Advanced Glycation End-Products and Its Receptors in Cancer Progression

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 703

Special Issue Editor


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Guest Editor
Department of Hematology and Oncology, Virginia Commonwealth University, Richmond, VA 23284, USA
Interests: advanced glycation end products; toxic advanced glycation end products; receptor for advanced glycation end products (RAGEs); glycosaminoglycans; cancer; cancer stem cells (CSCs); tumor immune microenvironment (TME)

Special Issue Information

Dear Colleagues,

Advanced glycation end products (AGEs) are a group of compounds formed when sugars react with proteins and lipids in the body. They have been implicated in various diseases, including cancer, through receptors for AGE (RAGEs), as well as dependent and independent mechanisms. An increasing body of literature implicates AGEs/RAGEs in various hallmarks of cancer, including the tumor immune microenvironment (TME), inflammation and cancer stem cells (CSCs). 

In this Special Issue, we aim to explore the latest research findings and advancements in understanding the role of AGEs in cancer. The issue will focus on the biochemistry and clinical detection of AGEs, their clinical relevance and biology, and the molecular mechanism of AGE/RAGE-induced carcinogenesis or therapeutic strategies targeting AGEs/RAGEs in cancer. We especially invite articles examining the role of glycosaminoglycans (GAGs) in regulating AGEs/RAGEs in cancer, as well as CSC biology and the role of AGEs/RAGEs in inflammatory TME and therapeutic targeting thereof. 

Dr. Bhaumik B. Patel
Guest Editor

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Keywords

  • advanced glycation end products
  • toxic advanced glycation end products
  • receptor for advanced glycation end products (RAGEs)
  • glycosaminoglycans
  • cancer
  • cancer stem cells (CSCs)
  • tumor immune microenvironment (TME)

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Published Papers (1 paper)

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11 pages, 1659 KiB  
Perspective
Perspective on Immunoglobulin N-Glycosylation Status in Follicular Lymphoma: Uncovering BCR-Dependent and Independent Mechanisms Driving Subclonal Evolution
by Gloria Pokuaa Manu, Mariette Odabashian and Sergey Krysov
Cancers 2025, 17(7), 1219; https://doi.org/10.3390/cancers17071219 - 4 Apr 2025
Viewed by 392
Abstract
Follicular lymphoma (FL) is a heterogeneous and incurable disease. One of the hallmark features of FL cells is the introduction of N-glycosylation (N-gly) amino acid sequence motifs into the immunoglobulin variable (IgV) region through ongoing somatic hypermutation (SHM) in the early stages of [...] Read more.
Follicular lymphoma (FL) is a heterogeneous and incurable disease. One of the hallmark features of FL cells is the introduction of N-glycosylation (N-gly) amino acid sequence motifs into the immunoglobulin variable (IgV) region through ongoing somatic hypermutation (SHM) in the early stages of lymphoma development. These N-gly motifs, containing oligomannoses, are rarely found in healthy B cells but evidently play a crucial role in the clonal evolution and survival of FL cells in the hostile environment of germinal centers. The random nature of the ongoing SHM in FL occasionally results in the loss of productive immunoglobulin (Ig) genes or the elimination of N-gly motifs in productive genes. Such events typically lead to clonal deletion, as demonstrated by the longitudinal analysis of FL samples. However, rare N-gly-negative subclones demonstrate prolonged survival with evidence of ongoing SHM, giving rise to new N-gly-negative subclones before eventual deletion. This observation suggests the presence of specific mechanisms supporting their survival and proliferation. This perspective examines the current literature and explores whether a detailed transcriptomic and functional comparison of FL subclones characterized by different N-gly statuses, with a particular focus on N-gly-negative subclones, will lead to a comprehensive understanding of both N-gly-dependent and independent pro-survival and proliferative transcriptional signatures. Specifically, it aims to deepen our understanding of FL pathobiology and identify novel therapeutic targets for better disease management. Full article
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