(Figure 2-1) Primitive Gut in a Sagital Section of a 4 Weeks Human Embryo

Plate 1 (Figure 2-1) Primitive gut in a sagital section of a 4 weeks human embryo. Broken lines: limit between foregut, midgut and hindgut. Plate 2 (Figure 2-3) Development of the pancreas in human embryos of 5(a), 6(b) and 7(c) weeks. Arrows indicate the sense of primitive intestine rotation around its longitudinal axis. Broken line: limit between foregut and midgut. Plate 3 (Figure 2-4) Histologic structure of the adult pancreas: (a) ac acini, iL islets of langerhans, (b) a arteria, v vein, n nerve, (c) ild interlobular duct, Arrowheads ductal cilindric epithelia, Broken arrows litle interlobular ducts, Arrows basophilic ergastoplasm of acini. Plate 4 (Figure 3-1) Normal pancreatic tissue. Acinar cells arranged in lobules constitute the majority of the parenchyma. These cells have apical lightly eosinophilic cytoplasm due to the presence of zymogen granules and basophilia in the basal aspect of the cytoplasm. To aid in their secretory activity, the nuclei are polarized to the periphery and the cells are arranged in round units creating the acinus. In the left middle part of the field, an islet of Langerhans consisting of round collection of endocrine cells is represented. Endocrine cells have moderate amphophilic cytoplasm and nuclei with finely stippled chromatin pattern. In the right upper part of the field an intralobular duct lined by cuboidal-low columnar epithelium is seen. Plate 5 (Figure 3-2) (a) Invasive ductal adenocarcinoma, macroscopic findings. A firm, sclerotic, poorly defined mass is seen in the head of the pancreas. The rounded pale structure (arrow) adjacent to the right lower border of the specimen represents a lymph node enlarged by metastatic adenocarcinoma. (b) Invasive ductal adenocarcinoma is characterized (and defined) by infiltrating tubular units embedded in desmoplastic stroma. Plate 6 (Figure 3-3) Invasive ductal adenocarcinoma, well differentiated. Well formed glandular structures lined by cuboidal cells closely mimic the non-neoplastic ducts. Plate 7 (Figure 3-4) Invasive ductal adenocarcinoma, moderately differentiated. There is a greater degree of cytologic and nuclear atypia. Loss of polarity can be seen as well. Plate 8 (Figure 3-5) Invasive ductal adenocarcinoma showing perineural invasion. Plate 9 (Figure 3-6) Vascular invasion of infiltrating ductal adenocarcinoma. Carcinoma cells line the luminal surface of vascular walls in such an organized and polarized fashion that they form a well-structured duct-like unit virtually indistinguishable from normal ducts or PanINs. Plate 10 (Figure 3-7) Isolated solitary ducts surrounded entirely by adipocytes without any accompanying islets, acini or other ducts are indicative of invasive carcinoma. This phenomenon of renegade ducts away from the main tumor is a peculiar manifestation of the insidious spread of pancreatic adenocarcinoma. Plate 11 (Figure 3-8) Undifferentiated carcinoma with osteoclast-like giant cells. Non-neoplasic multinucleated giant cells of histiocytic origin are mixed with neoplastic mononuclear spindle shaped epitheloid cells. The mononuclear cells have hyperchromatic, occasionally bizarre nuclei. Plate 12 (Figure 3-9) Colloid carcinoma (mucinous non-cystic carcinoma) characterized by large amounts of mucin pools. Detached fragments of tumor cells can be observed in these pools. Plate 13 (Figure 3-10) (a) PanIN-1B. In PanIN-1, the normal cuboidal to low columnar ductal epithelial cells are replaced by tall columnar cells containing abundant apical mucin. The nuclei are basally located. The epithelium can be relatively flat in PanIN-1A but papilla formation is well established in the PanIN-1B stage. (b) PanIN-2 usually is papillary. Cytologically, there is nuclear crowding, pseudo-stratification, loss of polarity, and enlarged nuclei. Mitoses are rare, but when present are not atypical. (c) PanIN-3 is characterized by severe cytologic atypia that is seen in full-blown carcinoma. Loss of polarity, nuclear irregularities and prominent (macro) nucleoli (inset) and mitoses, which may occasionally be abnormal, are usually prominent. Plate 14 (Figure 3-11) Intraductal papillary mucinous neoplasm (IPMN). Tall, exuberant papillary structures lined by columnar cells with abundant mucin and cigar-shaped nuclei filling and dilating the ducts (cystic transformation). The overall picture of the process is highly similar to that of villous adenomas of the colon. Plate 15 (Figure 3-12) Mucinous cystadenoma (MCN). The cyst lining is composed of tall columnar mucinous epithelium, surrounded by a cuff of distinctive hypercellular stroma, which shows all the characteristics of ovarian stroma. Plate 16 (Figure 3-13) Serous cystadenoma. Typical honeycomb (microcystic) pattern due to innumerable cysts of various sizes. The lining of these cysts compose of low cuboidal epithelial cells with clear (glycogen-rich) cytoplasm showing distinctive uniform, round, small nuclei with homogenous, dense chromatin (inset). Plate 17 (Figure 3-14) Pancreatic endocrine neoplasm. Uniform cells are arranged in nests and nuclear features show the characteristic clumped, ‘‘salt and pepper’’ chromatin pattern. Plate 18 (Figure 3-15) Acinar cell carcinoma. The tumor cells are highly atypical but at the same time fairly monotonous and round. They display markedly chromopholic cytoplasm, mostly reflecting the enzymatic granules and cytoplasmic organelles involved in their production. Single prominent nucleoli are also among the most distinctive histologic features of this tumor type. Plate 19 (Figure 3-16) Pancreatoblastoma. The acinar component predominates in most pancreatoblastomas as seen here. The most distinctive and characteristic finding in this tumor type is the squamoid corpuscles, which are well defined nests of plump to spindle-shaped cells that form a vague fascicular or whorled pattern highly similar to the ‘‘morules’’ seen in other malignant tumors related to beta-catenin pathway alterations. Plate 20 (Figure 3-17) Solid pseudopapillary tumor. Prominent pseudopapillary growth pattern is seen most cases, and is a characteristic feature of this enigmatic tumor. Plate 21 (Figure 4-1) Overview of pancreatic organogenesis. Schematics and photographs of embryonic pancreas depict development at stages indicated, from (a) bud evagination from the endoderm, (b) initiation of stratification or branching, (c) onset of the secondary transition, (d) exocrine and endocrine differentiation, and (e) the maturing anatomy of acinar, ductal and endocrine tissues and associated vasculature just prior to birth. Left panels depict the pancreatic epithelium at each stage (mesenchyme not shown). Note the alternative models for dense branching (left) versus stratification and microlumen formation (right) of the epithelium at 10.5 (B1) and 12.5 dpc (C1). Yellow, pancreatic epithelium; orange, multipotent precursor cells (MPCs); red, differentiating acini; light blue, newly emerged endocrine cells; dark blue, maturing endocrine cells. Middle panels show whole mount views of Pdx1-expressing (blue stain) dorsal and ventral pancreatic buds. At 12.5–15.5 dpc, the pancreas is associated with underlying stomach and duodenum. Right panels show sections through Pdx1-expressing epithelium (blue stain) surrounded by pancreatic mesenchyme (pink eosin staining). a, aorta; ac, acini; d, duodenum; dp, dorsal pancreas; du, duct; ec, endocrine cord; m, mesenchyme; p, portal vein; pa, proacinus; st, stomach; te, tubular precursor epithelium; vp, ventral pancreas. Plate 22 (Figure 4-4) Cell-cell signaling during pancreatic development. Developmental signaling depends on the proper spatiotemporal communication between embryonic tissues. Multiple sequential inductions between adjacent developing tissues are mediated by secreted or cell-tethered factors. During pancreatic bud development, sequential signals are produced by (1) the primitive streak during gastrulation (prior to the stage shown), which patterns the endoderm with a gradient of FGF4; (2) the notochord, which sends permissive signals (such as Fgf2 and activin-bB) that promote the pancreas domain; (3) the aorta, which provides endothelial signals (EC factors) required for Ptf1a induction, Pdx1 maintenance and first wave insulin expression; and (4) the lateral plate mesoderm, which produces Fgf10 and retinoic acid (RA) required for bud outgrowth. Reciprocally, structures such as the gut endoderm and somites produce VEGF, which is required for patterning the dorsal aorta. Plate 23 (Figure 4-6) The branched pancreatic epithelium in the middle of the secondary transition of an embryonic mouse pancreas. A section through the dorsal pancreas at late 14.5 dpc with immunolocalization of the transcription factor Pdx1 (green) displays the pancreatic epithelium during the secondary transition. At this stage, most of the cells of the epithelial tubules containing islet and ductal precursors (yellow outlines) and pro-acini (white indicators around the periphery) have nuclear Pdx1. Plate 24 (Figure 4-7) Multipotent precursors for acinar, ductal and islet cells initiate the secondary transition at epithelial tips. Yellow, precursors in the tubules for duct and islet cells. Orange, multipotent precursor cells (MPCs) [7]. Burnt orange, proacinar cells at the ends of branched tubules that have lost multipotency and committed to acinar differentiation. Red, differentiating acini that have revised their relationship with the terminal tubule cells, which will become centroacinar cells. Brown, domains in the tubules initiate ductal cell differentiation. Green

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