ReviewTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Insights into the molecular roles of heparan sulfate proteoglycans (HSPGs-syndecans) in autocrine and paracrine growth factor signaling in the pathogenesis of Hodgkin's lymphoma.
Review in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Multi-Omics and Single-Cell Dissection Reveals EXT1 as a Glycosylation-Linked Therapeutic Target in Cancer.Oncology research · 2026Article
- Gene expression profiling of venous malformations identifies the role of SDC1 in venous endothelial cells.Heliyon · 2024Article
- Modulation of Microenvironment Signals by Proteolytic Shedding of Cell Surface Extracellular Matrix Receptors.Frontiers in cell and developmental biology · 2021Review
- The lncRNA XIST regulates the tumorigenicity of renal cell carcinoma cells via the miR-302c/SDC1 axis.International journal of clinical and experimental pathology · 2017Article
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
Syndecans (SDC, SYND) comprise a group of four structurally related type 1 transmembrane heparan sulfate proteoglycans (HSPGs) that play important roles in tumorigenic processes. SDCs exert signaling via their protein cores and their conserved transmembrane and cytoplasmic domains or by forming complexes with growth factors (GFs). In classical Hodgkin's lymphoma (cHL), a lymphoid neoplasm of predominantly B cell origin, SDC1 and SDC4 are the active SDCs, and a number of GF (vascular endothelial growth factor, fibroblast growth factor, etc.) signaling pathways have been studied. However, despite extensive pre-clinical and clinical research on SDC-mediated GF signaling in many cancer types, there is very limited data for this interaction in cHL. Thus, this review highlights the relevant literature focusing on the potential interactions of SDCs and GFs in cHL pathogenesis. Also discussed are the pre-clinical and clinical studies targeting signaling through these pathways.
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Registered trials
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