Breast cancer (BC) is the second leading cause of cancer deaths in women. Mortality in BC patients is mainly due to metastasis to the lungs, bone, and brain. With the new estimates in 2019, 3 out of 10 women will develop BC in her lifetime and 1 in 7 will succumb to BC. In cancer patients, neoadjuvant chemotherapy, hormonal, biological therapies and/or radiotherapy can produce cancer cell death. However, resistance to such therapies arise through rewiring of signaling pathways, tumor cell heterogeneity, epigenetic mechanisms and also due to a small population of breast cancer stem-like cells (BCSCs) or tumor-initiating cells in the tumor. The ensuing therapy failure leads to poor overall survival and quality of life for BC patients. Thus, there is an unmet need for identifying novel targets and strategically targeting BC cells with novel approaches to overcome chemoresistance, eliminate minimal residual disease (MRD), and achieve better pathological complete response (pCR) in metastatic BC. By adopting transformative and transdisciplinary approaches to induce tumor cell death, we can launch development of novel anti-cancer therapies in drug-resistant situations with the aim of improving patient longevity.
Innovative approaches to study drug resistance in breast cancer involve studying tumor microenvironment which portrays paracrine interactions with malignant cells and the stromal cells. Identification of molecular / cellular subtypes, especially cancer stem-like cells and the deregulation of the complex mRNAs / ncRNAs expression patterns and their crosstalk with cellular signaling pathways may also lead to new target leads.
We welcome original preclinical, clinical, and translational research articles, reviews and mini-reviews on basic mechanisms involving:
-Induction of alternate forms of regulated cell death (RCD) such as ferroptosis, pyroptosis and immunogenic cell death including combination immunotherapy;
-Identification of the complex mRNAs/ncRNAs expression patterns in drug-resistant cells by innovative transcriptomic technologies (i.e. single cell-RNASeq) defining their role as anti-oncomiR or oncomiR in tumor development, identifying miRNA signatures related to prognosis in chemoresistant patients.
-Identification of deregulated CSC-related miRNAs which modulate BC stemness and favor drug resistance mechanisms;
-Description of crosstalk/feedback between signal pathways and miRNAs controlling drug resistance are welcome.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Breast cancer (BC) is the second leading cause of cancer deaths in women. Mortality in BC patients is mainly due to metastasis to the lungs, bone, and brain. With the new estimates in 2019, 3 out of 10 women will develop BC in her lifetime and 1 in 7 will succumb to BC. In cancer patients, neoadjuvant chemotherapy, hormonal, biological therapies and/or radiotherapy can produce cancer cell death. However, resistance to such therapies arise through rewiring of signaling pathways, tumor cell heterogeneity, epigenetic mechanisms and also due to a small population of breast cancer stem-like cells (BCSCs) or tumor-initiating cells in the tumor. The ensuing therapy failure leads to poor overall survival and quality of life for BC patients. Thus, there is an unmet need for identifying novel targets and strategically targeting BC cells with novel approaches to overcome chemoresistance, eliminate minimal residual disease (MRD), and achieve better pathological complete response (pCR) in metastatic BC. By adopting transformative and transdisciplinary approaches to induce tumor cell death, we can launch development of novel anti-cancer therapies in drug-resistant situations with the aim of improving patient longevity.
Innovative approaches to study drug resistance in breast cancer involve studying tumor microenvironment which portrays paracrine interactions with malignant cells and the stromal cells. Identification of molecular / cellular subtypes, especially cancer stem-like cells and the deregulation of the complex mRNAs / ncRNAs expression patterns and their crosstalk with cellular signaling pathways may also lead to new target leads.
We welcome original preclinical, clinical, and translational research articles, reviews and mini-reviews on basic mechanisms involving:
-Induction of alternate forms of regulated cell death (RCD) such as ferroptosis, pyroptosis and immunogenic cell death including combination immunotherapy;
-Identification of the complex mRNAs/ncRNAs expression patterns in drug-resistant cells by innovative transcriptomic technologies (i.e. single cell-RNASeq) defining their role as anti-oncomiR or oncomiR in tumor development, identifying miRNA signatures related to prognosis in chemoresistant patients.
-Identification of deregulated CSC-related miRNAs which modulate BC stemness and favor drug resistance mechanisms;
-Description of crosstalk/feedback between signal pathways and miRNAs controlling drug resistance are welcome.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
