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Glioblastoma multiforme (GBM) is characterized by a high mortality rate, high resistance to cytotoxic chemotherapy, and radiotherapy due to its highly aggressive nature. The pathophysiology of GBM is characterized by multifarious genetic abrasions that deactivate tumor suppressor genes, induce transforming genes, and over-secretion of pro-survival genes, resulting in oncogene sustainability. Synthetic lethality is a destructive process in which the episode of a single genetic consequence is tolerable for cell survival, while co-episodes of multiple genetic consequences lead to cell death. This targeted drug approach, centered on the genetic concept of synthetic lethality, is often selective for DNA repair-deficient GBM cells with restricted toxicity to normal tissues. DNA repair pathways are key modalities in the generation, treatment, and drug resistance of cancers, as DNA damage plays a dual role as a creator of oncogenic mutations and a facilitator of cytotoxic genomic instability. Although several research advances have been made in synthetic lethality modalities for GBM therapy, no review article has summarized these therapeutic modalities. Thus, this review focuses on the innovative advances in synthetic lethality modalities for GBM therapy.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11167713 | PMC |
http://dx.doi.org/10.1515/med-2024-0981 | DOI Listing |
Eur J Med Chem
September 2025
State Key Laboratory of Natural Medicines and Department of Medicinal Chemistry, School of Pharmacy, China Pharmaceutical University, Nanjing, 211198, PR China. Electronic address:
The Werner syndrome RecQ helicase (WRN) has recently emerged as a novel synthetic lethality target for microsatellite instability-high (MSI-H) cancers. However, available WRN inhibitors or degraders is still lacking so far. Particularly, chemically designed probes capable of degrading WRN irrespective of microsatellite status remain unexplored.
View Article and Find Full Text PDFJ Med Chem
September 2025
Repare Therapeutics, 7171 Frederick-Banting, Building 2, H4S 1Z9 Montréal, Québec, Canada.
DNA polymerase theta (Polθ) plays a critical role in repairing DNA double-strand breaks through microhomology-mediated end joining (MMEJ) and has emerged as a key synthetic lethal drug target in cancers with homologous recombination (HR) deficiencies. Its inhibition has shown a strong potential to synergize with PARP inhibitors, particularly in tumors with deleterious or mutations. Here, we describe the discovery and preclinical development of RP-2119, a selective, potent, and bioavailable Polθ ATPase inhibitor.
View Article and Find Full Text PDFCancer Genet
August 2025
National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India. Electronic address:
Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic and epigenetic alterations that drive uncontrolled cellular proliferation and survival. This review provides a comprehensive overview of key cancer driver genes, including oncogenes such as KRAS and PIK3CA, as well as tumor suppressor genes like TP53, PTEN, and CDKN2A, highlighting their molecular mechanisms and roles across various types of cancer. Leveraging insights from large-scale cancer genome initiatives and whole-genome sequencing, we examine the landscape of somatic mutations and their association with hallmark cancer pathways, including cell cycle regulation, apoptosis, metabolic reprogramming, and immune evasion.
View Article and Find Full Text PDFCell Rep
September 2025
Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China; Pôle de Recherches Sino-Français en Science du Vivant et Gé
RNA helicase DDX3X is generally implicated in inflammasome activation and anti-viral responses. We characterize the common features of scattered DDX3X mutations in lymphoid cancers using molecular dynamics simulation and crystallization, thereby demonstrating their crucial role in Epstein-Barr virus (EBV) lytic gene-driven oncogenic processes. The DDX3X mutation is significantly related to impaired stimulator of interferon genes (STING)/ interferon regulatory factor 7 (IRF-7)/interferon (IFN)-α/β-mediated innate immunity, overexpression of EBV lytic gene BNLF2b, and increased formation of R-loops.
View Article and Find Full Text PDFMol Cancer Ther
September 2025
David J. Sugarbaker Division of Thoracic Surgery, Michael E. DeBakey Department of Surgery and the Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas.
Diffuse mesothelioma is a rare but highly aggressive and treatment-resistant neoplasm with low survival rates. Effective therapeutic strategies are limited, and resistance to treatment is a major obstacle. Myeloid cell leukemia (MCL)-1 and B-cell leukemia (BCL)-xL are antiapoptotic B-cell lymphoma 2 (Bcl-2) family proteins that block cell-intrinsic apoptosis through interactions on the mitochondrial outer membrane which contribute to therapeutic resistance.
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