[A case of metastatic melanoma in the gallbladder].

Malignant melanoma is an aggressive tumor with a high potential for distant metastases. Autopsy studies have shown that gallbladder metastases are found in 15% of patients. However, metastatic melanoma of the gallbladder is rarely discovered in living patients. A 73-year-old man was reported. The patient underwent surgical removal of malignant melanoma on his back and lymphadenectomy of the axillary lymph nodes. In addition, the patient developed cutaneous metastases to the right axillary and the middle of the chest 1.5 years after the surgery. Consequently, nivolumab chemotherapy was started. A computed tomography (CT) scan showed a well-enhanced mass in the gallbladder 4 months after. Abdominal ultrasonography revealed a 13-mm hypoechoic heterogeneous mass in the gallbladder with a hyperechoic layer on the mass surface. Magnetic resonance imaging demonstrated that the gallbladder tumor showed high signal intensity on T1-weighted images, low signal intensity on T2-weighted images, and high signal intensity on diffusion-weighted images. Positron emission tomography-CT revealed the slight uptake of fluorodeoxyglucose at the tumor. Endoscopic ultrasonography showed a hypoechoic tumor infiltrating the submucosal layer. The patient underwent open cholecystectomy. Examination of the resected specimens revealed a black, nodular-type tumor in the gallbladder body. The histopathological diagnosis was malignant melanoma. It was judged as metastatic melanoma of the gallbladder.

Adenocarcinoma arising from a heterotopic pancreas in the first portion of the duodenum: a case report.

BACKGROUND: Heterotopic pancreas (HP) is defined as pancreatic tissue in organs with no anatomical continuity with the orthotopic pancreas. Based on the number of cases reported in the literature between the year 2000 and 2020, HP is rarely found causing malignant transformation of the duodenum. We herein report a case of adenocarcinoma arising from the HP in the first portion of the duodenum. CASE PRESENTATION: A 77-year-old Japanese man presented to our hospital with epigastric pain. Despite having undergone laparoscopic surgery for early sigmoid colon cancer a month earlier, serum levels of tumor-specific antigens, such as CA19-9, were elevated. After undergoing a series of radiologic examinations, the first portion of the duodenum was found thickened. However, a biopsy of the lesion showed no malignancy. Four months later, follow-up computed tomography (CT) scans showed that the lesion was thicker and involved the gastroduodenal artery (GDA), suggesting tumor invasion. A new biopsy did not detect the malignancy. However, serum tumor-specific antigen levels increased, especially duke pancreatic monoclonal antigen type 2 (5287 U/mL), in the absence of tumor in the orthotopic pancreas. The follow-up CT imaging showed a malignant tumor in the first portion of the duodenum. Five months later, we performed a subtotal stomach-preserving pancreaticoduodenectomy (SSPPD) for duodenal or HP cancer in the first portion of the duodenum, finding a lesion from the pyloric bulbs to the first portion of the duodenum, which invaded the adjacent pancreas and GDA. The pathological examination of the specimens revealed adenocarcinoma arising from HP. Nine months after surgery, no recurrence was found by radiologic imaging or tumor-specific antigen laboratory testing. CONCLUSIONS: HP adenocarcinoma is rare and difficult to diagnose preoperatively due to its submucosal location. Therefore, a careful follow-up with blood testing and radiologic imaging, as well as diagnostic surgery, is recommended.

Laparoscopic repair of a large perineal hernia after laparoscopic abdominoperineal resection: A case report.

A 75-year-old woman underwent laparoscopic abdominoperineal resection. Four months after abdominoperineal resection, the patient complained of a perineal bulge and urination disorder. Abdominal CT showed protrusion of the small intestine and bladder to the perineum. The patient underwent laparoscopic hernia repair with mesh. The size of the hernial orifice was 7.0 × 9.0 cm, and it had no solid rim. The mesh was tacked ventrally to the pectineal ligament and dorsally to the sacrum, and then sutured on the lateral side. The hernia has not recurred 10 months after the operation. Laparoscopic repair is a good treatment choice for secondary perineal hernia and fixing the mesh to the pectineal ligament, and the sacrum prevents the mesh from sagging.

Solitary choroidal metastasis from gastric adenocarcinoma: a case report.

BACKGROUND: Metastatic choroidal carcinomas that originated from the gastrointestinal tract are extremely rare. We report a case of suspected solitary choroidal metastasis from gastric adenocarcinoma. CASE PRESENTATION: The patient was a 60-year-old man who had undergone laparoscopic distal gastrectomy with D1+ lymphadenecetomy for gastric cancer. The clinical stage was T1bN0M0 (TNM classification), but the pathological stage was T4aN0M0 beyond expectation. Adjuvant chemotherapy with oral Tegafur, Gimeracil, Oteracil potassium (TS-1®) was initiated. But he suddenly complained of decreased visual acuity in his right eye about 8 months later. This was suspected to be caused by choroidal metastasis of gastric adenocarcinoma. Chemotherapy with paclitaxel (PTX) and intensity-modulated radiotherapy (IMRT) achieved complete remission and spared the patient from going blind. CONCLUSIONS: This case demonstrates that we should be aware of the possibility of choroidal metastases, when visual symptoms arise during treatment of gastric cancer.

Ubiquitin C-terminal hydrolase L1 (UCH-L1) acts as a novel potentiator of cyclin-dependent kinases to enhance cell proliferation independently of its hydrolase activity.

Dysregulation of cell proliferation and the cell cycle are associated with various diseases, such as cancer. Cyclin-dependent kinases (CDKs) play central roles in cell proliferation and the cell cycle. Ubiquitin C-terminal hydrolase L1 (UCH-L1) is expressed in a restricted range of tissues, including the brain and numerous types of cancer. However, the molecular functions of UCH-L1 remain elusive. In this study, we found that UCH-L1 physically interacts with CDK1, CDK4, and CDK5, enhancing their kinase activity. Using several mutants of UCH-L1, we showed that this enhancement is dependent upon interaction levels between UCH-L1 and CDKs but is independent of the known ubiquitin-related functions of UCH-L1. Gain- and loss-of-function studies revealed that UCH-L1 enhances proliferation of multiple cell types, including human cancer cells. Inhibition of the interaction between UCH-L1 and cell cycle-associated CDK resulted in the abolishment of UCH-L1-induced enhancement of cell proliferation. RNA interference of UCH-L1 reduced the growth of human xenograft tumors in mice. We concluded that UCH-L1 is a novel regulator of the kinase activities of CDKs. We believe that our findings from this study will significantly contribute to our understanding of cell cycle-associated diseases.

[Analysis of the eligibility of elderly colorectal cancer patients for adjuvant chemotherapy combined with polysaccharide K].

We enrolled 62 elderly patients( ≥70 years of age) with colorectal cancer who had undergone surgery and postoperative adjuvant chemotherapy at our department and analyzed the overall surviva(l OS) and disease-free surviva(l DFS) to identify the patients who responded to treatment. Postoperative adjuvant chemotherapy was performed with oral anticancer agents, including doxifluridine( 5'-DFUR), uracil/tegafur( UFT), and UFT/Leucovorin( LV); all patients also received polysaccharide K( PSK), an immunomodulator, in combination with chemotherapy. The 3-year OS and DFS rates for all patients were 83.4% and 78.6%, respectively, with no significant differences in these rates based on the chemotherapeutic agents used. The patients were assigned to low and high groups on the basis of the median cut-off values of each clinical laboratory parameter and the data obtained were subjected to univariate analysis. The results of the univariate analysis suggested that carcinoembryonic antigen (CEA) and cancer antigen 125 (CA125) levels were significant prognostic factors. Further multivariate analysis using Cox regression analysis identified the preoperative CEA level alone as an independent factor. When stratification analysis was performed using a preoperative CEA level of 4.0 ng/mL as the cut-off value, the results indicated that the outcome of patients with a high preoperative CEA level may be 8-fold worse than that of patients with a low preoperative CEA level. For these patients, the use of chemotherapeutic drugs that elicit a more potent antitumor effect should be considered.

[A case of AFP-producing gastric cancer with hepatic metastases that accompanied early gastric cancer treated effectively by chemotherapy].

We report a case of alphafetoprotein (AFP)-producing gastric cancer that accompanied early gastric cancer and was treated effectively by chemotherapy. The patient was a 73-year-old male. A type 1 tumor was observed in the upper gastric body and a 0-IIa tumor was noted on the anterior wall of the lower gastric body. Abdominal CT showed multiple metastatic lesions in the liver. A subtotal gastrectomy was performed, and the pathological examination revealed that the type 1 tumor was positive for AFP and the 0-IIa tumor was negative for AFP. After 5 courses of postoperative administration of S-1, hepatic metastatic lesions disappeared on imaging. The serum AFP level, which had increased to the maximum of 49,660 ng/ml, was normalized. After 60 months, there has been no sign of recurrence. We encountered a case of AFP-producing gastric cancer that accompanied early gastric cancer and was treated effectively by S-1. Various therapies for AFP-producing gastric cancer have been reported; however, a standardized regimen has not been established. Since the concurrence of AFP-producing gastric cancer and tubular adenocarcinoma is rare, and hepatic metastatic lesions disappeared, the case under study is considered to be of interest. Therefore, we report this case with a review of the literature.

Chemoembolization for the treatment of large hepatocellular carcinoma.

PURPOSE: To retrospectively evaluate the efficacy of chemoembolization for inoperable hepatocellular carcinoma (HCC) tumors larger than 5 cm in diameter. MATERIALS AND METHODS: Chemoembolization was performed in 30 patients with HCCs with a largest diameter of more than 5 cm with three or fewer lesions and no portal vein tumor thrombus. The mean maximum tumor diameter was 7.7 cm +/- 2.4. When the tumor was extremely large and had multiple feeding arteries, stepwise chemoembolization sessions at intervals of 3-10 weeks were performed. In addition, extrahepatic collateral supply was identified and embolized. Local therapeutic effects, survival rates, and complications were analyzed. RESULTS: The mean follow-up period was 33.8 months +/- 24.1. One to 13 chemoembolization sessions (mean, 4.0 sessions +/- 3.0) were performed in each patient. Additionally, 62 collateral vessels were embolized in 21 patients, including 22 vessels in 14 patients at the initial procedure. Early tumor response rate 2-3 months after treatment was 43.3% by Response Evaluation Criteria In Solid Tumors. Complete radiologic response was achieved in 19 patients. Eleven patients died between 4 and 61 months after treatment (mean, 27.2 months +/- 21.8), including four deaths unrelated to hepatic causes. Nineteen patients have survived for 6-103 months (mean, 37.5 months +/- 25.2). Overall and progression free-survival rates at 1, 3, and 6 years were 82.3% and 66.0%, 73.9% and 57.6%, and 32.9% and 34.2%, respectively. Three infectious complications developed and were managed by interventions. CONCLUSIONS: Chemoembolization was effective for large HCCs, although there is a risk of infectious complications after the procedure.

Aggressive recurrence of gastric cancer as a granulocyte-colony-stimulating factor-producing tumor.

A 62-year-old Japanese man presented with a 1-month history of inter-digestive epigastralgia. His family history included a sister with gastric cancer. Gastroendoscopy and gastrography demonstrated a type-2 tumor in the upper region of the stomach. CT scan and fluorodeoxyglucose-positron emission tomography (FDG-PET) scan demonstrated gastric cancer and its metastatic lymph nodes. The patient underwent total gastrectomy with splenectomy and extended lymph node dissection. Although postoperative adjuvant chemotherapy by S-1 was started, the deteriorating condition of the patient prevented drug administration and even eating meals. On the 19th postoperative day (POD), FDG-PET scan of the body demonstrated new uptake in the liver and lymph node around the aorta. Without any sign of infection, leukocytosis developed around the 30th POD. On the 49th POD, remarkable uptake in the whole upper abdomen was detected on FDG-PET scan. Finally, leukocyte count increased to 125,200 and granulocyte colony stimulating factor (G-CSF) was elevated to 28 pg/ml on the 54th POD. The patient died of multiple liver metastases and carcinomatous peritonitis only 56 days after surgery. G-CSF-producing tumor is a rare but aggressive disease, particularly as recurrent tumor. If leukocytosis is detected in relation to a non-lympho hematopoietic malignant tumor, G-CSF-producing tumor should be considered and FDG-PET scan is recommended for early detection. Chemotherapy for G-CSF-producing tumor must be conducted as soon as possible.

Identification of a novel chemical potentiator and inhibitors of UCH-L1 by in silico drug screening.

Ubiquitin-C-terminal hydrolase L1 (UCH-L1) is a de-ubiquitinating enzyme expressed in the brain and reproductive tissues as well as certain cancers. The hydrolase activity of UCH-L1 has been implicated in Alzheimer's disease and cancer invasion; therefore, it may represent a therapeutic target for these diseases. The present study was undertaken to identify novel chemical modulators for the hydrolase activity of UCH-L1. To identify chemicals that bind to the active site of UCH-L1, we carried out in silico structure-based drug screening using human UCH-L1 crystal structure data (PDB ID: 2ETL) and virtual compound libraries containing 26,891 and 304,205 compounds. Among the compounds with the highest binding scores, we identified one that potentiates the hydrolase activity of UCH-L1, and six that inhibit the activity in enzymatic assays. These compounds may be useful for research on UCH-L1 function, and could lead to candidate therapeutics for UCH-L1-associated diseases.

Large cell change of hepatocytes in chronic viral hepatitis represents a senescent-related lesion.

Large cell change involves the clustering of hepatocytes with hyperchromatism and cellular enlargement without an increase in the nuclear/cytoplasmic ratio. This study investigated whether large cell change in chronic viral hepatitis reflects cellular senescence because of morphological similarities between the 2 conditions. The expression of markers of senescence such as senescence-associated beta-galactosidase, senescence-associated heterochromatic foci, and p21, as well as markers of cell kinetics such as Ki-67, was examined in 26 frozen and 82 formalin-fixed liver specimens. Large cell change was frequently detected in chronic hepatitis B cases with advanced histologic staging, particularly those with hepatocellular carcinoma. Senescence-associated beta-galactosidase activity, senescence-associated heterochromatic foci, and p21 were frequently detected in areas of large cell change. Hepatocytes with large cell change showed no proliferative or apoptotic activity. The frequent expression of senescent features and the absence of proliferative or apoptotic activity suggest that large cell change represents senescence. The parallel increase in large cell change and hepatocellular carcinoma in chronic hepatitis B raises the possibility that cellular senescence develops as a safeguard against malignant transformation rather than as a precursor of hepatocellular carcinoma.

Bile ductular cell reaction with senescent hepatocytes in chronic viral hepatitis is lost during hepatocarcinogenesis.

Cellular senescence is defined as irreversible cell arrest and could work as a safeguard against tumorigenesis. This mechanism was examined in chronic viral hepatitis-related hepatocarcinogenesis. By using surgical resected or wedge biopsied liver specimens from 87 chronic viral hepatitis patients in whom 35 neoplastic nodules (dysplastic nodules and hepatocellular carcinoma) were complicated, P21 expression and senescence-associated beta galactosidase activity, a marker of senescence, were examined. All of these neoplastic nodules harbored portal tracts within the tumors. Hepatocytes expressing senescence markers and cytokeratin (CK)7-positive bile ductules including hepatic progenitor-like cells were increased in periseptal areas in cirrhosis. Interestingly, these cells appeared to form an anatomical complex that was completely lost in the periportal areas within the neoplastic nodules. In one-third of the neoplastic nodules, CK7-positive small neoplastic hepatocytes resembling hepatic progenitor cells proliferated zonally around the portal tracts. In conclusion, loss of a complex of senescent hepatocytes and ductular cell including hepatic progenitor-like cells in the periportal or periseptal areas may be associated with emergence of neoplastic hepatocytes and their proliferation followed by neoplastic nodules arising in liver cirrhosis. Zonal proliferation of CK7-positive small neoplastic hepatocytes resembling hepatic progenitor cells may develop during early hepatocarcinogenesis.

Histopathological findings after ultraselective transcatheter arterial chemoembolization for hepatocellular carcinoma.

AIM: To evaluate the histopathologic findings in the surgical specimen of hepatocelluar carcinoma after transcatheter arterial chemoembolization (TACE) at the most distal portion of the sub-subsegmental artery of the liver (ultraselective TACE). METHODS: Histolopathologic findings from nine tumors with a mean diameter of 3.1 cm +/- 1.7 from patients who underwent hepatectomy after ultraselective TACE were evaluated, especially with regard to the relationship between peritumoral liver parenchymal necrosis and portal vein visualization during TACE. Portal vein visualization was classified into three grades by a spot digital radiograph obtained just after TACE: 0, no obvious portal vein visualization; 1, visualization of the portal vein adjacent to the tumor; and 2, visualization in the whole embolized area or extending into the surrounding non-embolized areas. Unenhanced computed tomography (CT) was obtained 1 week later and surgical resection was performed 37 +/- 6.3 days after ultraselective TACE. RESULTS: Portal vein visualization during TACE was classed as grade 1 in 5 tumors and grade 2 in 4. Histopathologically, complete tumor necrosis was observed in 7 tumors (77.8%). In 2 tumors (1 of grade 1, the other grade 2), a small viable portion or viable daughter nodule was seen. Macroscopic parenchymal necrosis adjacent to the tumor was observed in all 4 grade 2 tumors including gas-containing areas on CT obtained 1 week after TACE. CONCLUSIONS: Ultraselective TACE induces not only complete tumor necrosis but also peritumoral parenchymal necrosis, similar to that after radiofrequency ablation, when the portal veins are markedly visualized during the TACE procedure.

Aberrant molecular properties shared by familial Parkinson's disease-associated mutant UCH-L1 and carbonyl-modified UCH-L1.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons. The I93M mutation in ubiquitin C-terminal hydrolase L1 (UCH-L1) is associated with familial PD, and we have previously shown that the I93M UCH-L1-transgenic mice exhibit dopaminergic cell loss. Over 90% of neurodegenerative diseases, including PD, occur sporadically. However, the molecular mechanisms underlying sporadic PD as well as PD associated with I93M UCH-L1 are largely unknown. UCH-L1 is abundant (1-5% of total soluble protein) in the brain and is a major target of oxidative/carbonyl damage associated with sporadic PD. As well, abnormal microtubule dynamics and tubulin polymerization are associated with several neurodegenerative diseases including frontotemporal dementia and parkinsonism linked to chromosome 17. Here we show that familial PD-associated mutant UCH-L1 and carbonyl-modified UCH-L1 display shared aberrant properties: compared with wild-type UCH-L1, they exhibit increased insolubility and elevated interactions with multiple proteins, which are characteristics of several neurodegenerative diseases-linked mutants. Circular dichroism analyses suggest similar structural changes in both UCH-L1 variants. We further report that one of the proteins interacting with UCH-L1 is tubulin, and that aberrant interaction of mutant or carbonyl-modified UCH-L1 with tubulin modulates tubulin polymerization. These findings may underlie the toxic gain of function by mutant UCH-L1 in familial PD. Our results also suggest that the carbonyl modification of UCH-L1 and subsequent abnormal interactions of carbonyl-modified UCH-L1 with multiple proteins, including tubulin, constitute one of the causes of sporadic PD.

Ultraselective transcatheter arterial chemoembolization with a 2-f tip microcatheter for small hepatocellular carcinomas: relationship between local tumor recurrence and visualization of the portal vein with iodized oil.

PURPOSE: To retrospectively evaluate the relationship between local tumor recurrence and iodized oil deposition in the portal vein by using ultraselective transcatheter arterial chemoembolization (TACE) for small hepatocellular carcinoma. MATERIALS AND METHODS: One-hundred twenty-three tumors smaller than 5 cm in diameter (mean diameter, 1.9 cm; median diameter, 1.6 cm) were treated with TACE by using a 2-F tip microcatheter at a distal portion of the subsegmental artery of the liver. Portal vein visualization at spot radiography during TACE was divided into three grades, as follows: 0 = not visualized, 1 = limited near the tumor, and 2 = whole or extended to the embolized area. Local recurrence rates of each grade group were compared. The recurrent pattern was divided into intratumoral and peritumoral recurrence. Complications were also analyzed. RESULTS: Of the 123 tumors, 53 (43.1%) were classified as grade 2, 52 (42.3%) were classified as grade 1, and 18 (14.6%) tumors were classified as grade 0. Overall local recurrence rates at 12, 24, and 36 months were 25.6%, 34.7%, and 34.7%, respectively. The local recurrence rates for the grades 2, 1, and 0 groups were 7.9%, 24.8%, and 85.7%, respectively, at 12 months and 17.7%, 38.9%, and 85.7% at 24 months. Recurrence rates in the grade 2 group were significantly lower than those in the grades 1 and 0 groups (P = .0485 and P < .0001, respectively). Intratumoral recurrence was observed in 21 tumors, most of which were in the grade 0 group. Peritumoral recurrence was noted in 16 tumors, most of which were in the grade 2 group. There were no major complications. CONCLUSION: Ultraselective TACE was safe and effective in a significant number of tumors. In particular, local recurrence was significantly lower when a greater degree of portal vein visualization was demonstrated during TACE.

Biliary papillary tumors share pathological features with intraductal papillary mucinous neoplasm of the pancreas.

Recently, attention has been drawn to papillary neoplasm of the pancreatobiliary systems. In the pancreas, the disease entity of intraductal papillary mucinous neoplasm (IPMN-P) is widely recognized. In contrast, the pathological characteristics of biliary papillary tumors, such as biliary papilloma(tosis) and papillary cholangiocarcinoma, have not yet been well documented. In this study, we compared the pathological features and post-operative prognosis among biliary papillary tumors (10 cases of biliary papilloma(tosis) and 22 cases of papillary cholangiocarcinoma), conventional non-papillary cholangiocarcinoma (15 cases), and IPMN-P (31 cases). Macroscopically, all biliary papillary tumors were characterized by the prominent intraductal papillary proliferation, and macroscopic mucin-hypersecretion was seen in 9 of 32 cases (28%). Histologically, biliary papillary tumors consisted of three types of tumor cells (pancreaticobiliary, intestinal and gastric types), whereas only the pancreaticobiliary type was observed in non-papillary cholangiocarcinoma. Immunohistochemically, biliary papillary tumors were characterized by the common expression of MUC2, CDX2 and cytokeratin 20. In addition, biliary papillary tumors could be associated with two types of invasive lesions: tubular adenocarcinoma (9 cases) and mucinous carcinoma (5 cases). Patients with tubular adenocarcinoma had a poor prognosis compared to non-invasive papillary tumor or papillary tumor with mucinous carcinoma. These pathological characteristics and the survival status of biliary papillary tumors were different from those of non-papillary cholangiocarcinoma, and rather closely resembled those of IPMN-P. In conclusion, biliary papillary tumors may be the biliary counterpart (intraductal papillary neoplasm of the bile duct) of IPMN-P.

Biliary cystic tumors with bile duct communication: a cystic variant of intraductal papillary neoplasm of the bile duct.

Biliary cystic tumors, which are also called biliary cystadenoma and cystadenocarcinoma, are thought to be a heterogeneous disease entity, and some of them are known to show a luminal communication to the bile duct. In this study, we examined the clinicopathological features of nine cases of biliary cystic tumors with bile duct communication. They were composed of five males and four females with an average age of 67 years (52-84 years). They were multilocular (eight cases) or unilocular (one case), and all cases contained mucinous fluid. A direct luminal communication with the bile ducts was identified in five cases on preoperative or intraoperative cholangiographies. Biliary cystic tumors examined in this study were histologically adenoma (one case), adenocarcinoma in situ (six cases), and adenocarcinoma associated with microinvasive mucinous carcinoma (two cases). One case of adenocarcinoma in situ also had the adenoma component (adenocarcinoma in adenoma). Dysplastic mucinous epithelium proliferated in flat, micropapillary and papillary fashions within the intracystic spaces. Intraepithelial neoplasm was observed within non-dilated adjacent bile ducts, suggesting a direct luminal communication between the cystic tumors and the bile duct. Ovarian-like stroma was not observed in their walls in any cases. Immunohistochemically, seven cases expressed MUC1 or MUC2 in the neoplastic biliary epithelium. All cases except one were alive without any evidences of tumor recurrence after total excision (3-156 months after surgery). These clinicopathological features resembled those of intraductal papillary neoplasm of the bile duct, which had been reported as a biliary counterpart of pancreatic intraductal papillary mucinous neoplasm. In conclusion, biliary cystic tumors with bile duct communication could be regarded as intraductal papillary neoplasm with a prominent cystic dilatation of the bile duct and mucin retention, rather than true biliary cystic neoplasms.

Multicystic biliary hamartoma: a hitherto undescribed lesion.

In this report, we presented 3 cases of unusual hamartomatous nodules of the liver. These nodules were located around hepatic capsule of the left hepatic lobe and characteristically protruded from the liver. Histologically, these nodular lesions consisted of ductal structures, periductal glands, and fibrous connective tissues containing blood vessels. Smooth muscle bundles focally surrounded ductal structures. Bile-like materials were observed within some ducts. Two cases were associated with xanthogranulomatous inflammation around bile-like materials, and this inflammatory process extended from ductal lumens to periductal connective tissues. In contrast, the remaining case, which was not associated with inflammation, showed a honeycomb appearance. Ductal epithelium and periductal glands resembled biliary epithelium and peribiliary glands, respectively, and they also expressed biliary-type cytokeratins such as cytokeratins 7 and 19. These nodules shared pathologic characteristics of ciliated hepatic foregut cysts, such as their location (around the falciform ligament) and periductal smooth muscle bundles, but did not fulfill the diagnostic criteria (no ciliated cells and multilocular lesions). These hamartomatous nodules of the liver did not fit into any of the described categories of hepatic nodular lesions. At present, we speculate that these lesions might be related to developmental abnormalities of the biliary tract or embryonal foregut.

Extrahepatic blood supply to hepatocellular carcinoma: angiographic demonstration and transcatheter arterial chemoembolization.

PURPOSE: To evaluate the incidence of each extrahepatic collateral pathway to hepatocellular carcinoma (HCC) and to assess technical success rates and complications of transcatheter arterial chemoembolization (TACE) through each collateral. METHODS: We retrospective evaluated extrahepatic collateral pathways to HCC on angiography in 386 procedures on 181 consecutive patients. One hundred and seventy patients had previously undergone TACE. TACE through extrahepatic collaterals using iodized oil and gelatin sponge particles was performed when a catheter was advanced into the tumor-feeding branch to avoid nontarget embolization. RESULTS: A single collateral was revealed in 275 TACE procedures, two were revealed in 74, and three or more were revealed in 34. Incidences of collateral source to HCC were 83% from the right inferior phrenic artery (IPA), 24% from the cystic artery, 13% from the omental artery, 12% from the right renal capsular artery (RCA) and left IPA, 8% from the right internal mammary artery (IMA) and right intercostal artery (ICA), and 7% from the right inferior adrenal artery (IAA). Technical success rates of TACE were 53% in the right ICA, 70% in the cystic artery, 74% in the omental artery, 93% in the left IPA, 96% in the right IPA, and 100% in the right RCA, right IMA, and right IAA. Complications included skin necrosis after TACE through the right IMA (n = 1), cholecystitis after TACE through the cystic artery (n = 1), and ulcer formation after TACE through the right gastric artery (n = 1), in addition to pleural effusion and basal atelectasis after TACE through the IPA and IMA. CONCLUSION: Our study suggests that TACE through extrahepatic collaterals is possible with high success rates, and is also relatively safe.