Endometrial cancer is the most common gynaecologic malignancy in high-income countries, with a rising incidence largely driven by reproductive factors, obesity, and prolonged exposure to unopposed oestrogens. Although most cases are sporadic, approximately 2–5% are associated with hereditary cancer syndromes, of which Lynch syndrome represents the most important contributor. Lynch syndrome results from germline mutations in DNA mismatch repair (MMR) genes and is associated with a substantially increased lifetime risk of endometrial cancer, reaching up to 71% in carriers of MutS homologue 6 (MSH6) mutations. Hereditary cancer predisposition typically follows an autosomal dominant inheritance pattern and may be suspected based on clinical warning signs such as early disease onset, multiple primary malignancies, a strong family history, or the presence of microsatellite instability in tumour tissue. In addition to Lynch syndrome, rarer genetic conditions—including Cowden syndrome (PTEN), Li–Fraumeni syndrome (TP53), polymerase proofreading–associated polyposis (POLE/POLD1), and hereditary breast and ovarian cancer syndromes (BRCA1/2)—also contribute to hereditary endometrial cancer risk. Recognition of these genetic backgrounds is essential for accurate diagnosis, personalised surveillance, and the implementation of targeted preventive and therapeutic strategies. Despite major advances in molecular diagnostics, hereditary endometrial cancer remains frequently underdiagnosed, leading to missed opportunities for cancer prevention among affected individuals and their families. This comprehensive review summarises current evidence on hereditary predispositions to endometrial cancer, with a particular emphasis on Lynch syndrome, and discusses underlying genetic mechanisms, inheritance patterns, diagnostic strategies, and clinical implications for screening, genetic counselling, and treatment optimisation.

Breast cancer remains the most commonly diagnosed malignancy among women worldwide and continues to pose significant therapeutic challenges, particularly in advanced and refractory disease. Although traditionally considered less immunogenic compared with other solid tumours, growing evidence demonstrates that subsets of breast cancer, particularly triple-negative and HER2-positive subtypes, exhibit immune-responsive features. This recognition has spurred the development and clinical evaluation of immunotherapeutic strategies, with immune checkpoint inhibitors (ICIs) emerging as the most prominent approach. This new class of drugs targeting the programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) axis has demonstrated meaningful clinical activity in select patient populations, leading to regulatory approvals in combination with chemotherapy for advanced triple-negative breast cancer. Despite these advances, response rates remain modest, and the benefits are largely restricted to patients with PD-L1-positive tumours. Ongoing studies are evaluating predictive biomarkers, optimal treatment combinations, and mechanisms of resistance to expand the efficacy of ICIs across broader breast cancer subtypes. Furthermore, novel checkpoint targets such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), lymphocyte-activation gene 3 (LAG-3), and T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains (TIGIT) are under investigation, with the potential to enhance or complement PD-1/PD-L1 blockade. This review summarises the current state of knowledge on breast cancer immunotherapy with an emphasis on ICIs, highlighting key clinical trial findings, as well as emerging biomarkers of response, and strategies to overcome therapeutic resistance, if cancer cells eventually develop resistance. By integrating preclinical insights with clinical progress, we aim to provide a comprehensive overview of the evolving role of checkpoint blockade in breast cancer and outline future directions to optimise patient outcomes.

Cancer precision medicine is moving beyond static, single-analyte profiling toward a dynamic view of tumour biology and treatment response. A multiomics approach, integrating genomic, transcriptomic, proteomic, metabolomic, and epigenomic information, offers a more comprehensive framework for understanding tumour heterogeneity and therapeutic vulnerability. This review examines the emerging landscape of clinically available, translational, and experimental approaches, spanning commercially available platforms such as CureResponse and Exacta, single-cell and spatial technologies, AI-assisted plasma multiomics, and functional platforms including BH3 profiling and patient-derived organoid drug screening. We also discuss longitudinal liquid biopsy approaches for minimal residual disease assessment and recurrence monitoring. Together, these technologies may extend conventional biopsy by enabling increasingly multidimensional, spatially resolved, and longitudinal assessment of cancer. However, their clinical implementation remains limited by challenges in analytical standardisation, data integration, biological interpretation, validation, and demonstrated clinical utility. The convergence of multiomics, single-cell and spatial profiling, artificial intelligence, and functional testing is therefore reshaping precision oncology, from describing what a tumour is to predicting how it may behave and respond to treatment.