The Promise of Research
The Promise of Research

BCRF has awarded the third annual David Yurman Award for Breast Cancer Research in the amount of $500,000 to Dr. Hayley McDaid, a New York-based scientist whose current research focuses on identifying new therapeutic options for triple-negative and BRCA-driven breast cancers, and Dr. Sarat Chandarlapaty, a New York-based medical oncologist and researcher studying how and why breast cancers become resistant to treatment.

These incredible researchers were kind enough to sit with us and share their specific areas of research, and explain why the funding from David Yurman and BCRF is instrumental in supporting their work.

BCRF has awarded the third annual David Yurman Award for Breast Cancer Research in the amount of $500,000 to Dr. Hayley McDaid, a New York-based scientist whose current research focuses on identifying new therapeutic options for triple-negative and BRCA-driven breast cancers, and Dr. Sarat Chandarlapaty, a New York-based medical oncologist and researcher studying how and why breast cancers become resistant to treatment.

These incredible researchers were kind enough to sit with us and share their specific areas of research, and explain why the funding from David Yurman and BCRF is instrumental in supporting their work.

Why did you decide to focus on breast cancer research?

Why did you decide to focus on breast
cancer research?

DR. McDAID: My laboratory studies cancer drugs known as tubulin inhibitors, of which paclitaxel and
docetaxel are best known. They are primarily used in the treatment of HER2+ and triple negative breast
cancers. Women with metastatic breast cancer respond well to paclitaxel, but some develop resistance
over time—I hope to help develop more efficacious, safe tubulin inhibitors for those patients.

DR. CHANDARLAPATY: I was working in the laboratory on a protein called HER2 that supports the
growth of many different types of cancer and is especially common in breast cancer. Then I saw patients
with breast cancer receiving anti-HER2 therapies that worked initially, but stopped working after a few
years. This became a major focus of our research: how and why do breast cancers develop resistance to
therapies that are designed to target their unique features?

DR. McDAID: My laboratory studies cancer drugs known as tubulin inhibitors, of which paclitaxel and docetaxel are best known. They are primarily used in the treatment of HER2+ and triple negative breast cancers. Women with metastatic breast cancer respond well to paclitaxel, but some develop resistance over time—I hope to help develop more efficacious, safe tubulin inhibitors for those patients.

DR. CHANDARLAPATY: I was working in the laboratory on a protein called HER2 that supports the growth of many different types of cancer and is especially common in breast cancer. Then I saw patients with breast cancer receiving anti-HER2 therapies that worked initially, but stopped working after a few years. This became a major focus of our research: how and why do breast cancers develop resistance to therapies that are designed to target their unique features?

What area of breast cancer research do you
focus on specifically?

Dr. McDAID: Triple negative breast cancer (TNBC)
remains one of the most recalcitrant forms of breast
cancer, particularly for patients who have inherited
mutations in the BRCA1/2 genes. While tubulin
inhibitors are still effective for these patients,
response rates are lower, and patients can relapse and
develop metastatic disease that is resistant to drugs.
Even after therapy, some breast cancer cells aren’t
killed, but become dormant, and resume growth at a
later stage. My lab is developing novel tubulin
inhibitors that induce cancer cell death even in
TNBCs that no longer respond to drugs like
paclitaxel. Another new benefit of these drugs is

inducing a very stable form of dormancy that limits the ability of surviving tumor cells to grow back, or
to metastasize. We are hopeful that this approach can help women with recalcitrant disease who need
additional treatment choices.

DR. CHANDARLAPATY: We focus on two major types of breast cancer: those that have the receptor
for the estrogen hormone, and those that have the HER2 receptor. Our lab is interested in
understanding how these cancers evolve and develop resistance to anti-estrogens and anti-HER2
therapies, and then devising ways to combat these patterns of resistance. For instance, we found that
breast cancers that are exposed to antiestrogen therapy develop mutations that cause the estrogen
receptor to remain active, even without any estrogen. So we developed and studied drugs that can
target those mutant estrogen receptors. At the same time, we’re studying the evolutionary process that
allowed the breast tumors to develop those mutations, so that we can develop treatments that will
prevent the mutations from occurring in the first place.

What area of breast cancer research do
you focus on specifically?

Dr. McDAID: Triple negative breast cancer (TNBC) remains one of the most recalcitrant forms of breast cancer, particularly for patients who have inherited mutations in the BRCA1/2 genes. While tubulin inhibitors are still effective for these patients, response rates are lower, and patients can relapse and develop metastatic disease that is resistant to drugs. Even after therapy, some breast cancer cells aren’t killed, but become dormant, and resume growth at a later stage. My lab is developing novel tubulin inhibitors that induce cancer cell death even in TNBCs that no longer respond to drugs like paclitaxel. Another new benefit of these drugs is inducing a very stable form of dormancy that limits the ability of surviving tumor cells to grow back, or to metastasize. We are hopeful that this approach can help women with recalcitrant disease who need additional treatment choices.

DR. CHANDARLAPATY: We focus on two major types of breast cancer: those that have the receptor for the estrogen hormone, and those that have the HER2 receptor. Our lab is interested in understanding how these cancers evolve and develop resistance to anti-estrogens and anti-HER2 therapies, and then devising ways to combat these patterns of resistance. For instance, we found that breast cancers that are exposed to antiestrogen therapy develop mutations that cause the estrogen receptor to remain active, even without any estrogen. So we developed and studied drugs that can target those mutant estrogen receptors. At the same time, we’re studying the evolutionary process that allowed the breast tumors to develop those mutations, so that we can develop treatments that will prevent the mutations from occurring in the first place.

“Over the last forty years, we’ve witnessed the
transformative power of breast cancer research.”
“Over the last forty years, we’ve
witnessed the transformative power
of breast cancer research.”
— Dr. Chandarlapaty
— Dr. Chandarlapaty
Why is BCRF’s support of breast cancer research so important right now?
Why is BCRF’s support of breast cancer
research so important right now?
DR. McDAID: Breast cancer survivorship is increasing, thanks to the unwavering commitment of
organizations like BCRF. But a proportion of survivors with more aggressive or recurrent disease will
require future therapy, and the available therapies may not work for them. We still need to develop
therapies that can kill cancer cells and spare normal cells. There are several approaches: creating cancer
drugs that target tumor cells, devising alternate dosing schedules to limit the cumulative toxicity of the
drugs, or developing drugs that are less toxic. BCRF remains steadfast in its support of these important
research endeavors.

DR. McDAID: Breast cancer survivorship is increasing, thanks to the unwavering commitment of organizations like BCRF. But a proportion of survivors with more aggressive or recurrent disease will require future therapy, and the available therapies may not work for them. We still need to develop therapies that can kill cancer cells and spare normal cells. There are several approaches: creating cancer drugs that target tumor cells, devising alternate dosing schedules to limit the cumulative toxicity of the drugs, or developing drugs that are less toxic. BCRF remains steadfast in its support of these important research endeavors.

DR. CHANDARLAPATY: Over the last forty years, we’ve witnessed the transformative power of breast cancer research—much of it conducted by BCRF-funded researchers. In the 1980s, it was discovered that the HER2 protein was over-expressed in breast cancers. By the 1990s, a new therapy had been developed to target that protein, and by the early 2000s that therapy was saving lives. The treatments continued to improve over the next two decades, and now we have an explosion of anti-HER2 therapies that can improve outcomes for many patients. However, there are many cancers that don’t have HER2 proteins, or that develop resistance to our best therapies, and we still need to find ways to help these patients. This requires time and innovation, and BCRF really fosters innovation in its research program.

DR. CHANDARLAPATY: Over the last forty years, we’ve witnessed the transformative power of breast cancer research—much of it conducted by BCRF-funded researchers. In the 1980s, it was discovered that the HER2 protein was over-expressed in breast cancers. By the 1990s, a new therapy had been developed to target that protein, and by the early 2000s that therapy was saving lives. The treatments continued to improve over the next two decades, and now we have an explosion of anti-HER2 therapies that can improve outcomes for many patients. However, there are many cancers that don’t have HER2 proteins, or that develop resistance to our best therapies, and we still need to find ways to help these patients. This requires time and innovation, and BCRF really fosters innovation in its research program.

How does the $250K research grant for each of you—funded by David Yurman—support your research?

DR. McDAID: We have developed molecules that can effectively treat paclitaxel-resistant cell and tumor models. Although this development is promising, we still need to expand testing to models that reflect the genetic diversity of TNBC tumors, and to evaluate the long-term response and toxicity. Furthermore, we want to understand the long-term dormancy effect of these novel drugs, so we will also use the funds to identify biomarkers that can help us see which types of TNBC are more likely to respond to these therapies.

DR. CHANDARLAPATY: These funds are instrumental in allowing us to conduct innovative research. First, good funding allows us to hire the brightest talent. Second, these funds enable us to explore new ideas—we can develop entirely new research approaches, rather than being restricted to making minor modifications to established paradigms. Third, it complements our federal funding, which is vital, because our federal funding has not been significantly increased in over 20 years.

How does the $250K research grant for
each of you—funded by David Yurman—support your research?

DR. McDAID: We have developed molecules that can effectively treat paclitaxel-resistant cell and tumor models. Although this development is promising, we still need to expand testing to models that reflect the genetic diversity of TNBC tumors, and to evaluate the long-term response and toxicity. Furthermore, we want to understand the long-term dormancy effect of these novel drugs, so we will also use the funds to identify biomarkers that can help us see which types of TNBC are more likely to respond to these therapies.

DR. CHANDARLAPATY: These funds are instrumental in allowing us to conduct innovative research. First, good funding allows us to hire the brightest talent. Second, these funds enable us to explore new ideas—we can develop entirely new research approaches, rather than being restricted to making minor modifications to established paradigms. Third, it complements our federal funding, which is vital, because our federal funding has not been significantly increased in over 20 years.

An image of a David Yurman pink ribbon pin.

*From now through July 31, 2024, while supplies last, David Yurman will donate 20% of the purchase price from designated designs, along with $16 of the $20 purchase price from the pink rubber cable bracelet to BCRF. Applicable to full-price sales in DY retail stores (excluding outlets and DY Saks concession) and online, within the US and Canada.

*From now through July 31, 2024, while supplies last, David Yurman will donate 20% of the purchase price from designated designs, along with $16 of the $20 purchase price from the pink rubber cable bracelet to BCRF. Applicable to full-price sales in DY retail stores (excluding outlets and DY Saks concession) and online, within the US and Canada.