That article wasn't actually useful, here is a better query
google.com
So I found this...
Human cancer is driven by the acquisition of genomic alterations. These alterations include amplifications and deletions of portions of one or both chromosomes in the cell. The localization of such copy number changes is an important pursuit in cancer genomics research because amplifications frequently harbor cancer-causing oncogenes, while deleted regions often contain tumor-suppressor genes. In this paper the authors present an expectation-maximization-based procedure that, when applied to data from single nucleotide polymorphism arrays, estimates not only total copy number at high resolution across the genome, but also the contribution of each parental chromosome to copy number. Applying this approach to data from over 100 lung cancer samples the authors find that, in essentially all cases, amplification is monoallelic. That is, only one of the two parental chromosomes contributes to the copy number elevation in each amplified region. This phenomenon makes possible the identification of haplotypes, or patterns of single nucleotide polymorphism alleles, that may serve as markers for the tumor-inducing genetic variants being targeted.
compbiol.plosjournals.org
I'm don't know if that answers my question, I might be getting closer...
Still, even if you genotype everything, maybe some
tumors respond to treatment while others don't, it
is all expensive and difficult. Seems mostly academic. |
