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Journal conference
Vincent T. DeVita, Jr., M.D., and Steven A. Rosenberg, M.D., Ph.D.
N Engl J Med 2012;366:2207-14.
R2 Seon-Hye Kim, Prof. Sun-kyung Beak
Advanced lung adenocarcinoma + EGFR mutation (+)
- the first-line erlotinib or gefitinib
- high objective response rate & long progression-free survival
and overall survival

All patients’ treatment eventually fails.
- resistance to EGFR tyrosine-kinase inhibitors (TKIs)
- characterised by the so-called gatekeeper mutation, T790M

Advanced lung adenocarcinoma + EGFR mutation (+)
- the first-line erlotinib or gefitinib
- high objective response rate & long progression-free survival
and overall survival

All patients’ treatment eventually fails.
- resistance to EGFR tyrosine-kinase inhibitors (TKIs)
- characterised by the so-called gatekeeper mutation, T790M

Advanced lung adenocarcinoma + EGFR mutation (+)
- the first-line erlotinib or gefitinib
- high objective response rate & long progression-free survival
and overall survival

All patients’ treatment eventually fails.
- resistance to EGFR tyrosine-kinase inhibitors (TKIs)
- characterised by the so-called gatekeeper mutation, T790M

Advanced lung adenocarcinoma + EGFR mutation (+)
- the first-line erlotinib or gefitinib
- high objective response rate & long progression-free survival
and overall survival

All patients’ treatment eventually fails.
- resistance to EGFR tyrosine-kinase inhibitors (TKIs)
- characterised by the so-called gatekeeper mutation, T790M



Irreversible ErbB-family blocker : Afatinib
: M/C mutations, L858R and deletion-19 & the exon 20
gatekeeper T790M mutation.
EVALUATION
: to assess its efficacy in patients with advanced lung adenoca.
with previous treatment failure on EGFR tyrosine kinase
inhibitors.


Irreversible ErbB-family blocker : Afatinib
: M/C mutations, L858R and deletion-19 & the exon 20
gatekeeper T790M mutation.
EVALUATION
: to assess its efficacy in patients with advanced lung adenoca.
with previous treatment failure on EGFR tyrosine kinase
inhibitors.
5-yr relative survival rate for all cancers
Late 1960s
Now
2015
38%
68%
80%
Overall rates of death from cancer


Late 1960s
Now
2015
100%
76%
62%
Most of the current declines are the result of the widespread
implementation of old technology for diagnosis, prevention, and
treatment.
However, the clinical application of the fruits of the extra-ordinary
molecular revolution is yet to come and cannot be measured with
the use of current statistics.




The sequencing of the human genome in 2000 has had a profound
effect on all of medicine.
The cost of sequencing will be much cheaper, putting in the realm of
a routine laboratory test.
Detected abnormalities will become targets of relatively simple drug
therapies, and if the effects mirror what we have seen in recent
years with targeted therapy, the ability to prevent or treat cancers
in the future will be impressive.
The economic and social consequences of converting cancer into a
curable or chronic disease will be both gratifying and daunting.