This symposium took place during the European Society for Medical Oncology (ESMO) Congress 2025 in Berlin, Germany. The aim of the symposium was to discuss strategic treatment sequencing and novel second-line and beyond (2L+) approaches for patients with oestrogen-receptor-positive (ER+), human epidermal growth factor receptor 2 negative (HER2-) advanced/metastatic breast cancer (a/mBC) after first-line (1L) treatment with endocrine therapy (ET) plus inhibitors of cyclin-dependent kinases 4 and 6 (CDK4/6i). Tiffany Traina from Memorial Sloan Kettering Cancer Center, New York, USA, described evolving standards in 2L+ ER+/HER2- mBC, including standard of care (SOC); primary and secondary endocrine resistance, emphasising that most patients with mBC will eventually develop resistance to ET; and ESMO guidelines for ER+/HER2- mBC, which are directed by endocrine sensitivity status and biomarkers. Sherko Kümmel from the Interdisciplinary Breast Unit, Kliniken Essen-Mitte, Germany, presented recommendations and strategies for treating ET-eligible patients after 1L ET plus CDK4/6i, including data from the EMERALD approval study with the selective oestrogen receptor degrader (SERD) elacestrant in patients with ESR1 mutations, and results for studies of the SERDs vepdegestrant, imlunestrant, and camizestrant. Frederik Marmé from University Hospital Mannheim and Medical Faculty Mannheim of Heidelberg University, Germany, discussed making biomarker-driven treatment decisions, including identifying mutations to drive therapeutic choices in mBC, the characteristics of ESR1 mutations, and the importance of timely ESR1 mutation testing at each progression during metastatic treatment, ideally by analysing circulating tumour DNA (ctDNA) from a liquid biopsy.

Lung cancer is one of the most common malignant tumours worldwide, with non-small cell lung cancer (NSCLC) accounting for the largest number of cases among both men and women. Poor patient prognosis due to therapeutic resistance remains a current issue, underscoring the need for a more comprehensive understanding of the underlying biology of the pathogenesis and progression mechanisms of NSCLC. Integrating multi-omics approaches, such as genomics, transcriptomics, proteomics, and metabolomics, has become crucial for studying the underlying biology of complex diseases like lung cancer. Applying these methods not only enhances knowledge of the mechanisms of lung cancer but also plays a pivotal role in identifying biomarkers and therapeutic targets for implementing personalised treatment plans. This review quantitatively analyses the predictive capability of integrated multi-omics models by synthesising findings from studies utilising clinical data (including survival outcomes and treatment response) with multi-omics technologies to pinpoint essential biomarkers and pathways associated with NSCLC. The author focused on comparing the reported predictive accuracy metrics of these models and the consistency of identified key biomarkers across different studies. The author highlights the importance of integrating multi-omics analyses in the development of targeted therapies, and offers a roadmap for future clinical applications, emphasising challenges in data integration and biomarker validation, alongside opportunities for novel clinical trial designs. This review aims to provide a comprehensive quantitative assessment of the current state of integrated multi-omics in NSCLC, ultimately informing the design of more effective personalised therapeutic strategies and future research directions.

Immune checkpoint inhibitors (ICI) targeting programmed death-ligand 1 have transformed the management of advanced malignancies, yet are associated with a spectrum of immune-related pulmonary toxicities, most notably checkpoint inhibitor pneumonitis (CIP). While CIP is a well-documented immune-related adverse event, the occurrence of hydropneumothorax as a manifestation of programmed death-ligand 1 inhibitor-induced pulmonary immune-related adverse event is exceedingly rare, with very limited prior reports. The authors present a case of hydropneumothorax in a 75-year-old Hispanic male with hepatocellular carcinoma who developed respiratory symptoms 3 weeks after initiating atezolizumab and bevacizumab, following extensive prior exposure to ICIs. Hydropneumothorax occurred after initiation of atezolizumab and bevacizumab, and CIP was favoured clinically after alternative causes, including bevacizumab, prior thoracic radiation, and talc pleurodesis were evaluated. This case contributes to the growing literature by presenting one of the earliest reports of ICI-associated hydropneumothorax with histopathological characterisation, while also highlighting potential contributing factors to this complication. Clinicians should be aware of hydropneumothorax as a potential manifestation of CIP as it may require acute surgical intervention and inform future diagnostic and therapeutic strategies.

Hepatocellular carcinoma (HCC) is the sixth leading cause of cancer-related mortality worldwide. Despite the availability of therapeutic options such as surgical resection, radiofrequency ablation, molecular-targeted agents, and liver transplantation, HCC shows a poor prognosis and limited responsiveness to conventional treatments. The tumour immune microenvironment (TME) influences key processes in HCC, including selection pressure on tumour cells, immune evasion, tumour evolution, treatment resistance, and recurrence. Among immune components within the TME, T cells, dominant among tumour-infiltrating lymphocytes (TIL), exert both suppressive and promotive effects on tumour growth. Thus, T cell-mediated immune responses are fundamental to cancer surveillance and elimination. Research highlights the crucial role of TILs in HCC prognosis, pathogenesis, and immunotherapy. Subpopulations such as Foxp3+ regulatory T cells, CD8+ cytotoxic T cells, and CD3+/CD4+ helper T cells show complex and often contrasting roles. However, the TME often induces T cell exhaustion or dysfunction, facilitating tumour progression and immune evasion. Understanding immune dysregulation is vital for improving anti-tumour immunity and refining T cell function. This review examines TIL subpopulation roles in HCC, emphasising their plasticity and therapeutic relevance. It also covers emerging T cell-based immunotherapies, especially TIL-based adoptive transfer and CAR-T cell therapy, both showing promise in preclinical and early clinical trials. These novel approaches offer new hope for enhancing immune-driven tumour eradication and improving HCC outcomes.