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My Breast Cancer

44 year old pre-menopausal female presents in January 2004 with inflammatory breast cancer.

The patient’s cancer was ER 3+, PR 3+ and HER-2-neu negative by FISH. She received chemotherapy with Cytoxan, Adriamycin, and Taxotere for 3 cy-cles, and then had surgery with bilateral mastectomy with reconstruction. Ge-netic testing demonstrated the patient to be BRAC-2 positive (BRAC analysis). Oopherectomy was performed in December 2004. The patient subsequently had recurrent disease and was treated at different times with several hormonal therapies which were poorly tolerated by the patient. In early 2009 the patient was treated in the Sarasota area with Herceptin and Abraxane with no response. Avastin and Gemzar were then administered with disease progression at multiple sites including lung, liver and bone.


The patient came to me for a second opinion in October 2009 stating “I want to be treated with a new experimental drug therapy for breast cancer called a PARP inhibitor at the National Institutes of Health. When I spoke to my current oncologist he initially told me that the treatment didn’t exist and after further investigation told me I didn’t qualify for the clinical trial.” Since conventional therapy did not work for treatment of my breast cancer, I need someone to help me to get enrolled in this clinical trial.

[tabs tab1=”Diagnosis” tab2=”Significant Findings” tab3=”Pharmacology” tab4=”Management” tab5=”Comments”]
[tab num=1]The patient at the time of her initial visit with us had Stage IV breast cancer and was heavily pre-treated. Her treatment included Herceptin, despite the fact that she had a HER-2 negative breast cancer.[/tab]
[tab num=2]The patient has a good performance status and desired aggressive therapy. CT PET scan in Nov 2009 demonstrated lung, liver, bone and nodal metastasis.[/tab]
[tab num=3]The patient qualified for a PARP inhibitor trial. PARP inhibitors (PARP= poly adenosine-diphosphate-ribose polymerase) are a new class of drugs which inhibit PARP. PARP-1 is a polymerase involved in DNA repair, particularly the repair of tumor cells in patients with the BRAC1 or BRAC2 mutation. In tumor cells that carry the BRAC1 or BRAC2 mutation homlogous recombination in nonfunctional.[/tab]
[tab num=4]This patient was placed on an oral PARP inhibitor prior to Thanksgiving 2009. On New Years Eve 2009 a repeat CT PET scan was completely normal.[/tab]
[tab num=5]Medical practices that participate in clinical trails do not participate in every clinical trial available. Practices choose trials based on whether they believe they can get a significant number of patient participants. Patients often don’t realize that while they may not qualify for a clinical trial offered within a medical practice that does NOT mean that they don’t qualify for a clinical trail at all. It is important to work with a physician that will go the extra mile and look outside their practice if necessary. Managing patients on clinical trails is time intensive. This heavily pre-treated patient with Stage IV breast cancer had perhaps the most rapid complete response for breast caner that I have seen in 30 years of practice. The patient effectively had no signifi-cant side effects, other then some malaise.[/tab]