Cancer cells: reduced death rate
✅
… rates are high in tumours because the cell environment is…
- Apoptosis is high due to inhospitable and cell signalling is
dysregulated. Apoptotic cells stimulate wound healing and responses
that promote tumour groth and regrowth after therapy
High cancer cell mitosis rates are balanced by…- ✅Programmed cell
death
although lytic necrotic cell death can also occurs, large sale normally
“tidy“ apoptosis can trigger inflammation and wound healing
Apoptosis can occur at any point in the tumour development to promote
the initial tumor growth or regrowth after cytotoxic therapy
✅
Apoptosis promotes wound healing- Effector caspase-3 cleaves
phosphoplipase A (iPLA) from cell membrane lipids, which produces
aranchodionic acid which is metabolised by COX2 into PGE2 which
promote the increase in vasodilation for cancer cell proliferation
Apoptotic bodies are coated with phosphatidylserine (PS) which isan eat
me signal for macrophage to come and ingest which then release
VEGF → angiogenesis
MMPs, PDGR, TGFb → extracellular matrix remodelling/ fibrosis
✅
Suppression of apoptosis- Individual malignant cells can suppress
apoptosis, which is important for the proliferation of cancer cells from
initiation → progression → treatment resistance
✅
Suppression of apoptosis at the premalignant stage- Extend lifetime of
cells so allow accumulation of potential “driver” mutation
Alters normal tissue homeostasis resulting in over production of cells
(hyperplasia)
✅
… rates are high in tumours because the cell environment is…
- Apoptosis is high due to inhospitable and cell signalling is
dysregulated. Apoptotic cells stimulate wound healing and responses
that promote tumour groth and regrowth after therapy
High cancer cell mitosis rates are balanced by…- ✅Programmed cell
death
although lytic necrotic cell death can also occurs, large sale normally
“tidy“ apoptosis can trigger inflammation and wound healing
Apoptosis can occur at any point in the tumour development to promote
the initial tumor growth or regrowth after cytotoxic therapy
✅
Apoptosis promotes wound healing- Effector caspase-3 cleaves
phosphoplipase A (iPLA) from cell membrane lipids, which produces
aranchodionic acid which is metabolised by COX2 into PGE2 which
promote the increase in vasodilation for cancer cell proliferation
Apoptotic bodies are coated with phosphatidylserine (PS) which isan eat
me signal for macrophage to come and ingest which then release
VEGF → angiogenesis
MMPs, PDGR, TGFb → extracellular matrix remodelling/ fibrosis
✅
Suppression of apoptosis- Individual malignant cells can suppress
apoptosis, which is important for the proliferation of cancer cells from
initiation → progression → treatment resistance
✅
Suppression of apoptosis at the premalignant stage- Extend lifetime of
cells so allow accumulation of potential “driver” mutation
Alters normal tissue homeostasis resulting in over production of cells
(hyperplasia)
