ReviewInternational journal of molecular sciences2014
Survivin as a preferential target for cancer therapy.
Review in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 2 of them syntheses 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
90 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The Radiosensitizing Potentials of Silymarin/Silibinin in Cancer: A Systematic Review.Current medicinal chemistry · 2024Pooled it
- Survivin and angiotensin-converting enzyme polymorphisms with risk of colorectal cancer: a systematic review and meta-analysis.World journal of surgical oncology · 2015Pooled it
- Silencing of NUP62 overcomes osimertinib resistance via ubiquitination of survivin in non-small cell lung cancer cells.British journal of cancer · 2026Article
- Survivin drives renal cell carcinoma tumorigenesis via proliferative and metabolic adaptation.Disease models & mechanisms · 2026Article
- Review
- Breaking the bonds: targeting protein dimerization for prostate cancer therapy.Endocrinology · 2026Review
- Mechanotherapeutic Potential of Survivin in Glioblastoma.bioRxiv : the preprint server for biology · 2026Article
- Survivin/BIRC5-derived peptide disrupts survivin dimerization and cell division and induces multifaceted anti-cancer effects.Molecular therapy. Oncology · 2026Article
- Expression of Survivin and HER-2 as Independent Predictive Factors for Treatment Response in Locally Advanced Breast Cancer: A Prospective Cohort Study.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Integrative Evaluation ofMolecules (Basel, Switzerland) · 2025Article
- MiR-101-3p targets the PI3K-AKT signaling pathway via Birc5 to inhibit invasion, proliferation, and epithelial-mesenchymal transition in hepatocellular carcinoma.Clinical and experimental medicine · 2025Article
- Pathogenetic therapeutic approaches for endocrine diseases based on antisense oligonucleotides and RNA-interference.Frontiers in endocrinology · 2025Review
- Effects of Resveratrol on Nonmelanoma Skin Cancer (NMSC): A Comprehensive Review.Food science & nutrition · 2024Review
- Functional Significance of miR-4693-5p in Targeting HIF1α and Its Link to Rheumatoid Arthritis Pathogenesis.Non-coding RNA · 2024Article
- Exploring the Therapeutic Effects ofNutrients · 2024Article
- Lotus seedFrontiers in chemistry · 2024Article
- [6]-Gingerol induces Caspase-Dependent Apoptosis in Bladder Cancer cells via MAPK and ROS Signaling.International journal of medical sciences · 2022Article
- Tumor relevant protein functional interactions identified using bipartite graph analyses.Scientific reports · 2021Article
- Arsenic trioxide-induced cell apoptosis and cell cycle arrest are potentiated by 1,25-dihydroxyvitamin D3 in human leukemia K562 cells.Oncology letters · 2021Article
- Discovery of Survivin Inhibitors Part 1: Screening the Harbor Branch Pure Compound Library.Marine drugs · 2021Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is typically a consequence of imbalance between cell death and proliferation in a way favorable to cell proliferation and survival. Most conventional cancer therapies are based on targeting rapidly growing cancerous cells to block growth or enhance cell death, thereby, restoring the balance between these processes. In many instances, malignancies that develop resistance to current treatment modalities, such as chemotherapy, immunotherapy, and radiotherapy often present the greatest challenge in subsequent management of the patient. Studies have shown that under normal circumstances, cells utilize different death mechanisms, such as apoptosis (programmed cell death), autophagy, mitotic catastrophe, and necrosis to maintain homeostasis and physiological integrity of the organism, but these processes often appear to be altered in cancer. Thus, in recent years developing various strategies for administration of cytotoxic chemotherapeutics in combination with apoptosis-sensitizing reagents is receiving more emphasis. Here, we review the properties of the anti-apoptotic protein, survivin, a member of the inhibitor of apoptosis protein (IAP) family and the clinical feasibility and anti-cancer potential of drugs targeting this protein. We also discuss some key points and concerns that should be taken into consideration while developing drugs that target apoptotic proteins, such as survivin.
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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.