Current Oncology Reports最新文献

Purpose of review: The gut microbiome (GM) has emerged as a pivotal modulator of melanoma pathogenesis and progression through its influence on systemic inflammation, immune surveillance, and antitumor immunity. Inter-individual variability in GM composition may underlie differences in immune checkpoint inhibitor (ICI) responsiveness and the development of immune-related adverse events (irAEs). This review aims to synthesize current knowledge on the complex interplay between the GM, host immunity, and melanoma, emphasizing its relevance to disease development, therapeutic response, and toxicity.

Recent findings: Both preclinical and clinical evidence have demonstrated that alterations in microbial diversity and composition can affect melanoma outcomes. Depletion or imbalance of specific microbial taxa has been linked to an increased risk of melanoma development or, conversely, to reduced tumor burden. In patients treated with ICIs, distinct taxonomic GM signatures have been correlated with therapeutic efficacy and the likelihood of developing irAEs. Emerging studies have also explored strategies to modulate the GM-including diet, antibiotics, probiotics, and fecal microbiota transplantation-to restore gut "eubiosis" and enhance antitumor immune responses. The intricate crosstalk between the gut microbiome, host immunity, and melanoma significantly influences disease biology and treatment outcomes. A deeper understanding of these interactions will be critical to the development of microbiome-informed, personalized approaches to melanoma management and immunotherapy optimization.

Purpose of review: To examine recent advances in understanding breast cancer brain metastases (BCBM), with emphasis on metastatic mechanisms, tumour-microenvironment interactions, receptor discordance between primary breast tumours and brain metastases, diagnostic innovations, and therapeutic strategies. The review sought to clarify how these developments inform precision management and identify priorities for future research.

Recent findings: Studies implicate JAK-STAT signalling, homologous recombination deficiency, c-MYC, PI3K/AKT/mTOR, and RET in BCBM progression. Tumour cells adapt via neuronal mimicry, metabolic reprogramming, and crosstalk with astrocytes and microglia. Receptor discordance between primary breast cancers and brain metastases occurs in up to one-third of cases and may alter systemic therapy. Emerging tools including liquid biopsy, spatial transcriptomics, and radiomics offer minimally invasive approaches for molecular profiling, spatial mapping, and imaging-based phenotyping to guide personalised management. Machine learning supports prognostication and imaging interpretation, though external validation is limited. BCBM reflect complex tumour-brain interactions. Advances in molecular understanding and diagnostics are beginning to inform the development of targeted therapies. Future work may benefit from integrating cancer neuroscience with computational modelling, standardise diagnostic platforms, and test the survival impact of receptor reassessment in prospective trials.

Purpose of review: For decades, ovarian cancer (OC) therapy has mainly relied on a regimen of tumor resection followed by treatment with cisplatin and paclitaxel. While this treatment is usually effective initially, resistance to this regimen in OC is widespread and is often the cause of death in OC patients. In the attempt to find new molecular targets for the treatment of chemoresistant OC, understanding the precise mechanisms of chemoresistance remains a paramount task. This review examines the critical roles of the lysosome in the instigation of chemoresistance in OC and explores possible clinical applications for overcoming chemoresistance.

Recent findings: Lysosomes contribute to chemoresistance through various mechanisms, including increased lysosomal biogenesis, resulting from the enhanced activity of transcription factor EB, a master regulator of the autophagy-lysosome pathway, which enhances cellular capacity for drug sequestration. Lysosomal exocytosis allows the cell to secrete chemotherapeutic agents from OC cells. Lysosomal autophagy pathways enable OC cells to selectively recycle cell components during chemotherapeutic stress. Finally, lysosomal signaling pathways disrupt various cell death mechanisms such as apoptosis, necroptosis, and ferroptosis, which allow cancer cells to evade death under chemotherapeutic stress. Targeting lysosomal biogenesis, stage-specific autophagy modulation, and lysosome-dependent metabolic vulnerabilities are promising avenues for sensitization of chemoresistant OC cells.