LITMIR.BIZ

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Ay Fawn/sable Aw Gray/wolf as Saddle at Bicolor (tan points) a Recessive black Black B Black b Liver Color C Color factor CC Full color cch Chinchilla c_e Extreme dilution cd White with dark eyes cb Blue eyes c Albinism Dilution D No dilution d Dilution (e.g., blue Doberman) Extension Em Black mask E Normal extension e Nonextension (yellow) Graying G Born black, turns blue g Born black, stays black Intensity INT Lightest tan intm Intermediate tan int Darkest tan Solid K Solid color in pigmented areas Br Brindle Y Allows yellow pigment to show Merle M Merle m Nonmerle Spotting S Solid color si Irish spotting sp Piebald sw Extreme white piebald S‐extension Se Black mask sese No black mask Ticking T Ticking t Nonticking

      3.3.6 Epigenetics

      Although many medical conditions are the result of gene mutations that have passed from generation to generation, evidence is mounting that the environment can not only have an impact on personal health but can also be conserved in the genes. These environmental “shocks” seem to be capable of leaving an imprint on the genetic material in eggs and sperm, which can pass along new traits in a single generation.

      The epigenome sits above the DNA sequence and provides a second layer of information, regulating several genomic functions, including when and where genes are turned on or off. New studies have shown that so‐called epigenetic marks are associated with genes, providing instructions such as telling them to switch on or off. These marks are normal and allow cells to differentiate, but if the marks do not work properly because of an environmental stressor, cancer or cell death might result, and, worst of all, could be transmitted to descendants. So, if some stressor such as a rich diet activates an epigenetic mark, which in turn modifies histones or adds methyl groups to DNA strands, it could result in disease or susceptibility to disease that not only affects the individual but can be passed on to future generations. This epigenetic influence may not even occur equally across both alleles, in some instances depending on genotype and in other instances depending on from which parent the allele was inherited. Nutrition is likely a major factor in epigenetics, and technological advances will likely lead to the identification of nutrient‐responsive genes and biological pathways, important nutrient–gene interactions, and genomic biomarkers of disease [1].

      While perhaps not as well known and discussed as the genome, the epigenome is believed to be much larger and more complicated than the genome of 20 000 or so genes. Medications are even available now that exert their effects through epigenetic marks. These developments are bound to assume more significance in the years ahead.

      3.3.7 Genetics and Cancer

      There is no doubt that many cancers have genetic associations [2] but there is still much to learn about the genetics of cancer. Solid evidence exists that some cancers, such as those associated with dermatofibrosis, have a genetic basis, and a DNA test can even be used for that particular disorder. Pugs are predisposed to viral pigmented plaques, associated with papillomavirus. Lymphoproliferative diseases also appear to have well‐defined heritable risk factors in at least some breeds. In many other instances, definite breed predispositions exist, but in many cases a definitive genetic basis is lacking. In other cases, epigenetics and environmental causes may coincide with genetics to promote cancer. For example, the incidence of transitional cell carcinoma (TCC) has been steadily increasing in dogs over the years, and the risk of Scottish terriers developing TCC is approximately 18 times the risk of mixed‐breed dogs [3]. Further studies have suggested that this breed‐associated risk may be due to differences in pathways that activate or detoxify carcinogens, and exposure to lawns or gardens treated with phenoxy herbicides could potentially be associated with the increased risk of TCC in Scottish terriers.

      Oncogenes

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