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.

Obstructive sleep apnea (OSA)-induced hypoxia modulates inflammatory mediators associated with atherosclerosis and cardiovascular diseases. ICAM-1, VCAM-1, TNF-α and IL-6 are involved in atherogenesis, but their expression in the aortic walls of OSA patients remains unknown. This study aimed to determine the relationship between OSA severity and inflammatory markers expression in aortic tissue from patients undergoing coronary artery bypass grafting (CABG). This study included 46 patients who underwent CABG. OSA severity was assessed using the WatchPAT™ home sleep apnea test, classifying patients into control and mild (0 < AHI < 15) and moderate-to-severe (AHI ≥ 15) OSA groups. Aortic wall samples were collected intraoperatively, and ICAM-1, VCAM-1, TNF-α and IL-6 expression was evaluated using immunohistochemistry. Statistical analysis compared protein expression across OSA severity groups. Compared with control and mild OSA, in aorta of the moderate-to-severe OSA group, significant differences for ICAM-1 (p = 0.001) and VCAM-1 (p = 0.006) expression were demonstrated. This study provides novel evidence of significantly increased ICAM-1 and VCAM-1 expression in the aortic walls of patients with moderate-to-severe OSA. No statistically significant differences were observed for TNF-α and IL-6. Our findings offer a rationale for integrating vascular inflammation markers into cardiovascular risk stratification in OSA. They also support the concept of OSA as a systemic inflammatory disorder, with tangible effects on large-vessel morphology.