Breast and prostate cancer are the most common tumors among people in Western countries. The incidence of sex-hormone related cancers is increased in developing nations and the reason remains unclear. It is well established that the presence of steroid receptor on the breast and prostate tumors specimens is considered a good biomarker to identify those patients who can respond to the anti-hormones therapy such as Tamoxifen or cyproterone acetate, respectively, or to reduction of the level of circulating estrogens or androgens such as aromatase inhibitors (anastrozole, letrozole, exemestane) and LHRH antagonist (goserelin, triptorelin, buserelin). However, more than 50% of those receptor positive breast cancers are resistant to endocrine therapy. In addition, most of hormone-responsive breast and prostate cancers that previously responded to endocrine therapy may become resistant over time. Therefore, the classical genomic model of steroid action, based solely on receptor mediated gene transcription, cannot be an exhaustive mechanism. Accumulating evidence indicates that rapid non nuclear-steroid signaling pathways regulate multiple biological processes such as differentiation, proliferation, survival and migration in target cells. Therefore, understanding the network complexity of non-genomic steroid hormones in cancer would be crucial to reduce the recurrence from breast and prostate cancer and to increase the relapse free-survival from cancer.
Potentials topics include, but are not limited to:
1. Role of steroid receptor in breast and prostate cancer
2. Non- transcriptional mechanisms of steroid receptor
3. Role of steroid receptor in epithelial-to-mesenchymal transition
4. Role of steroid receptor post translational modifications
5. New tool for prognostic significance and prediction to hormonal therapy and /or biological therapy
Breast and prostate cancer are the most common tumors among people in Western countries. The incidence of sex-hormone related cancers is increased in developing nations and the reason remains unclear. It is well established that the presence of steroid receptor on the breast and prostate tumors specimens is considered a good biomarker to identify those patients who can respond to the anti-hormones therapy such as Tamoxifen or cyproterone acetate, respectively, or to reduction of the level of circulating estrogens or androgens such as aromatase inhibitors (anastrozole, letrozole, exemestane) and LHRH antagonist (goserelin, triptorelin, buserelin). However, more than 50% of those receptor positive breast cancers are resistant to endocrine therapy. In addition, most of hormone-responsive breast and prostate cancers that previously responded to endocrine therapy may become resistant over time. Therefore, the classical genomic model of steroid action, based solely on receptor mediated gene transcription, cannot be an exhaustive mechanism. Accumulating evidence indicates that rapid non nuclear-steroid signaling pathways regulate multiple biological processes such as differentiation, proliferation, survival and migration in target cells. Therefore, understanding the network complexity of non-genomic steroid hormones in cancer would be crucial to reduce the recurrence from breast and prostate cancer and to increase the relapse free-survival from cancer.
Potentials topics include, but are not limited to:
1. Role of steroid receptor in breast and prostate cancer
2. Non- transcriptional mechanisms of steroid receptor
3. Role of steroid receptor in epithelial-to-mesenchymal transition
4. Role of steroid receptor post translational modifications
5. New tool for prognostic significance and prediction to hormonal therapy and /or biological therapy
