Greetings Francis,

Not sure if I understand your wording (in my book, a cancer cell is by definition malignant?), anyway there are a few ways this can occur:

1- Apparently the tunnel effect is sometimes responsible for the onset of cancer - a cell might become ionized through a passing cosmic ray's energy being boosted by tunnel effect, and thus becoming energetic enough to scramble the cell - which may then become a cancer seed. I remember reading somewhere that this scenario happens on average about 8 times a day in a normal earthling's body, but of course our immune systems are trained to squelch these seeds - a few slip through though.

2- Without a passing cosmic ray, quantum fluctuations would need to be rather energetic to scramble a cell, and statistically an energetic enough fluctuation is very rare. Incidentally, statistics of quantum fluctuations' energies can be inferred from different radioactive elements' half-lives (which, depending on the energy that needs to be be borrowed from the quantum vacuum to trigger decay, range from nano-squared seconds to millions of years.) So to do a calculation you'd have to estimate the energy needed to scramble a cell to turn it into a cancer seed, then compare with the element whose atoms need the same energy to decay, and back-calculate from the observed half-life to infer incidence in time. Scenario Nb 1 above would be the more frequent one by a very wide margin.

Not sure if I answered your question?

The driver mutation, which is essential for the development of cancer, causes the stochastic event. It is stochastic whether the genetic mutation is favorable for the survival and proliferation under the bad conditions (hypoxia, high redox stress, hyper-inflammation etc).  This is deeply related to the cell competition.

On the other hand, there is an emerging theory termed hierarchy model, in which cancer stem cells with higher potential of self-renewal exist at the top of the society of cancer cell population mainly composed of non-cancer stem cells with less potential of stemness.     

Given that tumor micro-environment is also the fundamental factor to predict which sub-population cells become predominant afterwards, a mathematical model has been proposed and widely accepted as reviewed in PLoS ONE 8(8): e71128. doi:10.1371/journal.pone.0071128.  The example of the mathematical application is shown in Scientific Reports 3, Article number: 2473 doi:10.1038/srep02473, which predict  what kind of sub-population of breast cancer stem cells (CD44+CD24− cells) become predominant in the time course.

Greeting Francis

I.

Your queston is a very important one, especially as the differentiation and distinction of sensing within the communication in as well as between cells and structures with its noise is one of the most investigated obstacles but still and largely incompletely understood. The theory by Christopher Govern ad Pieter Wolde is an interesting approach.

Govern CC, Ten Wolde PR: Optimal resource allocation in cellular sensing systems. Proc Natl Acad Sci U S A. 2014 Nov 24. pii: 201411524. [Epub ahead of print]

http://www.pnas.org/content/111/49/17486.abstract.html?etoc

II.

There is a misleading as mutations are not the proven cause for the mass of cancers, although many scientist re-cite the papers by some authors.

Among many cogent observations is a necessary distinction between the origins and ultimate manifestation of cancer. The implications for both early detection and treatment of the manifest disease are obvious and profound. This also is the reason, why we wont have real prevention within the near future. If we want preventing someting, we have identifying the cause at first. If thecause is not known, we cannot effectively prevent. 

The reality is the following, Cancer is triggered in

1) 5-10% by mutation

2) 15% by infection AND

3) 80% are (since 85y) sporadic, meaning unknown cause.

It makes very much sense, that mutations being the cause triggering carcinogenesis are increasingly questioned [Rosenfeld S, Cancer Inform 2013, 12:221–229; Versteeg R, Nature 2014, 506 (7489): 438–439].

You may be interested reading the following:

http://www.biomedcentral.com/content/pdf/1471-2407-14-331.pdf

And some more deeper explanations:

http://www.karger.com/Article/Pdf/362978

Both genetic and epigenetic events that lead to cancer could, in principle, be better understood if quantum theory is taken into account.

You might find the following publications interesting in this respect:

http://de.arxiv.org/abs/0805.4316

http://de.arxiv.org/abs/q-bio/0701050

http://de.arxiv.org/abs/0704.0034

http://de.arxiv.org/abs/0704.3957

http://de.arxiv.org/abs/0802.2271

http://de.arxiv.org/abs/0906.4279

http://de.arxiv.org/abs/1304.0683

http://de.arxiv.org/abs/1312.4440

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275479/

Regards,

Vasily

Certainly thermodynamics  can give explanations for carcinogenesis  e.g based on the 2nd Priciple of Thermodynamics and quantum mechaniscs may provide various opportunities to modify  the negative entropy import of tumor tissue and  the role of positive ntropy in the tumor progression. References from Schrödinger,  Szent-Györgyi, Watrhson, Molnar,  Thornton, Keisari etc

The public may have been misinformed about the real impact of observed / measured mutations / genetics due to wrongly mixing up observations and conclusions.

If I may be allowed, reminding us: it nearly seems that this had been in a comparable way, as cholesterol and heart disease were for decades wrongly be connected, and as we already had been thought by the primary results of the Framingham Heart Study, which to date is the longest-running and most comprehensive study on heart disease, it was clearly demonstrated that cholesterol intake in the diet had no correlation with heart disease. Interestingly, those scientists who reminded colleagues about the possibility abou a wrong direction were - before the results came up - ignored.

However, as above mentioned by this, some generations of scientists may have been misleaded into the wrong direction.

Contrary to the popular opinion, mutations and the majority of findings in cancer genetics so far reported are either late events or epiphenomena that occurs after the appearance of the pre-cancerous niche.

 The mutations have  important role in cancer in initiation and promotion. From the aspect of quantum mechanics , the tumor growth towards maximum entropy production. However the normal cells and tissues develop towards the minimum entropy production.  According to a new paradigm in oncology, the communication between cancer and normal cells basically changed between the cancer cells and stromal  and normal cells. The  changes in communication of the different cell populations might be similar to the   quorum sensing-  signal transmission among different bacterial species in biofilms.  Joseph Molnar, University of Szeged

Mutaitons are of importance in understanding paths in biology and nature. The main misleading was that observation measuing mutations in advanced tumor tissue had been mislead with wrong conclusions it would be "the" cause. As I mentioned elsewhere "an apple found in a car is not synonym of prove, apples grow in cars". 

However, mutations had been proven for some 5% of cancers triggering carcinogenesis, nothing more. The proposal mutations cause cancer was at first done in 1928 and the change of the proposed Knudson 1-hit onto a 2-hit theory did not change anything about this. We should start facing reality although it is understandable, that for those believin mutations are "the" cause of cancer is difficult. 

No question, the mathematical description by quantum mechanics is an interesting theory for explanation of the dual particle-like and wave-like behavior and interactions of energy. Further it may be also a kind of basic for bioelectrical networking, as we learned during the last decade, that this field is also completely underestimated. I therefore agree with @Joseph that this field will be of significance within the future and I am looking very forward to new discoveries in this topi of biophysics. In this regard someone may be interested in the paper from Stuart Baker / NCI "A Cancer Theory Kerfuffle Can Lead to New Lines of Research", J Natl Cancer Inst. 2014 Dec 20;107(2).

I completely agree with Björn's oppinion, that is the reason why we focus our experimets to cancer. and  try to find more and more complex systtems for modelling cancer - normal cell interactions and to improve the effectivity of chemotherapy  in vitro models, e.g with multidrug resistance modifiers. therapy.

http://www.nature.com/nature/journal/v517/n7536/full/517563a.html#comments

This is an interesting question and I am equally troubled by both the challenge it might pose to traditional models of cancer development and in finding where quantum mechanical models serve best.

A traditional view that DNA mutations are causative is very compelling, given the strong observational and experimental evidence linking mutagen exposures to chemically modified nucleotides, "hit" rates of such events within known oncogenes and tumour suppressors, the similarities and tumour inducing capacities of these genes whether the carcinogenic gene sequence is inherited, a somatic mutation, virus borne or deliberately induced by mutagens and then later isolated from the resultant tumours.

An obvious role for quantum mechanics applies in modelling traditional mutagenic "events".

When we consider the intracellular and extracellular signalling of the cell as a unique "quantum network" there could well be a powerful role for some aspects of quantum mechanics in modelling individual tumour progression. I am sorry to say I don't know enough about this to answer the original question, but could imagine a powerful understanding emerging. Best of luck!

A simple mutagen can induce cancer if promoting agent is applied in the experimental mouse skin carcinogenesis. However the  cancer in the population is continuously increasing from the beginning of the "industrial revolution".  Today  the cancer has  much higher incidence than one calculate  based on the frequency of mutations.

The environmental polutions can contribute  in cancer  as inducer, as promoter and  reducing the immune defence. The environmental tress changes  the communication , the cross talk between  normal and cells and  tissues. In case of co-existing normal and cancer cells the  signal transmission is disturbed if we compare to the  coexisting normal tissues, a predator- prey relationship can be observed. Cancer cell grow on the expense of normal cells. There is well defined direction of cancer-host relationhips. Cancer invades the normal tissue, but the opposite  never occurs. This means that the cancer grow as a superparasite. Cancer lives  on the energy and mass of the organism as  parasite  by metabolizing and destroying the tissues of the organism. Process develops according to the 2nd Law of thermodynamics. (Molnar et al.  LDDD 2,429(2005), Acta Sci-Nat.Univ.,NeiMong. 38/1,44-57, 2007 Current Cancer Ther.Rev 5,158-,2009).

Joseph, I think we are in furious agreement that mutagenesis is not the sole source of carcinogenesis. Despite my lack of recent experience in the field, I stuck my oar in because the question is a damn good one. Mutation of critical genes may be a process that "fixes" or ratchets otherwise reversible growth behaviour that originates from other sources. Environmental hormones might initiate a growth behaviour, or inflammation may, or endogenous enzymes that have been oddly induced. options abound. The old concept of "field cancerisation" may be a precurcursor state. My only regret is that I don't know enough to really answer the question.

Should we go back to epigenetics in embryogenesis for an explanation. How does such a complicated system get it right nearly all of the time.(25% pregnancies abort spontaeously but do not become malignant) The original definition of epigenesist  was development from simple to complex. For example form a single cell there develops  two layers (endoderm/ectoderm) then by inductive reaction a third layer appears(mesoderm) and a  fourth induces specialised layers to give organs. These inductions are spatially, temporally and physico-chemicaly dependent and must be done in the right place at the right time. Injury and inflammation induce changes in cells to revert to a primitive form before they re-organise themselves to grow again. Cancer cells show evidence of this by producing tumour markers which reflect reversion to a primitive state. For example the CEA tumour marker is carcino-embryonic antigen  (a cell adhesion glycoprotein) found in foetal Liver and gastrointestinal tract which disappears before birth. Regeneration in the adult tissue depends on stem cells over short and long periods of time and what random event deregulates them to become malignant. ?

I would like to share two publications for this discussion.

Evolutionary mechanism unifies the hallmarks of cancer

Link: http://www.ncbi.nlm.nih.gov/pubmed/24957955

Stochastic cancer progression driven by non-clonal chromosome aberrations

Link: http://www.ncbi.nlm.nih.gov/pubmed/16688757

It is a huge difference if we talk about

1) carcinogenesis 

or

2) cancer

Of course th majority of cancers will have mutations and I do not doubt that at all.

The mutation theory was first proposed in 1928 by Professor Karl-Heirich Bauer and it was for this time very brave doing so. Since some 5-10% of cancers had been proven being triggered by mutations.

I would assume, some 85 years are enough running behind false gods and making out of a opinion a dogma and holy grail. Critical thinking is much more important than overtaking opinions, although they mutated to dogma's. I can imagine that it is not easy for those who still believeand recognizing, this mutation theory did not change anything for the majority of cancer patients. Of course now it is additionlly started using promotional terms such as hallmarks, landscape etc, but let us be honest: does it change something? unfortunately not. 

If someone really wants taken into account stochastic views it should be even questioned, how would be the probility, if we take following into account: 

Fully 99.9% of all mutations that occur within the coding regions of the genome are not understood, nor have they been investigated.

The number of mutated genes and mutations per cancer are, a small percentage of mutations in a coding region varies greatly: 97% of mutations are single-base substitutions and about 3% are insertions or deletions.

Furthermore, of the reported single-base mutations, 90.7% are missense changes, 7.6% are nonsense, and 1.7% involve splice sites located in non-translated regions that immediately follow a start or stop codon.

The number of mutated genes varies, with a smaller number of somatic mutations observed in the population of younger patients with a cancer than that of older patients with the same cancer.

The number of observed mutations varies among tissues of the source cancer: tissue of cancers with high rates of cell division, such as the colon, exhibit more mutations per cell than that of cancers in slowly dividing tissues, such as the brain.

The enormous variability of mutations, combined with the fact that more than half of these occur even before the cancer phenotype is established, leads to an elevated “noise to signal” ratio in the exon sequencing data

.

Mutations are assumed to occur over long periods of time - even as long as several decades. Because of the long time frame, it is reasonable to assume that the data from sequencing vary greatly according to the time of sample collection. Investigation to understand mutations is of significant importance to understanding even more profound underlying biological processes.

If someone wants again telling that even genetic polymorphism would solve that someone may take the following numbers and facts of reality into account:

-is also important for understanding the processes, as two or more different phenotypes may exist in the same individual. Biologists usually investigate certain point mutations in the genotype, such as single nucleotide polymorphisms (SNPs) or variations in homologous DNA by restriction fragment length polymorphisms

(RFLPs), with chromatography, chromosome cytology, or by exploiting genetic data.

-neither the mechanisms nor the distribution of different polymorphisms among individual genes are well understood, although the latter is considered a major reason for the evolutionary disparity that survives

natural selection.

-polymorphisms are necessary to understanding biology - including tumor biology – but are not be the key to solving cancer genomics.

-the reasons why polymorphisms are not a viable route for unraveling cancer genomics are multiple:

(1) We do not understand how polymorphisms reflect a disease or respond to a treatment, or even if they react in coordination with other polymorphisms in other genes.

(2) On 23 July 2013, the number of SNPs published in the Single Nucleotide Polymorphism Database (dbSNP) was 62,676,337.

(3) Human beings have 23 paired chromosomes (46 in each cell) and, according to data from the Human Genome Project, humans probably have 21,000 haploid coding genes with approximately 3.3 × 109 base pairs.

(4) Chromosome 1 of the 46, with its 249,250,621 base pairs, has 4,401,091 variations.

(5) The mutation rate is estimated to be 10−6 to 10−10 in eukaryotes, a piece of data that could permit a calculation of the possible combinations.

(6) However, the number of pseudogenes - about 13,000 - and

(7) the wide variation of transposable (mobile) genetic DNA sequences complicate such a calculation. For example, Alu has about 50,000 active copies/genome, while another, LINE-1 (=long interspersed element 1), has 100.

(8) To the best of our knowledge, mobile genetic elements - classified under CLASS I DNA transposons as LTRs (long terminal transposanable retroposons) and non-LTRs, such as long interspersed elements (=LINEs) and short interspersed elements (=SINEs), and CLASS II DNA transposons - account for more than 40% of the total genetic elements.

I really can understand that it is difficult for those who researched for some 20 to 40 years finding the needle are disappointed and would may argue ‘there must be a way’, but independent of that understandable psychology and the mentioned reasons above, someone may note that neither the genetic information nor the different cells alone influence biological processes. Please face reality if someone declares mutations as being the cause:

measurements of the mutagenesis of cells grown in culture yield values of approximately 2×10−10 single base substitutions per nucleotide in DNA per cell division, or 1×10−7 mutations/gene/cell division.

An even lower number has been demonstrated in cultured stem cells.

The clinical reality is even more hard and tuff – and I know as I have staying honest, as it was shocking me, how this could happen during the last some 85 years:

only some 5% of cancers (and we are not talking about 95%) – we are talking about some 5% of cancers only, had been proven since 1928, being caused by mutations – we may start thinking of investing the majority of cancer funding in the majority of cancers and not in the minorities.

Observations made through my microscope while engaged in the duties of tissue culture in the mid-1970's, created these two questions:

1. Why do some cells begin to display cancerous behavior?

2. Why is this the correct response on the part of the cell?

It is my opinion that the expression of the process in which a cell transforms its energy production from aerobic to anaerobic is better explained by the Unified Field Theory than my Quantum Physics. Your question points in the correct direction and thank you for posing it.    

In case someone is interested that increasingly very honorable and recognized scientists reject as well such hype trains, such as mutations, epigenetics, and many others start getting on stage:

leading biologist, Adrian Bird, Edinburgh University:

he recently compared epigenetics with Lamarckian evolution and presented extensive discussion on why epigenetics is bad science and the claims are hyped up - you may want reading it (weblink below):

These views are not alone and had been echoed by Eric Davidson, Mark Ptashne and many others.

Of course those who earn money with hype trains will at first declare it as minor opinions, but I would assume they completely underestimate what is real going on, as if someone is awake, hecan see it nearly at every corner of the streets.

Of course my views may be biased as critical thinking by a human being.

http://www.sciencedirect.com/science/article/pii/S0092867413010040

I agree that the field of epigenetics became too fashionable and, as so many people try to hop on the train to get funding or publish in trendy journals, the scope of this field seems to widen beyond anything reasonable.

We tried to address this problem in this little review, which offers some clarifications of this term, and I hope will be helpful:

http://www.biopolymers.org.ua/content/30/1/003/

Man exposed to various effects from the environment. The mutation rate  of our body cells is much lower than the incidence of cancer.  There is " normal microflora"  with 10 -100 times more cells than our body cells between the environment and the man. We  cannot ignore the  consequences of the changes induced in this microflora  and "biofilms" as possible mediators of .conversion of  various extositions. to the biological processes.The  quantum mechanics or thermodynamics  can provide rational ideas based on the fact that the normal cells, tissues develop towards the minimum entropy production, however the cancer grow towards to entropy maximum, -to the opposite direction.  the second principle does not allow to make entropy barrier, however does not exclude to change the direction of some entropy flows by application of particular external forces.,We think that the cancer grow on the negative entropy of normal tissues as a parasite according to the 2nd Principle  of thermodynamics. Consequently we  may suppose that the direction of some components of  informational entropy flow can be reversed by external forces,.The process of  carcinogenesis can be characterized by the conversion  of order to chaos in the exposed tissue. The quatum field, thermodymics can lead to the development of new strategies  in  the explanation of cancer  growth and therapy.

Gunther Enderlein's work in Pleomorphism, laid the foundation for the correct understanding of cancer and its mechanism. It is time to abandon, in light of the Unified Field Theory, the idea of randomness, or chaos, or errors in metabolism as being causative for this mislabeled cell adapation to its degraded environment. Cancer is evolution or more correctly Natural Selection's answer to rampant toxicity in the ECF. Here is my quote: "If we do not attempt to kill the immune cell, when the body is responding to infection, then perhaps we should not try to kill the cancer cell when the body is responding to toxicity?"

Cancer is the correct response on the part of a unique cell - one that has a dual genome that enables it to respire with oxygen aerobically and without oxygen anaerobically. (Dr. Otto Warburg)  Quiz: What cell has the unique ability to respire both aerobically and anaerobically? The cancer cell. Which cell is that? Dr. John Beard wrote that paper in 1906. It remains buried, but is very worthwhile. Cancer research needs to emerge out from under the military strategy of kill it, kill it, kill it. Is it dead yet?

We need to change our thinking from broken stupid body to a more accurate view encompassing such dynamic processes as homeostasis. The cancer cell is correctly responding to the conditions of its environment. What we are seeing on the cellular level is what the Earth is experiencing to her atmosphere, water supply, food supply, and added radiation. In a closed system such as ours, where is the evidence of error on the part of the cell? There is none. The cell, having no brain by which to commit an error, does what it does because it is the thing to be done. Cancer is no mistake - in fact, cancer is not even a disease. Toxicity is the disease, cancer is the result or response to the environmental cues received by or driving the cell. It is actually time to reject allopathy as a whole. Allopathy may sell a lot of drugs and justify a lot of surgery, but it is holding back a wave of new research and understanding. Let's update disproven philosophy and misleading paradigms as well.  

Actual findings by Mehryar et al. WORLD GASTROENTEROL 2015 strongly supporting the new cancer hypothesis:

DNA of high-risk Human Papillomavirus (HPV) types 16 and 18 is present in 80% of esophageal squamous cell carcinoma (ESCC):

http://www.wjgnet.com/1007-9327/full/v21/i10/2905.htm

This indicates in terms of ESCC a strong epidemiological indication and in terms of the mass of cancers one strong important Domino stone for the paradigm of subclinical inflammation, an infectious agent and cancer genesis proposed in ‘Epistemology of the Origin of Cancer’ in BMC CANCER 2014:

http://www.biomedcentral.com/1471-2407/14/331

http://www.wjgnet.com/1007-9327/full/v21/i10/2905.htm

http://www.biomedcentral.com/1471-2407/14/331

Here another piece of evidence:

HPV – PROINFLAMMATORY MICROENVIRONMENT – CARCINOGENESIS in COLORECTAL CANCER / Li et al. PLoS ONE 2015

Someone may call the "proinflammatory microenviornment":   precancerous niche

Abstract

BACKGROUND:

Colorectal cancer (CRC) is a major burden of public health and healthcare worldwide. Microbiota has been suggested in promoting chronic inflammation in the intestine which, in turn, promotes tumor development. This study focuses on possible correlations of human papillomavirus (HPV) infection with proinflammatory Stat3 signaling activities and the resulting levels of its downstream proinflammatory cytokine IL-17 in CRC patients.

METHODS:

HPV was examined using HPV Genotyping Chip technology and constitutively active Stat3 (p-Stat3) and IL-17 levels were tested using immunohistochemistry (IHC) in paraffin-embedded cancerous and adjacent normal tissues (ANT) from a cohort of 95 CRC patients. Correlation analyses were performed between HPV infection and clinicopathological characteristics, Stat3 activities and IL-17 levels among these CRC patients.

RESULTS:

Three major findings were observed: (1) HPV infection existed in a high rate of CRC cases (48.4%, 46/95), of which 45 cases (45/46, 97.8%) were high-risk HPV16-positive and only one case was HPV53-positive. (2) HPV infection correlated with poorer clinical stages (III+IV) of CRC. (3) HPV infection strongly correlated with both constitutively higher Stat3 activities (P

Please find below strong evidence supporting the new cancer hypothesis:

Japanese scientists treat lung cancer patients with anti-inflammatory and –fibrotic atrial natruretic peptide and show that patients have by this lower recurrence rates

Personal summary:

Interesting approach from Japanese scientists: the authors published in 2011 a paper in which they could show, that circulating tumor cells in pulmonary veins during the manipulation of lung cancer surgery could be a prognostic indicator for early recurrence [Funaki et al. Eur J Cardiothorac Surg 2011;40(2):322–327]. Further this group showed, that ANP downregulates inflammatory response and having a prophylactic effect on postoperative complications due to lung surgery [Njiri et al. J Thorac Cardiovasc Surg 2012; 143(2): 488–494 Nojiri et al. Eur J Cardiothorac Surg 2013; 44(1):98–103; Eur J Cardiothorac Surg 2012; 41(6):1330–1334]. It is important to mention that ANP - besides an inhibition of the renin-angiotesin-aldosteron path through specific binding to the guanylyl cyclase-A (GC-A) receptor - has an anti-fibrotic effect (!) [Li et al. Curr Cardiol Rev 2001; 5(1):45–51 and Kishimoto et al. Curr Cardiol Rev 2009; 5(1):45–51]. Now the authors combined these findings and applicated ANP during curative lung cancer surgery and found that the recurrence rate (versus control) was lower.

Nojiri T et al.: Atrial natriuretic peptide prevents cancer metastasis through vascularendothelial cells. Proc Natl Acad Sci U S A. 2015 Mar 16. pii: 201417273. [Epub ahead of print]

http://www.pnas.org/content/112/13/4086.abstract.html?etoc

Independent of the support of the recent published new cancer paradigm: 

“Epistemology of the Origin of Cancer: a new paradigm"

BMC Cancer 2014; 14:331: 1-8”:

http://www.biomedcentral.com/1471-2407/14/331

and its its deeper explanations by 

“Cell-Cell Communication in the Tumor Microenvironment, Carcinogenesis, and Anticancer Treatment"

Cell Physiol Biochem 2014; 34: 213-243

http://www.karger.com/Article/FullText/362978

this could be a very useful approach for future peri-operative application in cancer surgery

- and that is the reason why we are here for.

http://www.pnas.org/content/112/13/4086.abstract.html?etoc

70% of cancers are [most assuredly not] known to occur by random mutations. The somatic mutation theory is very much in doubt these days, See, e.g., Coming full circle-from endless complexity to simplicity and back again. Weinberg RA. Cell. 2014 Mar 27;157(1):267-71.

In my recent book "Debating Cancer: The paradox in cancer research", I have discussed in detail about the key limitations of the gene mutation theory of cancer.  In addition, I have also reviewed many alternative theories/hypotheses in the field.  In particular, the role of the stochastic genome alteration mediated macro-cellular evolution has been illustrated, which represents a major core of the genome theory of the cancer evolution.

I welcome all of your comments/advice.

Please see the link:

http://www.worldscientific.com/worldscibooks/10.1142/8879#t=aboutBook

http://www.worldscientific.com/worldscibooks/10.1142/8879#t=aboutBook

http://www.worldscientific.com/worldscibooks/10.1142/8879#t=toc

Yes, the cancer  in thermodynamic terms, represents an open system that is connected to healthy tissues in the host..This open system exchanges nutrients, metabolites and energy with the environment. These exchanges are governed by two major principles e.g the tendency to equalize free energy and to maximize entropy, that measures the degree of disorder in the  patients. So the main difference between cancer and normal tissue is the magnitude of entropy production  by various entrpy currents. Some of these entropy currents can be modified by external forces as were calclculated in our studies  in collaborations when the rate of entropy production in healthy and cancer cells were compared.( Ref. LDDD 2005/2,255,, CCTR 2009/5, 158,,CCTR 2014/10, 234.)

I think quantum mechanics can indeed answer a lot of questions like how cancer becomes malignant. As for "why"...i don't think there is ever an answer in biology/or any study about life...

To start with i am a molecular biologist by training(no PhD yet)

According to my theory immortality is a natural inevitable consequence of evolution. And according to me cancer is really not a disease at all, it is evolution in process. The cell (which will later extend to organism level) is "searching" the "mutational-space" (i.e. space representing all possible mutations in humans) for the right combinations of mutations under different aspects like telomere-lengthening, apoptosis, tumour-suppressor, metabolism etc. which will make the cell grow forever in a controlled manner rather than the uncontrollable form we see now as the cancer disease. We are directing our own evolution and speeding it with anti-cancer drugs. Cancer develops resistance thereby taking another path in the mutational space. The longevity will result in brain size development and opening up other higher level functioning phenomenon of the brain. Coalescing of consciousness will take place. We will have hive mind. If One knows and every one else will know  immediately. Renewable energy resource and technology like mnemonics and the likes will help advance our species in leaps and bounds. Knowledge based society will prevail. We would have moved by the time our sun becomes a red giant., maybe to Mars first and then rest of the galaxy, universe. All this will take millions of years, of course. We will know everthing there is to know. And we will realize that sum of all knowledge - EVERYTHING and NOTHING is the same!....and then the cycle starts all over again. Like in Isaac Asimov's The last question. Try to read the Vedas if you can. Get hold of Sir Penrose's Cycles of time and Endless Universe by Steinhardt and Turok. You will see a lot of things matches. The ancient vedic texts even have quantum physics and string theory described in them. Even the noble laureate Schrödinger acknowledged the fact that the ancient Indians knew about Quantum physics and that we are just re-discovering it.

Coming back to cancer. You could argue that cancer is somatic and not a germline affecting disease which is passed on to the offsprings. Well. I have searched through literature and i have it in my hard disk (data which i searched through from countless entries from Sanger Research Institute's database)  that some oncogenes (cancer causing genes) are selected in the germline! Now why would nature select these terrible mutations to be passed on. If it is detrimental to the population, how is it selected in the germline??!!!  no one is able to come up with a convincing answer.

So basically we are headed there - immortality i mean, slowly but steadily. And i don't think future posthuman species will look anything like us.

it might sound like science fiction now but i thorougly believe that this is what is going to happen. today's science fiction is tomorrow's science. based on all the physics, biology, natural philosophy, sci&tech etc. i have come to this conclusion about life.  i just wanted this cancer/evolution idea to be "out there" so that people can think about it, know about it, spread the knowledge. I have searched for many people (scientists/biologists) who have ideas like me and have indeed come across a few people. I have done a lot of thought experiments in physics and biology and philosophy and develop theory and then i check if anybody else have come up with it. lots of it have already been published by other people. so i pat myself in the back saying "well if they came up with a accepted hypothesis, your thinking is on the right track"...so with similar belief i have confidence on the theory how human life is going to develop in the future.

I Thank you and RG for giving me an opportunity to put my idea out there and thank you for asking a question and letting me answer it.

Cancer cell is an object of information carrier and the information transfer can be activated under environmental conditions (e.g. hypoxia, acidity,, mutagenicity of the environment, immundepression etc). The thermodynamical explanation is based on the Second Law of thermodymics.  The cells and tissues live on the expense of negentropy of  healthy cells and tissues, cancer can be considered as  superparasite. The "spontaneous" process  increases the disorder  via invasion and metastasin formationin the host.

Cancer is primarily a metablic disease...metabolic derangements precede genetic changes...

I  should like to recommend to read the  one of our  paper.s,

Joseph Molnar et al: The role of stroma in tumor host co-existence: Some perspectives in stoma targeted therapy of cancer. Biochemistry and Parmacology: Open access, 2013,2/1

 The bioenergetic theory of carcinogenesis...

https://www.researchgate.net/publication/229325765_The_bio-energetic_theory_of_carcinogenesis

Article The bio-energetic theory of carcinogenesis

Stay tuned - a special issue is on it's way

For a practical framework see:

https://www.frontiersin.org/articles/10.3389/fonc.2017.00198/full

For the Special issue of carcinogenesis I should like to recommend to include old references from Royal Raymond Rife patents "universal virus microscop" and "frequence-, interference" questions from the beginning of 20th century dependind on the possible interests.

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Mechanochemical heterogeneity and mechanoemission chaos in malignant transformation during carcinogenesis

«What admits no doubt in my mind is that the Creator must have known a great deal of wave mechanics and solid state physics, and must have applied them. Certainly, He did not limit himself to the molecular level when shaping life just to make it simpler for the biochemist».

Albert Szent-Gyorgyi

(Introduction to a Submolecular Biology, Academic Press New York and London, 1960, page 15)

Regretfully, I have found such a captivating talk only today.

Many noted scientists have stucked their oars in determined chaos of malignant transformation based on the fundamental ideas of D'Arcy Wentworth Thompson (the growth and form), Theodor Boveri (the somatic mutation theory), Otto Heinrich Warburg (the cancer growth is caused by tumor cells generating bioenergy), Alan Turing (the chemical signals), Albert Szent-Györgyi (the connection between free radicals and the development of cancer), Alexander G. Gurwitsch (the morphogenetic field) and Ilya Prigogine (the order out of chaos),

Defining the malignant transformation only by the second law of thermodynamics would be a very difficult task. Much is known that to apply the second law of thermodynamics to living systems, as distinct from non-living, some definitive characteristics have to be first introduced. Meanwhile, one assumes, a part of colleagues would possibly agree the mutation theory, chaos theory and quantum mechanics are just the tip of the iceberg in this matter.

«Guess the devil really is in the details».

I propose to add that the malignant transformation phenomenon focus too on earlier observed practical aspects of mechanochemical heterogeneity (enzymatic, free radical and immunological reactions) and mechanoemission chaos (heat and electromagnetic emission) reported in:

https://www.researchgate.net/publication/263909869_SPATIAL_AND_MECHANOEMISSION_CHAOS_OF_MECHANICALLY_DEFORMED_TUMOR_CELLS

https://www.researchgate.net/publication/314270817_Heterogeneity_of_hypoxia_in_solid_tumours_and_mechanochemical_reactions_with_oxygen_nanobubbles

https://www.researchgate.net/publication/260797562_MECHANICAL_HETEROGENIZATION_OF_LEWIS_LUNG_CARCINOMA_CELLS_CAN_IMPROVE_ANTIMETASTATIC_EFFECT_OF_DENDRITIC_CELLS

https://rdms-cms.jinr.ru/drrr/Timofeeff/2000/TEsisis/evol/Orel1.htm

https://www.researchgate.net/publication/269763940_DNA_Triboluminescence_and_Carcinogenesis

The pilot experimental and clinical studies show promising results of above-mentioned phenomena in:

https://www.researchgate.net/publication/221906806_The_Effect_of_Spatially_Inhomogeneous_Electromagnetic_Field_and_Local_Inductive_Hyperthermia_on_Nonlinear_Dynamics_of_the_Growth_for_Transplanted_Animal_Tumors

https://www.researchgate.net/publication/294193530_CLINICAL_AND_IMMUNOLOGICAL_EFFECTIVENESS_OF_DENDRITIC_CELL_IMMUNOTHERAPY_IN_LUNG_CANCER_PATIENTS_5-YEARS_FOLLOW-UP_PERIOD

https://www.researchgate.net/publication/10978853_An_Algorithm_for_Estimating_Chaos_in_Mechanoemission_of_Blood_and_Magnetic_Resonance_Imaging_in_Patients_with_Gastric_Cancer

https://www.researchgate.net/publication/269687173_Electromagnetic_mechanoemission_of_whole_blood_from_cancer_patients

Valerii E. Orel

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Cancer is an exacerbated proliferation of cells that takes time to develop. I consider quantum mechanics to be a good tool because it studies the changes generated by this mutation at atomic resolution, but it does not help much to predict future changes. For a study focused on protein-level mutations, there are deep learning and machine learning tools that have algorithms that can generate heat maps. These diagrams show the comparison with the changes induced by 20 amino acids and the effect on the structure of the protein evaluated.

I disagree to the concept of cancer as a primarily genetic disease, I favor the concept of cancer as a primarily a metabolic disease.

Maybe this article can help with the answer:

Article Study on attractors during organism evolution

There is a big logical error in this question. Cancer cell is the name of the phenotype that already has malignant behavior

Article The bio-energetic theory of carcinogenesis

I should like to see chronological data (time series) that demonstrates that somatic mutations are causal to carcinogenesis and not just observed in cells/tissues already gone awry. This myth of somatic mutations as "causative" has been repeated so often over the past 75 years, it has become gospel, with little to no evidence!

set A of somatic mutations may cause carcinogenesis and the same set A of somatic mutations may not cause carcinogenesis (..)

Metabolic derangements precede genetic changes in malignancies...

bioenergetic disturbances precede metabolic derangements that precede genetic changes in malignancies...

"the apparently random events that occur during the pathogenesis of cancer development" - yes, in my opinion, cancer development is quasi-random

Thank you excellent reading

Prof Frank Cunningham

Yes in the sense that redox signaling plays a key role in the neoplastic process. Article Oxidative Stress in Cancer

Article The bio-energetic theory of carcinogenesis

Enhanced tumor growth under the influence of an inhomogeneous stationary magnetic field and magnetic nanoparticles involves magneto-mechanical modulation of free radical reactions and subsequent redox signaling. Quantum mechanics plays a role in a free radical mechanism in tumor redox-mediated pathways: external magnetic fields act on entangled states of electron spins in free radical pairs within the tumor and the microenvironmentArticle Magneto-mechanical effects of magnetite nanoparticles on Wal...

Furthermore, magnetic nanoparticles loaded with an antitumor drug combined with electromagnetic fields were shown to inhibit tumor growth based on singlet-triplet interconversions during magnetic resonance in the electron-nuclear spin states of a radical pair Article Nanomagnetic Modulation of Tumor Redox State

Different roles of quantum mechanics can be used to modulate the convergence of mechanochemical, magnetochemical effects, redox signals, gene regulation, cancer cell proliferation, the microenvironment, tumor growth and disseminationArticle Remote control of magnetic nanocomplexes for delivery and de...