Chemotherapy has opened a new window in cancer therapy. However, the resistance of cancer cells has dramatically reduced the efficacy of chemotherapy. Cisplatin is a chemotherapeutic agent and its potential in cancer therapy has been restricted by resistance of cancer cells. As a consequence, the scientists have attempted to find new strategies in elevating chemotherapy efficacy. Due to great anti-tumour activity, naturally occurring compounds are of interest in polychemotherapy. Quercetin is a flavonoid with high anti-tumour activity against different cancers that can be used with cisplatin to enhance its efficacy and also are seen to sensitise cancer cells into chemotherapy. Furthermore, cisplatin has side effects such as nephrotoxicity and ototoxicity. Administration of quercetin is advantageous in reducing the adverse effects of cisplatin without compromising its anti-tumour activity. In this review, we investigate the dual role of quercetin in enhancing anti-tumour activity of cisplatin and simultaneous reduction in its adverse effects.
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http://dx.doi.org/10.1080/13813455.2020.1773864 | DOI Listing |
Discov Oncol
January 2025
Division of Hematology/Oncology, The University of Texas Health Sciences Center at Houston, McGovern Medical School, 6431 Fannin Street, MSB 5.216, Houston, TX, 77030, USA.
The established protocol for the management of acute myeloid leukemia (AML) has traditionally involved the administration of induction chemotherapy, followed by consolidation chemotherapy, and subsequent allogeneic stem cell transplantation for eligible patients. However, the prognosis for individuals with relapsed and refractory AML remains unfavorable. In response to the necessity for more efficacious therapeutic modalities, targeted immunotherapy has emerged as a promising advancement in AML treatment.
View Article and Find Full Text PDFCancer Biol Ther
December 2025
Department of Pharmacology, Physiology, and Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER.
View Article and Find Full Text PDFMol Ther
January 2025
Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology and School of Life Sciences, East China Normal University, Shanghai, China, 200241. Electronic address:
CAR T-cell therapy has achieved remarkable clinical success in treating hematological malignancies. However, its clinical efficacy in solid tumors is less satisfactory, partially due to poor in vivo expansion and limited persistence of CAR-T cells. Here, we demonstrated that the overexpression of glucocorticoid-induced tumor necrosis factor receptor-related protein ligand (GITRL) enhances the anti-tumor activity of CAR-T cells.
View Article and Find Full Text PDFMethods Cell Biol
January 2025
Apoptosis, Immunity and Cancer Group, Aragón Health Research Institute (IIS-Aragón), University of Zaragoza, Zaragoza, Spain. Electronic address:
9-kDa Granulysin is a protein present in the granules of human activated cytotoxic T lymphocytes and natural killer cells. It has been shown to exert cytolytic activity against a wide variety of microbes: bacteria, fungi, yeast and protozoa. Recombinant isolated granulysin is also capable of inducing tumor cell death, so it could be used as an anti-tumor therapy.
View Article and Find Full Text PDFJ Control Release
January 2025
Medical 3D Printing Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou 450000, China. Electronic address:
Immune cells are sensitive to the perception of mechanical stimuli in the tumor microenvironment. Changes in biophysical cues within tumor tissue can alter the force-sensing mechanisms experienced by cells. Mechanical stimuli within the extracellular matrix are transformed into biochemical signals through mechanotransduction.
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