LT40-41
18 important questions on LT40-41
What did Mary Laskers philantrophy?
What did Sydney Farber?
What did Dr. Pinkel?
- more toxic chemicals
- radiotherapy brain and chemotherapy spinal fluid
- no success --> doubing dose
- cure rate (> 5 year survival) from 0,07% in 1962 to >50% in 1971 (later >70%)
Chance discovery of almost all drugs
Scant knowledge of how anti-leukemic drugs work in human
Sceptical that medical treatment alone could expalin the cure of ALL
- Higher grades + faster learning
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Tell something about Nixon's War on cancer
National cancer act 1971
Aim: cure more prevalent solid tumors (breast, lung, intestinal cancer)
Why was there a problem in curing solid tumors?
Solid tumors less sensitive to anti-cancer drugs than leukemia
What were discussion points in the cancer treatment development?
Realistic image: winding road of progress
Cure individual vs prevention population (endogenous vs exogenous): money politics
Ethical dilemmas, patient = research subject, doctor = researcher
What was the influence of non-medical factors in cancer treatment?
Many uncertainties -> many phiscians chose the most agressive, interventionist treatment (better safe than sorry_
Decline radical mastectomy 1970s: feminist and patient movement.
Wat is het verschil tussen complement dependent cytotxiicty and antibody dependent cytotoxicity van rituximab?
Binding anti-CD20 to B cell, Fc receptoren zorgt voor release of cytotxic molecules, called perforins.
Fc/CR-mediated opsonic phagocytosis door macrophagen
What is brentuximab vedotin?
Antibody drug conjugate (ADC)
Cojugated to monomethyl auristatin E (MMAE), potent antitubin agent protease-cleavable linker
ADC binds to CD30
ADC-CD30 complex traffics to lysosome
MMAE is released
MMAE disrupts microtubule network
G2/M cell cycle arrest
Apoptosis
What are side effects of the monoclonal antibodies, bites and CAR-T cells?
Allergic reactions at beginning of infusion (MoAbs)
Cytokine release syndrome: hypotension, fever, tachycardia, dyspnea.
Tumor lysis syndrome
- uric acid >> renal failure due to formation of uric acid crystals
- release LDH
MMAe: conjugated to anti-CD30: polyneuropathy
What cytokines are involved in monoclonal antibodies, bites, CAR-T cells, what are the side effects?
Cytokines:
- TNF-alfa
- IFN gamma
- IL6
- IL2
What side effects does MMAE give?
conjugated to anti-CD30
Polyneuropathy: damage of the sensory nerves in hands and feet
In what cancers can you use tyrosine kinase inhibitors?
CLL has constituitive activation of B cell receptor. You get down stream signaling and molecule was developed and was particular aiming ata the BTK molecule.
If you inhibit TK, you stop the constituitive signaling cascade.
Eg inhibitor of BR3 kinase, idelalisib, oral durgs., ibrutinb
You can take those drugs every day until resistance develops or until you get side effects and cannot tolerate the drugs any more.
Welke twee medicijnen zijn tyrosine kinase inhibitors?
idelalisib
What is a BRAF V600E inhibitor?
A molecule of the signalling cascade is attacked, which results in kill of the tumor cells
What is a FLT3 inhibitor?
You give an inhibitor to attack the growth factor receptor which is constituively active, and keeps on inducing signaling to the nucleus with increased proliferationd and decreased apoptosis.
After inhibition of this mutated molecule, you get decreased proliferation and increased apoptosis.
If you add midostaurin, you get an significant increase in the probability of survival.
What happens when PD-1L binds to PD-1?
What is the therapy for AML?
Non-classical chemotherapy
- gemtuzumab - ozagomycin
- FLT3 inhibitors PKC, other new drugs
- Allogeneic stem cell transplantation
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