"Uterine adenocarcinomas ($n = 30$) were classified histopathologically according to dominant growth patterns into two distinct subtypes: Papillary (Figure 1a) and Tubular/Solid (Figure 1b). The papillary subtype was identified in 53.3% of cases (16/30), characterized by delicate arborescent papillary projections lined by single or pseudostratified columnar epithelial cells with uniform nuclei. The tubular/solid subtype constituted 46.7% of cases (14/30), displaying crowded, back-to-back gland-like structures or solid sheets devoid of lumen formation."

Myometrial Invasion Data: Superficial myometrial invasion (<50% of wall thickness) was detected in 60% (18/30) of cases, whereas deep myometrial invasion ($\ge 50\%$ of wall thickness extending into the outer smooth muscle coat or serosa) was present in 40% (12/30) of cases. Mitotic activity ranged from low (<1 per 10 HPF in 20% of tumors) to high (>5 per 10 HPF in 43.3% of tumors).

"Using human FIGO staging adapted for lagomorph uterine histopathology, tumors were stratified into three tiers: Grade 1 (Figure 2a; 43.3%, 13/30), Grade 2 (Figure 2b; 36.7%, 11/30), and Grade 3 (Figure 2c; 20.0%, 6/30). Grade 1 lesions exhibited low-grade nuclear features with rare mitoses. Grade 2 cases demonstrated progressive loss of glandular architecture and moderate nuclear atypia. Grade 3 tumors were dominated by extensive solid growth ($>50\%$), widespread necrosis, marked nuclear pleomorphism, and brisk mitotic figures ($>5$ per 10 HPF)."

"Control non-neoplastic tissues comprised normal endometria from young healthy rabbits ($n = 10$; Figure 3a) and cases of cystic endometrial hyperplasia (CEH; $n = 7$; Figure 3b). Normal endometrial tissue presented uniform luminal lining with quiescent tubular glands embedded in compact stroma. In contrast, CEH demonstrated variable degrees of glandular enlargement, papillary infolding, and focal cystic dilatation. Importantly, hyperplastic glands maintained basement membrane integrity without cellular atypia or destructive myometrial invasion."

"COX-2 expression was quantified using the Immunoreactive Score ($\text{IHS} = \text{Staining Intensity} \times \text{Percentage of Positive Cells}$). Intensity was graded from 0 (negative) to 3 (strong). Percentage of positive cells was scored as 0 (0%), 1 (<10%), 2 (10–50%), 3 (51–80%), and 4 (>80%). All 30 uterine adenocarcinoma cases (100%) were positive for COX-2. Staining intensity ranged from weak (14/30, 46.7%; Figure 4a) to moderate (13/30, 43.3%; Figure 4b) and strong (3/30, 10.0%; Figure 4c). Technical negative controls (Figure 4d) confirmed antibody specificity, while active corpus luteum (Figure 4e) served as positive tissue control."

"In normal endometrial tissue (Figure 5a), COX-2 immunoreactivity was absent or confined to faint apical staining in luminal epithelial cells (mean IHS = $0.40 \pm 0.70$). In cystic endometrial hyperplasia (Figure 5b), weak-to-moderate apical cytoplasmic staining was observed in surface and hyperplastic glandular epithelial cells (mean IHS = $1.71 \pm 1.11$). Stromal cells, myometrium, and vascular endothelium were consistently negative in non-neoplastic specimens."

"Statistical analysis revealed a highly significant increase in COX-2 IHS in uterine adenocarcinomas (mean IHS = $8.27 \pm 2.86$) compared to both cystic endometrial hyperplasia (mean IHS = $1.71 \pm 1.11$; $p < 0.001$) and normal endometrium (mean IHS = $0.40 \pm 0.70$; $p < 0.0001$; Figure 6). No significant correlation was observed between COX-2 IHS and FIGO histological grade (Grade 1 mean = 8.15; Grade 2 mean = 8.45; Grade 3 mean = 8.17; $p > 0.05$), indicating that COX-2 overexpression occurs early during malignant transformation and remains consistently high across all evolutionary stages."