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Breast Cancer Case Studies

Kimberly Blackwell, MD: Clinical Trial Data Supporting These Choices

Kimberly Blackwell, MD
Published Online:Mar 31, 2016
Angela is a 56-year-old woman, who in 2013 was diagnosed with a 4 cm IDC of the left breast, ER positive at 50%, PR negative, and HER2 negative.

ER+/HER2-Breast Cancer with Adam Brufsky, MD, PhD and Kimberly Blackwell, MD: Case 1

Are there any clinical trial data that would inform this choice?

For this patient population, which is really they've had adjuvant endocrine therapy, they've progressed within roughly a year on first-line endocrine therapy, we really don't have a study that helps us with big decision making like is chemotherapy better than anti-estrogen strategies. In my own practice I try to milk out as much as I can out of the anti-estrogen strategies before going back to chemotherapy in incurable metastatic breast cancer. That's more based on minimizing the toxicities and hopefully prolonging the benefits of what I do for patients facing stage IV breast cancer.

We have very little data bout whethr we should switch to anti-estrogen therapy or stay on anti-estrogen therapy, or should we switch to chemotherapy, but my bias, and you would have to see a really quick response, would be to continue using anti-estogren strategies. Likewise, for this particular patient who's had a type 2 armoatase inhibitor and fulvestrant, we don't have a study that says what is best. Is it best to go back to a type 2 AI with a targeted agent, which many people would at least consider in the use of CDK inhibitors, or is it best to switch to a different anti-estrogen therapy, which exemestane is different than anastrozole, which the patient had received previously, and everolimus. We don't have any clinical trial data, nor do we have any molecular markers that say "okay, you have a PI3K kinase inhibitor and you should go on this, and if you have a CDK amplification you should go on this."

With that said, my bias is not to go back to the same anti-estrogen to jazz it up a little bit and use a different non-cross resistant agent. So we do know that exemestane works in patients who have had type 2 armoatase inhibitors, in this case anastrozole. I would also think about tamoxifen. I think people forget a lot about tamoxifen, and we do have very good data of tamoxifen being synergistic with everolimus. Not neccessarily in this line of therapy, but in the neoadjuvant setting, very good data that they work well together.

Although, like many of the decisions that we make every day in clinic, there is not a specific trial that this patient would have fit into. I think the switch into a non-cross resistant agent is attractive to me, so in this case exemestane or tamoxifen, and then adding in a targeted agent where the data would suggest that everolimus could be added to either one of those agents.

ER+/HER2-Breast Cancer: Case 1

Angela is a 56-year-old woman, who in 2013 was diagnosed with a 4 cm IDC of the left breast, ER positive at 50%, PR negative, and Her2 negative. She was treated with four cycles of neoadjuvant doxorubicin and cyclophosphamide, followed by twelve weeks of paclitaxel.

  • She then had a left MRM with AD, showing a residual 1.5 cm tumor with 3/10 LN positive
  • She received anastrozole, and in early 2015 she complained of low back pain and a bone scan revealed multiple areas of uptake in the lumbosacral spine
  • PET-CT revealed lytic lesions in the lumbosacral spine and pelvis, and a 2 cm low attenuation lesion in the liver with a PET SUV value of 10, indicating malignancy

She was placed on denosumab 120 mg SQ monthly, and fulvestrant 500 mg IM monthly. Her pain resolved within 2 months, and on follow-up CT qt 4 months her bone lesions appeared sclerotic and her liver lesion had reduced to 1 cm. Her fulvestrant and denosumab were continued.

  • In early 2016 she again complained of worsening low back pain and left hip pain
  • Repeat PET-CT demonstrated new lytic lesions in the left iliac crest as well as an enlargement of the liver lesion to 3 cm
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