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Kathy Miller, MD
KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified) )| Communities: Breast Cancer | Answers: 8 |
| Member Since: Aug. 2012 |
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Professional Statement
Dr Kathy Miller is Associate Professor and Sheila D. Ward Scholar at the Indiana University School of Medicine, Division of Hematology/Oncology. She is an active member of the American Society of Clinical Oncology, the Eastern Cooperative Oncology Group and the Hoosier Oncology Group.
She received her B.S. in biology Magna Cum Laude from the University of Miami, Coral Gables, Florida, and her M.D. from Johns Hopkins School of Medicine in Baltimore, Maryland. She completed her internship as well as her residency at Johns Hopkins School of Medicine followed by a Hematology/Oncology fellowship at Indiana University.
She received her B.S. in biology Magna Cum Laude from the University of Miami, Coral Gables, Florida, and her M.D. from Johns Hopkins School of Medicine in Baltimore, Maryland. She completed her internship as well as her residency at Johns Hopkins School of Medicine followed by a Hematology/Oncology fellowship at Indiana University.
Professional Info
Credential: MD
Primary specialty: Oncology - Hematology/Oncology
Medical school: Johns Hopkins School of Medicine
Residency: Johns Hopkins School of Medicine
Fellowship: Indiana University School of Medicine
Areas of expertise: Breast Cancer
Hospital affiliation: Indiana University Cancer Center
Practice address:
535 Barnhill Drive RT 473
Indianapolis, IN
46202
Practice phone number: (317) 944-0920
KathyMillerMD Activities
Angiogenesis is the growth of blood vessels. It is important for breast cancer and nearly all cancers. In order for a cancer to grow, they need a bigger blood supply to bring in more oxygen and nutrients, as well as to eliminate the tumors metabolic wastes. That bigger blood supply also provides more routes for the cancer to spread elsewhere in the body. In general the more aggressive the tumor, the greater the blood supply. In theory blocking the growth of those blood vessels should be a useful therapy. Unfortunately putting that theory into practice hasn’t been quite so simple.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
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8 months ago
Not as much as you might think. We would first determine the optimal treatment for each cancer individually, rarely do we need to make adjustments or changes. For example, it one tumor is ER- and requires chemotherapy and the other is ER+ and would only need antiestrogen therapy, we would use BOTH chemo and antiestrogen treatment.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
8 months ago
The most well studied drug is bevacizumab (Avastin), an antibody that blocks the growth of blood vessels stimulated by the vascular endothelial growth factor (VEGF for short). Adding bevacizumab to initial chemotherapy for metastatic disease resulted in more women who had their tumors improve and remain under control for a longer time but did not help women live longer. No one argues about that….the argument has been about how much longer a time of disease control is worthwhile and for what cost (both in terms of dollars and in terms of side effects). Bevacizumab was first approved based on a study that showed a fairly large benefit. When later studies found a benefit that was much shorter, the approval was withdrawn. Since those studies researchers have gotten closer (we think) to predicting which women might benefit. A large study is underway to test the agent in that group. Other anti-angiogenic agents tested thus afar haven’t been very successful. Those drugs inhibited many growth factors at the same time. With what I said earlier about the large number of growth factors at the tumors disposal, you would think that is a good thing right? Unfortunately it also increases the side effects and made it hard to combine those drugs with chemotherapy. Other antiangiogenic drugs that inhibit different growth factors seem very promising and are currently in clinical trials currently.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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8 months ago
It is a LONG list. We have identified over 40 genes that directly or indirectly stimulate the growth of blood vessels in breast cancer with another long list of genes that inhibit blood vessel growth. Most breast cancers have many of those genes activated by the time of diagnosis. This shouldn’t be surprising. Anything that is so crucial to the body (or cancer) is tightly regulated and very redundant. If we block the growth of blood vessels stimulated by one of those genes, the tumor has lots of other options.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
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8 months ago
Fairly limited. We have some imaging methods, namely some specialized PET scans (not the usual PET scan that uses sugar as the tracer) and MRI techniques that can measure the tumors blood supply BUT those imaging techniques haven’t been helpful in identifying which patients might benefit from treatments designed to block the growth of blood vessels.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
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8 months ago
I always (OK, almost always) biopsy the first site of disease to confirm that what we think is metastatic breast cancer really is metastatic breast cancer. That also allows us to repeat the tests for hormone receptors (ER and PR) as well as HER2. In some cases the initial ER and HER2 tests might have been wrong. In other cases the tumor might have changed or shifted over time. In my opinion those repeat tests should ADD to our list of treatment options, they shouldn’t eliminate options, So, if the tumor was initial ER+ but the biopsy of the metastatic site is ER-, a trial of hormone therapy would still be worthwhile. Similarly if the initial tumor was HER2- but the recurrence is HER2+, a trial of HER2 targeted therapy would be worthwhile.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
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8 months ago
At this point it doesn’t. However, when a treatment is clearly effective for patients with advanced disease that always leads to a simple question…”Perhaps if we used that treatment as a part of initial therapy it would prevent recurrence in the first place” It is important to remember that while this sounds logical, not all treatments that have a role in the advanced setting have been beneficial for patients with early stage disease. An international trial APHINITY is currently underway to test the role of pertuzumab in patients with early stage disease.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
1
Answer |
8 months ago
Pertuzumab is an antibody that recognizes the HER2 growth factor similar to trastuzumab (Herceptin). Here is the difference – it recognizes a different area of the HER2 growth factor allowing pertuzumab to stop HER2 from binding to other growth factors. Pertuzumab was approved based on the data from the CLEOPATRA trial. In that study women receiving their first chemotherapy for HER2 positive metastatic breast cancer were randomly assigned to docetaxel (Taxotere) + trastuzumab + pertuzumab or docetaxel (Taxotere) + trastuzumab +a placebo. Women treated with pertuzumab were more likely to have their cancer improve and remain under control for a longer time. Though we have not yet seen the detailed data, recent reports suggest women who received pertuzumab also lived longer. Pertuzumab should now be considered an important part of the treatment for most women with HER2 + metastatic breast cancer receiving chemo for the first time. So who shouldn’t receive pertuzumab – given the potential for heart damage women with poor heart function or a history of heart failure were excluded. Other studies will look at the role of pertuzumab in patients with more advanced disease and with other chemotherapy agents.
New answer by KathyMillerMD (Physician - Oncology - Hematology/Oncology (Verified))
1
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8 months ago
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