Mikel Portu

Systemic treatment of advanced renal cell carcinoma (RCC) after kidney transplantation requires balancing cancer control against allograft injury and immunosuppression. We searched PubMed, Ovid Embase, Scopus, Web of Science, and ClinicalTrials.gov in April 2026, with reruns on 13 August and 19 October 2026. We separated RCC-specific transplant reports from mixed-cancer transplant and non-transplant studies. Direct evidence comprised mainly case reports and retro-spective cohorts with incomplete outcomes and possible overlap. No prospective kidney-transplant-specific RCC study was identified. Vascular endothelial growth factor receptor–targeted tyrosine kinase inhibitors achieved tumor control in selected reports, but renal toxicity and interactions limited safety conclusions. Indications for mechanistic target of rapamycin in-hibitors (RCC treatment or immunosuppression) were often unclear. Concurrent therapies com-plicated response attribution. Immune checkpoint inhibitor outcomes ranged from tumor control with preserved graft function to rejection, irreversible graft loss, dialysis, graft intolerance, or nephrectomy. An unvalidated multidisciplinary framework integrates tumor site and lineage, histology, performance status, immunosuppression, and patient priorities. It distinguishes func-tioning or failing grafts, irreversibly failed retained grafts, and absence of allografts, states that change treatment trade-offs and outcome interpretation. Comparative evidence establishes nei-ther a preferred RCC sequence nor a graft-protective immunosuppressive regimen. Prospective studies should prioritize paired, state-specific cancer and transplant outcomes.

Pembrolizumab is standard adjuvant therapy for high-risk clear cell renal cell carcinoma, but serositis is an uncommon immune-related adverse event that may mimic recurrence or infection. We report a 55-year-old man who achieved no evidence of disease after nephrectomy and metastasectomy and developed anasarca, large bilateral pleural effusions, mild ascites, peripheral eosinophilia, and a small pericardial effusion after six cycles of adjuvant pembrolizumab. Pleural fluid was exudative and contained 20% eosinophils. Cytology showed inflammatory cells without evidence of malignancy; bacterial, mycobacterial, and fungal studies were negative; and mildly elevated adenosine deaminase did not support tuberculosis. Cardiac function and natriuretic peptides were preserved. Pembrolizumab was discontinued, thoracentesis and corticosteroids were administered, and symptoms, eosinophilia, renal function, and albumin improved rapidly. Follow-up through March 2026 showed no oncologic progression, although some residual pleural and abdominal fluid persisted alongside imaging findings suggestive of portal-hypertension physiology, which may have contributed to residual fluid but did not explain the eosinophilic pleural syndrome. In a targeted literature review, effusion eosinophil data were infrequently reported. This case highlights a likely underrecognized eosinophilic pleural-fluid phenotype within pembrolizumab-associated polyserositis and supports routine differential cell counts in drained serosal fluid when immune-related serositis is suspected.

Renal cell carcinomas (RCCs) driven by TFE3 rearrangement or TFEB alteration (MiT-RCC) account for up to 40% of pediatric RCCs but are rare in adults. MiT-RCC includes fusion-driven tumors with TFE3 or TFEB rearrangements (translocation RCC, tRCC) and TFEB-amplified RCC. Morphologic heterogeneity and historical exclusion from trials have limited evidence-based management. We reviewed the literature through January 2026 to summarize molecular biology, pathology, clinical behavior, and systemic therapy. MiT-RCC comprises biologically distinct entities: TFEB-rearranged tumors are often indolent in younger patients, whereas TFEB-amplified RCC, frequently co-amplifying VEGFA, behaves aggressively in older adults. In TFE3-rearranged RCC, fusion partner influences prognosis. Paradoxically, ASPSCR1::TFE3 fusions have the poorest natural history, yet fusion-annotated cohorts suggest these tumors may derive particular benefit from immune checkpoint inhibitor (ICI) plus VEGF receptor tyrosine kinase inhibitor (VEGFR-TKI) combinations. Diagnostic advances including GPNMB immunohistochemistry, TRIM63 RNA in situ hybridization, and sequencing-based fusion panels improve detection of cryptic alterations. First-line ICI + VEGFR-TKI combinations are increasingly favored for metastatic tRCC in eligible patients, while optimal management of TFEB-amplified RCC remains uncertain.

Renal cell carcinomas (RCCs) driven by TFE3 rearrangement or TFEB alteration (MiT-RCC) account for up to 40% of pediatric RCC but are rare in adults. MiT-RCC includes fusion-driven tumors with TFE3 or TFEB rearrangements (translocation RCC, tRCC) and TFEB-amplified RCC. Morphologic heterogeneity and historical exclusion from trials have limited evidence-based management. We reviewed literature through January 2026 to summarize molecular biology, pathology, clinical behavior, and systemic therapy. MiT-RCC comprises biologically distinct entities: TFEB-rearranged tumors are often indolent in younger patients, whereas TFEB-amplified RCC, frequently co-amplifying VEGFA, behaves aggressively in older adults. In TFE3-rearranged RCC, fusion partner influences prognosis. Paradoxically, ASPSCR1–TFE3 fusions have the poorest natural history, yet fusion-annotated cohorts suggest these tumors may derive particular benefit from immune checkpoint inhibitor (ICI) plus VEGF receptor tyrosine kinase inhibitor (VEGFR-TKI) combinations. Diagnostic advances including GPNMB immunohistochemistry, TRIM63 RNA in situ hybridization, and sequencing-based fusion panels improve detection of cryptic alterations. First-line ICI + VEGFR-TKI combinations are increasingly favored for metastatic tRCC in eligible patients, while optimal management of TFEB-amplified RCC remains uncertain.

Revista oficial de la Sociedad Española de Nutrición Parenteral y de la Sociedad Española de Nutrición. Está dedicada al estudio y divulgación de temas relacionados con la nutrición.

Real-World evidence on mesenchymal-epithelial transition exon 14 skipping mutations (METex14) in lung cancer remains limited. With an incidence of 3-4% across histological subtypes, METex14 is now an actionable target for MET inhibitors (METi) in advanced lung cancer, demonstrating response rates between 30-70%. Yet, its role in early stages and sensitivity to immune checkpoint inhibitors (ICIs) is still under exploration. We conducted a retrospective analysis of the clinical data of lung cancer patients presenting with METex14 across all stages. These patients were treated at two Swedish University Hospitals: Karolinska and Skåne, between the years 2014 and 2022. We identified a total of 63 patients, of which 50 met the inclusion criteria. The median overall survival (OS) with corresponding 95% confidence intervals (95% CI) according to the stage was not reached (NR) for stage I, NR for stage II, 15 months (95% CI, 5.4-24.6) for stage III, and 17 months (95% CI, 9.2-NR) for stage IV. The median OS for stage IV patients who received a METi was 17 months (95% CI, 9.5-NR) vs. 10 months (95% CI, 6.2-NR) in patients without METi (p = 0.92; Hazard Ratio [HR] = 1.07). The median OS for stage IV patients who received ICIs was 18 months (95% CI, 16.5-NR) vs. 6 months (95% CI, 2.5-NR) in patients without ICIs (p = 0.15; HR = 0.47). The median OS for stage IV patients who received chemotherapy was 17 months (95% CI, 9.7-NR) vs. 10 months (95% CI, 4.5-NR) in patients without (p = 0.97; HR = 0.98). Our data suggest limited survival benefits from METi, ICIs, and chemotherapy for METex14 lung cancer patients. While not statistically significant, these findings underscore the need for larger trials for validation. Identifying effective treatments for this challenging lung cancer subtype remains a priority.