Malignant peripheral nerve sheath tumor (MPNST) is an aggressive soft tissue sarcoma with limited therapeutic options and a poor prognosis. Although neurofibromatosis type 1 (NF1) and radiation exposure have been identified as risk factors for MPNST, the genetic and molecular mechanisms underlying MPNST pathogenesis have only lately been roughly elucidated. Plexiform neurofibroma (PN) and atypical neurofibromatous neoplasm of unknown biological potential (ANNUBP) are novel concepts of MPNST precancerous lesions, which revealed sequential mutations in MPNST development. This review summarized the current understanding of MPNST and the latest consensus from its diagnosis to treatment, with highlights on molecular biomarkers and targeted therapies. Additionally, we discussed the current challenges and prospects for MPNST management.
Cancer represents a major cause of death worldwide and is characterized by the uncontrolled proliferation of abnormal cells that escape immune regulation. It is now understood that cancer-associated fibroblasts (CAFs), which express specific fibroblast activation protein (FAP), are critical participants in tumor development and metastasis. Researchers have developed various FAP-targeted probes for imaging of different tumors from antibodies to boronic acid-based inhibitor molecules and determined that quinoline-based FAP inhibitors (FAPIs) are the most appropriate candidate as the radiopharmaceutical for FAPI PET/CT imaging. When applied clinically, FAPI PET/CT yielded satisfactory results. Over the past few years, the utility and effectiveness of tumor detection and staging of FAPI PET/CT have been compared with FDG PET/CT in various aspects, including standardized uptake values (SUVs), rate of absorbance and clearance. This review summarizes the development and clinical application of FAPI PET/CT, emphasizing the diagnosis and management of various tumor types and the future prospects of FAPI imaging.
Peripheral nerve diseases are significantly correlated with severe fractures or trauma and surgeries, leading to poor life quality and impairment of physical and mental health. Human dental pulp stem cells (DPSCs) are neural crest stem cells with a strong multi-directional differentiation potential and proliferation capacity that provide a novel cell source for nerve regeneration. DPSCs are easily extracted from dental pulp tissue of human permanent or deciduous teeth. DPSCs can express neurotrophic and immunomodulatory factors and, subsequently, induce blood vessel formation and nerve regeneration. Therefore, DPSCs yield valuable therapeutic potential in the management of peripheral neuropathies. With the purpose of summarizing the advances in DPSCs and their potential applications in peripheral neuropathies, this article reviews the biological characteristics of DPSCs in association with the mechanisms of peripheral nerve regeneration.
Bone fracture healing is a complex process involving various signaling pathways. It remains an unsolved issue the fast and optimal management of complex or multiple fractures in the field of orthopedics and rehabilitation. Bone fracture healing is largely a four-stage process, including initial hematoma formation, intramembrane ossification, chondrogenesis, and endochondral ossification followed by further bone remodeling. Many studies have reported the involvement of immune cells and cytokines in fracture healing. On the other hand, the Tumor Necrosis Factor (TNF) family and TNF receptor superfamily (TNFRSF) play a pivotal role in many physiological processes. The functions of the TNF family and TNFRSF in immune processes, tissue homeostasis, and cell differentiation have been extensively studied by many groups, and treatments targeting specific TNFRSF members are in progress. In terms of bone fracture management, it has been discovered that several members of TNFRSF have very distinct functions in different stages of fracture healing, including TNFR1, TNFR2, and receptor activator of nuclear factor kappa-B (RANK) pathways. More specifically, TNFR1 is associated with osteoclastogenesis and TNFR2 is associated with osteogenic differentiation, while RANK is in association with bone remodeling. In this review, we will discuss and summarize the involvement of members of TNFRSF including TNFR1, TNFR2, and Receptor activator of nuclear factor kappa-B (RANK) pathways in different stages of fracture healing and bone remodeling and the current treatment trend involving TNFRSF agonists and antagonists.
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