It may date from the 16th century.
Up to date, there is no evidence showing that a pathological point mutation may cause substantial structural differences in the PrP fold.
"This mutation may just increase the susceptibility to seizures".
This protean progression means that a drug targeted to one mutation may not work against cancer cells throughout the body.
Mutations may vary from one cancer cell to another in the same patient, and the same genetic mutation may cause cancers in different parts of the body.
Mutation is standard among viruses, and according to two cell model studies published in the journal Cell in November, an Ebola mutation may have allowed the virus to infect humans more easily than the original.
Given the small number of splice site mutations in malignant rhabdoid tumours reported to date (Biegel, 2006), it is interesting to note that our family and one other multigeneration family with RTPS (Taylor et al, 2000) demonstrate an INI1 mutation at a splice site, raising the possibility that carriers of such a mutation may be less likely to be affected.
Thus, this mutation would date back approximately to 2,200 years ago.
If positively selected, these mutations may have accumulated faster than the background rates assumed in our molecular dating calculations.
However, studies to date indicate that resistance to oseltamivir in influenza virus strains occurs rarely (32, 33 ) and that such mutations may have a fitness cost in terms of impaired growth and transmissibility (34, 35 ).
