ArticleCell reports2018
A Transient Pseudosenescent Secretome Promotes Tumor Growth after Antiangiogenic Therapy Withdrawal.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Therapy-induced secretion of spliceosomal components mediates pro-survival crosstalk between ovarian cancer cells.Nature communications · 2024Article
- Apatinib beyond first progression is associated with prolonged overall survival in patients with advanced breast cancer: Results from an observational study.Experimental and therapeutic medicine · 2024Article
- Machine-learning and mechanistic modeling of metastatic breast cancer after neoadjuvant treatment.PLoS computational biology · 2024Article
- Senescence and cancer - role and therapeutic opportunities.Nature reviews. Clinical oncology · 2022Review
- Resistance to tyrosine kinase inhibitors promotes renal cancer progression through MCPIP1 tumor-suppressor downregulation and c-Met activation.Cell death & disease · 2022Article
- Nutritional Niches of Cancer Therapy-Induced Senescent Cells.Nutrients · 2022Article
- IL-1 and senescence: Friends and foe of EGFR neutralization and immunotherapy.Frontiers in cell and developmental biology · 2022Review
- Overcoming the senescence-associated secretory phenotype (SASP): a complex mechanism of resistance in the treatment of cancer.Molecular oncology · 2021Review
- Adaptive response of resistant cancer cells to chemotherapy.Cancer biology & medicine · 2020Review
- New Insights into Therapy-Induced Progression of Cancer.International journal of molecular sciences · 2020Review
- A Novel 4-Gene Score to Predict Survival, Distant Metastasis and Response to Neoadjuvant Therapy in Breast Cancer.Cancers · 2020Article
- Y-box binding protein-1 is crucial in acquired drug resistance development in metastatic clear-cell renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2020Article
- Enhanced efficacy of sitravatinib in metastatic models of antiangiogenic therapy resistance.PloS one · 2019Article
- Tumor growth fueled by spurious senescence phenotypes.Molecular & cellular oncology · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
VEGF receptor tyrosine kinase inhibitors (VEGFR TKIs) approved to treat multiple cancer types can promote metastatic disease in certain limited preclinical settings. Here, we show that stopping VEGFR TKI treatment after resistance can lead to rebound tumor growth that is driven by cellular changes resembling senescence-associated secretory phenotypes (SASPs) known to promote cancer progression. A SASP-mimicking antiangiogenic therapy-induced secretome (ATIS) was found to persist during short withdrawal periods, and blockade of known SASP regulators, including mTOR and IL-6, could blunt rebound effects. Critically, senescence hallmarks ultimately reversed after long drug withdrawal periods, suggesting that the transition to a permanent growth-arrested senescent state was incomplete and the hijacking of SASP machinery ultimately transient. These findings may account for the highly diverse and reversible cytokine changes observed in VEGF inhibitor-treated patients, and suggest senescence-targeted therapies ("senotherapeutics")-particularly those that block SASP regulation-may improve outcomes in patients after VEGFR TKI failure.
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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.