cisplatin

We present the case of a 60-year-old non-smoking woman previously treated for luminal B human epidermal growth factor receptor 2 (HER2)-positive invasive breast carcinoma with surgery, AC60 chemotherapy, trastuzumab, breast radiotherapy, and hormone therapy at the Mohammed VI Oncology Center in Casablanca, Morocco. The patient received neoadjuvant vinorelbine-cisplatin chemotherapy followed by volumetric modulated arc therapy (VMAT) thoracic radiotherapy at 66 Gy, achieving clinical and radiological stabilization. This case highlights the occurrence of a second driver-negative primary lung adenocarcinoma in a non-smoker and underscores the importance of integrated histopathological, immunohisto chemical, and targeted molecular evaluation in distinguishing primary tumors from metastases, as well as the potential role of post-therapeutic carcinogenesis.

Consistently, decreasing WDR66 expression using CRISPR showed a reduction in tumorsphere formation, lower expression of pluripotency-related genes, decreased cell migration, and increased sensitivity to cisplatin...In this media, we identified several cytokines and growth factors related to inflammation and immune system modulation. In conclusion, WDR66 emerges as a potential biomarker of poor prognosis and a possible predictor of response to immunotherapy, given its impact on cellular pluripotency, treatment resistance and modification of the tumor microenvironment in head and neck cancer.

The enhanced cytotoxicity in leukemia cells was driven by oxidative stress: the general antioxidant N-acetylcysteine (NAC) and the mitochondrial ROS scavenger MitoTEMPO substantially reversed the combination effect. DNA damage markers (γH2AX and 8-OHdG) were also increased in MOLT-4 cells and attenuated by NAC and MitoTEMPO. Overall, cisplatin/PLB triggers selective and oxidative stress-dependent in leukemia cells while sparing normal macrophages, supporting the combination as a promising antileukemic approach with limited toxicity.

P3, N=568, Not yet recruiting, Sun Yat-sen University

We identified USP18 as a novel mediator of cisplatin resistance in ovarian cancer, acting through DNA repair modulation. Targeting USP18 may offer a therapeutic strategy to improve outcomes in platinum-resistant ovarian cancer.

Adjuvant therapy comprised paclitaxel (175 mg/m²) plus cisplatin (75 mg/m²) every 3 weeks for six cycles, combined with pembrolizumab (200 mg every 3 weeks). To our knowledge, this is one of the first reported cases of pembrolizumab combined with platinum-based chemotherapy in the adjuvant setting for primary triple-negative NEBC. This case provides hypothesis-generating evidence for chemo-immunotherapy in this rare, high-grade histologic subtype.

Importantly, RMAD1-vaccinated mice exhibited therapeutic efficacy comparable to cisplatin treatment, while demonstrating a favorable safety profile. Together, these findings position RMAD1 as a next-generation CPP platform that outperforms existing peptides in enhancing antigen delivery and anti-tumor immunity, offering a promising strategy for advancing cancer vaccine development.

These findings suggest that tamoxifen enhances cisplatin-based combination therapy by promoting cell death in canine osteosarcoma at reduced drug concentrations. Combination therapies targeting estrogen-independent pathways may represent a promising strategy for improving treatment response in metastatic canine osteosarcoma and warrant further investigation.

Silencing of AMPK eliminated the neuroprotective effects of LLL, confirming its key role in this mechanism. Overall, our findings suggest that LLL therapy exhibits robust neuroprotective effects against cisplatin-induced neuronal damage through AMPK-driven autophagy, offering a promising adjunctive strategy for managing chemotherapy-induced peripheral neuropathy.

CPAE exhibits potent hepatoprotective and anti-HCC activity, especially when combined with cisplatin. This combination modulates mitochondrial and inflammatory pathways while mitigating cisplatin-induced toxicity. These finding position CPAE as a promising natural adjuvant for integrative HCC management. Further translational studies are warranted to validate these findings and explore clinical applicability.

P3, N=0, Withdrawn, ImmunityBio, Inc. | N=494 --> 0 | Not yet recruiting --> Withdrawn

Moreover, we confirmed that PAF1c deficiency increases the cytotoxicity of several DNA-damaging agents, including hydroxyurea (HU), cisplatin (CDDP), methyl methanesulfonate (MMS), and bleomycin (BLM). Unexpectedly, PAF1c depletion confers tolerance specifically to topoisomerase inhibitors, such as camptothecin (CPT), etoposide (ETOP), and doxorubicin (DOX)...Collectively, our findings demonstrate that loss of PAF1c subunits not only promotes genomic instability through R-loop accumulation but also alters cellular responses to DNA-damaging agents, conferring resistance particularly to topoisomerase inhibitors. This study underscores the critical role of PAF1c in maintaining genome stability and provides a rationale for developing new therapeutic strategies in cancer treatment.