PMC7772033_01
Pleomorphic mantle cell lymphoma involves the spleen. (a) Diffuse infiltration of the splenic red pulp by large-sized tumor cells with clumped chromatin and conspicuous nucleolus (100x). (b) Immunostain for CD20 demonstrates membranous pattern positivity (200x). (c) Immunostain for CD5 reveals membranous pattern positivity (400x). (d) Immunostain for CD23 exhibits partial membranous pattern positivity (400x). (e) Immunostain for cyclin D1 demonstrates partial nuclear positivity (400x). (f) Immunostain for SOX11 presents with partial nuclear pattern positivity (400x).
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The microscopic study of the spleen displayed a diffuse involvement of the red pulp by a large lymphoid cell population with irregular nuclear contours and conspicuous nucleoli (Figure 1(a)). Ancillary testing performed on sections from the splenic tumor cells demonstrated strong immunoreactivity for CD20 (Figure 1(b)), PAX5, CD5 (Figure 1(c)), and BCL2; partial reactivity for CD23 (Figure 1(d)), CD45, BCL1 (Figure 1(e)), and SOX11 (Figure 1(f)); and negativity for AE1/AE3, BCL6, CD10, c-MYC, MUM1, p53, and S-100.
BCL1 FISH for splenic pleomorphic mantle cell lymphoma and esophageal adenocarcinoma. (a) The splenic mantle cell lymphoma shows red and green break-apart signals in 41% of cells by LSI BCL1 dual-color FISH probes (400x). (b) The lymphoma reveals BCL1/IGH dual-fusion signals in 65% of tumor cell nuclei with CCND1 and IGH gene copy numbers at 2 to 4 copies per cell (400x). (c) Esophageal adenocarcinoma exhibits no BCL1/CCND1 gene rearrangement in all the interphase tumor cells analyzed. However, aneuploidy with the single gene copy number of BCL1/CCND1 is observed in 24% of cells scored (400x).
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BCL1 Dual Color Break Apart, Abbott Molecular, Abbott Park, IL) for BCL1/CCND1 on 11q13 (Figure 2(a)). BCL1/IGH translocation fusion signals were detected in 65% tumor nuclei using probes for the CCND1 gene at 11q13 and the immunoglobulin heavy chain gene at 14q32 (Integrated Oncology, Phoenix, AZ) (Figure 2(b)). Both the CCND1 and IGH genes showed two to four copy numbers in lymphoma cells. The FISH for the BCL1/CCND1 gene performed on the esophageal tumor showed aneuploidy in 24% of the tumor cells scored (Figure 2(c)), without gene rearrangement or break-apart signals for the CCND1 gene.
Esophageal adenocarcinoma arises from Barrett's esophagus. (a) Poorly differentiated invasive adenocarcinoma involving the submucosa of the esophagus (200x). (b) The adenocarcinoma originates from overlying Barrett's esophagus with high-grade dysplasia (200x). (c) Immunostain for AE1/AE3 demonstrates strong cytoplasmic and membrane pattern positivity (200x). (d) Esophagus, immunostain for cyclin D1 demonstrates strong nuclear pattern positivity (200x).
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The esophagus was affected by a poorly differentiated adenocarcinoma infiltrating into the submucosal layer (Figure 3(a)). The adenocarcinoma arose from Barrett's esophagus with high-grade dysplasia (Figure 3(b)). The esophageal adenocarcinoma exhibited strong staining for AE1/AE3 (Figure 3(c)), BCL1 (Figure 3(d)), and p53 and was negative for synaptophysin and CD56.