Welcome To The Cancer Environment

“The organism can only be understood in its environments, and a cell can’t be understood without reference to the tissue and organism in which it lives.” Ray Peat PhD

When you listen to what the medical ‘experts’ say about cancer, you might come away with the impression that there has been complete agreement – in the vast amounts of scientific literature on the subject – regarding the nature of the disease and as such, the kinds of treatments worthy of consideration.

Even though that impression is not an accurate one, few people are aware of the fact that there is a long history of research and experimentation questioning the validity of the standard paradigm – which views cancer as a genetically driven disease of the cell – opening up the possibility for alternative forms of treatment.

“The somatic mutation theory of carcinogenesis has been the dominant force driving cancer research during the 20th century. In brief, it proposes that successive DNA mutations in a single cell cause cancer…”

“…its…continuous invocation of ‘programs’ and ‘mechanisms’ is a reflection of inadequate metaphors borrowed respectively from computer sciences and outdated physics; organisms are neither computers nor machines.”

The idea however, that cancer is not some kind of random genetic event – but is rather a systemic disease which can be the result of the effects of a wide variety of metabolic stressors – has faced great resistance in both the scientific and medical communities, regardless of the quality of the evidence supporting it.

“We argue that it is necessary to abandon the somatic mutation theory…We propose the adoption of an alternative theory, the tissue organization field theory of carcinogenesis…”

“…the tissue organization field theory…incorporates the premise that proliferation and motility are the default state of all cells, and that carcinogenesis is due to alterations on the reciprocal interactions among cells and between cells and their extracellular matrix…There are multiple examples of normalization of cells that once belonged to a cancer…”

The pushback to this theory arises in part because it threatens the status quo, suggesting that prevention and treatment of cancer need not focus upon discovering ‘responsible’ genes, and seeking out and destroying ‘guilty’ cells. It implies that the dominant approach may be more harmful than helpful.

“In the important realm of experimental cancer research, the proposed change would mean a switch from a subcellular, gene-centric approach to a tissue-based organicist one, in which a combined top-down and bottom-up strategy would include systems biology components.”

“The regulatory power of a mass of contiguous normal cells is expressed in its capacity to normalize the appearance and growth behavior of solitary homophilic neoplastic cells…”

Destroying or removing ‘cancer cells’ in the currently accepted way – surgery, chemotherapy and radiation – has been shown to have potentially dangerous repercussions, by increasing the cancer promoting capability of surrounding tissue environments.

“Put another way, cancer results from a breakdown of tissue organization that disrupts the normal inhibitions of proliferation that are inherent in the tissue architecture of a multicellular society of cells.”

Alternatively, it makes sense that any approach which can effectively improve tissue environments, is likely to have the opposite effect, preventing or perhaps even reversing the spread of cancer.

“One of the predictions of the tissue organization field theory is that carcinogenesis can potentially be reversed… Experimentally, the reversal of neoplastic behavior has been accomplished repeatedly when neoplastic cells were placed within the normal tissues from which they originated.”

“Normal growth behavior is reintroduced in solitary, carcinogen-initiated epidermal cells by contact with an excess of normal epidermal cells.”

The significance of this way of understanding is heightened by the knowledge that the worsening of tissue microenvironments influence the likelihood that tumors will spread or metastasize, a circumstance which is overwhelmingly responsible for cancer mortality.

“Metastases are defined as secondary tumors that develop at a distance from their primary originators; they are the cause of death for 90% of cancer patients…the prevailing consensus is that metastases are not explained accurately, and, more importantly, they are far from being successfully managed.”

“…behavior of normal cells is ordered by their topological relations in tissues and other homeostatic influences of the organism. Weakening of these ordering relations may contribute to malignant transformation…”

“…cancer metastases, as their primary cancers, are not cell-based events but represent, instead, tissue-based phenomena.”

Rather than random genetic mutations driving the creation of ‘cancer cells’, it makes sense – based on good quality evidence – to see biological stress as the central factor in the development of a cancer environment.

Continuous exposure to stress interfering with the provision of sufficient metabolic energy – or exceeding the amount required to cope with such stress – can be one general way of understanding how the conditions which can change the tissue, damage the cells (as well as DNA) and encourage cancer potential, come about.

“We challenge the notion that cancer is a cellular problem caused by mutated genes by assessing…an alternative view that regards carcinogenesis as a developmental process gone awry.”

“…interactions among different components of a tissue cannot be reduced to cellular events…carcinogenesis takes place at the tissue level of biological organization……while normal cells already carry mutations, they do not end up becoming cancer cells…From this perspective, these mutations would be irrelevant as suggested by the repeated instances where cells from diverse cancer types were normalized when placed within a normal field.”

The substances of stress – including cortisol, serotonin, endotoxin, nitric oxide, estrogen, lactate and various other inflammatory and fibrotic things – which often increase side by side with aging, directly and indirectly impact upon the ability of tissue environments to be able to function in a manner which protects against or even reverses cancer behaviour of the cell.

“…damage accumulates with age, as does an increasingly permissive local environment for tumor growth…The order that controls heterogeneity is weakened with age and contributes to the origin and progression of disordered growth.”

“…findings reveal unanticipated communication between stress-induced neural signalling and inflammation, which regulates tumour lymphatic architecture and lymphogenous tumour cell dissemination.”

Increased circulation of bacterial endotoxin LPS (lipopolysaccharide) is one thing that is known to promote the inflammatory conditions which can induce cancer development and metastasis.

“Inflammation has been known to be linked to invasion or metastasis of breast cancer, which has poor prognosis…Here we show that T-LAK cell-originated protein kinase (TOPK) mediates pro-inflammatory endotoxin lipopolysaccharide (LPS)-induced breast cancer cell migration and invasion.”

“NF-kappaB is one of the key factors connecting inflammation with cancer progression…LPS increased the invasive ability of pancreatic cancer cells, while blockade of NF-kappaB pathway decreased the LPS-dependent increased invasive ability…”

“Our findings suggest that inhibiting LPS-induced TLR4 signaling could improve therapeutic outcomes by preventing cancer metastasis during the perioperative period of CRC (colorectal cancer) resection.”

The polyunsaturated fats (PUFAs) which get stored in (and released from) the tissue, have been demonstrated to be a fundamental and powerful driver of inflammation, as well as the growth and spread of cancer.

“Arachidonic acid (ARA) is metabolized by cyclooxygenase (COX) and cytochrome P450 to produce proangiogenic metabolites. Specifically, epoxyeicosatrienoic acids (EETs) produced from the P450 pathway…promote angiogenesis, tumor growth, and metastasis.”

“…dietary fat promotes the growth of initiated cells, thus contributing to the higher risk of many human cancers…high-fat diets containing corn oil, soybean oil or safflower oil, which are 55–80% linoleic acid, increase the rate of growth of established tumors…”

“…we find that neutrophil-derived leukotrienes [metabolites of arachidonic acid] aid the colonization of distant tissue by selectively expanding the sub-pool of cancer cells that retain high tumorigenic potential.”

Endotoxin and PUFA promote nitric oxide (NO), and NO is another powerful mediator of inflammation, which has been shown to play a role in the development of a tissue environment which is increasingly capable of promoting cancer initiation and progression.

“…these data suggest that, in head and neck cancer, the increased NOS activity can be regarded as a novel biologic marker for tumor progression related to angiogenesis…”

“Inducible nitric oxide synthase (iNOS) is associated with poor survival in patients with breast cancer by increasing tumor aggressiveness…targeted therapy with iNOS inhibitors is able to inhibit not only tumor cell proliferation…self-renewal and migration, reducing tumor growth, tumor initiation, and the number of lung metastases.”

“…role for NO production from iNOS in human lung cancer because high concentrations of this short molecule may transform to highly reactive compounds such as peroxynitrite; moreover, through the upregulator NF-kB, they can induce a chronic inflammatory state representing an elevated risk for cell transformation to cancer.”

Exposure to chronic or acute levels of stress of many different kinds, wastes blood sugar reserves, and leads to the increased release of stress substances (including bacterial endotoxin), as well as a rise in systemic levels of polyunsaturated free fatty acids.

The combination of many of the above factors can be seen to be a major determinant of the stress conditions which promote tissue damage, genetic changes, blood sugar dysregulation, and the irregular cell activity of cancer and related metabolic illnesses.

“…chronic periods of stress can be detrimental to health by increasing inflammation and promoting the progression of diseases including cancer…we show that chronic stress restructures lymphatic networks within and around tumours to provide pathways for tumour cell escape.”

“Our findings provide a hitherto-undescribed direct role of increased aerobic glycolysis in inducing the cancer phenotype, in which increased glycolytic activity regulates the canonical oncogenic pathways…additional evidence for how hyperglycemia in diseases such as obesity and diabetes could provide a microenvironment that results in higher risk of some cancers.”

Estrogen levels are known to rise as a result of ongoing exposure to the inflammatory stress substances, potentially causing genetic changes and the development of cancer. Estrogen blood tests do not necessarily account for the amount of estrogen trapped in tissue where it can cause the most harm.

“…findings suggest that exposure to estrogen…is capable of driving genomic instability, a well-defined early event in breast cancer development. Given that estrogen levels in normal/benign breast tissue are known to be 6-7 times that of circulating estrogen levels, our findings suggest a mechanism through which BRCA1 carriers, through enhanced production of DNA damaging estrogen metabolites, may acquire the genetic alterations that initiate neoplastic transformation in breast tissue…Similarly, levels of estrogen in ovarian tissues greatly exceed that of circulating estrogen, suggesting that this model may also explain the substantially increased risk of ovarian cancer in BRCA1 carriers…”

“The knowledge that breast cancer in women is associated with prolonged exposure to high levels of estrogens gives relevance to this model of estrogen induced carcinogenesis…”

Avoiding consumption of the polyunsaturated fats and eating enough high quality protein – from milk, cheese and gelatinous cuts of meat – as well as plenty of simple and easy to digest sugars – from sweet ripe fruit, fruit juice, white sugar and honey – is one potentially powerful approach to suppressing stress, regulating blood sugar, and lowering exposure to dangerous fats (ingested and stored in tissue), and is a logical way to improve tissue organization, redirecting cellular behaviour away from cancer progression.

“…these observations may lead to a new paradigm for control and treatment of cancer in situ…it may be possible to redirect tumorigenic cells to normal cell function by exposure to substances present within normal tissues.”

“This provides a mechanism through which interaction with the normal mammary microenvironment may suppress tumorigenesis…the normal microenvironment redirects…tumorigenic cells to participate in the regeneration of a normal, functional mammary gland.”

Some other things which may be protective include increasing carbon dioxide levels (with bag breathing or adaptation to higher altitudes), exposure to daylight, therapeutic use of red light, pregnenolone and progesterone supplementation, vitamin E, vitamin A, caffeine, glycine, aspirin and a number of other anti-estrogen and anti-serotonin substances including the safe and effective antihistamine cyproheptadine.

Alternatively, anything that lowers stress – including therapeutic use of white sugar – and allows thyroid metabolism to function more effectively, has been shown to be very helpful.

“A deeper understanding of the role(s) of tissue and tumor microenvironments in the pathogenesis of cancer is essential to design more effective strategies for the management of this disease.”

“…if a cancer cell exists as a discrete entity distinguishable from a normal cell, it has certainly been very uncooperative in revealing what it has ‘invented’ to deserve the fame it has acquired. More to the point, cells isolated from cancers revert to normalcy when placed in a normal microenvironment.”

See More Here

Rethinking “Cancer as a Dynamic Developmental Disorder” a Quarter Century Later

What keeps cells in tissues behaving normally in the face of myriad mutations?

FoxA and LIPG endothelial lipase control the uptake of extracellular lipids for breast cancer growth

The death of the cancer cell.

Tumour hypoxia causes DNA hypermethylation by reducing TET activity

Ordered heterogeneity and its decline in cancer and aging.

Cyclooxygenase-derived proangiogenic metabolites of epoxyeicosatrienoic acids

Cell damage, aging and transformation: a multilevel analysis of carcinogenesis.

Lactate: a metabolic key player in cancer.

Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction

Lipopolysaccharide (LPS) increases the invasive ability of pancreatic cancer cells through the TLR4/MyD88 signaling pathway.

Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect

LPS Up-Regulates ICAM-1 Expression in Breast Cancer Cells by Stimulating a MyD88-BLT2-ERK-Linked Cascade, Which Promotes Adhesion to Monocytes

Dietary polyunsaturated fatty acids and cancers of the breast and colorectum: emerging evidence for their role as risk modifiers

Ras Involvement in Signal Transduction by the Serotonin 5-HT2B Receptor (*)

The significance of biological heterogeneity.

Inflammatory stimuli promote growth and invasion of pancreatic cancer cells through NF-κB pathway dependent repression of PP2Ac

Somatic mutation theory of carcinogenesis: why it should be dropped and replaced.

Lipopolysaccharide induces the interactions of breast cancer and endothelial cells via activated monocytes.

Novel interactions of vitamin E and estrogen in breast cancer.

Corn oil rapidly activates nuclear factor-κB in hepatic Kupffer cells by oxidant-dependent mechanisms

THE ROLE OF ESTROGEN IN THE INITATION OF BREST CANCER

Localization and activity of iNOS in normal human lung tissue and lung cancer tissue

Emergentism as a default: cancer as a problem of tissue organization.

Role of TOPK in lipopolysaccharide-induced breast cancer cell migration and invasion

Cancer Metastases: So Close and So Far.

Thymic involution and rising disease incidence with age

LPS-induced TLR4 signaling in human colorectal cancer cells increases beta1 integrin-mediated cell adhesion and liver metastasis.

Stromal Regulation of Neoplastic Development

BRCA1 DEFICIENCY EXACERBATES ESTROGEN INDUCED DNA DAMAGE AND GENOMIC INSTABILITY

Reprogramming metastatic tumour cells with embryonic microenvironments.

Reprogramming human cancer cells in the mouse mammary gland.

The Society of Cells: Cancer and control of cell proliferation

Neutrophils support lung colonization of metastasis-initiating breast cancer cells

Progesterone receptor modulates ERα action in breast cancer

Prostate enlargement: the canary in the coal mine?

Lipopolysaccharide-induced toll-like receptor 4 signaling in cancer cells promotes cell survival and proliferation in hepatocellular carcinoma.

Is dehydroepiandrosterone a hormone?

Chronic cellular hypoxia as the prime cause of cancer: what is the de-oxygenating role of adulterated and improper ratios of polyunsaturated fatty acids when incorporated into cell membranes?

Bivalent role of intra-platelet serotonin in liver regeneration and tumor recurrence in humans.

Function of inducible nitric oxide synthase in the regulation of cervical cancer cell proliferation and the expression of vascular endothelial growth factor

The tissue organization field theory of cancer: A testable replacement for the somatic mutation theory

Steroid hormone measurements from different types of assays in relation to body mass index and breast cancer risk in postmenopausal women: Reanalysis of eighteen prospective studies

Induction of proto-oncogene BRF2 in breast cancer cells by the dietary soybean isoflavone daidzein

Inhibition of arachidonate 5-lipoxygenase triggers massive apoptosis in human prostate cancer cells.

Identification of Cyproheptadine as an Inhibitor of SET Domain Containing Lysine Methyltransferase 7/9 (Set7/9) That Regulates Estrogen-Dependent Transcription.

Inhibition of iNOS as a novel effective targeted therapy against triple-negative breast cancer

Tumor-Associated Neutrophils and Macrophages Promote Gender Disparity in Hepatocellular Carcinoma in Zebrafish.

The microenvironments of multistage carcinogenesis.

The normal mammary microenvironment suppresses the tumorigenic phenotype of mouse mammary tumor virus-neu-transformed mammary tumor cells.

The aging of the 2000 and 2011 Hallmarks of Cancer reviews: A critique

Effects of fatty acids and eicosanoid synthesis inhibitors on the growth of two human prostate cancer cell lines.

Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine

Serotonin Activated Hepatic Stellate Cells Contribute to Sex Disparity in Hepatocellular Carcinoma

Positive Selection on a Regulatory Insertion–Deletion Polymorphism in FADS2 Influences Apparent Endogenous Synthesis of Arachidonic Acid

Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer

Role of Nitric Oxide in Angiogenesis and Tumor Progression in Head and Neck Cancer

Glycine as a potent anti-angiogenic nutrient for tumor growth.

Carcinoma cells induce lumen filling and EMT in epithelial cells through soluble E-cadherin-mediated activation of EGFR

Arginine starvation-associated atypical cellular death involves mitochondrial dysfunction, nuclear DNA leakage, and chromatin autophagy

Tumor microenvironment derived exosomes pleiotropically modulate cancer cell metabolism

Mitochondrial stress-induced p53 attenuates HIF-1α activity by physical association and enhanced ubiquitination

Androgen suppresses testicular cancer cell growth in vitro and in vivo

Aspirin blocks growth of breast tumor cells and tumor-initiating cells and induces reprogramming factors of mesenchymal to epithelial transition.

Retinyl acetate inhibits estrogen-induced mammary carcinogenesis in female ACI rats.

Chronic stress in mice remodels lymph vasculature to promote tumour cell dissemination

Inhibition of estrone sulfatase and 17 beta-hydroxysteroid dehydrogenase by antiestrogens.

[Relation of prolactin with nodular hyperplasia and carcinoma of the prostate].

Increased sugar uptake promotes oncogenesis via EPAC/RAP1 and O-GlcNAc pathways

#pufafeedscancer
#sugarblaming
#raypeat

Image: excluzive.net

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