Sep 2018 Science News - Cancer survives on Glucose

(Carpe salata!) #1

Science News : Realisation that cancer is surviving on our body glucose. The word is getting out - excess glucose can be harmful.

(Karen) #2

DUH. Sure takes them a long time to figure things out.

(Terence Dean) #3

Very interesting article, thanks for posting it.

(Raj Seth) #4

Otto Warburg knew this a hundred years ago

(Carpe salata!) #5

There is a whole litany of suppressed medical wisdom and success. The story of Rudolf Breuss’ court case is another one.

(Banting & Yudkin & Atkins & Eadeses & Cordain & Taubes & Volek & Naiman & Bikman ) #6

Some cancers. Other cancers eat protein. Other cancers even eat ketone bodies.

(Carpe salata!) #7

Great input - thanks!

(Bunny) #8

Cancer cells can survive on;

  1. glutamine (is an α-amino acid that is used in the biosynthesis of proteins),

  2. acetate (hypothesis: hydrogen cyanide adds across the carbon-oxygen double bond in aldehydes and ketones to produce compounds known as hydroxynitriles) Note: “… In the United States the Lovelock Caves in Nevada have yielded petrified animal and human faeces (fecoliths) that through carbon-dating have been found to go back many years. They showed numerous remnants of nitriloside-bearing plants. …”

  3. glucose (supplies a carbon source for biosynthesis)

  4. …other?

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Types of insulin seemingly a contributor to cancer growth proliferation:

  1. IGF-1 IGF-2

  2. Insulin

  3. Glucagon

  4. Hydrogen Peroxide (Depending on its intracellular concentration and localization, H2O2 exhibits either pro- or anti-apoptotic activities.)

  5. …other?

Question: Cancer cells can orchestrate metabolic reprogramming by altering the uptake and catabolism of nutrients, enabling them to maintain proliferative capacity, conferring resistance to oxidative stress, and promoting the evasion of immune-mediated destruction?

However, glucose only supplies a carbon source for biosynthesis; it cannot supply the amino acids and glutathione that rapidly proliferating cancer cells require for the synthesis of nucleic acids?

Data:

  1. “…Recent data indicate that: (1) insulin stimulates growth mainly via its own receptor and not the IGF-1 receptor; (2) in many cancer cells, the IR is overexpressed and the A isoform, which has a predominant mitogenic effect, is more represented than the B isoform. These characteristics provide a selective growth advantage to malignant cells when exposed to insulin. …” …More
  1. ”…A large body of evidences have shown that both the IGF-I receptor (IGF-IR) and the insulin receptor (IR) play a role in cancer development and progression. In particular, IR overactivation by IGF-II is common in cancer cells, especially in dedifferentiated/stem-like cells. In spite of these findings, until very recently, only IGF-IR but not IR has been considered a target in cancer therapy. Although several preclinical studies have showed a good anti-cancer activity of selective anti-IGF-IR drugs, the results of the clinical first trials have been disappointing. In fact, only a small subset of malignant tumors has shown an objective response to these therapies. Development of resistance to anti-IGF-IR drugs may include upregulation of IR isoform A (IR-A) in cancer cells and its overactivation by increased secretion of autocrine IGF-II. These findings have led to the concept that co-targeting IR together with IGF-IR may increase therapy efficacy and prevent adaptive resistance to selective anti-IGF-IR drugs. IR blockade should be especially considered in tumors with high IR-A:IGF-IR ratio and high levels of autocrine IGF-II. Conversely, insulin sensitizers, which ameliorate insulin resistance associated with metabolic disorders and cancer treatments, may have important implications for cancer prevention and management. Only few drugs co-targeting the IR and IGF-IR are currently available. Ideally, future IR targeting strategies should be able to selectively inhibit the tumor promoting effects of IR without impairing its metabolic effects. …” …More
  1. “…Glucagon, a 29-amino acid peptide, is secreted from the α-cells in the pancreas, and part of it is also secreted from the endocrine cells in the gastrointestinal tract [18]. … As for the role of glucagon in cancer, glucagon has been shown to enhance growth of cultured human colorectal cancer cells in vitro [21]. …” …More
  1. “… Cancer cells can orchestrate metabolic reprogramming by altering the uptake and catabolism of nutrients, enabling them to maintain proliferative capacity, conferring resistance to oxidative stress, and promoting the evasion of immune-mediated destruction (Hanahan and Weinberg, 2011). In early studies on cancer metabolism, dysregulated glucose metabolism, also called the “Warburg effect”, received much attention as a hallmark of cancer, since the glycolytic pathway produces ATP and metabolic intermediates for cancer cell proliferation. However, glucose only supplies a carbon source for biosynthesis; it cannot supply the amino acids and glutathione that rapidly proliferating cancer cells require for the synthesis of nucleic acids. …” …More
(Empress of the Unexpected) #9

Does anyone know at this point which tumors survive on sugar, and which on ketones? Not saying I believe it, but there are some studies out there, flawed or not.

(Carpe salata!) #10

There was a 2KD podcast I the last couple of months that had a guest, a doctor who was treating cancer with medical and diet protocols. Each patient was carefully evaluated for treatment protocol

Not sure of the details I mustn’t have been listening well.

(Bunny) #11

If the cancer biopsy tests positive for the BRAF V600E gene:

  1. Dietary fat promotes ketogenesis to enhance BRAF V600E tumor growth
  1. BRAF (V600E) mutation: A specific mutation (change) in the BRAF gene, which makes a protein that is involved in sending signals in cells and in cell growth. This BRAF gene mutation may be found in some types of cancer, including melanoma and colorectal cancer. It may increase the growth and spread of cancer cells. Checking for this BRAF mutation in tumor tissue may help to plan cancer treatment.
  1. “… Here we report evidence that the nucleocytosolic ACSS2 enzyme is of critical importance for mammalian cells to utilize acetate as a source of acetyl-CoA, and that mice lacking this enzyme exhibit a substantial reduction in tumor burden in two genetic models of liver cancer. …” …More
  1. ”… Should it be the case that humans, like mice, are not reliant on the ACSS2 enzyme, it is possible that chemical inhibitor of ACSS2 may be of use in either the treatment or prevention of cancer. …” “…Proceeding with these observations, a drug screen was performed in search of selective inhibitors of the ACSS2 enzyme. The screen yielded ACSS2 inhibitors that do not inhibit other acyl-synthetase enzymes, including ACSS1 and ACSS3. …” …More
(Empress of the Unexpected) #12

So Bunny, what is your take on all this. Do we just KCKO?

(Bunny) #13

Short and sweet answer:

Honest answer, we are walking on it; the cause, prevention and cure; it is the quality of the ground soil that we grow our plants on that the animals eat and we eat!

(Empress of the Unexpected) #14

I believe that - so I am way more comfortable growing my own vegetables. Meat I have less control over.

(Bunny) #15

All the endless walls of text and science man pours into the research trying to find a cure for something that man caused to begin with, without understanding the basic principles of his intricate nature; it is really a selfish attempt at self-annihilation in the mode of ignorance!

Processing everything in an attempt to preserve it; playing with chemicals and genes contrary to what is natural; it is like trying to put a square peg in a round hole is why nothing works anymore…