P=N/A, N=200, Recruiting, British Columbia Cancer Agency | Not yet recruiting --> Recruiting

P2, N=30, Recruiting, Northern Jiangsu People's Hospital

These findings identify ULK1-dependent phosphorylation as a novel regulatory mechanism governing Bax stability in CC. The study provides preclinical rationale for targeting the ULK1-Bax interface to overcome oxaliplatin resistance, while highlighting the need for further investigation into optimal therapeutic strategies.

In this study, we explored cytokines and macrophages that contribute to two chronic models of CIPN comparing paclitaxel (PTX)- and oxaliplatin (OHP)-induced CIPN in rats. On the contrary, OHP induced IL-6 and CCL2 expression in DRG. Since our results suggest that CXCL1 or IL-6 could be considered as critical lynchpins between inflammation pain and CIPN, targeting early inflammatory events could be a promising therapeutic approach.

In addition, Bev/oxaliplatin-treated FPR-L cases achieved better outcomes than those receiving the Bev/irinotecan regimen, particularly in the subgroup undergoing palliative resection. Cancer-derived inflammation appears to play a crucial role in mediating both intrinsic and acquired resistance to Bev. The FPR emerges as a robust, independent biomarker for predicting response to Bev, monitoring disease progression, and informing personalized therapeutic decision-making in patients with mCRC.

Resistance to chemotherapy, particularly to first-line regimens such as FOLFOX (5-fluorouracil, leucovorin, and oxaliplatin), remains a critical barrier to successful treatment. Elevated baseline ctDNA levels and persistent TP53 mutations are associated with chemoresistance in colorectal cancer. Early reduction in ctDNA during therapy may serve as a robust predictor of response, supporting its integration into personalized treatment strategies.

Additionally, it enhanced CRC cell sensitivity to first-line chemotherapies such as 5-fluorouracil (5-FU), oxaliplatin (OXA), and irinotecan (CPT-11). Moreover, in vivo studies confirmed the inhibitory role of GIPC1 in CRC growth and found that GIPC1-loaded lipid nanoparticles (GIPC1-LNPs) combined with 5-FU treatment had a more significant antitumor effect. In conclusion, this study reveals the GIPC1/TRIM21/TTC7B/mTOR/NF-κB tumor-suppressive axis in CRC and highlights the potential of GIPC1 for early diagnosis and overcoming chemoresistance in CRC patients.

Lastly, the stability and safety profiles are superior to that of oxaliplatin. OPA is a unique chemoimmunotherapeutic agent with a distinct mechanism of action and prominent efficacy on orthotopic colorectal cancer in mouse models.

Patients received 5-fluorouracil (5-FU) -based chemotherapy (with irinotecan or oxaliplatin), radiotherapy, or combined chemoradiotherapy. t1 values were higher in patients who relapsed (p < 0.001), whereas the within-patient change (Δ = t1 - t0) was not associated with outcome (p = 0.148); these post-treatment findings are exploratory. Evaluating DNA damage in PBLs, therefore, offers a valuable non-invasive biomarker for early detection, treatment monitoring, and short-term risk stratification in CRC, warranting validation in larger, stage-balanced cohorts.

P2, N=40, Active, not recruiting, University of Colorado, Denver | Trial primary completion date: Apr 2026 --> Jan 2026

P2, N=80, Active, not recruiting, University Hospital, Akershus | Recruiting --> Active, not recruiting | Trial primary completion date: Sep 2025 --> Jan 2028

These findings reveal that HF exerts anti-leukemic effects by modulating the p-eIF2α-S100A8/A9-Ca2⁺ signaling axis in AML cells. HF represents a promising therapeutic candidate for AML, particularly for patients with IDA-resistant disease.