Episode 31: Unleashing the future of cancer treatments - ASCO scientific highlights with past ASCO president Dr. Doug Blayney (Part 2)

Dr. Douglas Blayney, past ASCO president and oncologist, gives us his thoughts on some of the key scientific themes presented at the 2023 ASCO annual meeting. In the field of breast cancer, there are three key areas of interest Dr. Blayney discusses. First, there is growing attention towards the use of CDK 4/6 inhibitors in the treatment of hormone positive breast cancer. Second, the significance of somatic cell DNA testing is being recognized. This testing can inform treatment decisions at different stages of the disease and help identify when a change in treatment is necessary. Lastly, there is a focus on the emerging role of antibody drug conjugates, which can selectively kill cancer cells in a more targeted way. Samira and Dr. Blayney also discuss how patients learn from and use this new information in partnership with their physician.

Doug Blayney Stanford  oncologist ASCO

About our guest

Dr. Doug Blayney is an oncology physician who specializes in breast cancer. His research focuses on quality improvement in cancer care systems, new drug development, and patient experience improvement. At the American Society of Clinical Oncology (ASCO), he was founding Editor-in-Chief of its flagship practice journal, and as President, started the ASCO Quality Symposium and began planning for ASCO’s CancerLinq. He was a founding member of the National Comprehensive Cancer Network (NCCN) Growth Factor Guideline panel, and is a past member of the U.S. Food and Drug Administration’s Oncology Drugs Advisory Committee and the NCCN Board of Directors. Dr. Blayney leads the Manta Cares Scientific Advisory Board.

Watch the video of our episode on YouTube

  • 8 minutes:

    What is a CDK 4/6 inhibitor?

    In ER positive breast cancer, the estrogen receptor is stimulated by estrogen, it then goes to the nucleus and turns on the cell and says ‘grow and multiply’. Traditionally, there have been two approaches to inactivating the estrogen receptor. The first one was tamoxifen and similar drugs which bind to the estrogen receptor, lock it up, and prevent it from going to the nucleus to make the cell grow. The other mechanism for turning off estrogen stimulation of estrogen-positive cancer cells is by turning off estrogen production in the body. And that's typically the aromatase inhibitors, of which there are three….When that estrogen receptor growth pathway is shut down, the cell compensates, or many of the cancer cells compensate by this CDK 4/6 pathway. And it turns out that if you combine estrogen blockade with blockade of the CD46 pathway at various steps, you can have an augmented or more effective therapeutic approach.

  • 18 minutes:

    On the types of DNA and how they impact cancer treatment decisions.

    There are two kinds of DNA. There's germline DNA, which is present in every cell in our body. Then there is somatic mutation, which happens to various cells. Whether it's in a breast cell or a lung lining cell or a colon lining cell, an accumulation of those mutations in the right spot can lead to a cancer. So it's very important to distinguish germline DNA from somatic mutation or cancer cell mutation. Germline mutation, that's a whole other topic. Your viewers may have some knowledge of the BRCA1 which can predispose a person to cancer. Somatic mutations occur when we walk out in the sun or we take a high altitude airplane flight. We are exposed to ionizing radiation which can damage our DNA.

  • 33 minutes:

    On thinking about decision making with new scientific advances.

    Your listeners may remember that 20 or 30 years ago, there was an assay for circulating tumor cells. So in the blood where there's red blood cells, white cells and platelets, very rarely there can be circulating tumor cells, so an assay was developed to detect those circulating tumor cells. Randomized clinical trial looked at circulating tumor cells monitoring versus standard monitoring. And the circulating tumor cell DNA did not improve survival, probably because of the sensitivity of the test. Plus the treatments 20 or 30 years ago weren't as efficacious. There weren't as many of them. So if the cancer was growing, but you didn't have an effective treatment for it, so what? Looking at this now, the situation has changed. The test is probably more sensitive, and we have more treatments.

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