MDM2 (E3 ubiquitin protein ligase)

Emerging tools, such as radiomics and artificial intelligence-based approaches, are briefly addressed as evolving adjuncts. By integrating classical imaging principles with contemporary classification frameworks, this article aims to serve as a comprehensive and clinically relevant reference for radiologists involved in the assessment and management of fat-containing soft-tissue tumors.

P1, N=119, Completed, Boehringer Ingelheim | Active, not recruiting --> Completed

IHC and molecular analyses are crucial for an accurate diagnosis, particularly in tumors with heterologous elements that may mimic other sarcomas or germ cell tumors. Early recognition and multidisciplinary management optimize local control and surveillance planning.

P1/2, N=47, Active, not recruiting, Centre Leon Berard | Recruiting --> Active, not recruiting | Trial completion date: Jul 2026 --> Feb 2027 | Trial primary completion date: Jan 2026 --> Feb 2027

Brigimadlin is highly effective in MDM2-amplified GBM when adequate drug levels are achieved in tumor tissue. MDM2 amplification impacts both treatment efficacy and intratumoral drug accumulation.

This study presents genetic evidence supportive of a causal contribution of RACGAP1 to LUAD, highlighting it as a promising prognostic biomarker and candidate therapeutic target. By delineating a RACGAP1-driven axis that coordinates survival signaling and suppresses tumor surveillance, our findings highlight RACGAP1 as a promising therapeutic target for novel adjuvant strategies.

These findings provide a biological rationale to explore AKT1/HER2-targeted combinations with PARP inhibition in future studies for gBRCA-mutated breast cancer and provide the first evidence of PIK3CA-gBRCA mutual exclusivity in Chinese patients. The elevated HRD scores further underscore the presence of homologous recombination deficiency in the gBRCA group.

This study elucidates the critical role and molecular mechanism through which KLF11 drives radiotherapy resistance in ESCC by regulating the MDM2/E2F1 axis and enhancing HR repair, thereby providing a solid theoretical foundation and potential target for the development of KLF11-targeted radiosensitization therapies for ESCC.

APG-115 effectively inhibits proliferation, induces apoptosis, and enhances radiosensitivity in p53 wild-type colorectal cancer. These findings support APG-115 as a promising therapeutic candidate for colorectal cancers retaining functional p53.

Patients with/without MDM2 amplification receiving first-line therapy [cisplatin and gemcitabine (CisGem)] showed a median OS [95% confidence interval (CI)] of 18.4 months (12.3-19.9 months) and 17.8 months (12.3-19.9 months, P = 0.247), a median PFS (95% CI) of 5.3 months (2.7-8.9 months) and 6.0 months (5.3-6.8 months, P = 0.423), and an ORR of 21.4% and 29.6% (P = 0.762), respectively. Incidence of MDM2 amplification was similar to that described in other BTC cohorts. Comparable results in demographic/clinical characteristics, molecular profile, and survival outcomes between patients with/without MDM2 amplification was observed.

P1, N=119, Active, not recruiting, Boehringer Ingelheim | Trial completion date: May 2026 --> Feb 2026