P1, N=50, Active, not recruiting, University of Southern California | Trial primary completion date: May 2026 --> Dec 2026

LITAF interacted with PCMT1 and promoted ubiquitination-mediated degradation of PCMT1, thereby inhibiting COX-2-mediated AA metabolism, reducing the proliferation of PTX-resistant BC cells, and enhancing the sensitivity of BC cells to PTX in vivo. LITAF regulates the ubiquitination-mediated degradation of PCMT1 to inhibit COX-2-dependent AA metabolism, thereby enhancing the sensitivity of BC cells to PTX and providing a potential therapeutic strategy to overcome PTX resistance in BC.

Here, we show that silencing STC1 enhances CRT surface exposure in Lewis lung carcinoma (LLC) cells when combined with paclitaxel (PTX), converting dying tumour cells into an in-situ vaccine that drives immunoprevention of tumour growth...Moreover, siSTC1/LNP-PTX sensitizes tumours to PD-1 blockade. Our nanosystem, which unlocks ICD potential by silencing STC1, represents a paradigm-shifting approach to cancer immunotherapy.

Its effects were comparable to COX-2 gene silencing, with a favorable preclinical safety profile supporting long-term clinical use. These findings elucidate the neuroprotective mechanism of celecoxib, propose COX-2/PGE2 as a therapeutic target for CIPN, and lay a foundation for relevant combination therapy research, highlighting celecoxib's potential in CIPN management.

In vivo studies demonstrated significant tumor inhibition, stable body weight, and prolonged survival, associated with enhanced Caspase-3-mediated apoptosis. Overall, H@PLGA/PTX provides sustained local drug release with strong anti-tumor activity and low systemic toxicity, offering a promising strategy for adjuvant osteosarcoma chemotherapy.

Complementary computational analyses included the following: principal component analysis (PCA) revealing multivariate separation of treatment groups (PC1, 78.3% variance; PC2, 16.4%); Grad-CAM visualization localizing morphological features associated with apoptosis; and exploratory Random Forest modeling demonstrating time and formulation type as primary determinants of cytotoxic potency. Three-month stability assessment showed minimal drift in physicochemical parameters (particle size, + 10.2%; encapsulation efficiency, - 6.3%), supporting formulation robustness for preclinical studies.

P2, N=82, Recruiting, National Cancer Institute (NCI) | Trial completion date: Apr 2026 --> Apr 2027 | Trial primary completion date: Apr 2026 --> Apr 2027

In addition, overexpressing MARCH3 increased the PTX sensitivity of NPC in vivo. MARCH3 could block NPC progression and strengthen the sensitivity of NPC cells to PTX, possibly by advancing the ubiquitination degradation of HK2, providing a promising therapeutic target for NPC treatment.

The patient received neoadjuvant chemotherapy with carboplatin, paclitaxel, and bevacizumab, resulting in rapid symptomatic improvement, normalization of CA-125, and complete radiologic resolution of carcinomatosis. It also highlights the prognostic significance of robust chemotherapy response, as pathologic complete remission remains uncommon in high-grade serous Müllerian carcinomas. Overall, this case underscores the importance of recognizing atypical presentations of PPSC and shows that exceptional therapeutic outcomes are achievable with appropriately selected neoadjuvant therapy.

P4, N=500, Recruiting, Erasmus Medical Center | Not yet recruiting --> Recruiting

RTS exhibited superior selectivity compared with inorganic arsenic trioxide (ATO) and paclitaxel, significantly reducing the viability of TNBC cells (MDA-MB-231, BT-549, and MDA-MB-468) while sparing non-malignant MCF-10 A cells.. Collectively, these in vitro findings establish a "lysosome-mitochondria" signaling axis in which early pH perturbation represents a potential vulnerability in TNBC. While the multicomponent nature of RTS requires further characterization, this study provides preliminary insights into targeting organelle-specific Ca2+ hubs as a complementary strategy for refractory solid tumors.

P=N/A, N=84, Not yet recruiting, Necmettin Erbakan University | Trial primary completion date: Mar 2026 --> Oct 2026