Cancer Flashcards
What is Cancer?
uncontrolled cellular proliferation
cells divide when they shouldn’t
What causes cancer?
all known cancers are caused by damage to DNA
1-How DNA is regulated
- Sequence of DNA
- genes turning off and on- epigenetics
Cancer
• Mutations in cell’s own DNA–
cells getting ready to divide make an error-proof reading mechanisms aren’t full proof
Errors during replication and mitosis – Carcinogens
-tabacco, benzene, charred food, uv light
aspetis-used for insulation, x-rays
• viruses – Play a role in ~15% of cancers – Examples?
HPV-cervical cancer
virus that causes mono
How Many Mutations Does It Take?
• Number varies depending on which genes are mutated
-average 7 major genes mutated in tumors
;no sunscreen, mutation, cell divides possibility of another mutation( random error in replication
Why does the incidence of cancer increase with age?
around for longer. able to accumulate more mutuations, exposed to more carcinogens, immune system is not as great
What are the two types of genes most often associated with cancer? what do they act as?
- oncogenes -gas pedal OP
- tumor supressors -breaks TBS
• ____________ = Gene that when mutated or overexpressed can contribute to turning a normal cell into a cancer cell
protooncogene
tell to divide without a signal
Oncogenes
• Genes involved in growth and differentiation – Examples: growth factors, RTKs, GTPases, transcription factors
Oncogenes:3 basic types of activation ?
- Mutation that changes protein structure
- Increase in protein concentration
- Chromosomal Translocation
Mutation which changes protein structure
• Increase activity or cause loss of regulation
-change DNA, change shape, more stable, could be turned on all the time
– Increase in protein concentration
• Increase in expression, stability or gene duplication
-gene duplicated, always on, always making protein
-chromosomal translocation
- • Constitutively expressed fusion protein (Bcr‐Abl) or expression in wrong cell or at wrong time
- each genes on/off switch not controlled by own switch
can inhibit it with drug-cells continue to mutate —>have more mutations that develop
What are Tumor Suppressors?
• Genes which have a repressive effect on the regulation of the cell cycle or promote apoptosis
Tumor suppressors follow what hypothesis?
• Usually follow the “two‐hit hypothesis” – both copies of the gene must be non functional
-with one good copy-still have breaks
p53 is known as?
“The Guardian of the Genome”
What is P53?
Tumor suppressor
What does P53 do?
regulates the cell cycle-halts the cell cycle if there’s damage to the DNA/ stress on the cell
-mutated in 50% of human cancers
inherited mutations =Li Fraumens syndrome
diagnosed with first cancer very early in life-continue to develop malgnancies throughout life
-screened very often-inherit mutation-even if it’s not cancerous - predisposes you
What are the ten hallmarks of cancer
- Uncontrolled proliferation
- Evasion of growth suppressors (inactivation of tumor suppressors)
- Resistance to apoptosis
- Develop replicative immortality (activate telomerase)
- Induce angiogenesis
- Invasion and metastasis
- Genomic Instability
- inflammation
- Changed energy metabolism
- immune system invasion
What is uncontrolled proliferation?
uncontrolled cell division
• Resistance to apoptosis
damaged cells should die-cancer cells resistant -even w/o chemo they won’t die
Develop replicative immortality (activate telomerase)
continue to divide over and over again-normal cells divide-telomeres shorter reach critical length- apoptosis.
-loose more DNA-loose important information
enzyme telomyerase lengthens telemeres over and over again
• Induce angiogenesis
induce formation of new blood vessels as tumor larger cells inside can’t access nutrients, oxygen.
send signals for new blood vessels to form-new blood vessels difficult to remove because of blood vessels around the area
