Well these are fairly different processes, but your question does shed light on the biology. Mutagenesis is the process in which a cell’s genetic information undergoes a stable change, which may occur spontaneously, or as a result of exposure to environmental or endogenous mutagens. Carcinogenesis is initiation of cancer, which includes extensive mutagenic changes plus the interactions with the surrounding microenvironment, such as those that promote angiogenesis and inducing immune tolerance, Teratogenicity is abnormal development so involves cells, tissues and organisms. During rapid development in embryos the efficiency and coordination of DNA repair, cell cycle controls and apoptosis are far more critical to avoid damage than they are in adult organisms. Importantly, all of these - carcinogenic, mutagenic and teratogenic effects - can occur at much lower exposure levels than those required to exhibit toxicity. This is one reason that carcinogens, mutagens, and teratogens are so dangerous, as the harm they do is not necessarily evident in terms of any toxic response, which is a useful obvious warning when being exposed to dangerous substances. Overall, I agree with you that teratogenicity can be more insidious in the sense that small defects in replication, transcription, and repair may cause devastating defects during development. Thus some DNA repair knockouts are embryonic lethal, but if caused in adult animals by chemical knockout or SiRNA can have much milder phenotypes. This effect that rapidly developing cells require more efficient repair  than other cells means that some repair pathways essential to rapidly developing cells can be targets for anticancer drugs.

Mutagenicity & carcinogenicity are linked to DNA damages and/or chromosome changes (structure, numbers) and teratogenicity also in some cases but not only. Thus, many compounds are mutagenic and teratogenic or fetotoxic but several compounds are not mutagenic or carcinogenic but can be teratogenic at very low dose levels. Teratogens can also produce different malformations depending of the development stage the embryo is exposed to.

Many mutations or genomic changes in the embryo are lethal (e.g. among all human chromosomes only 3 types of trisomy are viable). Several human malformations are related to gene mutations either dominant or recessive and can affect many different human chromosomes. Some diseases are carried by sexual chromosomes (X or Y) or even by maternal mitochondrial DNA) but teratogenicity is also related to some differences in gene expressions during development without any genomic changes, as for example with vitamin A and RAR agonists (tretinoin and isotretinoin). Thus, any compound that might interfere with an enzymatic or metabolic pathway critical during development can be teratogenic or fetotoxic. Also, there exists several differences in species specificity and metabolism and distribution is critical to assess teratogenicity. Especially, the placental transfer is critical and some compounds were seen to accumulate in the embryo at much higher levels than plasma concentrations in dams.

Lastly, one single exposure (1 day) during pregnancy can cause malformation, whereas cancer might require more exposures. Also, for many human malformations/genetic diseases there is no available treatment as of today, except palliative ones.

This may be of interest:

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

I suggest readers use judgement and caution on the above citation to a commentary on  the Science paper by Tomasetti and Vogelstein - Science. 2015 Jan 2;347(6217):78-81. doi: 10.1126/science.1260825. The Science paper applies statistical analysis to argue that chance causes stochastic accumulation of mutations during DNA replication as  the major cause of variations in cancer incidence among tissues. They moreover  argue that this is therefore not impacted by environmental and heredity influences. Thus, press releases note "“Bad Luck of Random Mutations Plays Predominant Role in Cancer". This Nature commentary accepts the Tomasetti and Vogelstein  work and  extrapolates forward from it. There are two levels of problems to be cautious about in this work. There are statistical problems that are now being pointed out to the journal Science and will hopefully be published that will question parts of the analysis. More fundamentaly, the existence of a strong correlation between replication and cancer does not mean that mutagens and environmental factors do not greatly change this probability.  I expect that these issues will receive a lot of attention in upcoming months and that the idea that replication associated cancer risk is not changed by interventions will not stand in depth analysis. In fact, a strong correlation between replication and cancer makes good sense when we realize that replication is strongly impacted by DNA damage and furthermore takes DNA lesions into mutations by making them part of the cell's genetic information. 

I agree, that I adjust that readeers use caution and for this someone has to face reality:

Despite bad chosen semantic, oversimplification of conclusion, without explaining differences in absolute risk, as well as misunderstanding by the media as well as by some readers, it should be pointed out clearly why this paper lacks in general and this is not due to bad chosen semantics – agai, this is just one 'small and overestimated point.

Cristian Tomasetti and Bert Vogelstein basic methods:

1) Mutations trigger carcinogenesis,

2) The risk of mutations are relatively constant for a given cell division

3) Stochastic process.

Reality is, that Cancer is triggered in

1) 5-10% by mutation

2) 15% by infection and

3) 80% are sporadic, unknown cause.

Tomasetti ad Vogelstein took the 80% of sporadic cancers and declared such as mutation triggered cancers for having the majority of cancers, that their model works.

5 % of cancers only had been proven being triggered by carcinogenesis, an by this, the stochastic model as well as its results and as a Domino effect the conclusions are also wrongly approached to the majority of cancers.

My view may be biased, but this means, we do not have a need talking about cell division rates of any kind of cells in regard to the discussion of the content of the paper. The methods already lack and that – unfortunately – is enough.

And, if you or I would submit such a paper, esp. to that journal – although in general the approach reads itself interesting (but the paper is honestly on purpose complicated written) – every reviewer would reject it immediately or the paper would even not be reviewed and directly rejected without being peer-reviewed.

Teratogenic (English: Teratogenese) (from the Greek meaning monster teras) or traumatic to any environmental factor that refers to prenatal Jnyn, Only harm. Teratology studies on this phenomenon is probably congenital anomalies and identifying any teratogenic substance is defined. Possible teratogen is a chemical, pharmaceutical, infectious disease, pregnant or physical factors or changes in the metabolism of the embryo or fetus in the mother's body that cause structural or functional disabilities. Among these disorders, including some severe flaws and can be fatal for the baby Fvkvmlya, Cleft Palate (cleft lip) and cleft palate and defects and heart failure (such as changes in wall) cited. Since the medical knowledge of the harmful effects of some factors in overuse injuries in infants following the First Bdnyaamdn Brdhbvd can say that this knowledge has a long history that teratogens can cause damage yet simple to understand and not always depend on several factors.

Teratogen is so insidious than cancer

Dear Shaban

Thank you for your  papers.

regards

FADEL