Genetics: Ch 23 Genetics and Cancer

cancer

a genetic disease characterized by uncontrolled cell division due to mutations

why is cancer hard to cure

multiple mutations, genetic variation within tumors, and rapid evolution of cells

3 hallmarks of cancer cells

1. uncontrolled cell division

2. avoidance of apoptosis

3. maintenance of telomeres

clonal selection

process where mutated cells with growth advantages replicate more than others

proto-oncogenes

normal genes that promote cell cycle progression

oncogenes

mutated proto-oncogenes that drive excess cell division (gain of function)

tumor supressor genes

genes that inhibit cell cycle progression (loss of function leads to cancer)

DNA repair genes

genes that fix mutations defects increase mutation rate

cell cycle

ordered sequence of cell growth and division phases

cyclins

proteins that regulate progression thru the cell cycle

CDKs (cyclin-dependent kinases)

enzymes activated by cyclins to phosphorylate target proteins

cyclin-CDK complexes

act as “on/off switches” controlling cell cycle transitions

G1 checkpoint

determines if cell should enter DNA replication

G2 checkpoint

determines if cell should process to mitosis

M checkpoint (spindle assembly)

ensures chromosomes are properly aligned before division

RB protein

tumor suppressor that regulates E2F

E2F

transcription factor requires for S phase genes

MPF (maturation promoting factor)

cyclin B and CDK complex needed for mitosis

p53 (TP53)

tumor suppressor; “guardian of the genome”; regulates DNA damage response

BRCA genes

DNA repair genes involved in homologous recombination

Ras pathway

signal transduction pathway controlling cell growth

apoptosis

programmed cell death

metastasis

spread of cancer cells to other parts of the body

benign tumor

non-spreading tumor

malignant tumor

cancerous tumor capable of spreading

telomerase

enzyme that extends telomeres; active in cancer cells