Liver Neoplastic برای بزرگنمایی عکسها کلیک را روی ان نگه دارید Figure 20.1 A, Nodular regenerative hyperplasia features diffuse nodular transformation without fibrous septa. B, Reticulin stain highlights the nodularity, with intervening areas of atrophic parenchyma Figure 20.2 A, Focal nodular hyperplasia with typical stellate central scar in the center of the nodular lesion. B, This example is clearly nodular on cut surface but has a less prominent fibrous scar. (B, Courtesy of Dr. George F. Gray Jr.) Figure 20.3 A, Central portion of focal nodular hyperplasia showing the interface between the fibrous scar and the nodules. Vessels within the scar are often prominent (B), and may be thick-walled. C, Patchy ductular reaction is common, particularly at the interface between fibrous septa and liver parenchyma Figure 20.4 Map-like pattern of immunoreactivity with glutamine syn- thetase in focal nodular hyperplasia. (Courtesy of Dr. Sanjay Kakar.) Figure 20.5 A, Well-demarcated hepatocellular adenoma but without a well-defined capsule. It is paler than the surrounding liver. B, This case has a large central area of recent rupture and hemorrhage. (Courtesy of Dr. George F. Gray Jr.) Figure 20.6 A, Diffuse steatosis characterizes adenomas with HNF1α mutations. Note the transition between adenoma and nonneoplastic liver (arrows). B, Adenomas with CTNNB1 mutations show nuclear immunoreactivity (arrows) with B-catenin and lack fat and inflammatory features as is this case (C). D and E, Inflammatory (telangiectatic) adenomas feature telangiectatic sinusoidal spaces and marked inflam- mation. (B, Courtesy of Dr. Sanjay Kakar.) Figure 20.7 A, Regenerative nodule within a cirrhotic liver. B, The reticulin framework is intact, and there is a portal tract within the nodule (arrow) Figure 20.8 High-grade dysplastic nodule showing focal thickening of cell paltes, bile, and focal acinar architecture. Reticulin stain was intact Figure 20.9 Large cell change within a cirrhotic liver, featuring nuclear and cytoplasmic enlargement, nuclear pleomorphism and hyperchromasia, and multinucleated hepatocytes Figure 20.10 Small cell change, indicated by increased nuclear density, is seen in the right half of the picture; cirrhotic liver with hepatocytes of normal size is seen on the left Figure 20.11 A, Poorly encapsulated hepatocellular carcinoma consisting of two dominant nodules with multiple smaller satellite nodules, arising in a background of cirrhosis. B, Well-circumscribed, solitary mass with foci of hemorrhage and necrosis. C, Hepatocellular carcinoma with central necrosis and bile staining, arising in a patient with hereditary hemochro- matosis. A satellite nodule is present some distance from the main tumor mass (arrow). (A and C, Courtesy of Dr. George F. Gray Jr.) Figure 20.12 Typical growth patterns in hepatocellular carcinoma include pseudoglandular (A), trabecular (B), and solid (C). Note the diffuse small cell change in (C), as compared with the cirrhotic liver on the right Figure 20.13 A, Very well-differentiated HCC with numerous unpaired vessels (arrows). Note the lack of portal tracts within the tumor. B, Loss of the normal reticulin framework helps to make the diagnosis; compare with the cirrhotic liver with intact reticulin framework on the right. C, Poorly differentiated hepatocellular carcinoma that is difficult to recognize as such without stains Figure 20.14 The tumor cells of hepatocellular carcinoma may contain hyaline globules (A, arrows) or bile (B) Figure 20.15 Steatotic hepatocellular carcinoma with hepatocyte bal- looning, Mallory hyaline, and abundant fat Figure 20.16 Focal parenchymal invasion (arrows) of an adjacent regenerative nodule by an early well-differentiated hepatocellular carcinoma Figure 20.17 A, Diffuse cytoplasmic granular positivity with Hep Par-1 in hepatocellular carcinoma. This particular case had clear cell features, and the Hep Par-1 helped to confirm the diagnosis. B, Polyclonal CEA (pCEA) canalicular staining in a hepatocellular carcinoma Figure 20.18 A, A focus of clear cell hepatocellular carcinoma (HCC) adjacent to conventional-type HCC. B, Another case at higher power shows how closely clear cell HCC can mimic metastatic clear cell renal cell carcinoma Figure 20.19 Abundant dense fibrous stroma characterizes the scirrhous variant of hepatocellular carcinoma Figure 20.20 Large numbers of tumor-infiltrating lymphocytes are present in lymphoepithelioma-like hepatocellular carcin Figure 20.21 Sarcomatoid hepatocellular carcinoma comprised of sheets of neoplastic mesenchymal-type spindled cells and no features reminiscent of hepatocytes Figure 20.22 A, Grossly, fibrolamellar carcinoma is large, well circum- scribed, multinodular, and yellow. The adjacent nonneoplastic liver is noncirrhotic. B, Fibrolamellar HCC features nests of eosinophilic tumor cells surrounded by dense lamellar fibrosis. C, The tumor cells have abundant cytoplasm and prominent nucleoli Figure 20.23 A, This combined (mixed) hepatocellular carcinoma (HCC)/cholangiocarcinoma has areas with a phenotype intermediate between HCC and cholangiocarcinoma. B, This "collision tumor" had separate areas of cholangiocarcinoma and HCC within the same liver Figure 20.24 A, This Diff-Quik smear of an FNA of a hepatocellular carcinoma (HCC) shows a cellular lesion with golden-brown bile and nuclear pseudoinclusions (arrows). B, Another example shows thickened trabeculae of neoplastic hepatocytes with endothelial wrapping and capillaries traversing the cellular fragments. C, A cell block shows endothelial wrapping of neoplastic cell clusters, as well as nuclear pseudoinclusions. D, Reticulin stain can be useful even on small cell block specimens. (A, Courtesy of Dr. Asangi Kumarapeli; B, Courtesy of Dr. Susi Jeffus) Figure 20.25 A, Grossly evident (macroscopic) portal vein involvement in a hepatocellular carcinoma (HCC) with a diffuse pattern of growth (arrow). B, Microscopic involvement of a small vein Figure 20.26 Solitary Hepatoblastoma From a Young Child. A, The tumor has a variegated appearance with hemorrhage and necrosis. B, Pure fetal type of hepatoblastoma with abundant extra- medullary hematopoiesis. C, Embryonal elements with focal rosette formation (arrows). A focus of osteoid is in the upper right hand corner. D, Mixed type hepatoblastoma featuring fetal and embryonal elements, as well as mesenchymal elements in the form of osteoid. E, So-called macrotrabecular variant of hepatoblastoma. (A, Courtesy of Dr. George F. Gray Jr.) Figure 20.27 Simple biliary cyst with fibrous wall and overlying benign biliary epithelial lining Figure 20.28 Biliary microhamartoma consisting of fibrous stroma with ectatic, angular biliary channels lined by flattened cuboidal epithelium Figure 20.29 Peribillary gland hamartoma (bile duct adenoma) consisting of small tubular structures with little or no lumen embedded in dense fibrous stroma Figure 20.30 A, Biliary cystadenoma from a female patient, featuring multilocular cysts lined by a single layer of biliary-type epithelium with underlying cellular ovarian-type stroma. B, Cystadenocarcinoma consisting of multilocular cysts lined by markedly atypical neoplastic epithelium. There is necrotic debris within the cyst lumens. Note the absence of ovarian-type stroma Figure 20.31 Tubular and papillary neoplasm arising within the dilated lumen of an intrahepatic bile duct Figure 20.32 A, Large, multicentric intrahepatic cholangiocarcinoma with a firm, white cut surface secondary to the dense fibrous stroma. B, Tubular pattern with prominent fibrous stroma. C, In well-differentiated tumors, variation in nuclear size and irregularity of nuclear membranes may be helpful diagnostic features. D, Perineural invasion is common. E, Adenosquamous variant of intrahepatic cholangiocarcinoma. (A, Courtesy of Dr. George F. Gray Jr.) Figure 20.33 A, Typical spongy deep red cut surface in hemangioma of the liver. B, Tumor accompanied by large fibrin deposits secondary to thrombosis. C, An example with marked secondary fibrosis. D, Microscopically, there are dilated vascular spaces lined by flat endothelial cells, within dense fibrous stroma Figure 20.34 Infantile hemangioendothelioma featuring small thin-walled vascular channels within fibrous stroma. (Courtesy of Dr. Grace Kim.) Figure 20.35 A, Hepatic epithelioid hemangioendothelioma with multifocal growth pattern and marked parenchymal congestion due to involvement of the hepatic venous system by tumor. B, Epithelioid tumor cells with occasional intracytoplasmic lumens (arrow) are present within abundant stroma. Note involvement of the central vein in the middle of the photograph Figure 20.36 A, Hepatic angiosarcoma with areas of necrosis and hemorrhage. B, The sinusoids are dilated, and the liver parenchyma has essentially been replaced by malignant endothelial cells. A residual portal tract is in the center of the field Figure 20.37 Mesenchymal hamartoma of liver, which grossly may have a solid micronodular (A) or multicystic appearance (B). C, The microscopic appearance consists of abundant mesenchymal tissue with admixed blood vessels, bile ducts, and hepatocytes. (C, Courtesy of Dr. Grace Kim.) Figure 20.38 A, The solid pattern of growth and the epithelioid appearance of the tumor cells in angiomyolipoma, along with ballooned cytoplasm, may lead to a mistaken diagnosis of a hepatocellular neoplasm. B, Needle biopsy of another case with epithelioid smooth muscle cells, fat, and thin-walled vessels. Extramedullary hematopoiesis is also present Figure 20.39 A, Inflammatory myofibroblastic tumor showing a well- circumscribed nodule with admixed plasma cells, histiocytes, and spindled fibroblasts. B, High-power view showing spindle cells admixed with lymphocytes, plasma cells, histiocytes, myofibroblasts Figure 20.40 Large solitary fibrous tumor of the liver. Microscopically, the tumor had malignant features Figure 20.41 A, Grossly embryonal sarcoma is well circumscribed, largely solid, and has areas of cystic degeneration. B, Low power view shows undifferentiated spindle cells and giant cells, with prominent thin-walled vessels. C, Large eosinophilic hyaline globules are present within and between the tumor cells Figure 20.42 A, An anaplastic large cell lymphoma forms a large abscess-like mass that effaces the normal liver architecture. Portal involvement by Hodgkin disease. B, Note the mixed cellularity of the infiltrate, which has a vaguely granulomatous look and scattered large tumor cells Figure 20.43 Both portal and sinusoidal involvement are seen in this case of chronic lymphocytic leukemia Figure 20.44 Follicular dendritic cell tumor of the liver featuring spindled and epithelioid cells with ovoid nuclei and a sprinkling of lymphocytes Figure 20.45 Diffuse sinusoidal involvement by neoplastic plasma cells in a case of liver involvement by myeloma Figure 20.46 A, Large bowel carcinoma metastatic to liver. B, Leiomyosarcoma metastatic to liver. The primary tumor was located in the stomach. C, Choriocarcinoma metastatic to liver. The tumor has the highly hemorrhagic appearance that is characteristic of this entity. D, Malignant melanoma metastatic to liver. A portion of the tumor shows black melanin pigmentation
