ve talked about this a lot before, but I just feel like hitting it again on some of the interventions that we could deal with are very important. Your mTOR pathway, right here, is a major genetic metabolic pathway in your body on how you heal and how you deal with cell replication and deal with cell growth. Remember, when we talk about cancer, cancer is uncontrolled cell replication, but we don’t want to confuse that cell replication and cell growth and henceforth healing, as a bad thing. Of course, if we cut ourselves, we need to heal. Our body is constantly breaking down and growing new cells, that’s part of regeneration, that’s part of staying healthy. It is when a cell goes through rapid replication because something’s damaged in the DNA, which we’ve spoken about and bacteria, fungus, chemical, toxin gets in there and damages the DNA, damages different pathways, which are supposed to cause cell death, could damage pathways that proliferate cell growth, accelerate cell growth.

And that’s what we’re talking about. That’s what can cause cancer and it can lead to cancer. So anything that’s going to stimulate the mTOR pathway and the KRAS pathways, we want to look at what we’re dealing with a cancer patient. All these things up top up here. EMF cell tower, high fructose corn syrup, too much iron in your diet, taking methyl groups as a supplement. We see that a lot with our cancer patients coming in and they’re already on high methyl supplements. Problem with that is that can stimulate, it does stimulate, mTOR and stimulates growth. So think of mTOR as a major growth pathway. We don’t want to overstimulate mTOR if we have cancer. So is there anything wrong with taking, methyl B12 and methyl folate, if you don’t have cancer? Well, there can be, but technically there won’t be as far as growth goes. But certainly with somebody with cancer, we don’t want to stimulate that pathway.

MSG, glutamate, excess glutamine in bone broth, too much animal proteins, will stimulate that pathway and stimulate mTOR. Pesticide exposure, especially person has PON1 defects, is going to end up increasing mTOR. And again, MTHFR supplementation. Also, we look on this side, dairy, protein drinks, plastics exposure, all are going to stimulate different pathways that are going to stimulate growth. So we have to be careful of those things. This is a real nice chart. You can sit here and we could talk about it for hours, but we want to move on. But these are the things that we want to look at to know how we can shut down or slow down mTOR. Well, just a brief look at this chart, just eliminating or close to eliminating as many of these things on this list here, can help slow down mTOR.

Cut out dairy, try to eliminate my EMFs and stay away from sugar, stay away from iron supplements and methyl supplements and animal proteins, and glutamine supplements and pesticides and such, is going to slow down these growth pathways. Everything you’ve read here has to do with the genes that we look at because a person with PON1 gene defects is going to end up with problems, GAD and DAO defects. So that’s all our genetic workup that we do with cancer patients.

This is KRAS mutations, meaning KRAS is a gene, KRAS another growth pathway. People with KRAS mutations defects on that gene pathway and that’s why we look at them when we look at somebody’s genetics. KRAS also increases that growth pathway that we want to address. So, there’s different drugs that are in the market right now to help block this, but we look at some different supplementation that you could do to help block this too.

One of the major supplements that can help block this is curcumin. Curcumin is the product of tumeric, the active ingredient in tumeric. So using curcumin can help decrease that KRAS pathway. Here’s another slide I took for an article. It was actually on lung cancer. That’s why I talked about DNA damaging due to cigarette smoke components. What we could say, DNA damage, to any toxins within a cell that could cause cancer or any biotoxins in a cell that cause cancer, could stimulate certain pathways that cause survival proliferation. Think of that. Why would that be? You got a toxin inside the cell. Well, our body is trying to survive. That cell is trying to survive. They can stimulate different pathways that promote cell proliferation, but also stimulates the KRAS pathway, which can cause survival proliferation too. It blocks apoptosis, apoptosis is your normal programmed cell death.

Again, your body’s infinite wisdom is trying to keep the cell alive, but when there’s something that’s damaged the DNA of the cell and you’ve got rapid replication, well then the KRAS pathway is not our friend. So if it’s not a cancer that’s in the person’s body, well then the KRAS is our friend. But when a cell is in rapid replication, meaning that you have cancer in your body, KRAS is not our friend. KRAS also stimulates NF Kappa Beta. We’ve talked a lot about that in the past. That’s an inflammatory program that shuts down apoptosis and all the genes that will help stimulate apoptosis, again in order to keep the cell alive. Also even shuts down your P53. So KRAS could shut down your P53. Remember, your P53 is tumor suppressor pathway.

You have multiple tumor suppressor pathways, but P53 is your major tumor suppressor pathway inside the cell. That means when the cell goes into a rapid replication, P53 is kicked in and when P53 is kicked in, it is supposed to produce stimulation of cell death, your capsase pathway, and that will help stimulate apoptosis and kill the cell that is a cancer cell. And that’s why most of us don’t end up with a diagnosis of cancer because our tumor suppressor genes are doing their job. So when something is damaged inside the cell and the cell starts to go through rapid replication, your tumor suppressor pathways kick in and cause apoptosis, cause cell death. Well, if there are toxins inside the cell, they can damage the KRAS pathway, or if there are defects of the KRAS pathway, it can stimulate more KRAS production, increase nuclear factor, Kappa B, and can help in this way, hinder, the production, our stimulation of P53 and end up promoting cell survival, which is what we don’t want to do.

So we want P53 to kick in. So again, KRAS is not our friend in this scenario. There’s another great response, another great slide on the P53 pathway. Again, the P53 pathway is your major tumor suppressor pathway. So when the P53 pathway kicks in, you have growth arrest, meaning that growth will stop. Apoptosis will take place. Apoptosis protects the cell from continued growth. What apoptosis is, is normal programmed cell death, so it causes the cell to go through normal programmed cell death. P53 Also helps with DNA repair, which is quite interesting, but the KRAS pathway can block this. I kinda have messed that up, but this red thing, KRAS pathway will block P53. So when there’s overstimulation of that KRAS pathway, in this case, talking about a mutation or a defect of the KRAS genes, that causes hyper proliferation stress and it blocks the P53 pathway. So all of this is blocked if KRAS is a hyper active. So we want to do things that are going to slow this KRAS pathway and that’s where you can get back to the slides back up here.

Some things that could decrease mTOR and KRAS are dietary considerations on this list. Everything in yellow here, looking at all these little red boxes, which are your genes that are affecting KAS and mTOR secondarily that you could address those things. Again, there are some specific nutritional pieces, like curcumin and things that you could help when addressing those things too. So we can talk more about these, and I do want to talk more about these in individual little lectures on each one of these. That’s why we have things on the EMFs and sugar consumption or eating too much higher enriched foods when you have cancer and such. So, trying to give you the big picture of this. All right. Thanks so much.