Docetaxel is a chemotherapeutic agent widely used for breast cancer treatment; however, its efficacy is often limited by drug resistance and associated toxicity. This review examines the molecular mechanisms of docetaxel resistance in breast cancer and discusses research advances and future directions for overcoming this challenge. Key resistance mechanisms include alterations in drug targets (microtubules), increased drug efflux, suppression of apoptosis, activation of survival signalling pathways, epithelial-to-mesenchymal transition (EMT), and cancer stem cell enrichment. An evolutionary perspective distinguishes between intrinsic and acquired resistance, emphasising the need for adaptive therapeutic strategies. Recent advances in genomic profiling, non-coding RNA research, novel drug combinations, and biomarker-guided therapies have also been reviewed. Emerging approaches, such as targeting the tumour microenvironment, harnessing immunotherapy, and implementing adaptive dosing schedules, have been discussed. This review emphasises the understanding of resistance as a multifactorial phenomenon that requires multipronged interventions. Research has aimed to identify predictive biomarkers, develop targeted agents to reverse resistance, and design rational combination strategies to improve patient outcomes. Progress in deciphering and targeting docetaxel resistance mechanisms holds promise for enhancing treatment responses and extending survival in patients with breast cancer.

Vanishing bile duct syndrome (VBDS) is a rare but potentially fatal cause of intrahepatic cholestasis, usually associated with autoimmune, infectious or drug-induced etiologies. We present the first documented case of VBDS induced by Atezolizumab, an immune checkpoint inhibitor approved as adjuvant therapy in resected stage II-IIIA non-small cell lung cancer. A 63-year-old man developed cholestatic liver injury after three cycles of Atezolizumab, with progressive jaundice and elevated bilirubin despite immunosuppressive therapy. The diagnosis was confirmed by liver biopsy, which revealed intrahepatic bile duct leakage in more than 50% of the portal tracts. Despite initial stabilization, the patient’s bilirubin levels continued to rise and liver transplantation was contraindicated. He was discharged with immunosuppressive and supportive treatment, under close follow-up. This case highlights the need for greater clinical awareness of rare immunotherapy-associated immune-mediated hepatotoxicities, and underlines the importance of histological confirmation in severe or atypical presentations.

Background: Uveal melanoma is the most common primary intraocular cancer in adults; however, it remains rare. Despite its rarity, metastatic uveal melanoma poses significant treatment challenges. Tebentafusp, a T-cell receptor–bispecific molecule targeting glycoprotein 100 and CD3, has shown substantial survival benefits for HLA-A*02:01 positive patients. A notable complication associated with tebentafusp and similar immunotherapies is cytokine release syndrome (CRS), occurring in nearly 90% of tebentafusp-treated patients. Although typically mild, severe CRS (grade 3) affects around 1% of patients. The unpredictable nature of CRS complicates patient management during treatment. Methods: Monitoring cytokine levels, as key indicators of inflammation, may therefore be crucial for understanding and managing CRS. Advanced proteomic technologies enable the simultaneous measurement of multiple cytokines, providing a comprehensive view of inflammatory responses. Results: In this case, a patient with metastatic uveal melanoma developed CRS after tebentafusp treatment. A proteomic analysis tracked the cytokine changes from baseline to post-treatment, revealing significant elevations in inflammatory markers. Conclusions: These findings suggest potential strategies for more personalized CRS management in similar therapies.

Oligoprogression in MET Exon 14 skipping (METex14)–mutated non–small cell lung cancer (NSCLC) is clinically challenging, particularly when local therapies are contraindicated. We report the first documented case of a 62‐year‐old man with oligoprogressive METex14‐positive NSCLC who achieved a sustained metabolic response following the addition of docetaxel to ongoing tepotinib therapy after progression on tepotinib monotherapy. Due to prior thoracic irradiation, reirradiation and surgical interventions were deemed not feasible, prompting this systemic combination to maintain MET inhibition while targeting resistant tumor clones. This strategy resulted in a partial metabolic response at the primary lung lesion and a sustained complete metabolic response in an adrenal metastasis. The regimen was generally well tolerated; however, Grade 3 peripheral edema required dose reduction of tepotinib. This case supports the potential role of systemic therapy intensification in METex14‐driven NSCLC, highlighting the therapeutic value of continued MET inhibition beyond disease progression, particularly when local treatment and advanced molecular monitoring such as ctDNA are unavailable. Trial Registration: ClinicalTrials.gov identifier: NCT05439993