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Topic: Interrogating the Role of Metabolism in Acquired Drug Resistance

A special issue of Cancer Drug Resistance.

ISSN 2578-532X (Online)

Submission deadline: 30 Jun 2020

Guest Editor(s)

  • Ramandeep Rattan
    Associate Scientist, Division of Gynecology Oncology, Henry Ford Hospital and Assistant Professor, Department of Oncology, Wayne State University, Detroit, MI, USA.

    Website | E-mail

  • Shailendra Giri
    Associate Scientist, Department of Neurology, Henry Ford Hospsital, Detroit, MI, USA.

    Website | E-mail

Special Issue Introduction

Drug resistance remains a major obstacle to overcome to achieve successful cancer treatment. Despite the drug development, many patients relapse as treatment proceeds due to development of acquired chemoresistance. While acquired chemoresistance occurs due to diverse molecular mechanisms, emerging evidences indicate that resistance acquisition is coupled to metabolic reprogramming that may manifest as increased energy and substrate demands, along with gene expression changes. In addition, cancer cells can also reprogram the stromal cells that may deliver secreted metabolites that may create a unique metabolic microenvironment inducive to drug avoidance and escape. These changes can work together to rewire the metabolic phenotype of cancer cells when under drug pressure, which may result in development of tolerance to the drug and eventually resistance. However, it is not yet known whether the role of metabolism is linked to its maintenance or to its induction. Thus, a better understanding and identification of the metabolic changes induced by drugs that provide selective advantage to a cancer cell may represent a new target to avoid or to block the resistance mechanisms that have been impairing treatment success. This special issue will highlight the current understanding and emerging aspects of the diverse metabolic changes endured by cancer cells during the process of chemoresistance along with novel targets and prospects for improving cancer treatment.
The proposal welcomes original research and review articles that will illustrate and stimulate discovery and dissection of the role of metabolism in acquired drug resistance.

Keywords

Acquired drug resistance, metabolism, cancer, metabolic reprogramming, drug tolerance

Submission Deadline

30 Jun 2020

Submission Information

Articles of special issue are free of charge for article processing.
For Author Instructions, please refer to http://cdrjournal.com/pages/view/author_instructions
For Online Submission, please login at https://oaemesas.com/CDR/?IssueId=354
Submission Deadline: 30 Jun 2020
Contacts: Susan Song, Assistant Editor, susan@cdrjournal.com
Bill Li, Managing Editor, bill@cdrjournal.com or editorial@cdrjournal.com

Planned Papers

Type: Review

Title: Mechanisms of Resistance to PHGDH Inhibitors in Cancer

Authors: Brian A. Van Tine

Affiliations: Barnes and Jewish Hospital, Washington University in St. Louis

Abstract: The identification of biomarkers specific to certain types of cancer has lead to the development of novel, targeted therapies. Targeting components of cellular metabolism has brought a variety of new treatments to the forefront. However, metabolic reprogramming within cancer cells allows cells to quickly acquire resistance to these treatments. 3-phosphoglycerate dehydrogenase (PHGDH) is the rate-limiting enzyme of de novo serine biosynthesis, and has been shown to be elevated in a variety of cancers. Inhibitors of the enzymatic activity of PHGDH, including CBR-5884 and NCT-503, have shown promising effects in vitro, causing a decrease in cellular proliferation. However, these effects are minimal in vivo, suggesting that tumors that are otherwise susceptible to PHGDH inhibition can develop resistance to the inhibitors over time. This review will interrogate the role of PHGDH in the development and progression of cancer. With an understanding of the molecular mechanisms of PHGDH inhibition in cancer, we will then highlight mechanisms of resistance to PHGDH inhibition, and identify avenues for combatting PHGDH resistance for the development of more effective metabolic therapies.


Published Articles