Cancer is generally considered to be an abnormal growth of cells caused by mutations in DNA induced by carcinogenic substances, viral oncogenes, ionizing radiations etc. Although evidence has been insufficient, and it has also been argued that often this relationship was not seen, the mutational theory of cancer is the explanation we find in every textbook. A recent experiment raises doubts about the validity of the dogma. Investigators show that mutation in the Ha-ras-1 gene is sometime found in normal mammary gland and is absent in cancerous cells. Here is the abstract published in the Journal of Cell Science on March , 2 2004. THE STROMA AS A CRUCIAL TARGET IN RAT MAMMARY GLAND CARCINOGENESIS Maricel V. Maffini1, Ana M. Soto1,*, Janine M. Calabro1, Angelo A. Ucci2 and Carlos Sonnenschein1 A complex network of interactions between the stroma, the extracellular matrix and the epithelium drives mammary gland development and function. Two main assumptions in chemical carcinogenesis of the mammary gland have been that carcinogens induce neoplasia by causing mutations in the DNA of the epithelial cells and that the alterations of tissue architecture observed in neoplasms are a consequence of this primary mutational event. Here, we use a rat mammary tissue recombination model and the chemical carcinogen N- nitrosomethylurea (NMU) to determine whether the primary target of the carcinogen is the epithelium, the stroma or both tissue compartments. Mammary epithelial cells were exposed in vitro either to the carcinogen or vehicle before being transplanted into the cleared fat pads of rats exposed to carcinogen or vehicle. We observed that neoplastic transformation of these mammary epithelial cells occurred only when the stroma was exposed in vivo to NMU, regardless of whether or not the epithelial cells were exposed to the carcinogen. Mammary epithelial cells exposed in vitro to the carcinogen formed phenotypically normal ducts when injected into a non-treated stroma. Mutation in the Ha-ras-1 gene did not correlate with initiation of neoplasia. Not only was it often found in both cleared mammary fat pads of vehicle- treated animals and intact mammary glands of untreated animals, but it was also absent in some tumors. Our results suggest that the stroma is a crucial target of the carcinogen and that mutation in the Ha-ras-1 gene is neither necessary nor sufficient for tumor initiation. I am not predicting (although I am not excluding) that this will start a chain reaction of experiments designed to prove the EPIGENETIC origin of cancer, but it should make us rethink what is real (production of proteins) and what is fictious (determination of morphology, etiology of diseases, etc.) on the role of genes in biology.
<< Cancer is generally considered to be an abnormal growth of cells caused by mutations in DNA induced by carcinogenic substances, viral oncogenes, ionizing radiations etc. >> Let me say this cautiously. Yet it has also been found that many cancer patients share some basic psychological behaviors. Why would that be if those psychological behaviors didn't in some way connect with the disease? Anyone studying a chronic disease that develops over long periods of time, and that seems to have a strong psychological aspect accompanying it ; should take that into account when attacking the disease - everything should be on the table in attacking cancer IMO. In the case of some cancer (those not proven to be caused by carcinogens) there seems to often be a stoic behavior in the patient, an anger at self, a strong guilt, repressed fears in some cases, etc. Is that a reflection of the body's response to the disease, or a cause that is partially responsible. We know of cases of diseases in which the self not only attacks the non-self within the body, but it wrongly attacks the self within the body too as sort of an over protection that has gone amok. Where does cancer fit in here?
CNCabej <[email protected]> wrote or quoted: > Cancer is generally considered to be an abnormal growth of > cells caused by mutations in DNA induced by carcinogenic > substances, viral oncogenes, ionizing radiations etc. > Although evidence has been insufficient, and it has also > been argued that often this relationship was not seen, the > mutational theory of cancer is the explanation we find in > every textbook. A recent experiment raises doubts about > the validity of the dogma. Investigators show that > mutation in the Ha-ras-1 gene is sometime found in normal > mammary gland and is absent in cancerous cells. "[...] it was also absent in *some* tumors" is what they wrote. I.e. this particular mutation was probably not the sole causal factor. > Here is the abstract published in the Journal of Cell > Science on March , 2 2004. > > THE STROMA AS A CRUCIAL TARGET IN RAT MAMMARY GLAND > CARCINOGENESIS > > Maricel V. Maffini1, Ana M. Soto1,*, Janine M. Calabro1, > Angelo A. Ucci2 and Carlos Sonnenschein1 > > A complex network of interactions between the stroma, the > extracellular matrix and the epithelium drives mammary > gland development and function. Two main assumptions in > chemical carcinogenesis of the mammary gland have been > that carcinogens induce neoplasia by causing mutations in > the DNA of the epithelial cells and that the alterations > of tissue architecture observed in neoplasms are a > consequence of this primary mutational event. Here, we use > a rat mammary tissue recombination model and the chemical > carcinogen N-nitrosomethylurea (NMU) to determine whether > the primary target of the carcinogen is the epithelium, > the stroma or both tissue compartments. Mammary epithelial > cells were exposed in vitro either to the carcinogen or > vehicle before being transplanted into the cleared fat > pads of rats exposed to carcinogen or vehicle. We observed > that neoplastic transformation of these mammary epithelial > cells occurred only when the stroma was exposed in vivo to > NMU, regardless of whether or not the epithelial cells > were exposed to the carcinogen. Mammary epithelial cells > exposed in vitro to the carcinogen formed phenotypically > normal ducts when injected into a non-treated stroma. > Mutation in the Ha-ras-1 gene did not correlate with > initiation of neoplasia. Not only was it often found in > both cleared mammary fat pads of vehicle-treated animals > and intact mammary glands of untreated animals, but it was > also absent in some tumors. Our results suggest that the > stroma is a crucial target of the carcinogen and that > mutation in the Ha-ras-1 gene is neither necessary nor > sufficient for tumor initiation. > > > I am not predicting (although I am not excluding) that > this will start a chain reaction of experiments designed > to prove the EPIGENETIC origin of cancer, but it should > make us rethink what is real (production of proteins) and > what is fictious (determination of morphology, etiology of > diseases, etc.) on the role of genes in biology. I'm not sure I understand. Isn't cancer thought to be caused by (among other things) radiation. It seems to me that radiation qualifies as "EPIGENETIC" in origin. I certainly can't see anything very revolutionary in the study you cite. I don't see how it raises any doubts at all about the validity of the conventional explanations for cancer. -- __________ |im |yler http://timtyler.org/ [email protected] Remove lock to reply.
[email protected] (CNCabej) wrote in news:[email protected]: > Cancer is generally considered to be an abnormal growth of > cells caused by mutations in DNA induced by carcinogenic > substances, viral oncogenes, ionizing radiations etc. > Although evidence has been insufficient, and it has also > been argued that often this relationship was not seen, the > mutational theory of cancer is the explanation we find in > every textbook. A recent experiment raises doubts about > the validity of the dogma. Investigators show that > mutation in the Ha-ras-1 gene is sometime found in normal > mammary gland and is absent in cancerous cells. Here is > the abstract published in the Journal of Cell Science on > March , 2 2004. (snip) > Our results suggest that the stroma is a crucial target of > the carcinogen and that mutation in the Ha-ras-1 gene is > neither necessary nor sufficient for tumor initiation. > I am not predicting (although I am not excluding) that > this will start a chain reaction of experiments designed > to prove the EPIGENETIC origin of cancer, but it should > make us rethink what is real (production of proteins) and > what is fictious (determination of morphology, etiology of > diseases, etc.) on the role of genes in biology. The article, as I read it, has nothing to do with epigenetic origins of cancer.It simply says that the changes leading to the cancer occur in stromal cells rather than epithelial cells. Yours, Bill Morse
"CNCabej" <[email protected]> wrote in message news:[email protected]... > Cancer is generally considered to be an abnormal growth of > cells caused by mutations in DNA induced by carcinogenic > substances, viral oncogenes, ionizing > radiations etc. Although evidence has been insufficient, > and it has also been > argued that often this relationship was not seen, the > mutational theory of cancer is the explanation we find in > every textbook. A recent experiment raises > doubts about the validity of the dogma. Investigators show > that mutation in the > Ha-ras-1 gene is sometime found in normal mammary gland > and is absent in cancerous cells. Here is the abstract > published in the Journal of Cell Science > on March , 2 2004. <snip> It might be helpful, to people trying to understand cancers at the level of DNA, to look at that cancers as a legacy of a specific adaptative behaviour arisen in to-us-animals- ancestral populations of (in total a trillion^2 or so?) amoebic (single-celled) individuals. The thence arisen (and of cancer "prototypal") adaptive behaviour (or response pattern) in question, can be described as: - A 'last ditch' gamble on reproducing an offspring (mutant clone) that is genetically altered to the effect that the impact of the frequently occurring "Inescapable 'Irritating Cloud' Type Stressors/Situations", that trillions of amoebic individuals of ancestral population frequently got caught-up in, became neutral (not irritating), or even sometimes a source of nutrients, to the offspring's adaptively altered genophenotype. This 'inside-out' view of cancers came to me as a spin-off from when I tried to imagine a simplest possible case of being in a SHITS ["selective (as specific as synapse- situated) Hibernation" imploring type stressors/situations]. There is of course to be an emphasis on the unifying meaning of the word "Irritating", and on the meaning of the "Cloud" as being vast and longterm enough to cause an amoebic creatures reflexive recoils form the Cloud's constituent irritants to soon become a decidedly mal-adaptive behavioural response (IOW the irritants would cause a futile expenditure of vital, potentially reproductive, energy). ---- [Just for some SEPTIC humored and typically fuzzsilly logical EPT fun, try sounding the ICTS with a sloopy Cech pronounciation.%-].] ---- P
