OPEN FOR SUBMISSIONS: Interruption of Amino Acids Supply as Anti-Tumor Strategy

The fully OA Journal Amino Acids has launched a new Special Issue. Early-career researchers are especially encouraged to submit!
OPEN FOR SUBMISSIONS: Interruption of Amino Acids Supply as Anti-Tumor Strategy
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SUBMIT YOUR PAPER HERE

  • Fully OA Journal: Amino Acids
  • Guest Editors: Prof. Dr. Ellen Closs, Prof. Dr. Stefan Broer, Dr. Yilei Zhang
  • Submission Deadline: December 31, 2025
  • Special Issue title: Interruption of Amino Acids Supply as Anti-Tumor Strategy
  • Full waivers and a discount are available upon acceptance. Early-career researchers are especially encouraged to submit!

The interruption of amino acids supply has emerged as a promising anti-tumor strategy, with research focusing on the metabolic vulnerabilities of cancer cells. Depletion of essential amino acids necessary for tumor growth has shown potential in inhibiting cancer cell proliferation and inducing cell death. This approach has garnered significant interest in the field of cancer metabolism and targeted therapies, with studies exploring the mechanisms underlying amino acid depletion’s anti-tumor effects and its potential as a therapeutic strategy across different cancer types.

Advancing our collective understanding in this area is crucial for identifying novel therapeutic targets and developing effective anti-cancer interventions. Recent advances have elucidated the intricate metabolic pathways involved in amino acid utilization by cancer cells, shedding light on the potential for targeted disruption of amino acid metabolism and supply as a strategy to impede tumor growth.

Furthermore, studies have highlighted the interplay between amino acid depletion and the tumor microenvironment, offering insights into the broader implications of this approach for cancer therapy.

Original Research articles and reviews in this field are invited! 

This Collection supports and amplifies research related to SDG 3 (Good Health and Well-being). 

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Follow the Topic

Cancer Prevention
Life Sciences > Biological Sciences > Cancer Biology > Cancer Prevention
Cancer Metabolism
Life Sciences > Biological Sciences > Cancer Biology > Cancer Metabolism
Metabolic Pathways
Physical Sciences > Chemistry > Biological Chemistry > Metabolism > Metabolic Pathways
Protein Biochemistry
Life Sciences > Biological Sciences > Molecular Biology > Protein Biochemistry
Cancer Therapy
Life Sciences > Biological Sciences > Cancer Biology > Cancer Therapy
Cancer Microenvironment
Life Sciences > Biological Sciences > Cancer Biology > Cancer Microenvironment

Ask the Editor – Inflammation, Metastasis, Cancer Microenvironment and Tumour Immunology

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Interruption of Amino Acids Supply as Anti-Tumor Strategy

The interruption of amino acids supply has emerged as a promising anti-tumor strategy, with research focusing on the metabolic vulnerabilities of cancer cells. Depletion of essential amino acids necessary for tumor growth has shown potential in inhibiting cancer cell proliferation and inducing cell death. This approach has garnered significant interest in the field of cancer metabolism and targeted therapies, with studies exploring the mechanisms underlying amino acid depletion’s anti-tumor effects and its potential as a therapeutic strategy across different cancer types.

Advancing our collective understanding in this area is crucial for identifying novel therapeutic targets and developing effective anti-cancer interventions. Recent advances have elucidated the intricate metabolic pathways involved in amino acid utilization by cancer cells, shedding light on the potential for targeted disruption of amino acid metabolism and supply as a strategy to impede tumor growth. Furthermore, studies have highlighted the interplay between amino acid depletion and the tumor microenvironment, offering insights into the broader implications of this approach for cancer therapy.

Original Research articles and reviews in this field are invited.

This Collection supports and amplifies research related to SDG 3 (Good Health and Well-being).

Publishing Model: Open Access

Deadline: Dec 31, 2025

Incretin-Based Peptide Therapeutics: Advances in GLP-1 and GIP Receptor Modulation for Metabolic Disorders

Incretin-based peptide therapeutics, particularly those targeting GLP-1 (glucagon-like peptide-1) and GIP (gastric inhibitory polypeptide) receptors, have emerged as pivotal players in the management of metabolic disorders such as type 2 diabetes and obesity. These peptides are integral to the regulation of glucose metabolism and appetite control, making them ideal candidates for therapeutic intervention. Recent developments in peptide modulation have demonstrated promising results, with novel agonists and dual receptor modulators showing enhanced efficacy in clinical trials, paving the way for innovative treatment options.

Understanding the mechanisms underlying GLP-1 and GIP receptor modulation is crucial, as it not only provides insight into metabolic regulation but also reveals potential pathways for novel therapeutic strategies. Advances in this field have led to the development of long-acting formulations and combinatorial approaches that improve patient compliance and therapeutic outcomes. As the global prevalence of obesity and diabetes continues to rise, ongoing research in incretin-based therapies holds the promise of addressing these critical public health challenges.

Future research may lead to groundbreaking discoveries in incretin-based therapeutics, with a focus on personalized medicine approaches that consider individual patient profiles. Enhanced understanding of receptor interactions and the discovery of novel peptide structures could lead to the development of next-generation drugs that provide superior efficacy and safety profiles. Furthermore, advances in drug delivery systems may improve the bioavailability and effectiveness of these therapies, ultimately transforming the treatment landscape for metabolic disorders.

This Collection supports and amplifies research related to SDG 3 (Good Health and Well-being).

Publishing Model: Open Access

Deadline: Apr 03, 2026