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Figure 3.1.1 Menstrual endometrium. Markedly disrupted endometrium with loss of normal architecture and extensive stromal hemorrhage. |
Figure 3.1.3 Menstrual endometrium. Clusters of predecidualized stromal cells with inflammatory cells including numerous neutrophils. |
Figure 3.1.4 Menstrual endometrium. Diffuse stromal breakdown with fragmented late secretory glands. |
Figure 3.1.5 Interval endometrium with early stromal breakdown. Inset, higher magnification, some glands with subnuclear vacuoles indicating developing secretory changes. |
Figure 3.1.7 Disordered proliferative endometrium with early stromal collapse. Condensed subsurface stroma and surface epithelial metaplastic changes (fragment, upper right). |
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Figure 3.2.1 Artifactual glandular crowding. Proliferative endometrium with small tubular glands. Gland-to-stroma ratio appears increased due to stromal disruption. |
Figure 3.2.2 Artifactual glandular crowding. Focus of “molded” glands beneath the endometrial surface (center) due to stromal disruption, note extravasated blood. |
Figure 3.2.3 Artifactual glandular crowding. Proliferative endometrium. Stromal disruption creates a few foci with increased gland-to-stroma ratio. Glands are small and retain tubular shapes. |
Figure 3.2.5 Artifactual glandular crowding. “Telescoping” and crush, common artifacts seen in endometrial biopsies with tissue distortion. |
Figure 3.2.6 Complex endometrial hyperplasia. Increased gland-to-stroma ratio. Endometrial glands of different shapes and sizes. |
Figure 3.2.7 Simple hyperplasia. Despite some stromal disruption, most of the stroma is intact. Glands are crowded and irregularly shaped; some are cystically dilated. |
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Figure 3.3.1 Focal complex atypical hyperplasia (top) in a background of complex hyperplasia without atypia. Atypical glands appear pale compared to darker more basophilic glands without atypia. |
Figure 3.3.2 Focal complex atypical hyperplasia (top) in a background of complex hyperplasia without atypia. Same case as in Figure 3.3.1, higher magnification. Atypical glands (top) with nuclear enlargement, rounding, stratification, vesicular chromatin, and nucleoli. Compare with more elongated basophilic nuclei, aligned perpendicular to the basement membrane in glands without atypia (bottom). |
Figure 3.3.3 Complex atypical hyperplasia. Back-to-back glands with enlarged round nuclei with stratification and occasional nucleoli. |
Figure 3.3.5 Complex hyperplasia with tubal metaplastic changes. Evaluation of atypia is difficult in this setting. No definite atypia identified. |
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Figure 3.4.1 Complex hyperplasia with secretory changes. Haphazardly arranged irregularly shaped glands of varying sizes. |
Figure 3.4.2 Complex hyperplasia with extensive secretory changes. Markedly crowded endometrial glands with irregular shapes. |
Figure 3.4.3 Endometrioid carcinoma with extensive secretory changes. Confluent endometrial glands. Range of early (sub- and supranuclear vacuoles) to midsecretory changes. |
Figure 3.4.4 Complex atypical hyperplasia with extensive secretory changes. Same case as in Figure 3.4.2, higher magnification. Nuclei with vesicular chromatin and some stratification. Occasional nucleoli are seen. |
Figure 3.4.5 Secretory endometrium. Crowded endometrial glands without significant variation in size and shape. Ki 67 proliferative activity is essentially zero (inset). |
Figure 3.4.6 Early secretory endometrium. Irregular crowded endometrial glands with long axis parallel to each other. Note uniform subnuclear vacuoles reflecting early secretory phase. |
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Figure 3.5.1 Inactive decidualized endometrium, consistent with exogenous progestin therapy effect with focal residual glandular proliferation. |
Figure 3.5.2 Same case as in Figure 3.5.1, different area. Residual endometrial hyperplasia. Complex back-to-back glands of different sizes and shapes. |
Figure 3.5.3 Endometrial hyperplasia with progestin treatment effect. Irregular, merging glands with luminal secretions. |
Figure 3.5.6 Secretory endometrium. Crowded endometrial glands without significant variation in size and shape. A few small inactive glands are present for comparison (upper right). |
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Figure 3.6.1 Complex atypical hyperplasia. Focus of nearly back-to-back glands with some shape irregularity, surrounded by nearly normal endometrial stroma. |
Figure 3.6.5 Endometrioid carcinoma, FIGO grade 1. Altered, fibroblastic stroma with inflammation; small glands with some confluence. |
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Figure 3.7.1 Endometrioid carcinoma with extensive metaplastic changes. Confluent epithelial proliferation with some cribriform formations. Associated inflammation is commonly seen. |
Figure 3.7.3 Endometrioid carcinoma with metaplastic changes. Long papillary structures with well-developed fibrovascular cores. |
Figure 3.7.4 Endometrioid carcinoma with metaplastic changes. Same case as in Figure 3.7.3, higher magnification. Papillae are lined by epithelium with abundant eosinophilic and vacuolated cytoplasm. The nuclei are small and bland. |
Figure 3.7.5 Endometrioid carcinoma with metaplastic changes. Prominent papillary architecture with mucinous differentiation. Detached cell clusters. Mildly atypical vesicular nuclei. |
Figure 3.7.8 Fragmented endometrial tissue with prominent epithelial metaplastic changes. Same case as in Figure 3.7.7, higher magnification. Surface epithelium uniformly thickened and eosinophilic. |
Figure 3.7.9 Endometrial stromal breakdown and associated surface epithelial metaplastic changes. The nuclei can appear stratified. Note cilia on the surface. |
Figure 3.7.10 Fragmented endometrial tissue with prominent epithelial metaplastic changes. Same case as in Figure 3.7.7, higher magnification. Detached tangentially oriented fragment of eosinophilic epithelium may mimic papillary structure. Note lack of fibrovascular core. The nuclei are relatively uniform and mildly atypical. |
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Figure 3.8.1 Endometrioid carcinoma, FIGO grade 1 with squamous differentiation. Squamous areas (center) appear pale compared to more basophilic glandular areas at the periphery. |
Figure 3.8.5 Endometrioid carcinoma, FIGO grade 2. Solid and glandular areas have similar tinctorial properties at low power. |
Figure 3.8.7 Endometrioid carcinoma, FIGO grade 2. Same case as in Figure 3.8.5, higher magnification. Tumor cell nuclei are similar in solid and gland-forming areas. |
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Figure 3.9.1 Endometrioid carcinoma, FIGO grade 1 with papillary/villoglandular architecture. Papillary structures have smooth outlines. |
Figure 3.9.2 Endometrioid carcinoma, FIGO grade 1 with papillary architecture. Papillary structures with slightly irregular contours. The luminal borders are relatively smooth. |
Figure 3.9.3 Endometrioid carcinoma, FIGO grade 1 with papillary architecture and extensive surface metaplastic-like differentiation (squamous and eosinophilic). |
Figure 3.9.4 Endometrioid carcinoma, FIGO grade 1 with papillary/villoglandular architecture. Same case as in Figure 3.9.1, higher magnification. Papillae are lined by columnar cells with basally placed elongated nuclei arranged perpendicular to the basement membrane. Cytologic atypia is mild. |
Figure 3.9.5 Serous carcinoma. Markedly irregular luminal borders with detached cell clusters. Note debris in the background. |
Figure 3.9.6 Serous carcinoma. Irregular, scalloped luminal borders; occasional detached cell clusters. |
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Figure 3.10.1 Endometrioid carcinoma with small nonvillous papillae. Endometrial curettage, glandular proliferation with busy papillary architecture. |
Figure 3.10.2 Endometrioid carcinoma with small nonvillous papillae. Same case as in Figure 3.10.1, higher magnification, tightly packed intraglandular epithelial infoldings. |
Figure 3.10.3 Endometrioid carcinoma with small nonvillous papillae. Associated endometrial hyperplasia displays dilated glands with intraglandular papillary tufts and detached cell clusters. |
Figure 3.10.4 Endometrioid carcinoma with small nonvillous papillae. Same case as in Figure 3.10.2, higher magnification, intraglandular papillary infoldings composed of cells with abundant eosinophilic cytoplasm and round bland nuclei. Cells have metaplastic-like appearance. |
Figure 3.10.5 Endometrioid carcinoma with small nonvillous papillae. Weak and focal expression of p53 (left) and focally strong, but patchy expression of p16 (right). |
Figure 3.10.6 Serous carcinoma. Prominent intraglandular papillary infoldings; round and elongated detached intraluminal cell clusters. |
Figure 3.10.7 Serous carcinoma. Higher magnification, markedly atypical cells with vesicular pleomorphic nuclei with nucleoli. Numerous mitoses. |
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