More than 230,000 women and several thousand men in the U.S. will be diagnosed with breast cancer this year. Despite dramatic advances in detection and treatment, breast cancer is still one of the leading causes of cancer-related death for women in America and across the world.
On April 25, the annual Jefferson Breast Cancer Symposium – a day-long scientific and clinical conference at Jefferson’s Kimmel Cancer Center on our Center City campus – renowned specialists will explore the latest treatments and research.
“Treating breast cancer is a multidisciplinary effort, with input from a variety of specialists, such as pathologists, surgeons, radiation oncologists and medical oncologists, who make decisions about patient treatment and care,” says Richard Pestell, MD, PhD, director of the Kimmel Cancer Center at Jefferson.
Participants in the symposium will be eligible for continuing medical education (CME) credits.
Those in attendance are encouraged to share information from the conference and their thoughts and commentary on Twitter using the hashtag #KCCbreast14. You can follow along and join conversation using the same hashtag.
New research being presented at the symposium includes:
- Blocking Metastases with HIV Drugs
- Metabolic fingerprints of inflammatory breast cancer
- Novel biomarker for endocrine therapy
Blocking cancer metastases with HIV drugs
When breast cancer metastasizes, malignant cells break off from the original tumor and enter the blood stream, eventually landing in new areas of the body – often the lungs – to grow additional tumors. Researchers have shown that certain tissues release chemical beacons that attract metastatic cells expressing receptors for those homing signals.
Now, Richard Pestell, MD, PhD, director of the Jefferson’s Kimmel Cancer Center and colleagues have shown that they can block these homing receptors on cancer cells and reduce the risk of metastases in mouse models using drugs designed to treat patients with HIV.
Two drugs approved to treat HIV – Maraviroc, and Vicriviroc – work by blocking the same receptor, called CCR5, that metastatic breast cancer cells use to home to lung tissue. When the team blocked the CCR5 receptor with these drugs, the rates of metastases to the lung were reduced in the basal subtype of breast cancer in mice.
In addition, the team also showed that the CCR5 receptor is expressed in prostate cancer, and that these drugs can reduce the rates of metastasis to sites including the brain, bones, and lungs. The results not only demonstrate the role of the CCR5 receptor in cancer, but also suggest that a new – already approved – therapy could be useful in helping prevent metastases in two aggressive forms of cancer.
A metabolic fingerprint for inflammatory breast cancer
Inflammatory breast cancer (IBC) is an aggressive type of advanced breast cancer with a poor prognosis and lower survival rate than other types of breast cancer. The disease is resistant to standard treatments and has the capacity to spread very early through lymphatic channels and blood vessels. Currently, there are no targeted therapeutic options for IBC patients because there are few molecular markers unique to this disease.
In order to find out how inflammatory breast cancer differs from other breast cancers, medical oncologist Massimo Cristofanilli, MD, director of the Jefferson Breast Care Center and colleagues explored the biochemical signature of these cells in order to create a metabolic fingerprint of the disease that could be used to find novel therapeutic approaches.
The researchers found a number of differences in IBC cells including a reduction in cell proliferation, an increase in both inflammatory and anti-inflammatory signals, and slower metabolic rate, consistent with the lower rate of proliferation.
“Fast proliferation is usually associated with more aggressive disease, so it is somewhat surprising to find slower proliferation in this aggressive form of breast cancer,” says Dr. Cristofanilli.
The study is the first to show a difference in metabolic processes between breast cancer and IBC cells, and future studies to confirm these observations could help provide novel targets for more effective therapies for the treatment of IBC patients.
Novel biomarker and potential diagnostic method for endocrine therapy response in breast cancer
Anti-estrogen therapy, or endocrine therapy, has potential to be efficacious in one million patients diagnosed with estrogen receptor (ER)-positive breast cancer each year worldwide. Regrettably, up to one third of these patients will progress to endocrine resistant breast cancer.
Physician-research Hallgeir Rui, MD, PhD, a professor of cell biology at Jefferson’s Kimmel Cancer Center, and colleagues, report that loss of the tumor marker phospho-Stat5 in ER-positive breast cancer is associated with hormone therapy failure.
The protein STAT5 is often phosphorylated in cancer cells, promoting the cell’s survival despite genomic errors that should lead to its self-destruction. Surprisingly, in earlier retrospective clinical trials, Dr. Rui’s group showed that patients whose cancers no longer expressed phosphorylated STAT5, or Phospho-Stat5, also developed a resistance to hormone therapies such as tamoxifen. Although that 2011 study showed that phospho-Stat5 could have clinical value as a predictive marker, a robust assay to test the association was needed.
Now Rui and colleagues further confirm the association using a new patient cohort and show that two types of image-analysis software could be useful in speeding the detection of this change in cancer cells so that doctors can offer alternate therapies to patients sooner. The image-analysis software partially automates a pathologists’ job, thereby improving both the speed and accuracy of a test for this potential biomarker diagnostic in breast cancer.
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