[Music]
one out of eight women will be diagnosed
with breast cancer during her lifetime
the same is true for men one out of
1,000 men also will be diagnosed with
breast cancer during his lifetime per
year will lose 40,000 women to breast
cancer I am a breast cancer researcher
but I also worked very closely with
survivors who dedicate their time to
advocate for breast cancer research
what I have learned from those
incredible people is there a gap seems
to exist between the science behind
therapy and research and the patient why
is that from my perspective as a
researcher I know that we do not do
enough to reach out to you to tell you
about what we do so today I want to take
the opportunity to tell you a little bit
about breast cancer research
and the therapy we have come a long way
in breast cancer and the mortality rates
are steadily decreasing every year this
is largely due to better screening early
diagnosis but also to the targeted
therapies available in the area of
personalized medicine we have come to
realize however that not each cancer is
the same what do i mean by that
so we call this tumor heterogeneity a
tumor is made out of very different cell
types but not only that it also has each
cell has also different genetic makeups
now if you put this in a patient you can
be reassured that the metastases are
also different from the primary tumor to
the brain to the lung to the bone or to
the liver that is not all the cancer
also varies from patient to patient so
you can imagine that seems to be a big
problem and can be overwhelming however
we view this also as an opportunity and
let me tell you why
that is so we want now we can now
address tumor heterogeneity by doing
analysis like this we collect many many
patient issues we analyze them for the
level of gene expression and then
putting them in a mathematical analysis
we try to group the patients together
based on the gene expression level then
we are trying to take this group of
patients and see what do they share what
do they have in common a phenotype like
track response or survival but then the
hard part starts where we have to figure
out okay we know that group of patients
share shorter survival what is the gene
that is driving that and what are the
genes which are only bystanders that is
the hard part the goal however is and we
will get there is that we will have a
drug for each metastasis for each
primary tumor to eradicate cancer
completely now let me talk a little bit
about what we currently do with breast
cancer patients how do we treat them so
in breast cancer we treat patients based
on their subtype the majority of
patients progesterone positive breast
cancer another subtype of breast cancer
or breast cancers and they make roughly
20% of all the breast cancers are her2
positive the rest of the breast cancer
subtypes are triple negative they don’t
have estrogen receptor progesterone
receptor or the her2 receptor for Estrin
receptor positive cancers we know how to
treat them because we have learned that
the hormone estrogen binds to its
receptor which then sends a signal to
the cell to the DNA telling the cancer
cell to divide non-stop we can block
this with drugs like tamoxifen or
aromatase inhibitors for her2 positive
cancers we know that there’s a receptor
I thought of the cell which you see here
with the blue dark spots and when those
receptors are overexpressed when we have
too many of them signals are sent to the
cancer cell DNA to divide unstoppable
however we can
Octus with trucks likes like trust to
the map which shuts off that signaling
and kills the cancer cell with triple
negative breast cancer we don’t do so
well there are no receptors to be
targeted so the standard therapy for
those patients is still chemotherapy
radiation or surgery
however we have learned through
personalized medicine approaches in the
past years that those triple negative
breast cancer cell cells seem to share a
feature which is called genomic
instability so what does that mean the
DNA in those cancers is usually broken
which leads to fusion of chromosomes
there are a lot of mutations in no cells
which makes the tumor highly aggressive
why does this matter we know that once a
DNA is broken there is an army of
proteins which repair that DNA to
prevent the castell benign or cancer
cell from dying we will exploit however
this principle for triple negative
breast cancer cells in the following way
imagine those cancer cells sitting on a
stool and each leg represents a DNA
repair pathway we have four major DNA
repair pathways we cut off one leg the
cancer is still alive however once we
cut off the second leg of that stool the
stool tips over and crushes the cancer
cell now this is being used right now
nationwide internationally also in
Pittsburgh also in my lab to actually
exploit as a new therapy for triple
negative breast cancer by chemically
inducing the inhibition of DNA repair
pathways so the idea here is that we
have two drugs taking out two of those
tools so the stool will tip over and the
cancer cells will die how does this look
like I want to give you a little glimpse
from my lap here you see the blue dots
are nuclei of triple negative breast
cancer cells when we treat them with
ionizing radiation we are inducing DNA
damage and then this army of proteins
proteins rushes to the DNA damage and
tries to repair it with a new compound
we are working on this is not happy
there’s no DNA repair what then happens
in the cell in a cell which has not been
treated with the compound
the DNA is repaired and all the damage
goes away there is no red staining of
the nucleus however when we treat our
cancer cells with the compound the DNA
is not prepared the cancer cells die I
want to end my presentation by coming
back to the patients and I urge
everybody of you who is a patient who
knows a patient to educate educate
yourself know what your disease is know
what your options are know what your
treatments are seek out peer support
peer support is a powerful thing you
meet people human beings who have gone
through the cancer who will be able to
tell you how it feels like to worry
about dying not seeing your children
growing up this is not something a
physician can give to you or a science
this can give to you this is only
something you can learn from a peer
challenge challenge us challenge a
scientist challenge your doctors if we
are not able to explain to you what your
disease on the options are we are doing
a pretty bad job and then you have to
let us know consider a clinical trial
clinical trials are the essence of drug
progress right now they are truly the
accrual is very poor and that probably
has to do with the fact that many many
years ago clinical trials have been run
almost unethically where placebos have
been given and no other treatment versus
the the drug of choice but this is
different now everybody gets standard
treatment plus an experimental drug so
clinical trials are a good option
overall it is about to empower yourself
without empowering yourself you will not
be a good advocate for yourself and you
need to be with this disease thank you
[Applause] [Music]
one out of eight women will be diagnosed
with breast cancer during her lifetime
the same is true for men one out of
1,000 men also will be diagnosed with
breast cancer during his lifetime per
year will lose 40,000 women to breast
cancer I am a breast cancer researcher
but I also worked very closely with
survivors who dedicate their time to
advocate for breast cancer research
what I have learned from those
incredible people is there a gap seems
to exist between the science behind
therapy and research and the patient why
is that from my perspective as a
researcher I know that we do not do
enough to reach out to you to tell you
about what we do so today I want to take
the opportunity to tell you a little bit
about breast cancer research
and the therapy we have come a long way
in breast cancer and the mortality rates
are steadily decreasing every year this
is largely due to better screening early
diagnosis but also to the targeted
therapies available in the area of
personalized medicine we have come to
realize however that not each cancer is
the same what do i mean by that
so we call this tumor heterogeneity a
tumor is made out of very different cell
types but not only that it also has each
cell has also different genetic makeups
now if you put this in a patient you can
be reassured that the metastases are
also different from the primary tumor to
the brain to the lung to the bone or to
the liver that is not all the cancer
also varies from patient to patient so
you can imagine that seems to be a big
problem and can be overwhelming however
we view this also as an opportunity and
let me tell you why
that is so we want now we can now
address tumor heterogeneity by doing
analysis like this we collect many many
patient issues we analyze them for the
level of gene expression and then
putting them in a mathematical analysis
we try to group the patients together
based on the gene expression level then
we are trying to take this group of
patients and see what do they share what
do they have in common a phenotype like
track response or survival but then the
hard part starts where we have to figure
out okay we know that group of patients
share shorter survival what is the gene
that is driving that and what are the
genes which are only bystanders that is
the hard part the goal however is and we
will get there is that we will have a
drug for each metastasis for each
primary tumor to eradicate cancer
completely now let me talk a little bit
about what we currently do with breast
cancer patients how do we treat them so
in breast cancer we treat patients based
on their subtype the majority of
patients progesterone positive breast
cancer another subtype of breast cancer
or breast cancers and they make roughly
20% of all the breast cancers are her2
positive the rest of the breast cancer
subtypes are triple negative they don’t
have estrogen receptor progesterone
receptor or the her2 receptor for Estrin
receptor positive cancers we know how to
treat them because we have learned that
the hormone estrogen binds to its
receptor which then sends a signal to
the cell to the DNA telling the cancer
cell to divide non-stop we can block
this with drugs like tamoxifen or
aromatase inhibitors for her2 positive
cancers we know that there’s a receptor
I thought of the cell which you see here
with the blue dark spots and when those
receptors are overexpressed when we have
too many of them signals are sent to the
cancer cell DNA to divide unstoppable
however we can
Octus with trucks likes like trust to
the map which shuts off that signaling
and kills the cancer cell with triple
negative breast cancer we don’t do so
well there are no receptors to be
targeted so the standard therapy for
those patients is still chemotherapy
radiation or surgery
however we have learned through
personalized medicine approaches in the
past years that those triple negative
breast cancer cell cells seem to share a
feature which is called genomic
instability so what does that mean the
DNA in those cancers is usually broken
which leads to fusion of chromosomes
there are a lot of mutations in no cells
which makes the tumor highly aggressive
why does this matter we know that once a
DNA is broken there is an army of
proteins which repair that DNA to
prevent the castell benign or cancer
cell from dying we will exploit however
this principle for triple negative
breast cancer cells in the following way
imagine those cancer cells sitting on a
stool and each leg represents a DNA
repair pathway we have four major DNA
repair pathways we cut off one leg the
cancer is still alive however once we
cut off the second leg of that stool the
stool tips over and crushes the cancer
cell now this is being used right now
nationwide internationally also in
Pittsburgh also in my lab to actually
exploit as a new therapy for triple
negative breast cancer by chemically
inducing the inhibition of DNA repair
pathways so the idea here is that we
have two drugs taking out two of those
tools so the stool will tip over and the
cancer cells will die how does this look
like I want to give you a little glimpse
from my lap here you see the blue dots
are nuclei of triple negative breast
cancer cells when we treat them with
ionizing radiation we are inducing DNA
damage and then this army of proteins
proteins rushes to the DNA damage and
tries to repair it with a new compound
we are working on this is not happy
there’s no DNA repair what then happens
in the cell in a cell which has not been
treated with the compound
the DNA is repaired and all the damage
goes away there is no red staining of
the nucleus however when we treat our
cancer cells with the compound the DNA
is not prepared the cancer cells die I
want to end my presentation by coming
back to the patients and I urge
everybody of you who is a patient who
knows a patient to educate educate
yourself know what your disease is know
what your options are know what your
treatments are seek out peer support
peer support is a powerful thing you
meet people human beings who have gone
through the cancer who will be able to
tell you how it feels like to worry
about dying not seeing your children
growing up this is not something a
physician can give to you or a science
this can give to you this is only
something you can learn from a peer
challenge challenge us challenge a
scientist challenge your doctors if we
are not able to explain to you what your
disease on the options are we are doing
a pretty bad job and then you have to
let us know consider a clinical trial
clinical trials are the essence of drug
progress right now they are truly the
accrual is very poor and that probably
has to do with the fact that many many
years ago clinical trials have been run
almost unethically where placebos have
been given and no other treatment versus
the the drug of choice but this is
different now everybody gets standard
treatment plus an experimental drug so
clinical trials are a good option
overall it is about to empower yourself
without empowering yourself you will not
be a good advocate for yourself and you
need to be with this disease thank you
[Applause] [Music]
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