The Murine Double Minute 2 (MDM2) gene encodes an E3 ubiquitin ligase that negatively regulates the tumor suppressor p53, maintaining low p53 levels through ubiquitination and proteasomal degradation. MDM2 overexpression in various malignancies leads to reduced p53 activity, contributing to tumor initiation and resistance to therapies. As such, MDM2 is a promising target for drug development. Innovative small-molecule inhibitors are being designed to disrupt the MDM2-p53 interaction, thereby restoring p53’s tumor-suppressive functions. This review focuses on clinical trials evaluating MDM2 inhibition for cancer therapy. MDM2 exerts its oncogenic effects primarily through its interaction with p53 but also has p53-independent functions involved in cell cycle progression and DNA repair. Elevated MDM2 expression is associated with poor prognosis across various cancers, including dedifferentiated liposarcoma, breast cancer, and glioblastoma. Targeting MDM2 with inhibitors has shown promising potential in clinical development, aiming to reactivate p53’s functions in tumors with wild-type TP53, improving therapeutic outcomes in cancer treatment.

The Murine Double Minute 2 (MDM2) gene encodes an E3 ubiquitin ligase that negatively regulates the tumor suppressor p53, maintaining low p53 levels through ubiquitination and proteasomal degradation. MDM2 overexpression in various malignancies leads to reduced p53 activity, contributing to tumor initiation and resistance to therapies. As such, MDM2 is a promising target for drug development. Innovative small-molecule inhibitors are being designed to disrupt the MDM2-p53 interaction, thereby restoring p53’s tumor-suppressive functions. This review focuses on clinical trials evaluating MDM2 inhibition for cancer therapy. MDM2 exerts its oncogenic effects primarily through its interaction with p53, but also has p53-independent functions involved in cell cycle progression and DNA repair. Elevated MDM2 expression is associated with poor prognosis across various cancers, including dedifferentiated liposarcoma, breast cancer, and glioblastoma. Targeting MDM2 with inhibitors has shown promising potential in clinical development, aiming to reactivate p53’s functions in tumors with wild-type TP53, improving therapeutic outcomes in cancer treatment.

Background and Clinical Significance: Patent Blue V (PBV) is widely used for sentinel lymph node mapping but may rarely cause severe hypersensitivity reactions. These reactions can present atypically, with predominant cardiovascular collapse and minimal cutaneous manifestations, potentially delaying recognition and treatment. Case Presentation: We report the case of a 52-year-old woman who developed sudden and prolonged refractory hypotension shortly after PBV injection during melanoma surgery. The reaction initially occurred in the absence of bronchospasm or early significant cutaneous manifestations. Profound cardiovascular collapse preceded the delayed appearance of erythema and piloerection, making early recognition of perioperative anaphylaxis particularly challenging. Hemodynamic instability required aggressive fluid resuscitation and prolonged vasopressor support. Subsequent diagnostic work-up, including serum tryptase measurement and allergological evaluation, confirmed PBV-induced anaphylaxis. PBV-induced anaphylaxis may present with isolated cardiovascular collapse without typical clinical features. Conclusions: Early recognition and prompt hemodynamic support are essential to optimize outcomes in the perioperative setting.