Colorectal flat-type tumors include laterally spreading tumors (LSTs) and flat depressed-type tumors. The former of which shows a predominant lateral spreading growth rather than an invasive growth. The present study examined the morphological characteristics of LSTs, in comparison with polypoid- or flat depressed-type tumors, along with the expression of atypical protein kinase C (aPKC) λ/ι, a pivotal cell polarity regulator, and the hallmarks of cell polarity, as well as with type IV collagen, β-catenin and E-cadherin. In total, 37 flat-type (24 LSTs and 13 flat depressed-type tumors) and 20 polypoid-type colorectal tumors were examined. The LSTs were classified as 15 LST adenoma (LST-A) and nine LST cancer in adenoma (LST-CA). An immunohistochemical examination was performed on aPKC λ/ι, type IV collagen, β-catenin and E-cadherin. The LST-A and -CA showed a superficial replacing growth pattern, with expression of β-catenin and E-cadherin in the basolateral membrane and type IV collagen along the basement membrane. In addition, 86.6% of LST-A and 55.6% of LST-CA showed aPKC λ/ι expression of 1+ (weak to normal intensity staining in the cytoplasm compared with the normal epithelium). Furthermore, ~45% of the polypoid-type adenomas showed 2+ (moderate intensity staining in the cytoplasm and/or nucleus) and 66.7% of the polypoid-type cancer in adenoma were 3+ (strong intensity staining in the cytoplasm and nucleus). A statistically significant positive correlation was observed between the expression of aPKC λ/ι and β-catenin (r=0.842; P<0.001), or type IV collagen (r=0.823; P<0.001). The LSTs showed a unique growth pattern, different from the expanding growth pattern presented by a polypoid tumor and invasive cancer. The growth characteristics of LST appear to be caused by adequate coexpression of β-catenin, type IV collagen and aPKC λ/ι.
We report a case of hepatic mesenchymal hamartoma in an adult; this condition is extremely rare, with only 15 cases having been reported in the English-language literature worldwide. The patient was a 36-year-old woman who was seen at her local hospital for upper abdominal distension. A giant multilocular cystic tumor, which had almost entirely replaced the normal parenchyma of the right lobe of the liver, was diagnosed. She was referred to our hospital, where, with a diagnosis of biliary cystadenoma, the tumor was successfully removed by right hemihepatectomy. After an uneventful postoperative course, the patient was discharged from our hospital. On histological examination, the tumor consisted of numerous cystic lesions without epithelial lining cells; hepatocytes, bile duct, and vascular components, without either lobular structure or atypia, were observed in the pseudocyst wall, leading to a diagnosis of hepatic mesenchymal hamartoma. There have been a few previously reported cases of multifocal hepatic mesenchymal hamartoma reappearing in the remaining liver after hepatectomy, although these cases are considered to be extremely rare. Therefore, periodic follow-up will be necessary for the patient.
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