ArticleCancer gene therapy2026
Zoledronic acid enhances the antitumor efficacy of the PSMA CAR-T cells for bone tumors, but impedes the ability to control metastases of prostate cancer in mice.
Article in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
The chimeric antigen receptor (CAR)-T cell therapy has shown promise for the treatment of hematological and solid tumors. Although CAR-T cells targeting PSMA showed robust antitumor efficacy for prostate cancer in preclinical studies, the clinical benefits of PSMA CAR-T cells are unsatisfactory. To maximize the efficacy of this immunotherapy, we combined zoledronic acid (ZOL), a first-line prophylactic drug against skeletal-related events (SREs) and for bone pain management in patients with advanced prostate cancer, with PSMA CAR-T cells for the treatment of prostate cancer. In mice with intratibial inoculation of 22Rv1 prostate tumor, ZOL treatment after PSMA CAR-T cells infusion inhibited growth of the primary intratibial tumor, while it increased the extraskeletal metastasis, demonstrating that ZOL impedes the long-term immunosurveillance, albeit it enhances the short-term antitumor capability of the CAR-T cells. Mechanistically, ZOL showed no increase in the frequency of γδT cell phenotype. Finally, we found that ZOL induced hyperactivation and eventually led to exhaustion of the PSMA CAR-T cells, elucidating the impediment clues of ZOL on the T cell therapy. Our study demonstrates the necessity to balance the contribution of ZOL when combined with CAR-T cell therapy for prostate cancer.
Indexed as
Identifiers
41927852What 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.