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Hello, I am Ramaswamy Govindan,
a medical oncologist at
the Washington University School
of Medicine in St. Louis.
I'm an expert in lung cancer and
cancer genomics.
Today we are going to talk about
the genomics of lung cancer.
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I have no conflicts relevant
to this presentation.
I'm a consultant for BMS, BI,
Pfizer, Mallinckrodt Medical,
Genentech, Novartis, and GlaxoSmithKline.
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I want to acknowledge the investigators
from the Cancer Genome Atlas project.
I specifically want to thank Dr.
Matthew Meyerson and Dr.
Steve Baylin, my two co-chairs,
for their support.
I also want to thank my colleagues at the
Washington University School of Medicine,
specifically those at the Genome
Institute, Dr. Richard Wilson, Dr.
Elaine Mardis, and Dr.
Li Ding, for their collaboration.
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I want to begin with a story.
This is a patient of mine with
advanced non-small cell lung cancer,
who came to see me after receiving
multiple lines of chemotherapy.
When we saw her,
she had advanced disease and
she had a lot of symptoms related to her
cancer, she was unable to work full-time.
We biopsied her tumor, as you can
see here she has a fairly large and
impressive tumor on the right side.
The biopsy showed a 12 base-pair
insertion in exon 20 of the ERBB2 gene.
This is a known oncogenic alteration
seen in a small number of patients
with non-small cell lung cancer.
When we treated her as a part of
the phase 1 study with neratinib and
temsirolimus, she had an impressive
response, as you can see here,
from before to after treatment, she had
a very nice decrease in the tumor size and
had significant benefit clinically
as well as radiographically.
She in fact went back to work full-time,
and worked for nearly a year before
the cancer progressed, she's now
currently on salvage chemotherapy but
she had a very good one year with
the combination of neratinib and
temsirolimus, because of
the recognition that her tumor had this
activating mutation in the ERBB2 gene.