# Impact of adding carboplatin to docetaxel chemotherapy on testosterone levels and treatment outcomes in metastatic docetaxel-resistant prostate cancer

**Authors:** Hejar Atalan, Michael A. Morgan, Philipp Ivanyi, Paula Kappler, Florian H. Heidel, Christoph W. M. Reuter

PMC · DOI: 10.1038/s41598-025-04667-0 · Scientific Reports · 2025-06-20

## TL;DR

Adding carboplatin to docetaxel chemotherapy lowers testosterone levels and improves outcomes in prostate cancer patients resistant to docetaxel.

## Contribution

This study shows that combining carboplatin with docetaxel enhances treatment effectiveness in docetaxel-resistant prostate cancer.

## Key findings

- Salvage DC chemotherapy significantly reduced free and total testosterone levels in most patient groups.
- Low free testosterone was an independent predictor of better progression-free and overall survival in two patient groups.
- Adding carboplatin may improve therapeutic effects in a castration-dependent setting for resistant prostate cancer.

## Abstract

Docetaxel resistance, particularly post-androgen-receptor targeted therapy (ART), undermines its clinical utility in metastatic castration-resistant prostate cancer (mCRPC). This study explores the impact of docetaxel plus carboplatin (DC) chemotherapy on serum testosterone levels in metastatic docetaxel-resistant prostate cancer (mDRPC) patients. 123 mDRPC patients were categorized into three groups: (1) no previous ART (n = 65), (2) previous ART with serum free testosterone (FT) > detection limit (DL) at baseline (n = 31), and (3) previous ART with FT < DL at baseline (n = 27). Salvage DC chemotherapy led to significant reductions in FT and total testosterone (TT) levels in groups 1 and 2 (p < 0.05). Group 1 saw FT decrease from 0.85 pg/mL to below the DL (< 0.18 pg/mL) with 54.3% achieving complete reduction (CR); group 2 showed FT decrease from 0.28 pg/mL to below the DL with 67.7% achieving CR; group 3 had baseline FT values already below the DL with 96.3% maintaining this level. TT reductions to below the DL occurred in all groups. Low FT was an independent predictor for better PFS and for improved OS in groups 1 and 2. Our data indicate that adding carboplatin may improve the therapeutic effects of docetaxel in a castration-dependent setting.

The online version contains supplementary material available at 10.1038/s41598-025-04667-0.

## Linked entities

- **Chemicals:** docetaxel (PubChem CID 148124), carboplatin (PubChem CID 426756)
- **Diseases:** prostate cancer (MONDO:0005159)

## Full-text entities

- **Genes:** AR (androgen receptor) [NCBI Gene 367] {aka AIS, AR8, DHTR, HPCX3, HUMARA, HYSP1}
- **Diseases:** castration-resistant prostate cancer (MESH:D064129), mDRPC (MESH:D011471)
- **Chemicals:** TT (MESH:D013739), Docetaxel (MESH:D000077143), carboplatin (MESH:D016190), DC (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12181351/full.md

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Source: https://tomesphere.com/paper/PMC12181351