The importance of steroid receptors in the etiology and therapy of breast cancer has been well established during the past few decades. Similarly, tumor suppressor proteins such as p53 and Rb have also been shown to be involved in various mechanisms underlying breast oncogenesis. While the pro-proliferation/pro-tumorigenic roles of steroid receptors and the anti-proliferation/anti-tumorigenic roles of p53 and Rb have been studied intensively, whether these two classes of proteins with opposing functions crosstalk to control both normal and abnormal cancer physiology has not been addressed systematically until recently. Recent reports reveal the fascinating biology of the interaction between these two classes of proteins and point to the hitherto unnoticed diagnostic, therapeutic, and prognostic opportunities they present. This Research Topic will focus on recent developments in this field.
Breast cancer heterogeneity is being defined more precisely at the molecular level. This provides an unprecedented opportunity to understand how differential expression of steroid receptors, p53, Rb and other tumor suppressor proteins and interaction/crosstalk among them drive different subtypes of breast cancer. How do steroid receptors influence tumor suppressor pathways and vice-versa in breast cancer? What are the underlying mechanisms of this interaction? How do mutations in these proteins affect the interaction and downstream signaling? How does gain-of-oncogenic function mutations in tumor suppressor proteins impact this crosstalk? How can this information be exploited for the development of novel therapeutic strategies based on molecular stratification and novel biomarkers?
This Research Topic thus welcomes Original Research and Review articles addressing, but not limited to, the following themes:
-Role of estrogen receptors alpha and beta (ERa, ERß) progesterone receptor (PR), glucocorticoid receptor (GR), androgen receptor (AR), and Vitamin D receptor (VDR) in breast cancer
-Functions of wild type (WT) and mutant p53, Rb and other tumor suppressor proteins in different molecular subtypes of breast cancer
-Major pathways (involved in tumor growth, invasion, and metastasis) impacted by the interaction/crosstalk between different steroid receptors, and WT and mutant tumor suppressor proteins
-Role of p53 context (WT versus mutant) in determining opposite functions of the same steroid receptor
-Exploiting signaling crosstalk to develop novel personalized therapies, for patients with breast cancer
-Importance of steroid hormone receptors and p53 in designing prospective clinical studies on breast cancer
-Regulation of tumor cell metabolism by steroid receptor-tumor suppressor signaling crosstalk
-Estrogen receptors, p53 and tumor micro/immune environment
The importance of steroid receptors in the etiology and therapy of breast cancer has been well established during the past few decades. Similarly, tumor suppressor proteins such as p53 and Rb have also been shown to be involved in various mechanisms underlying breast oncogenesis. While the pro-proliferation/pro-tumorigenic roles of steroid receptors and the anti-proliferation/anti-tumorigenic roles of p53 and Rb have been studied intensively, whether these two classes of proteins with opposing functions crosstalk to control both normal and abnormal cancer physiology has not been addressed systematically until recently. Recent reports reveal the fascinating biology of the interaction between these two classes of proteins and point to the hitherto unnoticed diagnostic, therapeutic, and prognostic opportunities they present. This Research Topic will focus on recent developments in this field.
Breast cancer heterogeneity is being defined more precisely at the molecular level. This provides an unprecedented opportunity to understand how differential expression of steroid receptors, p53, Rb and other tumor suppressor proteins and interaction/crosstalk among them drive different subtypes of breast cancer. How do steroid receptors influence tumor suppressor pathways and vice-versa in breast cancer? What are the underlying mechanisms of this interaction? How do mutations in these proteins affect the interaction and downstream signaling? How does gain-of-oncogenic function mutations in tumor suppressor proteins impact this crosstalk? How can this information be exploited for the development of novel therapeutic strategies based on molecular stratification and novel biomarkers?
This Research Topic thus welcomes Original Research and Review articles addressing, but not limited to, the following themes:
-Role of estrogen receptors alpha and beta (ERa, ERß) progesterone receptor (PR), glucocorticoid receptor (GR), androgen receptor (AR), and Vitamin D receptor (VDR) in breast cancer
-Functions of wild type (WT) and mutant p53, Rb and other tumor suppressor proteins in different molecular subtypes of breast cancer
-Major pathways (involved in tumor growth, invasion, and metastasis) impacted by the interaction/crosstalk between different steroid receptors, and WT and mutant tumor suppressor proteins
-Role of p53 context (WT versus mutant) in determining opposite functions of the same steroid receptor
-Exploiting signaling crosstalk to develop novel personalized therapies, for patients with breast cancer
-Importance of steroid hormone receptors and p53 in designing prospective clinical studies on breast cancer
-Regulation of tumor cell metabolism by steroid receptor-tumor suppressor signaling crosstalk
-Estrogen receptors, p53 and tumor micro/immune environment
