T16: Senescence and Cancer

G1 checkpoint

G1 checkpoint

environment, damage

G2 checkpoint

replication, damage

M checkpoint

attached to spindle

cyclin-dependent kinase (Cdks) induce

cell cycle

telomere role

prevent chromosome from fusing

telomerase

keeps telomere long (found in cancer, stem cells)

proto-oncogene

normal, dominant

oncogene

mutated, unregulated growth

RAS oncogene

bad: inhibit p53 and Rb -> cell cycle progress

mutated: keep going cell cycle

Tumor suppressor gene

normal, inhibit cell division, suppress growth, recessive

p53

good, detect damage, trigger repair or apoptosis

retinoblastoma (Rb)

good, control transcription

Quiescence goes to phase ______ and is ______

G0; reversible

Senescence is

irreversible

short term advantages of senescence

tumor suppression, limit tissue damage and wound healing, embryonic development

long term disadvantages of senescence

aging, cancer

senescent cell release

SASP

monocyte become senescent ->

plaque instability (atherosclerosis)

adipocyte become senescent ->

insulin resistance (type 2 DM)

astrocyte become senescent ->

neuron death and less neurogenesis (Parkinson's)

bone become senescent ->

induce osteoclast, inhibit osteoblast -> bone resorption (osteoporosis)

chondrocyte become senescent ->

cartilage degradation (osteoarthritis)