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Hello, my name is Dr. Dieter Wolf.
I'm a professor in the Tumor Initiation and Maintenance
Program at Sanford Burnham Prebys Medical Discovery Institute in La Jolla, California.
I also hold an appointment in the school of
Pharmaceutical Sciences of Xiamen University in China.
This lecture is going to be about
"Mitochondrial Inhibition as a Novel Therapeutic Approach in Drug-Resistant Cancer".
Drug resistance is one of the major problems in cancer therapy.
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While scientists and physicians avail of plenty
of drugs that kill cancer cells often in a selective manner,
typically tumors develop resistance to these drugs relatively quickly.
In our studies, we have addressed prostate cancer as a paradigm of drug resistance.
Prostate cancer is the most common male malignancy
and the second most common cause of death from cancer in men.
There are approximately 250,000 new cases diagnosed each year.
And there are over two million patients living in the US with numbers increasing steadily.
Due to the large number of patients,
the prostate cancer drug market is huge and has
doubled from 8 to 16 billion US dollars in the past five years.
The main problem with prostate cancer comes when the standard of care drugs stop working.
This is when the disease progresses to drug resistance,
or so called castration resistant prostate cancer or CRPC.
So as the naming is saying,
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castration resistant prostate cancer is
resistant to a form of therapy that is known as castration.
Castration aims at the withdrawal of male sex hormone or androgen.
And it can be achieved in a number of ways including
surgical orchiectomy or chemical castration using a series of drugs.
Now let me explain why castration also known
as androgen deprivation is a therapy for prostate cancer.
It has been well-established for decades,
that the androgen receptor or AR which is bound and activated by
androgens is the main oncogenic driver in hormone-sensitive prostate cancer.
AR activation leads to growth and survival signals that spur cancer growth.
Conversely, androgen locate through ADT,
or androgen deprivation therapy has
profound therapeutic benefit by stopping
the growth and promoting the death of prostate cancer cells.
Two main approaches are used in ADT of hormone-sensitive prostate cancer,
removing androgen from the circulation and secondly,
AR blockers or anti-androgens.
The situation is somewhat different in castration resistant prostate cancer,
