Twelve dogs with oral malignant melanomas (MM) were evaluated in this study, with demographic details indicating a balanced distribution of gender, age, and weight among various breeds. Tumor locations varied, with diverse surgical procedures being performed, including mandibulectomies and maxillectomies. Lymphadenectomies were conducted, revealing a 16.66% metastatic rate in regional lymph nodes. At the time of surgery, clinical staging identified stages I, II, and III, with most cases having non-infiltrated margins and a high mitotic index. Follow-up revealed local recurrences and metastases, prompting additional surgeries and affecting survival rates. This study reports varying outcomes, with some dogs completing one year without recurrence, while others experienced progressive disease, leading to six oral melanoma-related deaths. The characteristics of melanotic melanoma and amelanotic melanoma are observed in order to study differences between them, the degree of aggressiveness, the mortality rate and the possibility of future therapeutic targets. Although high pigmentation has been correlated with a better outcome, we could not find any significant correlation between survival and achromia. Oral benign melanomas might exist, and this could justify variabilities between stage and survival; however, carefulness is required due to their unpredictable behavior. The findings underscore the complexity of oral melanoma cases and highlight the need for further research on effective management strategies.

Humanin (HN) and MOTS-c are mitochondrial-derived peptides (MDPs) known for their neuroprotective and metabolic functions. Their circulating and tissue levels decline with age and in neurodegenerative diseases such as Alzheimer’s disease (AD). This study aimed to evaluate whether blood and plasma gene expression and plasma protein levels of HN and MOTS-c are associated with AD markers, their role in the conversion from mild cognitive impairment (MCI) to AD, and their overall association with the disease. A case–control study was conducted, including patients with AD and MCI, and individuals with subjective cognitive decline (SCD) as controls. Gene expression levels were quantified from total RNA isolated from blood and plasma, normalised to mitochondrial DNA copy number (mtDNA-CN). ELISA was used to measure plasma HN and MOTS-c protein concentrations. HN and MOTS-c transcript levels differed significantly among study groups, whereas plasma protein concentrations did not discriminate between AD and MCI. In silico and RNA decay assays revealed faster degradation of HN mRNA and delayed but stable recovery of MOTS-c mRNA. Overall, blood and plasma transcript levels—but not circulating protein levels—of these MDPs were significantly reduced in AD compared to SCD, suggesting their potential as early biomarkers of Alzheimer’s disease.

Background: Canine oral melanoma (COM) is an aggressive and often fatal neoplasm in dogs, with clinical and molecular similarities to human melanoma. Despite its relevance as a comparative oncology model, the molecular mechanisms underlying COM remain poorly understood. This study aimed to characterize gene expression profiles in COM to identify differentially expressed genes (DEGs), potential biomarkers, and therapeutic targets. Methods: In this pilot study, we performed RNA sequencing (RNA-seq) on tumor and healthy oral tissue samples from dogs. Two independent analytical pipelines—Bowtie2-DESeq2 and HISAT-StringTie-Ballgown—were used to ensure robustness in DEG detection. We also conducted pathway enrichment and isoform-level analyses to investigate biological processes and alternative splicing events. Results: Both approaches identified a core set of 929 common DEGs. Key oncogenic pathways, including MAPK/ERK and cell cycle regulation, were significantly affected, with notable upregulation of BRAF, NRAS, CDK4, and MITF (log2FC = 2.86, p < 0.001). The transcription factor SOX10 and the cytokine IL-33, both previously implicated in melanoma progression, were consistently overexpressed. Additionally, NF1, a known RAS pathway inhibitor, was also upregulated. Isoform analysis revealed novel transcript variants, suggesting a complex layer of post-transcriptional regulation in COM. Many DEGs remained uncharacterized, and chromosomal distribution analysis highlighted potential genomic influences. Conclusions: Our findings provide new insights into the molecular landscape of COM, reinforcing its utility as a model for human melanoma. The identification of conserved oncogenic pathways and novel transcript variants opens avenues for further functional studies and the development of targeted therapies in both veterinary and human oncology.

Primary hepatic masses in dogs represent a heterogeneous group of lesions with variable biological behavior and challenging preoperative characterization. The objective of this retrospective study was to describe the clinical presentation, diagnostic findings, surgical management, and outcome of dogs with primary hepatic masses treated surgically. Ten dogs with resectable hepatic lesions and no evidence of extrahepatic metastasis were included. Clinical records, imaging findings, histopathological diagnoses, treatment, and follow-up data were reviewed. Histopathological diagnoses included hepatocellular carcinoma (n=3), nodular hyperplasia (n=2), lobular hyperplasia (n=1), hepatocellular adenoma (n=1), undifferentiated sarcoma (n=1), osteosarcoma (n=1), and one case without definitive histological diagnosis. Tumor size ranged from 3.3 to 18 cm and was not associated with biological behavior. Preoperative cytology showed poor concordance with final histopathological diagnosis in all sampled cases. Abdominal ultrasound identified solitary lesions in all evaluated dogs, although surgery revealed previously undetected multifocal disease in two cases. Most lesions were located in the right hepatic lobes, differing from the predominance of left-sided lesions commonly reported in the literature. All dogs underwent surgical resection. Two perioperative deaths occurred secondary to postoperative renal failure. In the remaining dogs, surgery resulted in complete remission of clinical signs and prolonged survival, including dogs with malignant tumors. Four dogs remained alive and disease-free at the end of the follow-up period (>730 days). These findings highlight the limitations of preoperative diagnostic techniques for predicting the biological behavior and extent of canine hepatic masses. Surgical resection provided substantial clinical benefit and prolonged survival in most cases, supporting its consideration whenever complete excision is technically feasible.

Background/Objectives: Chemotherapy-induced peripheral neuropathy (CIPN) affects up to 85% of patients receiving neurotoxic regimens, often leading to dose reduction and impaired quality of life, yet effective preventive or therapeutic options remain scarce. Emerging evidence implicates chemotherapy-induced gut microbiota dysbiosis in CIPN pathogenesis via a gut–nerve axis. Concurrently, rectal ozone insufflation (ROI) has been shown to modulate the gut microbiota and reduce inflammation in preclinical models. This article critically examines the evidence on the role of gut dysbiosis in CIPN, evaluates the microbiota-modulating capacity of rectal ozone therapy (OT), and assesses the biological plausibility of ozone as a microbiota-targeting intervention for CIPN, while explicitly distinguishing between established evidence and hypothetical mechanisms. Evidence synthesis: Neurotoxic agents induce dysbiosis marked by reduced microbial diversity, loss of short-chain fatty acid-producing bacteria, and expansion of pro-inflammatory taxa. Preclinical models demonstrate a causal role for specific microbial communities in CIPN, with microbiota depletion or fecal transplantation modulating neuropathic phenotypes. In human cohorts, dysbiosis severity correlates with CIPN symptoms. Preclinical studies show that ROI restores microbial balance, enhances short-chain fatty acid levels, and strengthens intestinal barrier function via Nrf2/HO-1 and SIRT1 pathways. Preliminary retrospective data from small case series (n = 7 and n = 15) report sustained symptom improvement in CIPN patients receiving OT. However, no human study has directly linked ozone-induced microbiota changes to clinical outcomes, and the clinical evidence for OT in CIPN remains limited to uncontrolled observations. Conclusions: Convergent preclinical evidence supports a biological rationale for investigating ROI as a microbiota-targeting intervention in CIPN. However, this rationale remains largely hypothetical in the clinical setting. High-quality randomized controlled trials with longitudinal microbiome profiling are urgently needed to establish mechanistic causality and to determine whether the promising preclinical findings translate into clinically meaningful benefits. Until such evidence is available, the framework presented here should be regarded as hypothesis-generating rather than as a basis for clinical practice.

Background: Feline mammary carcinoma (FMC) is an aggressive neoplasm in cats and has attracted interest in comparative oncology because selected clinicopathological and molecular features overlap with human breast cancer. Methods: This integrative review synthesized literature was identified in PubMed/MEDLINE, Scopus, and Web of Science from database inception to 30 March 2026, focusing on epidemiology, pathology, biomarkers, tumor microenvironment, omics, therapy, and comparative oncology. Feline-derived evidence was distinguished from the human breast cancer literature, and findings were synthesized qualitatively because of substantial methodological and clinical heterogeneity. Results: FMC shows recurrent associations with aggressive histological features, hormone receptor-negative phenotypes, HER2-related signaling, immune checkpoint pathways, and emerging molecular and liquid-biopsy biomarkers. However, differences in molecular classification, methodology, treatment, cohort size, and clinical validation limit direct cross-species inference. Conclusions: FMC may serve as a complementary, question-specific comparative oncology system for studying selected aspects of aggressive mammary tumor biology, metastasis, tumor–host interactions, biomarkers, and therapeutic response. Its translational relevance remains hypothesis-generating and requires standardized methods and independent clinical validation.