Sharon’s story – coping with metastasized hormone-receptor-positive breast cancer | oncotest
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Sharon’s story – coping with metastasized hormone-receptor-positive breast cancer

In 2003, when Sharon was 42, she was diagnosed with breast cancer. She immediately underwent surgery to excise the tumor and the pathological findings showed that this was a penetrating tumor that was positive for hormone receptors.
About two thirds of breast cancer tumors are hormone-receptor-positive, which means that the growth of these tumors depends on the female hormone estrogen. Therefore, the treatments offered for tumors of this type are based on an estrogen-receptor inhibitor (such as Tamoxifen and Faslodex) or estrogen-production inhibitors (aromatase inhibitors).
During Sharon’s surgery, it was discovered that the tumor had spread to seven glands. Therefore, after surgery, she began receiving adjuvant chemotherapy that included AC and later Taxotere for about six months. When she finished the chemotherapy, Sharon underwent a doubt mastectomy and an oophorectomy to remove her ovaries, followed by treatment with Tamoxifen as adjuvant hormone therapy. In 2005, the preventive therapy was replaced and she received aromatase-inhibitors. At the end of 2007, metastases were discovered in her bones, and she began receiving chemotherapy with Xeloda. A year and a half later, new metastases were discovered and the therapy was replaced with a different chemotherapy. Until the end of 2008, Sharon was treated with Avastin and aromatase-inhibitors, but unsuccessfully. In 2009, she continued to receive a combination of chemotherapy, biological therapy and hormone therapy without any significant improvement in her condition.
By mid-2012, Sharon had already managed to receive 15 different treatment lines within four years, with each line being beneficial for two to four months at the most, and she was repeatedly informed that the treatment had failed.
At the beginning of 2012, a physician suggested that she underdo genomic DNA sequencing of the tumor tissue.
During the test, hundreds of genes are sequenced simultaneously on the basis of a new, highly sensitive DNA sequencing technology. The test discovered that Sharon has a mutation in the gene encoding the estrogen-receptor. As a result of the test, a new mechanism was discovered that explained why the tumor had been resistant to hormone therapy. The mutation was what caused the estrogen-receptor to continue to be active despite the estrogen hormone and caused its resistance to treatment.
During a trial conducted in Israel at the laboratory of Dr. Ido Wolf, and concurrently at laboratories in the United States on cells taken from the tumor, it was discovered that the tumor is resistant to a large number of compounds, except for a high dose of Tamoxifen. This discovery constituted a breakthrough and gained wide acclaim in leading medical journals.
Based on the results of the trial, Sharon began receiving combined treatment of a high dose of Tamoxifen and a biological drug called Afinitor.
For the first time since she was diagnosed, the drug therapy succeeded in arresting the disease for a long period of nearly a year.
After the progression of her cancer resumed, Sharon began receiving treatment with a progesterone-receptor antagonist, together with Afinitor. Since then, more than a year later, Sharon has been continuing her treatments, and is functioning and working normally.
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