concept 18.5: cancer results from genetic changes that affect cell cycle control

what can mutations to genes that regulate cell growth and division be caused by

spontaneous mutation or environmental influences such as chemicals, radiation, and viruses

oncogenes

mutagens in genes protooncogenes that code for proteins that stimulate normal growth and division

when does an oncogene arise

from a change that either increases the amount of the proto-oncogenes product or in the activity of the protein

what can the conversion of a proto-oncogene to an oncogene lead to

abnormal stimulation of the cell cycle

what are the 4 different ways proto-oncogenes can be converted to oncogenes

epigenic changes - mutation of the gene of chromatin modifying enzyme that can lead to loosening of chromatin and inappropriate expression of proto-oncogene

translocations- movement of DNA within the genome

gene amplification- amplifications of a protooncogene that increases the number of copies of the gene

point mutations- mutations in the protooncogene of its control elements that causes an increase in gene expression

tumor suppressor genes

inhibit cell divisions, they are good at preventing cancer

what do tumor suppressor genes do

they repair damaged DNA, control cell adhesion, and act in cell-signaling pathways that inhibit the cell cycle

multistep mutations

needed for fully active cancer

why does changes of cancer increase with age

because of multistep mutations,

what characterizes a cancer cell at the DNA level

they will have one active oncogene and the mutation of several tumor supressor genes

that gene mutation commonly indicates breast cancer

mutations in the MRCA1 or BRCA2 gene

what is adenomatous polyposis coli (APC)

the tumor suppressor gene