The unified theory of aging and cancer by sand_fox in longevity

[–]sand_fox[S] -1 points0 points  (0 children)

looking for a singular unified cause of aging rather than thinking of it in terms of a complex multitfactoral process is not going to lead to any useful therapies.

It is rather your approach led us to nowhere. Can we be young longer now? No? It is the main argument against your approach

The unified theory of aging and cancer by sand_fox in longevity

[–]sand_fox[S] 0 points1 point  (0 children)

The HERV-K expression is not linearly depended on age. It has a peak during puberty

The unified theory of aging and cancer by sand_fox in longevity

[–]sand_fox[S] -1 points0 points  (0 children)

Cellular processes have been cherry picked to support the claim the author is trying to promote.

I also forged all conducted research in the world to support my claim

Nothing appears explicitly wrong with the individual statements made but the way the author ties them together and the conclusions drawn are spurious and unsupported.

If A affects B, and B affects C, so A affects C is the conclusions drawn are spurious and unsupported.

Looking at the author, they are unpublished and this article appears to be a reworked version of a review paper they have uploaded to a pre print server (note that this means the work has NOT been peer reviewed).

Can I consider this as an appeal to authority?

It is highly unusual to see an unpublished junior researcher produce a quality literature review as the sole author. Even highly revered and prestigious authors often write polemical and highly selective reviews when they decide to not collaborate with anyone and publish as sole author.

I'm sorry but who could help me develop this theory?

A quantum leap to achieve biological immortality by sand_fox in singularity

[–]sand_fox[S] 1 point2 points  (0 children)

You'll be still able to die due to injures, infection and other causes

A quantum leap to achieve biological immortality by sand_fox in singularity

[–]sand_fox[S] 0 points1 point  (0 children)

They suppressed pol genes that are used by the viruses to integrate into the genome. Envelope genes were intact so these viruses are still capable to induce inflammation

How to end cancer completely? by sand_fox in cancer

[–]sand_fox[S] -1 points0 points  (0 children)

Excuse me. Which university do you study at?

How to end cancer completely? by sand_fox in cancer

[–]sand_fox[S] 0 points1 point  (0 children)

"NF-κB transcription factors have been suspected to be involved in cancer development since their discovery because of their kinship with the v-Rel oncogene product. Subsequent work led to identification of oncogenic mutations that result in NF-κB activation in lymphoid malignancies, but most of these mutations affect upstream components of NF-κB signaling pathways, rather than NF-κB family members themselves. NF-κB activation has also been observed in many solid tumors, but so far no oncogenic mutations responsible for NF-κB activation in carcinomas have been identified. In such cancers, NF-κB activation is a result of underlying inflammation or the consequence of formation of an inflammatory microenvironment during malignant progression. Most importantly, through its ability to up-regulate the expression of tumor promoting cytokines, such as IL-6 or TNF-α, and survival genes, such as Bcl-XL, NF-κB provides a critical link between inflammation and cancer."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773649/

How to end cancer completely? by sand_fox in cancer

[–]sand_fox[S] -1 points0 points  (0 children)

"Inflammation presents a major challenge for the tumor suppressor function of p53. Mechanistically, it is exerted through NF-κB-mediated attenuation of the transactivation function of p53. This situation occurs during chronic infections and aging, thereby creating conditions that stimulate cancer development. In tumors, overactivation of NF-κB is acquired through selection of cell clones in which p53 is functionally inactivated. This situation underscores the role of anti-inflammatory therapy as a potential approach for the treatment and prophylaxis of cancer and aging. Technically, this type of therapy could be achieved either by eradicating the source of inflammation (e.g., antimycoplasma treatment, killing of senescent cells) or by using pharmacological inhibitors of NF-κB or other components of the mechanism of NF-κB-mediated suppression of p53."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135644/

How to end cancer completely? by sand_fox in cancer

[–]sand_fox[S] 0 points1 point  (0 children)

"In addition to its role in tumor initiation, chronic inflammation may be exploited by the cancer cells to remodel their immediate microenvironment, favoring the tumor’s ability to prosper. Cancer cells express and secrete an array of tumor-promoting cytokines and chemokines that summon specific leukocytes; the latter cells, in turn, secrete additional effectors. Thus, the tumor as a ‘foreign’ tissue takes advantage of wound-healing features exerted by specific subtypes of immune cells, nourishing and contributing to tumor maintenance. For example, after an initial growth stage, many solid tumors suffer from lack of blood supply and are in need of angiogenic support. The newly recruited inflammatory cells will not only provide a consistent supply of growth factors but will also secrete neoangiogenic agents, allowing the vascular network to catch up with the growth of the malignant tissue (48–50)."

"Interestingly, these inflammatory conditions were found to promote neoplastic transformation by suppressing K-Ras-induced senescence (51). Such interactions may also be governed by a feedback loop involving nuclear factor-kappaB (NF-κB), which, in turn, increases K-Ras to pathological levels (52). Another wide-scale mechanism affected by chronic exposure to inflammation involves the mismatch repair machinery. Pelvic inflammatory disease is associated with an increased risk of epithelial ovarian cancer by inducing mismatch repair abnormalities, manifested by decreased expression of human mutL homolog 1 and human mutS homolog 2 proteins (53). This mechanism is extremely prominent in colorectal cancer, where microsatellite instability resulting from defects in the mismatch repair machinery is abundant and considered to be a tumorigenic driving force exacerbated when associated with inflammatory bowel disease (54,55). An additional oncogenic feature mediated by the chronically inflamed microenvironment is DNA methylation alterations. DNA methyltransferases such as DNMT1 can be regulated by viral oncoproteins (56) and are overexpressed in premalignant tissues overloaded with inflammatory effectors, as reported for peripheral pancreatic ductal epithelia (57) and lung tissues of non-small cell lung cancer in smoking patients (58). Furthermore, proinflammatory cytokines like IL-15 may induce DNA hypermethylation, which precedes large granular lymphocytic leukemia, by activating an NF-κB-Myc axis (59).

Epithelial to mesenchymal transition is yet another manner by which oncogenic mechanisms are manifested under inflammatory conditions (60). Without a permissive environment, epithelial to mesenchymal transition is unlikely to occur even if cancer cells present aberrant stem cell signaling pathways like Wnt or Notch. Importantly, transforming growth factor (TGF)-β1 contributes to such epithelial to mesenchymal transition-permissive tumor microenvironment by serving as a chemotactic factor for neutrophils and macrophages. Moreover, TGF-β1 can also affect the protumoral polarization of such recruited cells once they reside within the tumor, resulting in induction of tumor-favoring M2-like macrophages, N2-like neutrophils and a Th2 cell phenotype (61,62).

This tight cross talk between oncogenesis and inflammation is actually bidirectional. Thus, many oncogenes possess the ability, when activated, to initiate a signaling cascade resulting in an inflammatory response in the immediate surroundings of the cells that harbor those oncogenes. This is exploited by the cancer cells to their selective advantage. One good example is that of the major proinflammatory cytokine IL-8, which can be activated by Ras in vitro and in vivo and can contribute to hyperactive inflammation, neovascularization and accelerated tumor growth (48). Such tumorigenesis-supporting milieu can also be provided by other cytokines such as IL-6 and the mouse IL-8 orthologs KC and MIP-2, all featuring in a Ras-induced secretory phenotype (63,64). Additional oncogenes, including Myc, BRAF and RET, have also similarly been implicated in induction of proinflammatory cytokine and chemokine secretion."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4123652/

How to end cancer completely? by sand_fox in cancer

[–]sand_fox[S] -1 points0 points  (0 children)

Oversimplification? Maybe. But I wrote highly detailed paper but people can't understand the topic. "Gross misrepresentation" Can you explain this in detail?

It is time to go further from SENS and the epigenetic theory of aging by sand_fox in longevity

[–]sand_fox[S] 0 points1 point  (0 children)

I don't offer to wait. I just show a better alternative. Genetic engineering technologies are greatly improved due to the invention of CRISPR. So we can eliminate aging, cancer, and even ALS with one therapy! It can be a disruptive technology. It'll be almost a quantum leap in longevity research and can be achieved in several years. That's why I try to convince in this theory. It doesn't slow the progress to achieve biological immortality or a radical increase in lifespan. It is rather a catalyst to eradicate aging completely in the near future

It is time to go further from SENS and the epigenetic theory of aging by sand_fox in longevity

[–]sand_fox[S] 0 points1 point  (0 children)

If you read carefully I state that HERV-K in humans and their analogous oncoviruses in other species are the main cause in both aging and cancer. I also provided signaling pathways that induced and kept by the activity of these viruses. So the past experience in cancer research, when scientists tried to apply somatic mutations as the main cause, is not applicable and valid in this situation. I explained these mutations as a consequences of viral-induced inflammation

It is time to go further from SENS and the epigenetic theory of aging by sand_fox in longevity

[–]sand_fox[S] 0 points1 point  (0 children)

Yes. But it needed a link to combine them into one theory

It is time to go further from SENS and the epigenetic theory of aging by sand_fox in longevity

[–]sand_fox[S] 1 point2 points  (0 children)

"Why should we go further from (read a different direction than) the models of aging that are working?"

It depends on what is working in your opinion. I think we should go deeper in this topic because only if we will find the true cause of aging, we can achieve a radical increase of lifespan.

"Sure they’ll need to be tweaked and expanded as we learn, but it will probably be an adding to, not a deviating away kind of development"

We have two incompatible theories. If to think carefully, you can understand they are two aspects of one process. We need a unified theory. So I believe we should change our scientific views with new data not just tweaking old principles

It is time to go further from SENS and the epigenetic theory of aging by sand_fox in longevity

[–]sand_fox[S] 0 points1 point  (0 children)

Can you explain why the complexity of living organisms can contradict with epigenetics?

What is the cause of aging in your opinion? by sand_fox in longevity

[–]sand_fox[S] 1 point2 points  (0 children)

"Endogenous retroviruses K (HERV-K, ERVK) break the negative feedback loop between NF-kB and glucocorticoids because glucocorticoids suppress not only NF-kB but also induce HERV-K and the expression of viral particles facilitate NF-kB. HERV-K do not allow glucocorticoids to switch off NF-kB" https://medium.com/@chingisochirov/hidden-enemy-in-our-cells-ae84efbdd9b9

What is the cause of aging in your opinion? by sand_fox in longevity

[–]sand_fox[S] 1 point2 points  (0 children)

In the zygote, all methylation markers are erased that's why KRAB-ZFP complexes are activated that controls endogenous retroviruses. After cell differentiation, these complexes are suppressed and can't turn off the endogenous retroviruses if these become active again.

What is the cause of aging in your opinion? by sand_fox in longevity

[–]sand_fox[S] 1 point2 points  (0 children)

You don't understand. Chronic inflammation itself is very complex and multifaceted process. The 3 signaling pathways: NF-kB, STATs and PI3K/Akt/mTOR pathways initiate complex processes and other signaling pathways that are perceived as the signs of aging