Therapeutic Options in Cancer Flashcards
Prevention
environmental /behavioral change Diet Screening Genetics medication/vaccination
Treatment
Surgery
Radiotherapy
Systemic therapy
Immunotherapy
what drug is given to women who are at risk of developing primary breast cancer?
tamoxifen - has dangerous side effects
in what cancer is applying 3 times the dose for radiotherapy a good thing
head and neck cancer
5 R’s of radiotherapy
radiosensitivity repair repopulation reoxygenation reassortment
what specific breast cancer does tamoxifen target?
ER positive breast cancer
interleukin 2 (IL-2)
acts as cell signalling btw WBCs and help the immune system grow more quickly and fight off cancer
how does interferon alpha treat cancer?
innate immunotherapy - helps boost the ability of certain immune cells to attack cancer cells
where is PD1 and PDL 1
PD1 is on T cells
PDL1 is on tumor cells and other normal body cells
what are the 3 immunomodulating drugs
thalidomide
lenalidomide
pomalidomide
examples of specific immunotherapy
monoclonal antibodies
CAR T cell therapy
checkpoint blockage
what does rituximab target
binds to CD20 receptors of B cells to treat NHL B cell lymphomas
what does transtuzumab target
treats HER2 positive breast and gastric cancer
intravasation vs extravasation
intra - cancer cells entering blood flow
extra - cancer cells leaving the blood flow to be arrested in another tissue else where
3 enzymes related to tumor invasion to the EC matrix
- MMP (like gelatinases)
- plasmin
- cathepsin
3 enzymes related to cell adhesion of tumor
- cadherins
- intergrins
- CD44
what does bevacizumab do? (anti-VEGF MAb Avastin)
monoclonal antibody, prevents the interaction of VEGF with its receptors (VEGF receptor-1 and 2) on the surface of vascular endothelial cells. This prevents activation of downstream signalling pathways which will lead to angiogenesis and stops cancer growth
what does nivolumab do?
inhibits PD1
tumor suppressor genes summary
during G1, the cell would slowly accumulate cyclin, which will bind to CDKs and form complexes. when the concentration of these complexes reach a threshold, G1 phase will end and DNA replication of S phase begins.
G1/S checkpoint is basically tumor suppressor proteins like Rb. when unphosphorylated, it will bind to E2F transcription factor and stop the cell cycle from moving forward.
the cyclin/CDK complex will phosphorylate Rb and release E2F.
p16 reinforces Rb action by binding to CDK complex and inhibiting its kinase phosphorylating action. This halts cell cycle in G1 phase.
p53 works at the G1 checkpoint.
it also induces transcription of p21 that binds to cyclins to prevent formation of CDK complexes that will prompt the cell cycle.
how does transcription factor work?
it will move along the DNA until it encounters a wrong sequence which it will bind tightly to. this binding will induce expression of tumor suppressor genes that will halt the cell cycle until the damage is fixed.
in cancer cells, this mistake is not recognized by the transcription factor
