Natural killer (NK) cells contribute to tumor immunosurveillance, yet their heterogeneity across cancer types remains incompletely understood. Transcriptomic, spatial, and functional assays reveal that non-small cell lung carcinoma (NSCLC) is enriched in NK cells that mediate clinically relevant effector functions, whereas high-grade serous ovarian carcinoma (HGSOC) contains dysfunctional NK cells that express co-inhibitory receptors including NKG2A. Analysis of HGSOC patient samples and syngeneic mouse models indicates a crosstalk between NK cells and CD8⁺ T cells critical for effective antitumor immunity. Depletion of either population leads to phenotypic impairment of the reciprocal one. Blocking NKG2A restores NK cell cytotoxicity and promotes CD8⁺ T cell responses, significantly improving the efficacy of PD-1 blockade in murine HGSOC models. Thus, NK cells and CD8⁺ T cells engage in a functional interplay of immunological relevance. Moreover, the NKG2A–HLA-E axis represents a clinically actionable immunological checkpoint in tumors with impaired NK cell functions.

Introduction and Hypothesis: Endometrial cancer therapy may affect lower urinary tract function and quality of life (QoL). We prospectively evaluated short-term urodynamic and QoL outcomes after surgical treatment with or without adjuvant radiotherapy. Methods: Women with biopsy-confirmed endometrial cancer underwent standardized urodynamic testing before surgery and 6 months after treatment completion. Parameters included detrusor pressure, bladder capacity, compliance, and post-void residual (PVR) urine volume. QoL was assessed using EORTC QLQ-C30 and QLQ-EN24 questionnaires. Pre- and post-treatment data were compared using nonparametric tests (α = 0.05). Surgery was performed either robotically or via the open abdominal approach. Results: Of the 101 participants, 55 received adjuvant radiotherapy and 46 were treated with surgery alone. No clinically significant urodynamic deterioration was observed post-surgery. Median PVR urine volume decreased from 50 to 40 mL ( p = 0.002) and detrusor pressure from 30 to 28 cmH ₂ O ( p = 0.08) following surgery; other parameters remained stable. No acute radiation cystitis occurred. QoL scores were high at baseline and follow-up, with no domain showing a ≥ 10-point change. Sexual and urinary symptom scores remained unchanged. Conclusions: Within 6 months after endometrial cancer treatment, urodynamic parameters and QoL remained stable. These results suggest short-term functional safety of contemporary surgical and radiotherapy protocols, warranting longer-term follow-up.

To determine how often lymph node assessment alters post-operative risk classification or adjuvant therapy in p53-abnormal endometrial carcinoma and to calculate the number needed to stage to obtain 1 management-changing result. This multicenter retrospective study included patients with biopsy-confirmed p53-abnormal endometrial carcinoma who underwent pre-operative expert ultrasound, molecular classification, and definitive surgery. Pre-operative risk groups were based on ultrasound-assessed invasion and molecular subtype; post-operative groups incorporated final pathology and lymph node status. The number needed to stage was defined as the number of patients staged divided by the number with management-changing results. Among 120 patients, lymph node status was evaluable in 107, with metastases identified in 19 (17.8%) cases. Concordance between pre-operative and post-operative risk groups was 84.2%. Reclassification occurred in 15.8% of patients and was driven entirely by uterine pathological findings. Lymph node findings altered guideline-based post-operative management in only 2 of 107 patients (1.9%; 95% confidence interval 0.2% to 6.6%), both through treatment de-escalation based on negative nodal status. No escalation of adjuvant therapy was triggered by nodal metastases. The number needed to stage was 53.5. In this multicenter cohort of p53-abnormal endometrial carcinoma, lymph node assessment had a limited impact on guideline-based post-operative management, with treatment decisions largely driven by molecular subtype and uterine pathological factors. Prospective, molecularly stratified studies are needed to clarify the optimal role of nodal staging in this patient population.