For stage Ⅲ and above mismatch repair-deficient (MMRd) endometrial cancer, postoperative paclitaxel plus carboplatin chemotherapy combined with ICIs and maintenance therapy are recommended. Many issues remain to be resolved, such as whether MMRd endometrial cancer caused by MLH-1 methylation or mutations in MMR-encoding genes has consistent responses to ICIs, and how to predict treatment efficacy. The reduced cost and rapid popularization of high-throughput technologies, as well as the continuous expansion and improvement of evidence from prospective cohorts, will provide high-quality evidence for further refinement of molecular characteristics and risk stratification of endometrial cancer, and guide the implementation of precision treatment for this disease.

LINC00963 downregulation could block PC cell progression and elevate their sensitivity to carboplatin through accelerating miR-495-3p level.

NFE2L2 rs35652124C > T was identified as an independent predictive genetic factor for Grade 4 neutropenia in esophageal cancer patients treated with DCF chemotherapy.

Management is predominantly based on adequate surgery and chemotherapy with carboplatin and paclitaxel, with the addition of anti-angiogenic therapy as indicated. Other molecular characteristics are important in distinct types of EOC, but the use of matched targeted therapies remains under investigation, as does the role of immunotherapy for EOC, for which trial data have been disappointing to date. Translationally enriched clinical trials will be important to further explore and validate accurate biomarkers to better guide clinical care.

The patient therefore underwent adjuvant carboplatin/paclitaxel chemotherapy followed by vaginal brachytherapy and has remained recurrence-free for five years. This case demonstrates molecular classification of an unusual histological type of EC exhibiting an extremely short-term risk of early distant metastasis and its implication on aggressive adjuvant therapeutical approach. It, furthermore, exemplifies the pronounced heterogeneity of the NSMP subgroup.

By co-encapsulating COL and the chemotherapeutic agent docetaxel (DTX) into bovine serum albumin (BSA) nanoparticles, an "enzyme-enhanced penetration" strategy combined with chemo-immunotherapy synergy was achieved...The COL-mediated penetration strategy enables low-dose DTX to effectively induce ICD in deep tumor regions, resulting in a synergistic effect between chemotherapy and immunotherapy. This work provides a new reference for collagenase-based drug delivery strategies targeting deep tumors and expands the application prospects of low-dose chemotherapy-induced ICD in nanomedicine.

P2, N=56, Not yet recruiting, Tianjin Medical University Cancer Institute and Hospital

Doxorubicin or carboplatin treatment of adipogenic differentiating MSC led to an increased percentage of mature BMA confirmed by increased gene expression of the adipocyte marker, PPARG. As FGF2 is a secreted protein we tested and confirmed that transfer of conditioned media from doxorubicin-treated BMA enhanced proliferation of tumour cells in vitro, a phenotype that was partially abrogated when FGF2 was depleted from adipogenic differentiating MSC. Our findings suggest that chemotherapy actively promotes adipogenesis, in part by alteration of FGF2 in the context of doxorubicin treatment, which directly enhances adipogenesis and in turn leads to enhanced tumour cell growth as a result.

Inhibition of cFLIP in combination with either TRAIL or docetaxel has the potential to be used as a novel therapeutic approach to provide more potent, long-lasting benefits to men with prostate cancer.

P=N/A, N=30, Recruiting, Queen Mary University of London | Trial completion date: Oct 2025 --> Oct 2028 | Trial primary completion date: Oct 2025 --> Oct 2028

P2, N=106, Completed, University of Michigan Rogel Cancer Center | Active, not recruiting --> Completed

Mice were randomized to receive vehicle, docetaxel, or KLS-3021, administered on day 9 (prostate-confined) or day 29 (visible/locally invasive) after implantation of luciferase-labeled PC-3 cells. Mechanistic analyses revealed extracellular matrix degradation, enhanced viral spread, increased immune cell infiltration, M1 macrophage polarization, and features of immunogenic cell death in KLS-3021-treated tumors. These results collectively demonstrate the translational potential of KLS-3021 as a minimally invasive or neoadjuvant therapeutic strategy for prostate cancer, especially in patients for whom early, localized intervention is medically feasible.