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Wednesday, 27/10/2021
Week 5
Lecture
Prof. Mike Lynn
Systemic Anticancer Therapy
Part Two
By the late 1980s it became apparent that cytotoxic therapy had reached the glass
ceiling
Not going to produce the gains required
Progress came from studying the cancer cells in depth
Possible points of intervention
Complexities around this
All cells have receptors which have an extra/trans/intra cellular domains
Phosphorylation
Sets off a cascade of signals
Leads to increased proliferation
BRAF inhibitors come to the fore in melanomas
In many cancers components of cell signal pathways don’t require a stimulus
EGFR
Epidermal growth factor receptor
Found in embryonic growth
Later found it was present in many cancer cells especially in the lungs
When these drugs were taken into the European population they didn’t work while
they had in Japan
Patients who did well had never smoked, were of eastern or Asian origin and were
female
Due to a mutation
In an area called the ATP binding cassette this process is short circuited, and the ATP
is bound tightly
The drugs competitively inhibit the binding of ATP
EGFR mutation status the response rate to gefitinib was very high
High rates of survival
Many patients become resistant due to a mutation on the EXON20
Now a third generation called Osimertinib
Given to those who have relapsed
Those shown to have the mutation do much better with this also
Chromosome 2 – EML4 and ALK
EML4 gene is inverted through 180 and stuck by the ALK gene – found in lung
cancers
Many ways to diagnose
o FISH
o PCR/Sequencing
o Using dyes
Does it work?
Study looked at no treatment and locally advanced non-small cell lung cancer
Very common to see brain metastases
Randomised crizotinib or chemotherapy
Medium duration of treatment was longer with crizotinib
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