ArticlePloS one2013
Cabozantinib inhibits growth of androgen-sensitive and castration-resistant prostate cancer and affects bone remodeling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 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
44 citing papers in PubMed.
- Phase II Study of Cabozantinib in Patients With Bone Metastasis.The oncologist · 2022Trial
- Efficacy and Effect of Cabozantinib on Bone Metastases in Treatment-naive Castration-resistant Prostate Cancer.Clinical genitourinary cancer · 2020Trial
- Cabozantinib Versus Mitoxantrone-prednisone in Symptomatic Metastatic Castration-resistant Prostate Cancer: A Randomized Phase 3 Trial with a Primary Pain Endpoint.European urology · 2019Trial
- A phase II study of GW786034 (pazopanib) with or without bicalutamide in patients with castration-resistant prostate cancer.Clinical genitourinary cancer · 2015Trial
- Cabozantinib in chemotherapy-pretreated metastatic castration-resistant prostate cancer: results of a phase II nonrandomized expansion study.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014Trial
- Modulating metabolic signatures to mitigate cabozantinib resistance in FLT3-ITD acute myeloid leukemia cell models.Cell death discovery · 2026Article
- Bone Effects of Anti-Cancer Treatments in 2024.Calcified tissue international · 2025Review
- Prostate Cancer: A Review of Genetics, Current Biomarkers and Personalised Treatments.Cancer reports (Hoboken, N.J.) · 2024Review
- PSMA-Targeted 2-Deoxyglucose-Based Dendrimer Nanomedicine for the Treatment of Prostate Cancer.Biomacromolecules · 2024Article
- PSMA-targeted dendrimer as an efficient anticancer drug delivery vehicle for prostate cancer.Nanoscale · 2024Article
- Augmented antitumor effects of erlotinib and cabozantinib on A549 non-small cell lung cancer:Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Angiogenesis as Therapeutic Target in Metastatic Prostate Cancer - Narrowing the Gap Between Bench and Bedside.Frontiers in immunology · 2022Review
- Article
- Article
- Reprogramming of the FOXA1 cistrome in treatment-emergent neuroendocrine prostate cancer.Nature communications · 2021Article
- Review
- Cabozantinib can block growth of neuroendocrine prostate cancer patient-derived xenografts by disrupting tumor vasculature.PloS one · 2021Article
- c-Met expression in renal cell carcinoma with bone metastases.Journal of bone oncology · 2020Review
- Article
- A Selective FGFR inhibitor AZD4547 suppresses RANKL/M-CSF/OPG-dependent ostoclastogenesis and breast cancer growth in the metastatic bone microenvironment.Scientific reports · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cabozantinib is an inhibitor of multiple receptor tyrosine kinases, including MET and VEGFR2. In a phase II clinical trial in advanced prostate cancer (PCa), cabozantinib treatment improved bone scans in 68% of evaluable patients. Our studies aimed to determine the expression of cabozantinib targets during PCa progression and to evaluate its efficacy in hormone-sensitive and castration-resistant PCa in preclinical models while delineating its effects on tumor and bone. Using immunohistochemistry and tissue microarrays containing normal prostate, primary PCa, and soft tissue and bone metastases, our data show that levels of MET, P-MET, and VEGFR2 are increasing during PCa progression. Our data also show that the expression of cabozantinib targets are particularly pronounced in bone metastases. To evaluate cabozantinib efficacy on PCa growth in the bone environment and in soft tissues we used androgen-sensitive LuCaP 23.1 and castration-resistant C4-2B PCa tumors. In vivo, cabozantinib inhibited the growth of PCa in bone as well as growth of subcutaneous tumors. Furthermore, cabozantinib treatment attenuated the bone response to the tumor and resulted in increased normal bone volume. In summary, the expression pattern of cabozantinib targets in primary and castration-resistant metastatic PCa, and its efficacy in two different models of PCa suggest that this agent has a strong potential for the effective treatment of PCa at different stages of the disease.
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.