Tumour lysis syndrome (TLS) is a potentially fatal oncological emergency characterised by rapid cellular breakdown resulting in hyperkalaemia, hyperphosphataemia, hyperuricaemia, and hypocalcaemia, with subsequent acute kidney injury, cardiac dysrhythmias, and multi-organ dysfunction. It most commonly occurs following initiation of anti-cancer therapy in highly proliferative haematological malignancies. Spontaneous tumour lysis syndrome (STLS), occurring in the absence of a therapeutic trigger, is considerably rarer, particularly in solid tumours. We report a 55-year-old female presenting with progressive abdominal distension, pain, constipation, and oliguria progressing to anuria. Investigation demonstrated a 14 × 12 cm pelvic mass with extensive peritoneal and omental metastatic disease and large-volume ascites. During admission, prior to any anti-cancer therapy, she developed severe refractory hyperkalaemia, peaking at 8.1 mmol/L, alongside hyperphosphataemia >1.45 mmol/L (peaking at 2.44 mmol/L), hyperuricaemia of ≥476 µmol/L (peaking at 784 mmol/L), ionised hypocalcaemia ≤1.12 mmol/L (1.06 mmol/L), and rapidly progressive acute kidney injury, with creatinine rising from a baseline of 54 µmol/L to 310 µmol/L. These abnormalities fulfilled the Cairo-Bishop criteria for both laboratory TLS by achieving two or more deranged serum biochemical markers or changes >25% from baseline, as well as clinical TLS with the presentation of acute kidney injury and eventual death. Histopathological and genetic assessment ultimately identified a dedifferentiated endometrial carcinoma. Despite appropriate intravenous hydration, rasburicase, and repeated correction of electrolyte abnormalities, renal function and multi-organ dysfunction progressively deteriorated. The patient died nine days after admission, before anti-cancer therapy could be commenced. It was this absence of anti-cancer therapy and the trigger for the TLS that led us to classify this patient's presentation as STLS. STLS is exceptionally uncommon in solid malignancies but may occur in aggressive tumours with a high disease burden and rapid cellular turnover. This case is particularly notable because biochemical evidence of TLS preceded biopsy and any oncological treatment, supporting a genuinely spontaneous presentation. Furthermore, conventional risk stratification classified this patient as low risk, demonstrating the limitations of existing approaches when applied to rare, aggressive solid malignancies. STLS should be considered in patients with newly diagnosed or suspected solid malignancy who develop otherwise unexplained hyperkalaemia, hyperphosphataemia, hyperuricaemia, hypocalcaemia, or acute kidney injury, even before anti-cancer treatment. Early recognition and application of TLS diagnostic criteria are essential to facilitate prompt hydration, urate-lowering therapy, and correction of life-threatening metabolic abnormalities; however, it is key to note that, despite this, this condition remains to possess a poor prognosis. Greater awareness of STLS in aggressive solid tumours may enable earlier intervention and potentially improve outcomes for this fulminant condition.

Oral melanoma is a rare form of melanoma that typically presents as a black-brown macule or nodule with variable pigmentation and occasional depigmented areas. Oral melanoma typically affects the maxillary gingiva, palate, and retromolar trigone, and tends to be aggressive with high propensity for distant spread and poor prognosis. We report a patient with metastatic visceral melanoma who, upon presentation for dental care, was found to also have advanced gingival melanoma with bone involvement. This may support the oral cavity as the primary site and represents a missed opportunity for early diagnosis.

Anastasis is a newly identified cellular recovery process that enables cells to regain viability after progressing into execution-phase apoptosis. In cancer, this process may allow tumor cells to survive transient cytotoxic stress and subsequently acquire more aggressive phenotypes, including enhanced migration, invasion, and resistance to therapy. Although anastasis has attracted increasing attention, its biological significance and contribution to cancer progression remain incompletely understood. In this review, we summarize the defining features and biological processes of anastasis and critically evaluate current evidence linking post-apoptotic recovery to cancer-associated phenotypes, including apoptosis regulation, metastasis, angiogenesis, oxidative-stress adaptation, and epithelial-mesenchymal transition. We further discuss molecular pathways implicated in anastatic recovery and examine potential therapeutic strategies aimed at limiting post-apoptotic survival in cancer cells. Finally, we highlight major challenges in the field, including the need for more specific biomarkers, physiologically relevant in vivo models, and direct clinical validation, and outline key unresolved questions that should guide future investigation.

In contrast to the well-documented phenomena of inter-male aggression and competition in nature, the long-term consequences for females involuntarily exposed to persistent male-initiated social threat remain inadequately understood. In the present study, we demonstrate that C57BL/6J female mice co-housed with CD1 male mice for 14 days developed anxiety-like behaviors and cognitive deficits, without exhibiting depressive-like phenotypes. Concurrently, these females displayed a significant decrease in serum estrogen levels and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Furthermore, co-housing with CD1 males profoundly disrupted sleep architecture in C57BL/6J females, as evidenced by reduced wakefulness and prolonged durations of both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Mechanistically, these behavioral and physiological alterations were associated with substantial a reduction in cell density in the CA1 and CA3 subregions of the ventral hippocampus, accompanied by a marked downregulation of brain-derived neurotrophic factor (BDNF) within these same areas. Collectively, our findings provide experimental evidence for the adverse effects of chronic exposure to persistent male-initiated social threat on female recipients in a mammalian model, thereby offering a theoretical framework for understanding the enduring psychological trauma that may arise from sustained environments of psychological harassment, domestic violence, or sexual coercion-circumstances frequently encountered by women in human society.