ReviewCell death discovery2025
Perspectives on cancer therapy-synthetic lethal precision medicine strategies, molecular mechanisms, therapeutic targets and current technical challenges.
Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Zebrafish tumor xenograft models for drug-screening: a systematic review of methods for treatment assessment.Journal of translational medicine · 2026Pooled it
- Expanding Synthetic Lethality in DNA Damage Response-Defective Cancers Through Stress Phenotype-Guided Kinase Targeting.International journal of molecular sciences · 2026Review
- Patient-Derived Organoid-Based CRISPR Screens in Cancer Research: Applications, Advances, and Challenges.Cancer medicine · 2026Review
- Targeted therapeutic strategies forTranslational lung cancer research · 2026Review
- Overcoming Resistance in Triple-Negative Breast Cancer: A Translational Perspective on Next-Generation DNA Damage Response Inhibitors and Synthetic Lethality.Molecules (Basel, Switzerland) · 2026Review
- Molecular landscape and clinical translation of DNA damage response alterations in solid tumors: A pan-cancer perspective on precision oncology.Neoplasia (New York, N.Y.) · 2026Review
- Article
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Multifaceted anticancer mechanisms of tribenzyltin carboxylates: DNA minor groove targeting and inhibition of key enzymes in DNA replication, nucleotide synthesis, and redox homeostasis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Cell-intrinsic and tumor microenvironmental determinants of platinum resistance in epithelial ovarian cancer.Discover oncology · 2026Review
- PARP1 trapping activates cGAS-STING pathway to induce immunogenic cell death in multiple myeloma.Cancer cell international · 2026Article
- Insights into the olaparib-mediated cell death mechanisms in canine hematological malignancies: a different fate for CLBL-1 and GL-1 cell lines.Frontiers in veterinary science · 2026Article
- Unlocking the undruggable spliceosome: generative AI and structural dynamics in cancer therapy.Frontiers in cell and developmental biology · 2026Review
- Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026Review
- A pathway-informed mutual exclusivity framework to detect genetic interactions in pediatric cancer.BMC medical genomics · 2025Article
- Design, development, and therapeutic applications of PARP-1 selective inhibitors.Future medicinal chemistry · 2025Review
- Integrative multidimensional analysis of age-associated synthetic lethal genes and development of a prognostic model in breast cancer.Frontiers in immunology · 2025Article
- Targeting replication stress in glioblastoma: From genotoxic treatment and inhibitors of the DNA damage response to immunotherapy.Neuro-oncology advancesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, synthetic lethality has become an important theme in the field of targeted cancer therapy. Synthetic lethality refers to simultaneous defects in two or more genes leading to cell death, whereas defects in any single gene do not lead to cell death. Taking advantage of the genetic vulnerability that exists within cancer cells, it theoretically has no negative impact on healthy cells and has fewer side effects than non-specific chemotherapy. Currently, targeted cancer therapies focus on inhibiting key pathways in cancer. However, it has been found that over-activation of oncogenic-related signaling pathways can also induce cancer cell death, which is a major breakthrough in the new field of targeted therapies. In this review, we summarize the conventional gene targets in synthetic lethality (PARP, ATR, ATM, WEE1, PRMT) and provide an in-depth analysis of their latest potential mechanisms. We explore the impact of over-activation of pathways such as PI3K/AKT, MAPK, and WNT on cancer cell survival, and present the technical challenges of current research. Important theoretical foundations and insights are provided for the application of synthetic lethal strategies in cancer therapy, as well as future research directions.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.