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The TGF-β Family in Glioblastoma. Int. J. Mol. Sci. 2024, 25, 1067. [https://](https://)[ ](https://)[doi.org/10.3390/ijms25021067](doi.org/10.3390/ijms25021067)  \nReceived: 14 November 2023  \nRevised: 3 January 2024  \nAccepted: 9 January 2024  \nPublished: 15 January 2024  \nCopyright: © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \nDepartment of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, SE-75123 Uppsala, Sweden; [irene.golan@imbim.uu.se](irene.golan@imbim.uu.se)  \n* Correspondence: [laia.caja@imbim.uu.se](laia.caja@imbim.uu.se)  \nAbstract: Members of the transforming growth factor β (TGF-β) family have been implicated in the biology of several cancers. In this review, we focus on the role of TGFβ and bone morphogenetic protein (BMP) signaling in glioblastoma. Glioblastoma (GBM) is the most common malignant brain tumor in adults; it presents at a median age of 64 years, but can occur at any age, including childhood. Unfortunately, there is no cure, and even patients undergoing current treatments (surgical resection, radiotherapy, and chemotherapy) have a median survival of 15 months. There is a great need to identify new therapeutic targets to improve the treatment of GBM patients. TGF-βs signaling promotes tumorigenesis in glioblastoma, while BMPs suppress tumorigenic potential by inducing tumor cell differentiation. In this review, we discuss the actions of TGF-βs and BMPs on cancer cells as well as in the tumor microenvironment, and their use in potential therapeutic intervention.  \nKeywords: TGF-β; BMP; glioblastoma  \n1. Glioblastoma  \nGlioblastoma (GBM) is the most common primary central nervous system malignancy in adults; it has an incidence of 5 cases per 100,000 people per year. The median survival of GBM patients who have received standard care involving surgical resection followed by treatment with radiotherapy and temozolomide (TMZ) is 15 months [1–3] . In 2016, the World Health Organization (WHO) classified GBM according to the isocitrate dehydrogenase (IDH) mutation status, IDH-mutant (IDH-mt) or IDH-wild-type (IDH-wt) GBM; however, this classification has been reconsidered, as the IDH-mutant GBM aligns more closely with aggressive anaplastic astrocytomas; therefore, the Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy (cIMPACT-NOW) has since proposed that the previously defined IDH-mt GBM now be referred to as astrocytoma, IDH-mt, grade 4 [4] . The current WHO 2021 classification defines glioblastoma as IDH-wt, and describes it as involving frequent alterations associated with mutations in the telomerase reverse transcriptase (TERT) promoter, amplifications of the epidermal growth factor receptor (EGFR), and single-copy loss of chromosome 10 and gain in chromosome 7 [5] . GBMs are characterized as invasive, vascularized, and necrotic, with high intratumoral heterogeneity. In 2010, they were classified into different molecular subtypes according to their transcriptomic profiles, proneural (PN), mesenchymal, and classical [6,7] . These subtypes can co-exist in the same tumor in different regions or at different times [7,8] . PDGFRA amplification can be found in all of the subtypes, but is most abundant in the PN subtype [9]; the mesenchymal subtype has a high NF1 mutation burden, and the classical subtype displays high levels of EGFR amplification and few TP53 mutations [4] .  \nThe cancer stem cell (CSC) hypothesis is the basis for many solid tumors, including brain tumors. It has been seen that a small group of glioma stem cells (GSCs) ca","cbCaid4gzESRGVkw","https://ap.wps.com/l/cbCaid4gzESRGVkw","pdf",1447739,22,"English","# Glioblastoma\n## Incidence, survival, and classification\n## Molecular subtypes and genomic features\n# TGF-β Signaling\n## Role in cellular transformation and anchorage-independent growth\n# Cancer stem cells and glioblastoma plasticity\n## GSC identification and marker sets\n## Signaling pathways shaping fate and differentiation\n# Tumor microenvironment and therapeutic intervention\n## Actions of TGF-βs and BMPs in cancer cells and TME","[{\"question\":\"What roles do TGF-β and BMP signaling play in glioblastoma?\",\"answer\":\"TGF-β signaling promotes tumorigenesis in glioblastoma, whereas BMP signaling suppresses tumorigenic potential by inducing tumor cell differentiation.\"},{\"question\":\"Why is glioblastoma difficult to treat, and what survival is reported?\",\"answer\":\"Glioblastoma has no cure, and even with standard treatments such as surgical resection, radiotherapy, and chemotherapy, patients have a median survival of about 15 months.\"},{\"question\":\"How are glioblastoma molecular classifications and subtypes described?\",\"answer\":\"The review notes that earlier WHO and molecular frameworks have been reconsidered; current WHO 2021 defines glioblastoma as IDH-wild-type and describes frequent alterations such as TERT promoter mutations, EGFR amplification, and chromosome 10 loss with chromosome 7 gain, along with transcriptomic subtypes (proneural, mesenchymal, and classical).\"},{\"question\":\"What are glioma stem cells (GSCs) and how are they identified?\",\"answer\":\"GSCs are a small cell population capable of recapitulating the original tumor through clonogenicity and oncogenic potential, with high proliferation, self-renewal, and multilineage differentiation. They are identified using markers including CD133, CD24, and CD44, as well as intracellular markers such as SOX4, Nanog, SOX2, and others.\"}]","The TGF-β Family in Glioblastoma - Review | PDF",1789995275,55]