The use of heparin and heparin-like molecules in cancer treatment: a review
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Elsevier Ltd
Abstract
Background: Heparin and heparin-like molecules have shown some promise in the treatment of several cancers. These molecules have roles in angiogenesis, cell proliferation, immune system modulation, cell migration, and cellular invasion. The pathways and mechanisms used by these molecules to inhibit the proliferation of cancer cells aid in understanding the utilization of these molecules in potential treatments. Our aim is to review the use of heparin and heparin-like molecules in cancer treatment, explore the results, and discuss their potential downfalls. Methods: Publications on heparin and heparin-like molecules and compounds were collected from the PubMed and EMBASE databases. Boolean operators and MeSH terms related to heparin, heparin-like molecules, and cancer were used to conduct this search. The articles were reviewed by the authors. Results: Several heparin mimetics are showing promise in cancer treatment. Various studies using mimetics alone or in combination with chemotherapy have been conducted and have yielded mixed results. They work on multiple target molecules, mostly receptors such as fibroblast growth factor and endothelial growth factor. The main types of cancers targeted by these drugs are multiple myeloma, pancreatic cancer, hepatocellular carcinoma (HCC), and other solid tumors. Conclusion: Although limited clinical evidence of efficacy and potential pitfalls are present, heparin and heparin-like molecules have shown potential in the management of cancer patients. Additional research is required to fully understand the biological mechanisms utilized by these molecules in cancer treatment. © 2020 The Author(s)
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Keywords
Heparin, Heparin like, Heparin sulfate, Oncology, Treatment, Antineoplastic combined chemotherapy protocols, Cell proliferation, Clinical trials as topic, Humans, Medical oncology, Neoplasms, Neovascularization, pathologic, Treatment outcome, Tumor microenvironment, Fibroblast growth factor, Focal adhesion kinase, Glucuronic acid, Glycosaminoglycan, Heparin derivative, Iduronic acid, Low molecular weight heparin, Muparfostat, Necuparanib, Phospholipase c, Pixatimod, Protein kinase b, Proteoglycan, Roneparstat, Uronic acid, Vasculotropin, Antineoplastic agent, Ampk signaling, Angiogenesis, Cancer therapy, Carcinogenesis, Cell invasion, Cell migration, Cell polarity, Cellular distribution, Chemotherapy, Fibroblast, Human, Immune system, Liver cell carcinoma, Mammalian tissue, Molecular size, Molecular weight, Multiple myeloma, Pancreas cancer, Pathogenesis, Phase 1 clinical trial (topic), Phase 2 clinical trial (topic), Phase 3 clinical trial (topic), Pi3k/akt signaling, Priority journal, Review, Solid malignant neoplasm, Tumor angiogenesis, Tumor growth, Clinical trial (topic), Drug effect, Mortality, Neoplasm, Neovascularization (pathology), Pathology, Procedures, Vascularization