Home Products Most Popular Contact
No items in your cart.
The page below is a sample from the LabCE course Hallmarks and Signaling of Cancer Cells. Access the complete course and earn ASCLS P.A.C.E.-approved continuing education credits by subscribing online.

Learn more about Hallmarks and Signaling of Cancer Cells (online CE course) »
How to Subscribe
MLS & MLT Comprehensive CE Package
Includes 111 CE courses, most popular
$95 Add to cart
Pick Your Courses
Up to 8 CE hours
$50 Add to cart
Individual course$20 Add to cart

Cancer Hallmark #10: Unstable Genome

A genome is the collection of all genes for a given species. Sequencing of the human genome has been completed and approximately 25,000 coding sequence genes (genes that code proteins, or protein-coding genes) have been discovered.
Genome instability refers to a high frequency of mutations within a species' genome. Cancer occurs from cumulative mutations of genes that promote cell proliferation, apoptosis, and migration as well as genes that function to suppress tumors and/or repair DNA damage.
It is thought that in cancer there are an average 60-70 mutated genes. Of course, only a small handful are the "driver" genes whereas the rest are "passenger" genes which may not be pathogenic. Among the many challenges in studying cancer is how one can distinguish between "driver" and "passenger" genes. Understanding these differences should allow for the development of new treatment strategies for cancers.
Single nucleotide polymorphisms (SNPs)
There are four building blocks of DNA designated as: Adenine (A), Thymine (T), Guanine (G), and Cytosine (C). These building blocks are called nucleotides. Molecular rules of complimentary pairing of A-T and G-C must be followed to maintain DNA fidelity.
A single nucleotide polymorphism (SNP) takes place when a nucleotide normally found at a specific locus on a gene segment is replaced by a different nucleotide. SNP is a type of DNA variation among individuals and marks individual differences. Depending on the location and genes affected, SNPs can interact with environmental factors that collectively drive tumorigenesis.