Can FDG PET/CT monitor the response to hormonal therapy in breast cancer patients?

Excerpt

As breast cancer becomes metastatic, it becomes incurable and the goals of treatment are palliation of symptoms, prolongation of survival, and maintenance or improvement of the quality of life. The median survival of women with metastatic disease is approximately 2 years, but it may be longer than 10 years in some patients with slowly progressive skeletal or nodal metastases. Advanced breast cancer is mostly treated with endocrine therapies or cytostatic agents, or palliative radiotherapy/systemic metabolic radiotherapy in those with painful bone metastases and ulcerative tumours. Hormonal therapy is a cancer treatment that removes hormones or blocks their action and stops cancer cells growing. Endocrine therapy has often been employed in breast cancer patients as neoadjuvant or adjuvant treatment, significantly improving the outcomes in women with breast cancer positive for oestrogen receptors (ER), while in women with ER- negative cancer, systemic chemotherapy remains the best choice for decreasing disease recurrence and death. Hormonal drugs produce their effects in various ways: (1) by blocking the effect of a specific enzyme, (2) by suppressing hormone production, and (3) by inactivating the target receptors. A number of pharmacological agents have been developed that modulate tumour cell ER function or reduce the levels of circulating oestrogens. Among these compounds are the selective ER modulators (SERMs; tamoxifen, raloxifen), pure antioestrogens (fulvestrant/Faslodex), luteinizing hormone-releasing hormone agonists (leuprolide, goserelin), and third-generation selective aromatase inhibitors (AIs; anastrozole/Arimidex, letrozole/Femara, exemestane/Aromasin). Tamoxifen acts as an antioestrogen against breast cancer cells through competitive inhibition of oestrogen binding to the ER and inhibition of the expression of oestrogen-modulated genes. The result is a slowing of cell proliferation and therefore the arrest in G1 phase of the proliferative process. AIs act by inhibiting the cytochrome P-450 enzyme that promotes the conversion of androstenedione and testosterone to oestrone and oestradiol, respectively, resulting in a fall in circulating oestrogens to very low levels. …