Chemotherapy Flashcards
What type of therapies is cancer treatment moving towards?
Targeted therapies
How is cancer categorized?
By origin and mutational status
What is the 2 part definition of cancer?
Cells that divide uncontrollable and can invade nearby tissues
Sarcomas affect what tissues?
Fat, bone, muscle
What are the 6 hallmarks of cancer?
Limitless replication, evading apoptosis, self-sifficient growth hormone production, insensitivity to anti-growth signals, angiogenesis, and tissues invasion/metastasis
In what way are cancer cells able to avoid apoptosis?
Normally, damage to DNA will cause the cell to undergo apoptosis. In cancer cells, many mutations exist, including those to allow it to avoid apoptosis and to grow more rapidly.
How are cancer cells able to invade and metastasize?
Because of the other properties of cancer cells (self-sufficiency of growth hormones and loss of contact inhibition). Normally, healthy cells rely on neighboring cells for signals to grow and stop growing, however, cancer is able to survive on it’s own as long as it has a blood supply.
How are cancer cells able to replicate without limit?
Active telomerase. In healthy cells, telomerase is usually inactive. In cancer cells, telomerase is actively lengthening telomeres, rendering the cell immortal. This makes the cell more prone to mutations and more prone to pass those mutations on to daughter cells.
In normal cells, shortening of the telomere causes the cell to enter this state
Replicative senescence
Are tumor suppressor genes dominant or recessive?
Recessive. Tumor suppressor genes generally follow the “two-hit hypothesis,” which implies that both alleles that code for a particular protein must be affected before an effect is manifested. This is because if only one allele for the gene is damaged, the second can still produce the correct protein. In other words, mutant tumor suppressors’ alleles are usually recessive whereas mutant oncogene alleles are typically dominant.
Give an example of a tumor suppressor gene
p53
What is the role of p53?
p53 prevents cells with damaged DNA from proliferating. It is known as the “guardian of the genome.” About 50% of people with cancer have a mutate p53 gene.
How does p53 work?
Certain damage to the DNA will cause p53 to activate. There is a checkpoint between the G1 and S (synthesis) phases, where p53 will be activated if need be. p53 will then decide if the damage is repairable or irreparable. If repairable, the cell goes into cell cycle arrest, during which DNA repair occurs. If irreparable, p53 activates apoptosis.
Are you able to inherit somatic mutations?
No.
What is Li-Fraumeni Syndrome?
A germline mutation of the p53 gene. People with this mutation are about 25x more likely to have cancer by age 50, and are more likely to get cancer at an early age.
Are germline mutations found in all of your cells?
Yes.
What is the typical signal transduction cascade leading to DNA transcription and proliferation?
RAS -> RAF -> MEK-> ERK
ERK then enters the nucleus to stimulate transcription factors.
Are RAS, RAF, MEK, and ERK tumor suppressor genes or proto-oncogenes?
Proto-oncogenes
Are proto-oncogenes dominant or recessive?
Dominant
What is an oncogene?
A proto-oncogene that has undergone a mutation
