Acquired therapy resistance is a major factor leading to cancer-associated mortality, therefore, understanding how resistance can be prevented or targeted is crucial to improve cancer therapy. In the last decades, the metabolic reprogramming of cancer cells, one hallmark of cancer, has been highlighted as an important mediator of resistance toward anticancer therapies. Different discoveries have highlighted intriguing insights into how metabolic rewiring is critical for tumor aggressiveness and drug resistance, thus, opening new opportunities to treat therapy-insensitive tumors. A variety of experimental compounds inhibiting key metabolic pathways emerged as a promising approach to target cancer cells and potentiated the standard treatments.
In addition, many studies show an association between drug resistance and the metabolic symbiosis inherent to cancer cells and stroma. Various metabolites are released by the tumor cells into the microenvironment, conferring resistance towards chemo-radio and immunotherapy. Thus, molecular hallmarks of cancer cell metabolism are potential therapeutic targets, not only to eliminate malignant cells but also to boost the efficacy of anticancer therapies.
The past decades have brought numerous advances to our knowledge about how metabolic heterogeneity of tumors represents therapeutic vulnerabilities, therefore, understanding how metabolic programs and which mechanism underlie therapy resistance is urgently needed.
In this Research Topic, we will highlight the relationship between metabolic reprogramming of cancer cells and cancer therapy resistance and how manipulating key metabolic enzymes can enhance the efficacy or overcome resistance to classical chemotherapy, oncogene-targeted therapies, and T cell-based therapies.
In this Research Topic, we welcome Original Research, Reviews, and Mini-Review articles focusing on the following subtopics:
1. The relationship between cell metabolism and drug resistance in cancer cells;
2. How metabolic symbiosis between cancer cells and stroma sustain cancer aggressiveness and therapy resistance;
3. The role of metabolites in inducing drug resistance;
4. Metabolic plasticity and heterogeneity in cancer, associated with resistance to therapy;
5. Metabolic alterations underlying oncogene targeted therapies resistance;
6. Metabolic prognostic biomarkers for drug response;
7. How targeting key metabolic enzymes improve the efficacy of cancer therapies such as chemotherapy, radiotherapy and immunotherapy;
8. Molecular mechanisms of resistance to identify novel metabolic targets that can be used for combinatorial therapy;
Note: Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
Acquired therapy resistance is a major factor leading to cancer-associated mortality, therefore, understanding how resistance can be prevented or targeted is crucial to improve cancer therapy. In the last decades, the metabolic reprogramming of cancer cells, one hallmark of cancer, has been highlighted as an important mediator of resistance toward anticancer therapies. Different discoveries have highlighted intriguing insights into how metabolic rewiring is critical for tumor aggressiveness and drug resistance, thus, opening new opportunities to treat therapy-insensitive tumors. A variety of experimental compounds inhibiting key metabolic pathways emerged as a promising approach to target cancer cells and potentiated the standard treatments.
In addition, many studies show an association between drug resistance and the metabolic symbiosis inherent to cancer cells and stroma. Various metabolites are released by the tumor cells into the microenvironment, conferring resistance towards chemo-radio and immunotherapy. Thus, molecular hallmarks of cancer cell metabolism are potential therapeutic targets, not only to eliminate malignant cells but also to boost the efficacy of anticancer therapies.
The past decades have brought numerous advances to our knowledge about how metabolic heterogeneity of tumors represents therapeutic vulnerabilities, therefore, understanding how metabolic programs and which mechanism underlie therapy resistance is urgently needed.
In this Research Topic, we will highlight the relationship between metabolic reprogramming of cancer cells and cancer therapy resistance and how manipulating key metabolic enzymes can enhance the efficacy or overcome resistance to classical chemotherapy, oncogene-targeted therapies, and T cell-based therapies.
In this Research Topic, we welcome Original Research, Reviews, and Mini-Review articles focusing on the following subtopics:
1. The relationship between cell metabolism and drug resistance in cancer cells;
2. How metabolic symbiosis between cancer cells and stroma sustain cancer aggressiveness and therapy resistance;
3. The role of metabolites in inducing drug resistance;
4. Metabolic plasticity and heterogeneity in cancer, associated with resistance to therapy;
5. Metabolic alterations underlying oncogene targeted therapies resistance;
6. Metabolic prognostic biomarkers for drug response;
7. How targeting key metabolic enzymes improve the efficacy of cancer therapies such as chemotherapy, radiotherapy and immunotherapy;
8. Molecular mechanisms of resistance to identify novel metabolic targets that can be used for combinatorial therapy;
Note: Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
