Each mitochondrion contains about 2-10 copies of the mitochondrial DNA (mtDNA), which unlike the nuclear DNA, is circular like the DNA molecules of bacteria. mtDNA codes for 13 proteins involved in energy production, plus specific proteins involved in its own replication, including polymerases. The nucleus supplies many other proteins for mitochondrial function. When a cell is ready to divide it replicates its mitochondria. The DNA is duplicated in much the way that it is in bacteria, using what is called a D-loop mechanism: one strand replicates until it reaches the origin of replication of the other strand, and then the process continues in the opposite direction.
“The term 'monoclonal gammopathy of undetermined significance' denotes the presence of a monoclonal protein in patients without evidence of multiple myeloma, macroglobulinemia, amyloidosis or related plasma cell proliferative disorders. The disorder has been found in approximately 3% of persons older than 70 years and in approximately 1% of persons older than 50 years. A population-based study included 1384 patients from south-eastern Minnesota who had the disorder diagnosed at the Mayo Clinic from 1960 through 1994. Risk of progression was about 1% per year, but patients were at risk of progression even after 25 years or more of stable monoclonal gammopathy of undetermined significance. The risk for development of multiple myeloma was increased 25-fold; the risk of macroglobulinemia, 46-fold; and the risk of primary amyloidosis, 8.4-fold. Concentration and type of monoclonal protein were the only independent predictors of progression. The presence of a urine monoclonal protein and the reduction of one or more uninvolved immunoglobulins were not risk factors for progression. Monoclonal gammopathy of undetermined significance may be associated with various disorders, including lymphoproliferative diseases, leukemia, von Willebrand disease, connective tissue diseases and neurologic disorders.” Therefore, discuss the plan carefully with your doctors.
Single nucleotide polymorphisms can easily be measured on “gene chips” some of which can compare 5 million or more SNPs between different people’s genomes.
Yes, there are many mutations that take place between the initiation and final development of cancer.
Yes, we can repair genes in mouse embryos, and can add new ones, for example, normal or mutated human genes to see the effects on mouse development and learn what they might be doing in humans. We have not yet tried adding or changing human embryonic genes.
Well-differentiated refers to the overall look of the tissue; does it look like a normal tissue, or very abnormal? So a well-differentiated adenocarcinoma looks a lot like normal glandular tissue. It is usually a good prognostic sign.
Absolutely, we already do this, for example by screening all newborns for phenylketonuria (PKU) which is devastating, unless it is diagnosed early and the patient put on a phenylalanine-free diet; then they can be perfectly normal.
There are routine screens of newborns, when identification can lead to prevention. And there are adult human genetics labs that can screen for genetic variants that can be significant, for example certain variants of the BRCA gene with high association to breast cancer. The uncoiling is brief and not in itself associated with increased mutation; but only when DNA replicates do mutations become “locked in."