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The macrotrabecular (MT) pattern of hepatocellular carcinoma (HCC) has been suggested to represent a distinct HCC subtype. We retrospectively reviewed 231 HCC cases. Detailed pathologic evaluation for histologic patterns, including MT-pattern, was performed for each case and recorded as percentage involved at 10% intervals. MT-pattern was defined as having trabeculae6 cells thick. After excluding all recognized HCC subtypes, remaining cases were deemed conventional HCC (CV-HCC) and served as controls. HCCs with a component of ≥10%, ≥30% and ≥50% MT-pattern were identified in 41 (17.7%), 24 (10.4%) and 4 (1.7%) cases, respectively. The clinicopathologic features of HCCs with 10% to 29% MT-pattern (n=17, 7.4%) were largely similar to CV-HCC. No significant difference was observed between the 30% and 49% (n=20) and ≥50% (n=4) MT groups, hence these were combined for further analysis as MT-HCC. MT-HCCs (≥30% MT-pattern) were larger tumors (5.5 vs. 3.1 cm), were less likely to be associated with cirrhosis (54% vs. 79%), were more likely to have hepatitis B (21% vs. 5%) and less likely hepatitis C infection (33% vs. 58%) compared with CV-HCC. MT-HCC was associated with the presence of anaplastic tumor cells (42% vs. 14%), higher alpha-fetoprotein level, higher AJCC stage, and higher histologic grade. Compared with patients with CV-HCC, patients with MT-HCC had poorer overall survival. Patients with MT-HCC who underwent primary resection or transplantation had a higher recurrence rate and worse recurrence-free survival. Our findings suggest that ≥30% MT-pattern could be used as the more appropriate cut-off for defining MT-HCC, which represents a unique and aggressive HCC histologic subtype.

Calcifying nested stromal-epithelial tumor is a rare entity that has gone by a variety of names in the literature: ossifying malignant mixed epithelial and stromal tumor, ossifying stromal-epithelial tumor, and desmoplastic nested spindle cell tumor of the liver. To our knowledge, approximately 38 cases have been reported in the literature. The histogenesis is still largely unknown but histopathologically is characterized by nests of spindle and epithelioid cells in an organoid arrangement surrounded by a prominent dense myofibroblastic stroma with occasional psammomatous calcification and focal heterotopic ossification. Vascular invasion is rare and tumoral recurrence is uncommon with only a single reported case of metastasis leading to death. Treatment is mainly by surgical intervention with the role of chemotherapy seeming limited, but lack of data hinders a true recommendation. It is important to rule out other processes such as hepatoblastoma, calcified hemangioma, synovial sarcoma, metastatic gastrointestinal stromal tumor, desmoplastic small round cell tumor, among others, which appear similar radiographically and histopathologically.

Objectives Gastric adenocarcinoma of the fundic gland type (GA-FG) is a newly described entity with a lack of awareness amongst general surgical pathologists and this review highlights the key features and controversies associated with this uncommon neoplasm. Methods A literature search through PubMed using synonyms for GA-FG was conducted to obtain 111 cases. Results GA-FG is a well-differentiated neoplasm of oxyntic mucosa, that is comprised of chief cells and parietal cells. Chief cell differentiation is highlighted with Muc-6, RUNX3, and pepsinogen. Parietal cells are highlighted with H+/K+ ATPase and PDGFRA-α. Association with Helicobacter infection, chronic gastritis, intestinal metaplasia, or gastric atrophy is not seen. Most GA-FGs are confined to the mucosa. Deeper invasion, lymphovascular invasion, nodal metastasis, and extragastric spread are uncommon. Conclusions GA-FGs are rare lesions that typically follow a benign course. However, despite features of malignancy in some cases, complete surgical excision, sometimes with endoscopic mucosal resection, seems adequate treatment.

Abernethy malformation, also termed congenital portosystemic shunt and congenital absence of portal vein is the result of malformation of the splanchnic venous system. Congenital portosystemic shunts are divided into extra- and intrahepatic shunts. Two shunts have been defined: Type I is characterized by the complete diversion of portal blood into the vena cava with an associated congenital absence of the portal vein. Type II is defined by an intact but diverted portal vein through a side-to-side, extrahepatic connection to the vena cava. The clinical manifestations of Abernethy malformation are diverse with a typical presentation consisting of hypoxia and hepto-pulmonary syndrome. Histologically, focal nodular hyperplasia, nodular regenerative hyperplasia, liver adenoma, hepatoblastoma, and hepatocellular carcinoma have all been reported. Herein, we report a case of Abernethy malformation, type Ib, in a 12-month-old male who was found to have a small hepatocellular carcinoma at the time of explant. The immunohistochemical characteristics in relation to the genetic aspects are discussed. To our knowledge, this is the first reported case of hepatocellular carcinoma developing in a patient who is under the age of 5 years with Abernethy malformation.

Papillary thyroid carcinoma is a common malignancy to affect the thyroid and is typified by a nonaggressive nature and low rates of mortality. In contrast, anaplastic thyroid carcinoma is the most aggressive thyroid malignancy with a mortality rate of nearly 90% and survival typically of only six months after the diagnosis is made. The transformation of papillary thyroid carcinoma to anaplastic thyroid carcinoma is well documented in the literature but is uncommon and in most instances is reported as a case report or small series only. Transformation of papillary thyroid carcinoma to anaplastic thyroid carcinoma usually takes place in the thyroid itself or in the adjacent lymph nodes. Only on rare occasions does a transformation occur in a papillary thyroid carcinoma metastasis outside of these locations. In the present case report and subsequent discussion we highlight an unusual case of PTC with transformation to anaplastic thyroid carcinoma, which is shown to involve numerous locations to include near total lung parenchyma obliteration. We also discuss the differential diagnostic challenges when faced with a thyroid malignancy that is negative for thyroglobulin.

[Figure][1] An asymptomatic 66-year-old woman presented with an elevated total protein of 9.1 g on routine blood work. Serum protein electrophoresis showed an immunoglobulin A (IgA) κ (kappa) M-spike measuring 3570 mg/dL with depression of immunoglobulins M and G (IgM and IgG). Renal

Colorectal carcinoma (CRC), as the third most common new cancer diagnosis, poses a significant health risk to the population. Interval CRCs are those that appear after a negative screening test or examination. The development of interval CRCs has been shown to be multifactorial: location of exam-academic institution versus community hospital, experience of the endoscopist, quality of the procedure, age of the patient, flat versus polypoid neoplasia, genetics, hereditary gastrointestinal neoplasia, and most significantly missed or incompletely excised lesions. The rate of interval CRCs has decreased in the last decade, which has been ascribed to an increased understanding of interval disease and technological advances in the screening of high risk individuals. In this article, we aim to review the literature with regard to the multifactorial nature of interval CRCs and provide the most recent developments regarding this important gastrointestinal entity.

Eccrine spiradenomas are uncommon, benign lesions, which are thought to originate from the eccrine sweat glands. They are common in young adults and are without a sex predilection. Here we report a case of eccrine spiradenoma of the breast skin in a 39-year-old woman who presented with a breast nodule for 10 years. It is crucial to take eccrine spiradenoma into consideration in superficial, well-circumscribed, breast skin/subcutaneous lesions. It is useful to recognize the two-cell populations constituting this tumor: small, dark, basaloid cells with hyperchromatic nuclei, which are immunoreactive for P63 and calponin, and larger cells with a pale nucleus, often near the center of the cluster (inner cells), which are immunoreactive for CK7 and CD117 (C-kit).

It is widely accepted that hyperglycemia per se incites and perpetuates the diabetic state be adverse effects on β cell insulin secretion and peripheral insulin action. Examination of the latter locus has revealed glucose-related abnormalities in facilitated glucose transport. Beyond the plasma membrane, however, there is scant data examining whether hyperglycemia influences important intracellular metabolic events. We recently described a sizable reduction in post-transport, in situ metabolism in permeabilized fat cells from streptozocin-induced diabetic rats. Of importance, the diabetes-related deficit was entirely ameliorated by insulin therapy. In this study we examined whether hyperglycemia per se contributes to this altered intracellular metabolic effect. By infusing phlorizin, near euglycemia was achieved for at least four days in streptozocin-induced diabetic rats. The phlorizin-treated diabetic rats had improved (intact cell) rates of insulin-stimulated 2-deoxyglucose uptake. Despite this, permeabilized fat cell studies revealed non improvement or deterioration in diabetic intracellular metabolism as measured by both the oxidation of [6- 14 C]glucose-6-phosphate via the citric acid cycle or its incorporation into triglyceride. We conclude that hypoinsulinemia, and not hyperglycemia, mediates the disturbance in porous diabetic adipocyte cellular metabolism.