I will rather say chronic inflammation is initiating factor in many tumors...and also associated with tumor promotion and progression...

Chronic inflammation causes a hypermethylation of tumor suppressor genes termed as CIMP (CpG island methylator phenotype), and genetic mutations of driver genes for carcinogenesis. This is frequently observed in the multi-step development of colon cancer with adenoma-adenocarcinoma sequence also referred to as Vogelstein’s hypothesis. (Attached File1)

On the other hand, some of the cancers arise independently of chronic inflammation characterized by the hereditary tumor syndromes such as Li-Fraumeni syndrome lack of p53 expression, and HNPCC (hereditary non-polyposis colorectal cancer syndrome) lack of DNA-mismatch repair genes such as MSH2 and MLH1. Microsatellite instability seen in these syndromes cause central nervous system tumors as well as ovarian, gastric, and colon cancers in a simultaneous manner. GBM (glioblastoma multiforme) is a very aggressive de novo tumor with multiple genetic alterations, leading to EGFR/PTEN/Akt/mTOR pathway. Craniopharyngioma occurs due to the remnant of pituitary gland precursor cells in sella turcica. Medulloblastoma in the cerebellum arises based on BCL6/BCOR/SIRT1 axis. BCL6 is a transcriptional repressor and lymphoma oncoprotein, which is required for neurogenesis of granule progenitor neurons, expected to tumor-initiating cells of medulloblastoma (Attached File2). Collectively, the genetic failure to repair the damaged DNA or  the remnant of ectopic precursor cells are mainly responsible for the de novo carcinogenesis without inflammation.

http://www.ncbi.nlm.nih.gov/books/NBK1211/

I will rather say chronic inflammation is initiating factor in many tumors...and also associated with tumor promotion and progression...

The exceptions that I can think of are the cancers arising from viral pathogens such as Liver cancer (Hepatitis B virus) or Cervical cancer (Human papilloma virus HPV),  cancers that are due to chromosomal translocation such as CML or APL, and cancer arising from mutations without inflammation being involved (refer to first answer).

But certainly inflammation contributes greatly to the process of carcinogenesis and it is for sure context dependent. 

I agree with DR. Patrick. In not a few cases, the role of inflammation in the tumor development is difficult to determine whether the cause or effect. Surely, chronic inflammation causes epigenetic changes, but inflammation occurs due to the tumor central necrosis or apoptosis accompanied by the lack of tumor-associated new blood vessels.

Dear Mohit Sharma,

Whether do you think that inflammatory processes with dissipation energy into Environment causing high temperature of an organism is the similar expression of energy operation as abundance of huge proliferative processes in cancer metabolism causing accelarated cellular cycle and irrepressible tissue (tumor) growth? As concern to my point of view these processe should be considered via different expression of energy operation. Is it not so?

Chronic inflammation is one sequence out of 6 sequences triggering carcinogenesis:

1) Hypothesis for the Origin for the Mass of Cancer “Epistemology of the Origin of Cancer”:

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

and the following paper with a deeper explanation: 

2) “Cell-Cell Communication in the Tumor Microenvironment, Carcinogenesis, and Anticancer Treatment” (Chemotherapy, Radiotherapy, Immunotherapy) with its physiology and biochemistry explanations:

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

Genetics and / or mutations analyis failed being of significant help in diagnosing or treating cancer patients.

It was very forward thinking that mutations were proposed as being a cause for cancer in 1928. Since then some 5 to 10% hereditary tumors have been shown to be caused by mutations but some 80% of all human cancer are labeled as being “sporadic”- meaning they are of an unknown etiology. There are measurable mutation rates in different cancers cited correctly by @Daniel, but these observations are associations and not so far shown to be causative-which in science means being synonymous with proof of etiology.

As pointed out by Professor Vladimir Matleev elsewhere, genes are of importance for metabolism and changes of those would need a sufficient quantity of mutations. Even the clonal theory which is proposed to explain the rapid proliferation of cancer cells cannot account for the number of mutations observed in human cancers.

If someone does not accept also a kind of genetic metabolism pathway, and would say that these control everything, why has it been now proven, that genes are controlled from the outside (epigenetics)? We know the mechanism of gene control by long non-coding RNA (lncRNAs) mediated repressor occlusion; this group also identified the COX-2-lncRNA, PACER, as a new potential target for COX-2-modulation in inflammation and cancer [Kramczyk et al. Elife. 2014 Apr 29;3:e01776].

http://elifesciences.org/content/3/e01776

Some predominant lepidic pulmonary adenocarcinomas of the lungs with proven activating ERFR mutations aris in almost "normal" lungs without obvious inflammation.

Absolutely correct, but at first these are part of the some 5% of cancers triggered by mutations and the other important field is, that until now no-one concentrated on mutation triggered cancers looking in detail for different forms of inflammation.

Dear Björn L.D.M. Brücher,

Unfortunately I have meant in my works acute inflammatory process causing high temperature of an organism which mechanism of the metabolic pathway is differed from mechanism of metabolic pathway of oncogenesis drastically, that gave me possibility to oppose these two pathways each other considering their inflamation on an organism (Ponizovskiy M.R., (2013), Biophysical and biochemical models of cellular development mechanisms via cellular cycle as in normal tissue and as well as in cancer tissue and in inflammatory processes, Critical Reviews in Eukaryotic Gene Expression, 23 (2), 171 – 193). However the local mechanism of the metabolic pathway of chronic inflammatory process is differed from the mechanism of the cataboloic aerobic pathway of acute inflammatory process. Therefore I consider your researches as important work. I think that maybe it should be examined the appearance even weak signs of Warburg effect in different stages of chronic inflammatory processes. I wish you further success. Thank you for this information and let me know your published works.

Dear Philipp Albert Schnabel,

Dear Philipp Albert Schnabel,

Unfortunately I have meant in my works acute inflammatory process causing high temperature of an organism which mechanism of the metabolic pathway is differed from mechanism of metabolic pathway of oncogenesis drastically, that gave me possibility to oppose these two pathways each other considering their inflamation on an organism (Ponizovskiy M.R., (2013), Biophysical and biochemical models of cellular development mechanisms via cellular cycle as in normal tissue and as well as in cancer tissue and in inflammatory processes, Critical Reviews in Eukaryotic Gene Expression, 23 (2), 171 – 193). However the local mechanism of the metabolic pathway of chronic inflammatory process is differed from the mechanism of the cataboloic aerobic pathway of acute inflammatory process. Therefore I consider your researches as important work. I think that maybe it should be examined the appearance even weak signs of Warburg effect in different stages of chronic inflammatory processes. I wish you further success. Thank you for this information and let me know your published works.

Dear Björn L.D.M. Brücher,

Unfortunately I have meant in my works acute inflammatory process causing high temperature of an organism which mechanism of the metabolic pathway is differed from mechanism of metabolic pathway of oncogenesis drastically, that gave me possibility to oppose these two pathways each other considering their inflamation on an organism (Ponizovskiy M.R., (2013), Biophysical and biochemical models of cellular development mechanisms via cellular cycle as in normal tissue and as well as in cancer tissue and in inflammatory processes, Critical Reviews in Eukaryotic Gene Expression, 23 (2), 171 – 193). However the local mechanism of the metabolic pathway of chronic inflammatory process is differed from the mechanism of the cataboloic aerobic pathway of acute inflammatory process. Therefore I consider your researches as important work. I think that maybe it should be examined the appearance even weak signs of Warburg effect in different stages of chronic inflammatory processes. I wish you further success. Thank you for this information and let me know your published works.

In short acute inflammation is anticancer while chronic inflammation is procancerous?

Yoshida's information is relevant for some 5% of cancers which are triggered by mutation - nothing more. 

We may come to the polit being critical and asking if we shold invest the mass of cancer research funding still in the minority of cancers or in the mass. Further this view of mutations triggered cancers was not created by Vogelstein, it was done in 1928, some 85 years ago.

This answer reflects our problem these days in science: less people are aware about the findings of our scientific grandfathers, they do not re-cite those references, and by this they create their own biased view. At least to me, this is not of help, not for science and ersp. not for the cancer patients and their relatives and they - and not the shining star of someone - are "the" reason, why we should make progress instead of continuing investing into a road which is a one way street without any benefit for cancer patients. 

The next point an increasing number needs reflecting is, that people read increasingly receptively, by means overreading instead of reading with critical reflection of each single sentence. However this quite funny even if someone performs a down-voting here - independent of whom, it is not of help.

Someone who still tries being a lawyer of the mutation analysis may read the section "mtation an polymorphism" of the paper 'Epistemology of the origin of cancer', as within the realiy of our knowledge and impact of it is reflected and not the wishes of some.

What really shoudl grasp us to exist in science is critical thinking. Unfortunately this seems to be less and less common as people fall easily in love with gold idols.

Dear Mohit Sharma,

I agree with this your Query, and you can become familiar with my point of view on the mechanism of metabolic pathway of chronic inflammatory process in my answers to Prof. Björn L.D.M. Brücher and to Prof. Philipp Albert Schnabel (see above). Just really the mechanism of metabolic pathway of chronic inflammatory process is differed as from acute inflammatory  process as well as from cancer process although this pathway can be  transitional pathway between catabolic aerobic exoergonic pathway of acute inflammatory processes and anabolic endoergonic pathway of cancer metabolism that should be examined. It is the my point of view.

Dear Mohit Sharma,

Maybe you are right that "the short acute inflammation is anticancer while chronic inflammation is procancerous". However this thought should be proved although I have opposed in my pubished works the catabolic exoergonic pathway of acute inflammatory processes and anabolic endoergonic pathway of cancer metabolism: (Ponizovskiy M.R., (2013), Biophysical and biochemical models of cellular development mechanisms via cellular cycle as in normal tissue and as well as in cancer tissue and in inflammatory processes, Critical Reviews in Eukaryotic Gene Expression, 23 (2), 171 – 193).

This may be of interest: 

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

As concern to Vogelstein’s hypothesis and chronic inflammatory processes as well as the Domanik Wodarz & Ann G. Zauber note "developing cancer in different tissues is mostly down to random mutations" in article entitled "Cancer: Risk factor and random chances", all of these different mechanisms in various cells and tissues should be considered from the point of view of Warburg effect mechanism (aerobic glycolysis) taking into accout So: Firtly vital for an organism balance catabolic exoergonic & anabolic endoergonic processes causing stability Internal Energy (temperature 36,6gradC), Secondly excessive shift balance catabolic & anabolic processes into excessive anabolic endoergonic processes of cancer tissue causing suppression normal catabolic exoergonic aerobic processes with simultaneously reserving some catabolic processes for survival of cancer tissue metabolism (Apoptosis Resistance) as in local mechanism of camcer tissue and as well as local mechanism of chronic inflammatory which can be transitional pathway between nornal balance catabolic & anabolic processes of an organism and excessive anabolic processes of cancer metabolism; Thirdly it should consider the differed mechanisms of anabolic processes in various cels of various tissue of various states of an organism and cells of an organism. However the general mechanism of all these different mechanisms are subjected to common biophysical and biochemical laws of oncogenesis, i.e. Warburg effect mechanism: [Ponisovskiy M.R., (2010), “Cancer metabolism and the Warburg effect as anabolic process outcomes of oncogene operation”, Critical Reviews in Eukaryotic Gene Expression, 20 (4), 325 – 339]

Tuberculosis is chronic inflammatory state by not pre-malignant......does not cause cancer

Really, there are the different chronic inflammatory processes having different especial mechanisms which depend on causative agent of a disease. However they are subjected to common principle of the chronic inflammatory mechanism corresponding to biophysical and biochemical laws. Therefore the chronic inflammatory tubercular process is not pre-malignant!

a large number of other disorders are als in list like amyloidosis, rheumatoid arthritis, scleroderma......

The mechanisms of such diseases as cardiovasculary diseases, amyloidosis, scleroma etc. should be considered as violation of minimization gain of entropy due to violation substances flows causing violation stability Stationary State of an organism via violation Internal Energy and Internal Medium of an organism according to famous Prigogine theorem that lead to negative fluctuations entropy (-∆xβ) according to Glansdorff and Prigogine theory and to Quasi-stationary pathologic State of thermodynamic system of an organism. Unlike of cardiovasculary diseases, amyloidosis, scleroma etc. the mechanisms of oncologic diseases and inflammatory diseases are characterized as violation of minimization gain of entropy due to violation energy flows causing violation stability Stationary State of an organism via violation Internal Energy and Internal Medium of an organism according to famous Prigogine theorem that lead to negative fluctuations entropy (-∆xβ) according to Glansdorff and Prigogine theory and to Quasi-stationary pathologic State of thermodynamic system of an organism. Thus the crucial difference between mechanisms of these pathologic processes consists in either violation of substances flows or violation of energy flows. Thus the machanisms of these diseases should not be compared. Apropos, rhumatoid arthritis is the chronic inflammatory disease about which already there were discussed.

Dear Mr. Mohit Sharma and Mr. Sandeep Rajput,

I ask your Pardon and respond to the both notes: Mohit Sharma's note "Chronic inflammatory states promotes cancers by modifying the microenvironment" and Sandeep Rajput's note "I will rather say chronic inflammation is initiating factor in many tumors...and also associated with tumor promotion and progression". Firstly, really chronic inflammatory processes modify the microenvironment, but What is the mechanism of the modifed microenvironmeny which promotes mechanism of oncogenesis, i.e. connection between mechanism of modifing the microenvironment and mechanism of oncogenesis? Secondly, really I agree to associate some chronic inflamations with tumor promotion and progression, but I don't know the factor of chronic inflammation which initiate oncogenesis in many tumors: Please, give the citation of a literature, if it is. Thus I try to offer my assumption of the biochemical mechanism oncogenesis inducing by some chronic inflammatory processes. Just  the some causative agents of chronic inflammation such as some viruses get over the barriers as of the local inflammatory nidus and as well as accross cellular wall and accross nuclear envelope intruding into nuclear DNA - the main center of anabolic processes and causing excessive anabolic processes leading to exertion G1/S phases cellular cycle resulting in accelerated cellular cycle that induces irrepressible proliferative processes of cancer development. Also some coccal chronic infectious processes can occur with viruses which provoke oncogenesis (see above). Unlike operation of these causative agents, a lot of microbal chronic inflammatory processes and some of viral chronic inflammatory processes operate only in cellular mitochondria - the main center of catabolic processes, i.e. on the level catabolic pathway. Just these chronic inflammations don't create oncogenesis. 

My point of view and answer to your question MR Ponizovskiy I have attached a picture summary

maybe we should take into account, that energy metabolism is much more complicated as it had been proposed for the last decades, as it was recently shown by Renato et al 2014 in plants, that cellular energy is not coming exclusively from the mitochondrium which may show us that this under influence of different variables: 

Renato M, Pateraki I, Boronat A, Azcón-Bieto J: Tomato fruit chromoplasts behave as respiratory bioenergetic organelles during ripening. Plant Physiol. 2014;166(2):920-933.

http://www.plantphysiol.org/content/166/2/920.long

Yet another way chronic inflammation can be correlated with promtion of cancers 

Dear Colleaque Mohit Sharma,

Unfortunatelly I don't see in your schema the driving mechanism causing  Aerobic Glycolysis, which is the mail characteristic of Warburg effect versus Pasteur effect in norm! Just the arrow, showing the pathway to Warburg effect, should  begin from the point of Lactic acid formation, the crucial marker of Glycolysis, but this arrow should not begin from mitochondria [main center only aerobic oxidation] as in your schema. Please, see the mechanism of Warburg effect: * Ponisovskiy M.R., (2010), “Cancer metabolism and the Warburg effect as anabolic process outcomes of oncogene operation”, Critical Reviews in Eukaryotic Gene Expression, 20 (4), 325 – 339 and * Ponizovskiy M.R., (2013), Biophysical and biochemical transmutation of mitochondrial function in cancer genesis, Biochemistry & Analytical Biochemistry, Volume 2, Issue 3, doi:10.4172/2161-1009.1000137. 

Dear Prof. Björn Brücher,

Really energy is much more complicated as it had been presented.as well as substance structure and substances metabolism which can not exist without energy flows. But it should share energy flows into two pathways [anabolic endoergonic pathway and catabolic exoergonic pathway] which balance of anabolic processes & catabolic processes defines States of thermodynamic system an organism considering that States of all thermodynamic systems is an entropy determinations according to Boltzmann theory, e.g. gaseous - liquid - solid of substance State, as well as balance catabolic & anabolic processes defines an able-bodied organism's State; the excessive shift of balance catabolic & anabolic processes into excessive anabolic endoergonic processe defines the State of excessive proliferative processes of cancer diseases; shift balance catabolic & anabolic processes into excessive catabolic exoergonic processe defines the State of acute inflammatory and infectious processes.

References:

* Ponizovskiy M., (2014), The mechanisms operation of thermodynamic system of a human organism, European Journal of Biophysics, 2 (4), 29 – 37, doi: 10.11648/j.ejb.20140204.11.

* Ponizovskiy M.R., (2013), Biophysical and biochemical models of cellular development mechanisms via cellular cycle as in normal tissue and as well as in cancer tissue and in inflammatory processes, Critical Reviews in Eukaryotic Gene Expression, 23 (2), 171 – 193.

Brain cancer, primary tumours of the brain arise in the absence of inflammation

Thank you @Janice, if you do not mind, I would like providing the facts

You may read the following paper:

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

and you may also take into account the following references:

Versteeg R: Cancer: tumours outside the mutation box. Nature 2014, 506(7489):438–439.

Mack SC, Witt H, Piro RM, Gu L, Zuyderduyn S, Stütz AM, Wang X, Gallo M, Garzia L, Zayne K, Zhang X, Ramaswamy V, Jäger N, Jones DT, Sill M, Pugh TJ, Ryzhova M, Wani KM, Shih DJ, Head R, Remke M, Bailey SD, Zichner T, Faria CC, Barszczyk M, Stark S, Seker-Cin H, Hutter S, Johann P, Bender S et al: Epigenomic alterations define lethal CIMP-positive ependymomas of infancy. Nature 2014, 506(7489):445–450.

Other aspects:

Viral infections and chronic inflammation already had been associated with brain cancer:

Kofman A, Marcinkiewicz L, Dupart E, Lyshchev A, Martynov B, Ryndin A, Kotelevskaya E, Brown J, Schiff D, Abounader R: The roles of viruses in brain tumor initiation and oncomodulation. J Neurooncol. 2011 Dec;105(3):451-66.

Pu Y, Li S, Zhang C, Bao Z, Yang Z, Sun L: High expression of CXCR3 is an independent prognostic factor in glioblastoma patients that promotes an invasive phenotype. J Neurooncol. 2014 Dec 20. [Epub ahead of print]

Further, variables reflecting chronic inflammation had been shown being associated with brain cancers: IGF-1, IL-6, TNF-α, VEGF and chronic viral infection had been associated with malignant brain neoplasms. The findings could not be associated with survival but that is not synonym of prove, no chronic inflammation occurred.

I would assume: just because pathologists did not concentrate on searching and proving chronic inflammation in brain cancer tissue slides, this may should not result in the argumentation brain cancers arise in the absence of chronic inflammation.

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

As Dr. Yoshida commented:  "On the other hand, some of the cancers arise independently of chronic inflammation characterized by the hereditary tumor syndromes such as Li-Fraumeni syndrome lack of p53 expression, and HNPCC (hereditary non-polyposis colorectal cancer syndrome) lack of DNA-mismatch repair genes such as MSH2 and MLH1. Microsatellite instability seen in these syndromes cause central nervous system tumors as well as ovarian, gastric, and colon cancers in a simultaneous manner. GBM (glioblastoma multiforme) is a very aggressive de novo tumor with multiple genetic alterations, leading to EGFR/PTEN/Akt/mTOR pathway. Collectively, the genetic failure to repair the damaged DNA or  the remnant of ectopic precursor cells are mainly responsible for the de novo carcinogenesis without inflammation."

Given that hereditary cancers such as cited represent approximately 5% of cancers, their mechanisms are not relevant to the approximately 80% of adult cancers labeled as "sporadic", i.e., of "unknown etiology". These majority of cancers are the ones we have been trying to unravel in terms of their mechanisms of transformation from a normal cell to a cancerous one. As stated by Prof. Brucher (above), the observation of mutations in cancerous tissue/biopsies says nothing about the role of mutations in initiating cancers.

Really, chronic inflammations are the pathologic sates of an organism in which the local mechanisms of catabolic anaerobic processes prevail over mechanisms of catabolic aerobic processes that cause local partial obstacle for free exoergonic dissemination of catabolic generated energy into Environment. This rest of energy can been consumed for anabolic endoergonic processes creating local sift balance catabolic & anabolic processes into anabolic endoergonic processes which induce the vulnerable local metabolism for v-oncogene operation in cellular genome. Thus it occurs the possible exertion irrepresible proliferative processes of cancerous mutation of this pathologic focus.

NORMAL CELL TRANSITION INTO CANCER CELL – http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117986 - Prove of 6th sequence of new cancer paradigm http://www.biomedcentral.com/1471-2407/14/331

attached below the actual prove of the 6th sequence of the new proposed cancer paradigm:

The transition from one cell function to another, as well as the transition of one cell type to another seems to be a routine event rather than a rare one. It has been shown that an epithelial mesenchymal transition (EMT) in embryogenesis/morphogenesis acts in a direction opposite to that of a mesenchymal-epithelial transition (MET) [Cell 2009, 139(5):871–890]. Furthermore, EMT can induce non-cancer stem cells to become cancer stem cells [Cell 2008, 133(4):704–715 & PLoS One 2008, 3(8):e2888].

Braun recognized some 60 y ago that a gram negative bacterium Agrobacterium tumefaciens could initiate the in vitro transformation of normal plant cells into tumor cells; he showed that transformation occurs in a short time period, resulting in tumor cells with slower growth and less progression [Am J Biol 1947, 34(4):234–240 & Proc Natl Acad Sci U S A 1958, 44(4):344–349 & Phytopathology 1951, 41:963–966]. Zaenen et al. revealed, and Mary-Ann Chilton’s group subsequently proved, that a small DNA plasmid within A. tumefaciens was responsible for the transformation [J Mol Biol 1974, 86(1):109–127.]: tumor inducing DNA (Ti-DNA), after infection, was integrated into the plant genome in tobacco plants [Cell 1977, 11(2):263–271]. Chilton also showed that Braun’s findings were based on the same principle: although the T-DNA from the A. tumefaciens Ti-plasmids was not at first detected [Proc Natl Acad Sci U S A 1974, 71(9):3672–3676], it was later proven to be in the nuclear DNA fraction of crown-gall tumors [Proc Natl Acad Sci U S A 1980, 77(7):4060–4064]. More evidence comes from research on mesothelial cells. In 1966, Eskeland, based on silver-staining electron microscopy studies, first suggested that injured or destroyed mesothelial cells are replaced in location and function by free-floating “peritoneal macrophages,” which are transformed from their original role to that of mesothelial cells [Acta Pathol Microbiol Scand 1966, 68(3):379–395 & Acta Pathol Microbiol Scand 1966, 68(3):353–378.].

As a consequence of a pathogenic stimulus such as inflammation or wound healing, EMT can change MCs into cells with mesenchymal or epithelial characteristics [Int J Biochem Cell Biol 1997, 29(1):5–17]. Recently it was reported that the transition from one cell function to another, as well as the transition of one cell type to another seems to be a routine event rather than a rare one [BMC Cancer. 2014 May 10;14:331] AND due to the above findings within the human, animal and plant kingdom it was proposed that carcinogenesis occurs by a multistep sequence and that its last step is a transition of a normal cell into a cancer cell. The actual paper in PLoS ONE 2015 proves the proposed 6th sequence of the new cancer paradigm http://www.biomedcentral.com/1471-2407/14/331 as chronic lung injury results into a transition of a normal cell into a cancer cell: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117986

Dear Prof. Björn L.D.M. Brücher,

I am grateful you for presented interesting researches in field of oncogenesis, including your and Dr. Ijaz S. Jamall work. I have carefully familiarized myself with these works and don't found the contradictions between my short description mechanisms transmutation of  chronic inflammations into cancer metabolism and as your hypothesis as well as your estimations of various concepts of oncogenesis. You present hypothesis of such sequence of oncogenesis: 1) pathogenic stimulus (biological or chemical carcinogens): You estimate as different factors of cancerogenesis [X-ray, cancer hereditary, infectious, sporadic malignant mutations] as well as possible mechanisms of chemical oncogenesis via two-step process: in the first step, called “initiation,” the carcinogen changes or binds to nuclear DNA; in the second step, called “promotion,” some chemical objects [different aromatic polycyclic hydrocarbons (PAHs), such as benzopyrene and benzoanthracene and so on] or physiologic v-oncogenes and oncogenes [c-Sis, EGFR, PDFR, VEGFR, HER, BTK (family of tyrosine kinases) etc.] cause the aberrant growth resulting in cancer.expression. 2) Chronic inflammations: My short descriptions of mechanisms transmutaton of chronic inflammation don't contradict your note "Cancer has been linked to various pathogens, including the Epstein-Barr virus (EBV) in Burkitt’s lymphoma and nasopharyngeal carcinomas [100] and human papilloma virus (HPV) in cervical cancer and the other".  3) Fibrosis and changes in the microenvironment. Discussing the mechanism of cancerous desmoplasia I have compared desmoplasia with extracellular mechanism cancerous angiogenesis formation due to anabolic endoergonic processes of connective tissue biosythesis which chemical potential interacts with  intracellular chemical potential. This mehcanism corresponds to your description this topic. 4) and 5) Pre-cancerous niche and Chronic-Stress-Escape-Strategy (CSES). Your note "The microenvironment of an acute inflammatory condition differs significantly from that of chronic inflammation" is developed in detail in the article: Ponizovskiy M.R., (2013), Biophysical and biochemical models of cellular development mechanisms via cellular cycle as in normal tissue and as well as in cancer tissue and in inflammatory processes, Critical Reviews in Eukaryotic Gene Expression, 23 (2), 171 – 193. Further short explanation of chronic inflammation mechanism is "chronic inflammations are the pathologic sates of an organism in which the local mechanisms of catabolic anaerobic processes prevail over mechanisms of catabolic aerobic processes that cause local partial obstacle for free exoergonic dissemination of catabolic generated energy into Environment. This rest of energy can been consumed for anabolic endoergonic processes creating local sift balance catabolic & anabolic processes into anabolic endoergonic processes which induce the vulnerable local metabolism for v-oncogene operation in cellular genome. Thus it occurs the possible exertion irrepresible proliferative processes of cancerous mutation of this pathologic focus". 6) Normal Cell-Cancer Cell Transition (NCCCT). This topic is described in detail in two articles: *Ponisovskiy M.R., (2010), “Cancer metabolism and the Warburg effect as anabolic process outcomes of oncogene operation”, Critical Reviews in Eukaryotic Gene Expression, 20 (4), 325 – 339; and *Ponizovskiy M.R., (2013), Biophysical and biochemical transmutation of mitochondrial function in cancer genesis, Biochemistry & Analytical Biochemistry, Volume 2, Issue 3, doi:10.4172/2161-1009.1000137.

                                               Sincerely yours,

                                               Dr. M.Ponizovskiy

Inflammation is one of several things that produce chronic oxidative stress.    In turn,  this promotes the cancer process by inducing genetic instability and by modulating the whole alphabet soup of cell growth and check factors.  E.g. BRCA1, p53, HIVs, etc.   As noted above,  it ties in with the Warburg effect.    

There is significant evidence that much of this is in the local microenviorrnment.   Might even be a therapeutic target. . E.g.,  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552923/

BTW,  I have a US patent to use the agent in the above paper, TEMPOL, in the treatment of fibrocystic disease of breast (FD).   FD is not precancerous itself,  but may reflect local microenviornmental oxidative stress.   Some manifestations are associated with a higher incidence of breast cancer.

I want to notify that today I leave from the house and I shall be away from 20.02.2015 to

26.03.2015.

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

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

Dear Prof. Björn L.D.M. Brücher,

I familiarized myself with the your Hypothesis and the interesing published works offered by you and repeat that I don't found the contradictions between my short description mechanisms transmutation of chronic inflammations into cancer metabolism and your hypothesis. Indeed these outstanding experimental published works confirm your hypothesis. Just I think that some local chronic inlammations are mediators between general acute inflammation and cancer although you and Jamall I.S. noted that 10% of all cancers are hereditary; cancers caused by infection are some 15% of the non-hereditary cancers and 70 to 80% are called "sporadic cancer" [article entitled “Epistemology of the Origin of Cancer: a new paradigm"]. However this percent (15%) does not eliminate your hypothesis as a new paradigm of cancer genesis via chronic inflammation processes. As concern to your and Jamall I.S. published work entitled “Cell-Cell Communication in the Tumor Microenvironment, Carcinogenesis, and Anticancer Treatment", you considered cells communicate by direct and indirect signaling creating indirect intercellular communication and local communication over short distances. I am sorry but I would want to supplement this interesting work with elucidation physical mechanisms of direct and indirect signaling which were put into this effect by cellular capacitors due to resonance waves across distance causing remote cellular reactions (accross distance) transiting into contact cellular reactions [see article - Ponisovskiy M.R., (2011), Driving mechanisms of passive and active transport across cellular membranes as the mechanisms of cell metabolism and development as well as the mechanisms of cellular distance reactions on hormonal expression and the immune response, Critical Reviews in Eukaryotic Gene Expression, vol.21 (3), 267-290].  Considering prevention of cancer metastasis by Atrial natriuretic peptide (ANP) described in published work Nojiri T et al., "Atrial natriuretic peptide prevents cancer metastasis through vascularendothelial cells", this outcome can be explained due to blocking by ANP of guanylyl cyclase-A (GC-A) receptor causing suppression the variable capacitor of this receptor [see above mentioned article].

kindly have look at the schema.May this may ....?

https://www.researchgate.net/publication/274712018_Linking_chronic_inflammation_and_warburg_effect

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Dear Dr. Mohit Sharma,

I have familiarized myself with your schemas. Unfortunately I can not agree with involving ATP into cancer genesis because ATP is driving mechanism of only oxidative phosphrilation exerting catabolic exoergonic processes leading to dissipation energy into environment, but Cancer metabolism and Warburg effect display anabolic endoergonic processes creating consumption and absorption energy for synthetic processes. Also I don't agree with UCP-1 /Thermogenin/ due to the similar cause. And beta-oxidation of free fatty acids release Acetyl ion which form Acetyl-CoA which is consumed in great quantity with huge quantity energy for anabolic endoergonic processes of cancer metabolism.[see 2 articles: 1. Ponisovskiy M.R., (2010), “Cancer metabolism and the Warburg effect as anabolic process outcomes of oncogene operation”, Critical Reviews in Eukaryotic Gene Expression, 20 (4), 325 – 339, and 2. Ponizovskiy M.R., (2013), Biophysical and biochemical transmutation of mitochondrial function in cancer genesis, Biochemistry & Analytical Biochemistry, Volume 2, Issue 3, doi:10.4172/2161-1009.1000137]

Dear Colleagues, 

Studying Oncogenesis I interest myself in the driving mechanisms which cause transmutations leading to cancer pathology, e.g. such queries: What is it the mechanism of chronic inflammation exerting hypermethylation of tumor suppressor genes termed as CIMP (CpG island methylator phenotype) and gene mutation for carcinogenesis? Similar query is concerning hereditary tumor syndromes due to lack of DNA-mismatch repair genes such as MSH2 and MLH1. What is the driving mechanisms of this oncogenesis which arise independently of chronic inflammation? And so on......!