ArticleCancer research2020
Therapy-Induced Senescence Drives Bone Loss.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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
77 citing papers in PubMed, 123 citations in OpenAlex.
- Cellular senescence and the SASP in skeletal ageing: convergent mechanisms of progressive bone loss in osteoporosis.Biogerontology · 2026Review
- Targeting cellular senescence mitigates chemotherapy-induced bone loss in young and aged mice.GeroScience · 2026Article
- Tumor survivors' musculoskeletal health assessment: advances in imaging biomarkers for cancer treatment-related sequelae.Journal of orthopaedic surgery and research · 2026Review
- Later menopause confers no additional protection against osteoporosis in older women.Endocrine connections · 2026Article
- Systemic Treatments Impact Bone Quality in a Preclinical Model of Mixed Femoral Metastases.Annals of biomedical engineering · 2026Article
- Targeting breast cancer senescence in 3D models of bone metastasis.Breast cancer (Tokyo, Japan) · 2026Article
- Juvenile Doxorubicin Exposure Causes Lasting Trabecular Bone Loss in Mice: A Preclinical Model of Long-Term Skeletal Damage.Cancers · 2026Article
- DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Doxorubicin induces bone loss and modifies multiple cell populationsJournal of bone oncology · 2026Article
- Engineered bone matrix models for understanding breast cancer skeletal metastasis.Cancer metastasis reviews · 2026Review
- Review
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Chemotherapy-induced adipo-lineage cell senescence drives bone loss.Nature communications · 2025Article
- Human dental pulp stem cells-derived small extracellular vesicles prevent osteoradionecrosis of the jaw in a rat model.Nagoya journal of medical science · 2025Article
- Autophagic-active nanosystem for senile bone regeneration by in-situ mitochondrial biogenesis and intercellular transfer.Bioactive materials · 2025Article
- Multi-omics Mendelian randomization integrating RNA-seq, eQTL and pQTL data revealed CPXM1 as a potential drug target for osteoporosis.Hereditas · 2025Article
- Critical Review of Hearing Rehabilitation in Pediatric Oncology: Specific Considerations and Barriers.Current oncology (Toronto, Ont.) · 2025Review
- Targeted delivery of liposomal senolytics to alleviate cellular senescence-induced bone loss.Fundamental research · 2025Article
- Abaloparatide increases bone mass without affecting growth of bone-disseminated cancer cells.JBMR plus · 2025Article
- Review
17 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
14 authors at 3 institutions in 1 country.
Funding
Abstract
Chemotherapy is important for cancer treatment, however, toxicities limit its use. While great strides have been made to ameliorate the acute toxicities induced by chemotherapy, long-term comorbidities including bone loss remain a significant problem. Chemotherapy-driven estrogen loss is postulated to drive bone loss, but significant data suggests the existence of an estrogen-independent mechanism of bone loss. Using clinically relevant mouse models, we showed that senescence and its senescence-associated secretory phenotype (SASP) contribute to chemotherapy-induced bone loss that can be rescued by depleting senescent cells. Chemotherapy-induced SASP could be limited by targeting the p38MAPK-MK2 pathway, which resulted in preservation of bone integrity in chemotherapy-treated mice. These results transform our understanding of chemotherapy-induced bone loss by identifying senescent cells as major drivers of bone loss and the p38MAPK-MK2 axis as a putative therapeutic target that can preserve bone and improve a cancer survivor's quality of life. SIGNIFICANCE: Senescence drives chemotherapy-induced bone loss that is rescued by p38MAPK or MK2 inhibitors. These findings may lead to treatments for therapy-induced bone loss, significantly increasing quality of life for cancer survivors.
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.