Assessing cancer risk - from mouse to man. See the attached case study and pleas

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Assessing cancer risk - from mouse to man. See the attached case study and please answer question 1.

ASSESSING CANCER RISK FROM MOUSE TO MAN Cancer is a frightening disease. The biological process | been an emphasis in public policy on assessing cancer that creates cancerous cells from healthy tissue is poorly understood at best. Much research has been conducted into how external conditions relate to cancer. For example, we know that smoking leads to one group of people to the chemical while keeping substantially higher incidence of lung cancer in humans. Cancer appears spontaneously, however, and its onset seems to be inherently probabilistic, as experiments performed on animals, usually mice or shown by the fact that some people smoke all thei ats. The laboratory animals in the experimental lives without developing lung cancer risks from a variety of chemicals. Scientifically speaking, the best way to determine cancer risk to humans would be to expose others away from it. But such experiments would not be ethical. Thus, scientists generally rely on group are exposed to high doses of the substance Some commentators claim that the use of new being tested. High doses are required because low and untested chemicals is leading to a cancer epidemic. As evidence they point to the increase innoticeable effect on the relatively small experimental cancer deaths over the years. Indeed, cancer deaths group. After the animals die, cancers are identified have increased, but people generally have longer life by autopsy. This kind of experiment is called a spans, and more elderly people now are at risk for the bioassay. Typical cancer bioassays involve 600 disease. When cancer rates are adjusted for the increased life span, cancer rates have not increasedseveral hundred thousand dollars. substantially. In fact, when data are examined this way, some cancer rates (liver, stomach, and uterine assessments, two important extrapolations are made cancer) are less common now than they were 50 years First, there is the extrapolation from high doses to low ago (1986 data of the American Cancer Society) Nevertheless, the public fears cancer greatly. The Delaney Amendment to the Food, Drug, and Cosmetics Act of 1954 outlaws residues in processed extrapolations, assessments are made regarding the foods of chemicals that pose any risk of cancer to incidence of cancer when humans are exposed to the animals or humans. One of the results of this fear has substance doses probably would not have a statisticall animals, require 2 to 3 years to complete, and cost When bioassays are used to make cancer risk doses. Second, it is necessary to extrapolate from effects on test species to effects on humans. On the basis o data from laboratory experiments and these

Explanation / Answer

The two extrapolation mentioned here are change on the subjects body due to a high dose i.e. estimating what kind of effect low dose of medication would have on humans given the effects of high dose on animals and estimation of effect of drug on humans given that the test subjects were animals. But to asses these estimations without any method or form could result in bias which could potentialy be devastating for humans. A probabilistic approach makes sense as it sets a bench mark from earlier drugs produced which were not harmful and would require any new drug to equal or exceed earlier probabilities in apositive manner. In the extrapolation of effect of low dose we need to consider that there could be short term as well as long term side/adverse effects. Since lab animals die of the high dose we can only estimate any long term effect the medication may have. It is well known that chemical composition of humans differ from that of animals and some chemicals which may not be found in animals could be in human. We need to assess seperately the effect of the drug on such chemicals and the neccesary proabilistic level achieved from this must be used in research purposes.

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