<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">JCT</journal-id><journal-title-group><journal-title>Journal of Cancer Therapy</journal-title></journal-title-group><issn pub-type="epub">2151-1934</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/jct.2018.95034</article-id><article-id pub-id-type="publisher-id">JCT-84367</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine&amp;Healthcare</subject></subj-group></article-categories><title-group><article-title>
 
 
  A Novel Model of Cancer
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Hans</surname><given-names>W. Giertz</given-names></name><xref ref-type="aff" rid="aff1"><sub>1</sub></xref></contrib></contrib-group><aff id="aff1"><label>1</label><addr-line>GiertzTech, Gnesta, Sweden</addr-line></aff><author-notes><corresp id="cor1">* E-mail:</corresp></author-notes><pub-date pub-type="epub"><day>07</day><month>05</month><year>2018</year></pub-date><volume>09</volume><issue>05</issue><fpage>383</fpage><lpage>387</lpage><history><date date-type="received"><day>2,</day>	<month>February</month>	<year>2018</year></date><date date-type="rev-recd"><day>5,</day>	<month>May</month>	<year>2018</year>	</date><date date-type="accepted"><day>8,</day>	<month>May</month>	<year>2018</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p>
 
 
  This study describes a novel model of cancer. Cancer is caused, according to this model, by two toxic molecules, COF
  <sub>2</sub>
   (carbonyl fluoride) and CS
  <sub>2</sub>
   (carbon disulfide). COF
  <sub>2</sub>
   acts as a catalyst and produces CS
  <sub>2</sub>
  . CS
  <sub>2</sub>
   acts as a catalyst and produces COF
  <sub>2</sub>
  . Hence, the molecules COF
  <sub>2</sub>
   and CS
  <sub>2</sub>
   have the ability to reproduce each other, 
  i.e.
   to create a chain reaction where COF
  <sub>2</sub>
   and CS
  <sub>2</sub>
   are multiplied. COF
  <sub>2</sub>
   and CS
  <sub>2</sub>
   are toxic. It is proposed that long-term cell exposure to COF
  <sub>2</sub>
   and CS
  <sub>2</sub>
   may disturb cell apoptosis and cause uncontrolled cell growth, 
  i.e.
   cancer. Consequently, cancer is caused by a disease causing mechanism or agent and not by a pathogen. However, cancer can be initiated by e.g. a bacteria or virus that contain
  s
   the molecules COF<sub>2</sub> and CS<sub>2</sub>, wherein these molecules start a chain reaction producing COF<sub>2</sub> and CS<sub>2</sub> in the infected area and where the result can be cancer. The study describes why Fe<sub>2</sub>O<sub>3</sub> (iron
   
  (III) oxide) may have a therapeutic effect on cancer.
 
</p></abstract><kwd-group><kwd>Cancer Model </kwd><kwd>Cancer Marker</kwd><kwd> Cancer Therapy</kwd><kwd> Catalyzes</kwd><kwd> Carbonyl Fluoride</kwd><kwd> Carbon Disulfide</kwd><kwd> Fe2O3</kwd><kwd> Ferumoxytol</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>The present report describes a novel model of cancer. According to this model cancer is caused by a mechanism consisting of two toxic molecules. It is proposed that they impair the immune system. A new method is described that facilitates non-invasive analyses of these two molecules in cancer cell lines and tumors in vivo. These molecules create catalyzes, also in a test tube positioned outside the cell line or tumor. The result is analyzed and provides a description of the mechanism causing cancer.</p><p>Within medicine enzyme catalyzes is the increase in the rate of a chemical reaction by the active site of a protein. However, the human organism, pathogens, molecules and chemical elements encompass a much larger range of different types of catalyzes. Catalyzes can create new molecules and where the catalyst is another molecule, compound or chemical element [<xref ref-type="bibr" rid="scirp.84367-ref1">1</xref>] . Molecules and chemical elements can act as catalysts where the catalytic reaction is reduction (destruction) of molecules [<xref ref-type="bibr" rid="scirp.84367-ref2">2</xref>] . Catalyzes is caused by radiated energy from molecules and chemical elements and generates reactions also at distance, similar to the electrons field [<xref ref-type="bibr" rid="scirp.84367-ref3">3</xref>] .</p><p>Recent development displays that many pathogens (e.g. bacteria, virus) as well as autoimmune diseases contain a generic part that consists of the molecules COF<sub>2</sub> and CS<sub>2</sub>. This will be reported in separate studies.</p><p>An overwhelming body of evidence displays that relationship among certain bacteria and cancer exists [<xref ref-type="bibr" rid="scirp.84367-ref4">4</xref>] . Chronic gastritis induced by Helibacter pylori is the strongest known risk factor for gastric cancer [<xref ref-type="bibr" rid="scirp.84367-ref5">5</xref>] . An estimated 15% of all human cancers worldwide may be attributed to viruses [<xref ref-type="bibr" rid="scirp.84367-ref6">6</xref>] [<xref ref-type="bibr" rid="scirp.84367-ref7">7</xref>] . Several studies have shown that a history of autoimmune diseases increases the risk of cancer [<xref ref-type="bibr" rid="scirp.84367-ref8">8</xref>] , despite the fact that cancer and autoimmune diseases are fundamentally different pathological conditions [<xref ref-type="bibr" rid="scirp.84367-ref9">9</xref>] .</p><p>Numerous reports display that the molecule Fe<sub>2</sub>O<sub>3</sub> increases cellular necrosis, increases the rate of apoptosis [<xref ref-type="bibr" rid="scirp.84367-ref10">10</xref>] and significantly inhibits cellular growth [<xref ref-type="bibr" rid="scirp.84367-ref11">11</xref>] . Fe<sub>2</sub>O<sub>3</sub> is the active substance in Ferumoxytol [<xref ref-type="bibr" rid="scirp.84367-ref12">12</xref>] . Ferumoxytol is an FDA-approved therapeutic for the treatment of anemia. However, reports display that it also may be effective in treatment of various forms of cancer [<xref ref-type="bibr" rid="scirp.84367-ref13">13</xref>] [<xref ref-type="bibr" rid="scirp.84367-ref14">14</xref>] .</p></sec><sec id="s2"><title>2. Novel Model of Cancer</title><p>Cancer is caused, according to this model, by two molecules COF<sub>2</sub> and CS<sub>2</sub>. Presence of COF<sub>2</sub> and CS<sub>2</sub> in cancer cell lines and tumors/metastases in vivo can be measured by their radiated frequency spectrum (using frequency spectrometry). However, they can also be measured using catalyzes and that is described below.</p><p>COF<sub>2</sub> acts as catalyst and where it creates CS<sub>2</sub> in cell lines and in tumors in vivo. CS<sub>2</sub> also acts as catalyst and where it creates COF<sub>2</sub> in cell lines and in tumors in vivo. Consequently, a small amount of COF<sub>2</sub> acts as catalyst and creates CS<sub>2</sub>, which in its turn creates more COF<sub>2</sub> and which in its turn creates more CS<sub>2</sub>. Hence, COF<sub>2</sub> or CS<sub>2</sub> generates a chain reaction that produces an increasing amount of COF<sub>2</sub> and CS<sub>2</sub>. The molecule CS<sub>2</sub> is toxic and the molecule COF<sub>2</sub> is extremely toxic. It is proposed that long-term cell exposure to COF<sub>2</sub> and CS<sub>2</sub> may result in reduced apoptosis and uncontrolled cell growth, i.e. cancer.</p><p>COF<sub>2</sub> and CS<sub>2</sub> in a cell line or tumor also act as catalysts outside the cell line and outside the human body by means of their radiated energy [<xref ref-type="bibr" rid="scirp.84367-ref3">3</xref>] . A test tube was positioned outside the cell line or outside the body in the vicinity of the tumor. The test tube contained C (carbon), F (fluoride) and S (sulfur) dissolved in H<sub>2</sub>O (water). The radiated energy from COF<sub>2</sub> acted as catalyst and created CS<sub>2</sub> in the test tube. The radiated energy from CS<sub>2</sub> acted as catalyst and created COF<sub>2</sub>. Catalyzes of COF<sub>2</sub> and CS<sub>2</sub> in a test tube can be used as a cancer marker and where the method is non-invasive. Alternatively the test tube may contain only C, F and H<sub>2</sub>O wherein only COF<sub>2</sub> was created. Alternatively the test tube may contain only C, S and H<sub>2</sub>O wherein only CS<sub>2</sub> was created. Catalyzes in a test tube can be used as a method to analyze presence of COF<sub>2</sub> and CS<sub>2</sub> in cell lines or tumors.</p><p>COF<sub>2</sub> can be analyzed using FTIR (Fourier Transform Infrared Spectrometer), GC (Gas Chromatography) or GC/MS (Gas Chromatography-Mass Spectrometry). CS<sub>2</sub> can be analyzed using GC or LC (Liquid Chromatography).</p><p>The following types of cancer have been analyzed and they all contain the molecules COF<sub>2</sub> and CS<sub>2</sub>: brain cancer, breast cancer, colon cancer, larynx cancer, leukemia, liver cancer, lung cancer, lymphatic cancer, melanoma, pancreatic cancer, prostate cancer, squamous cell carcinoma, testicular cancer and uterine cancer.</p><p>The following cancer cell lines have been analyzed and they contain the molecules COF<sub>2</sub> and CS<sub>2</sub>: cellosaurus cell line Mutu-3, lymphoblastic cell line LCL and epithelial cell line HONE-1.</p></sec><sec id="s3"><title>3. Discussion</title><p>A novel model of cancer is presented. Cancer is created by a mechanism that contains two toxic molecules: COF<sub>2</sub> and CS<sub>2</sub>. They have the ability to reproduce each other wherein a chain reaction occurs that produces vast amounts of COF<sub>2</sub> and CS<sub>2</sub>. CS<sub>2</sub> is toxic and COF<sub>2</sub> is extremely toxic. It is proposed that they impair the immune system and where the result can be impaired apoptosis and uncontrolled cell growth, i.e. cancer.</p><p>Empiric results display that cancer cell lines and cancer tumors act as catalysts wherein they produce COF<sub>2</sub> and CS<sub>2</sub>, also at a distance, i.e. in a test tube positioned outside the cell line or outside the body close to the tumor. Catalyzes of COF<sub>2</sub> and CS<sub>2</sub> can be used as cancer marker. The method can also be used in order to analyze content of cell lines and tumors, i.e. the cancer causing mechanism.</p><p>Reports display correlation between bacterial infections and cancer [<xref ref-type="bibr" rid="scirp.84367-ref5">5</xref>] [<xref ref-type="bibr" rid="scirp.84367-ref6">6</xref>] , between viral infections and cancer [<xref ref-type="bibr" rid="scirp.84367-ref7">7</xref>] [<xref ref-type="bibr" rid="scirp.84367-ref8">8</xref>] and between autoimmune diseases and cancer [<xref ref-type="bibr" rid="scirp.84367-ref9">9</xref>] [<xref ref-type="bibr" rid="scirp.84367-ref10">10</xref>] . Recent findings display that many pathogenic bacteria, virus and autoimmune diseases contain a generic part that consists of the molecules COF<sub>2</sub> and CS<sub>2</sub>. These findings will be reported elsewhere. Cancer cannot occur on its own, i.e. without presence of COF<sub>2</sub> and/or CS<sub>2</sub>. Presence of COF<sub>2</sub> and/or CS<sub>2</sub> is mandatory in order to start the chain reaction where the long-term result is production of vast amounts of COF<sub>2</sub> and CS<sub>2</sub>. Many pathogenic bacteria and viruses as well as autoimmune diseases contain a generic mechanism that consists of the molecules COF<sub>2</sub> and CS<sub>2</sub>. It is proposed that chronic bacterial, viral and autoimmune diseases may start catalyzes of COF<sub>2</sub> and CS<sub>2</sub> in the infected area. The result is, eventually, a chain reaction that produces vast amounts of COF<sub>2</sub> and CS<sub>2</sub> and, sometimes, subsequent cancer. Hence, bacterial, viral and autoimmune diseases can initiate a chain reaction where the result is cancer. They are not carcinogenic by their own.</p><p>Reports display that Fe<sub>2</sub>O<sub>3</sub> in nanoparticles had a therapeutic effect on cancer cells in vitro and xenograft liver cancer in mice and where the result was increased inhibitory rate and ratio of apoptosis [<xref ref-type="bibr" rid="scirp.84367-ref11">11</xref>] . Another report describes the therapeutic mechanism of treating SMMC-7721 liver cancer cells using Fe<sub>2</sub>O<sub>3</sub> nanoparticles. It was shown that it could cause cellular necrosis, induce cellular apoptosis and significantly inhibit cellular growth, all of which appeared to be dependent on the concentration of the Fe<sub>2</sub>O<sub>3</sub> nanoparticles. Fe<sub>2</sub>O<sub>3</sub> is the active substance in Ferumoxytol [<xref ref-type="bibr" rid="scirp.84367-ref12">12</xref>] . Stanford researchers discovered that Ferumoxytol triggered the immune system to destroy tumor cells [<xref ref-type="bibr" rid="scirp.84367-ref13">13</xref>] . Another study suggests that Fe<sub>2</sub>O<sub>3</sub> nanoparticles in Ferumoxytol could be applied “off label” to protect the liver from metastatic seeds and potentiate macrophage-modulating cancer immunotherapies [<xref ref-type="bibr" rid="scirp.84367-ref14">14</xref>] .</p><p>The above studies display a correlation between Fe<sub>2</sub>O<sub>3</sub> and therapeutic effect on cancer and in particular the therapeutic effect of Ferumoxytol. The following is proposed. Fe<sub>2</sub>O<sub>3</sub> acts as a catalyst where it reduces (destroys) the molecule COF<sub>2</sub> contained in cancer tumors and metastases. However, the molecule CS<sub>2</sub> is not destroyed. Destruction of (only) COF<sub>2</sub> inhibits further production of CS<sub>2</sub> and which limits toxic exposure in cancer tumors and metastases and where the result is increased cellular necrosis and apoptosis. This type of catalyzes can be demonstrated in the following experiment. A test tube containing COF<sub>2</sub> was positioned close to 10 grams of Fe<sub>2</sub>O<sub>3</sub> during 15 minutes. Then the test tube was removed and its content of COF<sub>2</sub> was analyzed; the result was zero content of COF<sub>2</sub>.</p></sec><sec id="s4"><title>4. Conclusion</title><p>The overall conclusion is that it has been difficult to analyze the cause of cancer using state of the art technique. The present report displays a novel method. Molecules in cancer cell lines and tumors can be analyzed because they radiate energy that causes catalyzes outside the cell line and outside the body in a test tube wherein specific molecules are created (COF<sub>2</sub> and CS<sub>2</sub>). These molecules can be analyzed using conventional measurement techniques such as FTIR, GC, GC-MS and LC. The conclusion is also that Fe<sub>2</sub>O<sub>3</sub> reduces the molecule COF<sub>2</sub> and hence, Fe<sub>2</sub>O<sub>3</sub> may have an important role in cancer therapy.</p></sec><sec id="s5"><title>Cite this paper</title><p>Giertz, H.W. (2018) A Novel Model of Cancer. Journal of Cancer Therapy, 9, 383-387. https://doi.org/10.4236/jct.2018.95034</p></sec></body><back><ref-list><title>References</title><ref id="scirp.84367-ref1"><label>1</label><mixed-citation publication-type="other" xlink:type="simple">Garcia-Viloca, M., Gao, J., Karplus, M. and Thrular, D.G. (2004) How Enzymes Work: Analysis by Modern Rate Theory and Computer Simulations. 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