Galbanic acid (GBA), as a natural compound has potential anticancer properties. It has been documented that GBA shows promising therapeutic potential against various types of cancer, including breast, lung, colon, liver, and prostate cancer. Several mechanisms involve im anti-tumor effects of GBA include apoptosis induction, cell cycle arrest, inhibition of angiogenesis, suppression of metastasis, and modulation of immune responses. Furthermore, the synergistic effects of GBA along with chemotherapeutic agents led to has enhancing efficiency with reduction in toxicity. Moreover, GBA through antioxidant and anti-inflammatory properties possess indirect anti-tumor effects. In this review, we will summarize the anti-tumor effects of GBA acid along with involve mechanisms.
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http://dx.doi.org/10.1016/j.prp.2023.154686 | DOI Listing |
Nanomedicine (Lond)
January 2025
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI, USA.
Aim: To develop pH (pHe)-triggered membrane adhesive nanoliposome (pHTANL) of CD40a to enhance anti-tumor activity in pancreatic cancer while reducing systemic toxicity.
Materials And Methods: A small library of nanoliposomes (NL) with various lipid compositions were synthesized to prepare pH (pHe)-triggered membrane adhesive nanoliposome (pHTANL). Physical and functional characterization of pHTANL-CD40a was performed via dynamic light scattering (DLS), Transmission Electron Microscopy (TEM), confocal microscopy, and flow cytometry.
Background: -related schwannomatosis ( -SWN) is a debilitating condition that calls for robust treatment options. The defining feature of -SWN is the presence of bilateral vestibular schwannomas (VSs), which grow over time and can result in irreversible sensorineural hearing loss, significantly affecting the quality of life for those affected. At present, there are no FDA-approved medications specifically for treating VS or related hearing loss.
View Article and Find Full Text PDFB7-H3 (CD276), a member of the B7-family of immune checkpoint proteins, has been shown to have immunological and non-immunological effects promoting tumorigenesis [1, 2] and expression correlates with poor prognosis for many solid tumors, including cervical, ovarian and breast cancers [3-6]. We recently identified a tumor-cell autochthonous tumorigenic role for dimerization of the 4Ig isoform of B7-H3 (4Ig-B7-H3) [7], where 4Ig-B7-H3 dimerization activated tumor-intrinsic cellular proliferation and tumorigenesis pathways, providing a novel opportunity for therapeutic intervention. Herein, a live cell split-luciferase complementation strategy was used to visualize 4Ig-B7-H3 homodimerization in a high-throughput small molecule screen (HTS) to identify modulators of this protein-protein interaction (PPI).
View Article and Find Full Text PDFRadiopharmaceutical therapy (RPT) enhances tumor response to immune checkpoint inhibitors (ICI) in preclinical models, but the effects of different radioisotopes have not been thoroughly compared. To evaluate mechanisms of response to RPT+ICI, we used NM600, an alkylphosphocholine selectively taken up by most tumors. Effects of Y-, Lu-, and Ac-NM600 + ICIs were compared in syngeneic murine models, B78 melanoma (poorly immunogenic) and MC38 colorectal cancer (immunogenic).
View Article and Find Full Text PDFFront Immunol
January 2025
Leeds Institute of Medical Research, School of Medicine, University of Leeds, St. James University Hospital, Leeds, United Kingdom.
Background: There has been limited success of cancer immunotherapies in the treatment of ovarian cancer (OvCa) to date, largely due to the immunosuppressive tumour microenvironment (TME). Tumour-associated macrophages (TAMs) are a major component of both the primary tumour and malignant ascites, promoting tumour growth, angiogenesis, metastasis, chemotherapy resistance and immunosuppression. Differential microRNA (miRNA) profiles have been implicated in the plasticity of TAMs.
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