ReviewJournal of the National Cancer Institute2010
Therapy-induced senescence in cancer.
Review in Journal of the National Cancer Institute, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 481 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
481 citing papers in PubMed, 1 synthesis or guideline pooled it, 819 citations in OpenAlex.
- Non-oncologic to oncologic drug: A systematic review of drug repurposing in cancer.Cancer chemotherapy and pharmacology · 2025Pooled it
- The Relationship Between Immunogenic Cell Death and Cellular Senescence in Cancer Immunotherapy.Life (Basel, Switzerland) · 2026Review
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- Senescence and Hypoxia Regulate Colon Cancer Cell Transcriptome and Secretome: Insights into Cancer Cell Senescence Pathophysiology.Biomolecules · 2026Article
- On the Edge of Benefit and Harm: Reactive Oxygen Species in Cancer.International journal of molecular sciences · 2026Review
- Therapy-induced senescence rewires the melanoma secretome to promote antitumor immune response and augment cell therapies.Journal for immunotherapy of cancer · 2026Article
- Small molecule activators of the mitochondrial protease ClpP induce senescence in triple-negative breast cancer cells and sensitize cells to the Bcl-2 inhibitor venetoclax.Cell death & disease · 2026Article
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Polyploid Giant Cancer Cells as a Senescence-Linked State in the Tumor Microenvironment.Cancers · 2026Review
- Senescent endothelial cell-derived extracellular vesicles promote neoadjuvant chemoresistance in colorectal cancer via GPX4.Communications biology · 2026Article
- Stress-induced CXCL13 regulates pancreatic exocrine homeostasis, age-related chronic inflammation, and cancer progression.Science advances · 2026Article
- Subclonal β-catenin/YAP signaling heterogeneity accelerates ovarian cancer metastasis through a senescence-associated secretory phenotype.Cell death & disease · 2026Article
- IAP Antagonists Selectively Eliminate Therapy-Induced Senescent Cancer Cells via TNFα-Independent Apoptosis.Cancer science · 2026Article
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- NFATC2-mediated CST1 upregulation drives cholangiocarcinoma growth and metastasis.Cell death discovery · 2026Article
- Disproportionality Analysis of Hematologic Adverse Event Signals Associated with Venetoclax in Combination with Senescence-Inducing Chemotherapy.Journal of clinical medicine · 2026Article
- AKG-TET axis is central to senescence plasticity.iScience · 2026Article
- Crosstalk between TGF-β and Wnt/β-catenin signaling drives fibrogenic and stem-like phenotypes in senescent MDA-MB-231 breast cancer cells.npj aging · 2026Article
- Differential responses to the combination of navitoclax and venetoclax with doxorubicin in murine models of triple negative breast cancer.Frontiers in cell and developmental biology · 2026Article
- Molecular and Biochemical Evidence of Edaravone's Impact on Dasatinib-induced AGS Cell Senescence: A Promising Strategy for Gastric Cancer Therapy.Current medicinal chemistry · 2026Article
421 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence is a response to nonlethal stress that results in persistent cytostasis with a distinct morphological and biochemical phenotype. The senescence phenotype, detected in tumors through the expression of mRNA and protein markers, can be generated in cancer cells lacking functional p53 and retinoblastoma protein. Current research suggests that therapy-induced senescence (TIS) represents a novel functional target that may improve cancer therapy. TIS can be induced in immortal and transformed cancer cells by selected anticancer compounds or radiation, and accumulating data indicate that TIS may produce reduced toxicity-related side effects and increased tumor-specific immune activity. This review examines the current status of TIS-regulated mechanisms, agents, and senescence biomarkers with the goal of encouraging further development of this approach to cancer therapy. Remaining hurdles include the lack of efficient senescence-inducing agents and incomplete biological data on tumor response. The identification of additional compounds and other targeted approaches to senescence induction will further the development of TIS in the clinical treatment of cancer.
Indexed as
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.