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Purpose: Laparoscopic liver resection (LLR) has gained acceptance as an effective treatment for colorectal liver metastases (CRLM) in selected patients, providing similar oncologic outcomes compared to open liver resection (OLR). The aim of this study was to determine prognostic factors for survival outcomes associated with LLR for CRLM. Methods: A single-center retrospective analysis of a prospectively maintained database was performed. The inclusion period ranged from September 2011 until mid-March 2020. Results: Two hundred consecutive LLRs were included. The 5-year overall survival (OS) and disease-free survival (DFS) rates equalled 54.8% and 49%, respectively. A pushing (HR = 5.42, 95% CI 1.56–18.88, p = 0.008), as well as a replacement (3.87, 1.05–14.2, p = 0.04) growth pattern of the CRLM, poor differentiation of the primary colorectal cancer (CRC) (3.72, 1.72–8.07, p < 0.001) and administration of neoadjuvant chemotherapy (NAC) (2.95, 1.28–6.8, p = 0.01) were identified as independent predictors of a worse OS. Requirement of more than 6 cycles of NAC (6.17, 2.37–16.03, p < 0.001), a replacement (4.96, 1.91–12.87, p < 0.001), as well as a pushing (4.3, 1.68–11, p = 0.002) growth pattern of the CRLM and poor differentiation of the primary CRC (2.61, 1.31–5.2, p = 0.006) were identified as independent predictors of a worse DFS. Conclusion: LLR for CRLM offers adequate long-term oncologic outcomes. OS and DFS rates are negatively affected by the administration of NAC and by pathological features, including the differentiation grade of the primary CRC and the histological growth pattern of the CRLM. [ABSTRACT FROM AUTHOR]

A Belgian ring trial for pan-TRK immunohistochemistry (IHC) staining was organised to harmonise pan-TRK IHC staining protocols and interpretation. As a reference method, the VENTANA pan-TRK Assay (clone EPR17341) on the Benchmark Ultra platform was selected. Six samples were selected: 2 negative, 2 fusion positive and 2 samples with wild-type endogenous TRK expression. Each participating laboratory stained the slides using their routine pan-TRK IHC and reported their results. In addition, they were asked to return one TRK-stained slide from each case. The coordinating lab evaluated these slides, compared them with the reference method and scored them. Two clones were used during the ring trial: A7H6R (Cell Signaling) and EPR17341 (Abcam/Ventana). Seven protocols achieved a sufficient performance mark, and three labs were advised to further optimise the protocol. Interpretation of pan-TRK IHC proved to be challenging in cases with physiological TRK expression. In addition, depending on the NTRK fusion partner, the staining can vary strongly in both intensity and staining pattern. Labs using the Ventana ready-to-use system based on the EPR17341 clone and using the recommended protocol settings scored best. However, given some small optimisation, all labs scored well on the technical staining and the succeeding evaluation. [ABSTRACT FROM AUTHOR]

Lymphatic malformations (LMs) are debilitating vascular anomalies presenting with large cysts (macrocystic) or lesions that infiltrate tissues (microcystic). Cellular mechanisms underlying LM pathology are poorly understood. Here we show that the somatic PIK3CAH1047R mutation, resulting in constitutive activation of the p110α PI3K, underlies both macrocystic and microcystic LMs in human. Using a mouse model of PIK3CAH1047R-driven LM, we demonstrate that both types of malformations arise due to lymphatic endothelial cell (LEC)-autonomous defects, with the developmental timing of p110α activation determining the LM subtype. In the postnatal vasculature, PIK3CAH1047R promotes LEC migration and lymphatic hypersprouting, leading to microcystic LMs that grow progressively in a vascular endothelial growth factor C (VEGF-C)-dependent manner. Combined inhibition of VEGF-C and the PI3K downstream target mTOR using Rapamycin, but neither treatment alone, promotes regression of lesions. The best therapeutic outcome for LM is thus achieved by co-inhibition of the upstream VEGF-C/VEGFR3 and the downstream PI3K/mTOR pathways. Lymphatic malformation (LM) is a debilitating often incurable vascular disease. Using a mouse model of LM driven by a disease-causative PIK3CA mutation, the authors show that vascular growth is dependent on the upstream lymphangiogenic VEGF-C signalling, permitting effective therapeutic intervention. [ABSTRACT FROM AUTHOR]

Although the prognostic and predictive significance of human epidermal growth factor receptor 2 (HER2) in invasive breast cancer is well established, its role in ductal carcinoma in situ (DCIS) remains unclear. Reports on combined evaluation of both HER2 protein expression and HER2 amplification status in pure DCIS and DCIS adjacent to invasive ductal carcinoma (i.e., admixed DCIS) are scarce. In this study, immunohistochemistry and fluorescence in situ hybridization (FISH) were used to assess HER2 status in 72 cases of pure DCIS, 73 cases of DCIS admixed with invasive ductal carcinoma (IDC), and 60 cases of pure IDC. HER2 copy number-based amplification was present in 49% of pure DCIS, 16% of admixed DCIS, 18% of admixed IDC, and 8% of pure IDC. Amplified pure DCIS with clusters of HER2 signals showed a significantly lower HER2 copy number than amplified admixed DCIS with clusters. Whereas pure DCIS and admixed DCIS presented significant differences, the in situ and invasive component of admixed tumors showed striking similarities regarding mean HER2 and chromosome 17 centromere (CEP17) copy number, grade, and estrogen and progesterone receptor expression. The discrepant prevalence of HER2 amplification among breast cancer subgroups indirectly suggests that HER2 may not play a crucial role in the transition of in situ to invasive breast cancer. The similarities in HER2 amplification status between the in situ and invasive component of admixed tumors hint at a common biological pathway for both components. Our data support the theory that pure DCIS, pure IDC, and admixed lesions have a common progenitor, but can progress as separate lineages. [ABSTRACT FROM AUTHOR]

Endoscopic submucosal dissection (ESD) allows en-bloc resection of superficial gastrointestinal tumors, providing specimens on which lateral margin analysis can be performed reliably. Positive lateral margins have been linked to higher rates of recurrence/residual tumor. There are no guidelines for macroscopic processing of lateral margins. Currently, most institutions use parallel lateral sections, which are difficult to interpret. We use perpendicular lateral sections, hypothesizing that it decreases potential artifactually positive lateral margins. We analyzed positive lateral margin rates in colorectal ESD specimens according to sectioning method. We also looked at morphological factors associated with margin positivity as a function of technique used. We studied 166 ESD specimens, on which parallel sectioning practiced from 2006 to 2011 (n = 75). Perpendicular sectioning was used from 2010 to 2015 (n = 91). We recorded the number of positive margins, along with grade of dysplasia/carcinoma. Other information such as histopathological type, specimen size, lesion location, and patient follow-up was also recorded for evaluation. Forty of seventy-five (63%) margins were positive for parallel sections. In contrast, perpendicularly cut margins were significantly less frequently positive: 22/91 (24%) (p = 0.0001). Positive margins were found significantly more frequently in tubulo-villous lesions compared to tubular lesions in both the parallel and perpendicular groups (p = 0.03 and p = 0.02, respectively). Specimen size was not significantly associated with positive margins. Using perpendicular sectioning of colorectal ESD specimens, the proportion of cases with a positive lateral margin was significantly lower than when parallel sectioning was used. We suggest perpendicular sectioning to improve accuracy in histopathological analysis. This method is particularly important to use in future studies, as it may prevent authors from making conjectures based on overestimation of positive lateral margins. [ABSTRACT FROM AUTHOR]

Objective: To analyse the characteristics of prostate cancers (PrCa) detected following negative multiparametric magnetic resonance imaging (mpMRI).Materials and Methods: Eight hundred and thirty patients with elevated prostate-specific antigen (mean 11.9 μg/l) underwent mpMRI of the prostate at 1.5 Tesla with endorectal coil. The characteristics of all PrCa detected within 2 years after a negative mpMRI were analysed. Primary Gleason grade 4 or any grade 5 PrCa were considered high-grade (HG), Gleason score 3 + 4 intermediate grade (IG) and Gleason score ≤3 + 3 low-grade (LG). Tumour size was considered 'small' when <1 cm on radical prostatectomy specimen or limited to ≤2 cores on prostate biopsy.Results: mpMRI was negative in 391 patients (47.1 %). In 124 patients (31.7 %) PrCa was detected within 2 years. Eighty-four (67.7 %) were LG, 22 (17.7 %) IG and 18 (14.5 %) HG. 119 (96.0 %) of the missed PrCa were organ-confined. The negative predictive value was 95.4 % (373/391) for HG PrCa. Among the 18 missed HG PrCa, 15 (83.3 %) were organ-confined and 12 (66.6 %) were small.Conclusion: The majority of missed tumours on mpMRI were low grade and organ-confined. In patients with elevated PSA and a negative mpMRI, consideration could be given to continued surveillance rather than immediate biopsy.Key Points: • The majority of missed prostate cancers were low grade and organ-confined. • In patients with a negative mpMRI a biopsy may be postponed. • mpMRI had a negative predictive value of 95.4 % for high-grade prostate cancer. [ABSTRACT FROM AUTHOR]

Background: The relationship between the width of surgical margins and local and distant recurrence of colorectal liver metastases (CRLM) remain controversial. We analyzed the impact of surgical margins in laparoscopic liver resections (LLR) for CRLM, using the parenchymal-sparing approach on overall (OS) and recurrence-free survival (RFS). Methods: From January 2005 to October 2012, 114 first LLR for CRLM were performed and retrospectively analyzed. The ultrasonic aspirator was used for parenchyma division. R1 margins were defined when the tissue width was <1 mm. Results: After a mean follow-up of 30.9 ± 1.71 months, OS was 97.1-73.9-58.9 % and the RFS 64.2-35.2-31 % at 1-3-5 years, respectively. The major resection rate was 7 %. The median margin width was 3 (0-40) mm, and R1 resection was recorded in 14 (12.3 %) cases. Twenty-two patients (33.3 %) with hepatic recurrence underwent a repeat hepatectomy. R1 margins were significantly related to lower RFS survival ( p = 0.038) but did not affect OS. Multivariate analysis showed that lesions located in postero-superior segments (HR = 2.4, 95 % CI 1.24-4.61, p = 0.009) as well as blood loss (HR = 3.2, 95 % CI 1.23-7.99, p = 0.012) were independent risk factors for tumor recurrence. The carcinoembryonic antigen level >10 mcg/L affected OS (HR = 4.2 95 % CI 2.02-16.9, p = 0.001), and the resection of more than two tumors was significantly associated with R1 margins (HR = 9.32, 95 % CI 1.14-32.5, p = 0.037). Discussion: Laparoscopic parenchymal-sparing surgery of CRLM does not compromise the oncological outcome, allowing a higher percentage of repeat hepatectomy. R1 margins are a risk factor for tumor recurrence but not for overall survival. The presence of multiple lesions is the only independent risk factor of R1 margins and also the major disadvantage of this technique. [ABSTRACT FROM AUTHOR]

Purpose: Recent studies have reported that margins alone do not predict survival in patients with a positive chemotherapy response. The aim of this retrospective study is to analyze the surgical and oncological outcomes of patients who underwent chemotherapy and liver resection for colorectal liver metastases (CRLM) with lesions detached from the main hepatic veins, comparing the vein-preserving (VP) approach with traditional surgery. Methods: Fourteen patients undergoing VP surgery from January 2006 to January 2013 were matched in a 1:2 ratio with a control group (CG) of 28 patients undergoing traditional resection. Results: The median follow-up was 43 months. The radiological response was classified as 'partial response' in eight VP patients and 11 controls (57 vs. 39 %, p = 0.249) and as 'stable disease' in three VP patients and 9 controls (21 vs. 32 %, p = 0.465). Ten VP (71.4 %) and twenty CG patients (71.4 %) experienced tumor relapse ( p = 0.99). No venous edge recurrences were recorded in the VP group, whereas 1/13 (7.7 %) was observed in the control group ( p = 0.99). The pathological response rate was 64 vs. 39 % ( p = 0.037) in VP and CG patients, respectively. The 5-year recurrence-free survival rate was 24 % for VP patients and 25 % for CG patients ( p = 0.431). Conclusion: In patients with a positive CT response, CRLM can be detached from the hepatic veins, as the oncological outcome is similar to that of a larger resection. The VP approach offers the possibility to enlarge the surgical indications, thus optimizing future surgical treatment chances. [ABSTRACT FROM AUTHOR]

Most patients with rectal cancer receive neoadjuvant radiochemotherapy (RCT), causing a variable decrease in tumor mass. We evaluated the prognostic impact of pathologic parameters reflecting tumor response to RCT, either directly or indirectly. Seventy-six rectal cancer patients receiving neoadjuvant RCT between 2006 and 2009 were included. We studied the association between disease-free survival (DFS) and the 'classical' clinicopathologic features as well as tumor deposits, circumferential resection margin (CRM), Dworak regression grade, and tumor and nodal downstaging. Patients with tumor downstaging had a longer DFS ( p = 0.05), indicating a more favorable prognosis when regression was accompanied by a decrease in tumor infiltrative depth, referred to as tumor shrinkage. Moreover, tumor downstaging was significantly associated with larger CRM and nodal downstaging ( p = 0.02), suggesting that shrinkage of the primary tumor was associated with a decreased nodal tumor load. Higher Dworak grade did not correlate with tumor downstaging, nor with higher CRM or prolonged DFS. This implies that tumor mass decrease was sometimes due to fragmentation rather than shrinkage of the primary tumor. Lastly, the presence of tumor deposits was clearly associated with reduced DFS ( p = 0.01). Assessment of tumor shrinkage after RCT via tumor downstaging and CRM is a good way of predicting DFS in rectal cancer, and shrinkage of the primary tumor is associated with a decreased nodal tumor load. Assessing regression based on the amount of tumor in relation to stromal fibrosis does not accurately discern tumor fragmentation from tumor shrinkage, which is most likely the reason why Dworak grade had less prognostic relevance. [ABSTRACT FROM AUTHOR]

Background: Functional disturbances of the endoplasmic reticulum (ER) lead to activation of the unfolded protein response (UPR), which is involved in the consecutive steps of carcinogenesis. In human hepatocellular carcinoma (HCC), the UPR is shown to be activated; however, little is known about the UPR kinetics and effects of UPR modulation in HCC. Methods: We sequentially monitored the UPR over time in an orthotopic mouse model for HCC and explored the effects of UPR modulation on cell viability and proliferation in vitro and in the mouse model. Results: The expression of ER-resident chaperones peaked during tumor initiation and increased further during tumor progression, predominantly within the nodules. A peak in Ire1 signaling was observed during tumor initiation. The Perk pathway was activated during tumor progression, and the proapoptotic target Chop was upregulated from week 5 and continued to rise, especially in the tumors. The Atf6 pathway was modestly activated only after tumor initiation. Consistent with the UPR activation, electron microscopy demonstrated ER expansion and reorganization in HCC cells in vivo. Strikingly, under ER stress or hypoxia, the Perk inhibitor and not the Ire1 inhibitor reduced cell viability and proliferation via escalating proteotoxic stress in vitro. Notably, the Perk inhibitor significantly decreased tumor burden in the mouse model. Conclusion: We provide the first evaluation of the UPR dynamics in a long-term cancer model and identified a small molecule inhibitor of Perk as a promising strategy for HCC therapy. [ABSTRACT FROM AUTHOR]

This study aimed to characterize ductal carcinoma in situ (DCIS) according to human epidermal growth factor receptor 2 (HER2) amplification status and molecular subtype. In addition, we performed a detailed HER2 and CEP17 copy number analysis and we assessed the impact of recent changes in the American Society of Clinical Oncology/College of American Pathologists (ASCO/CAP) guidelines on HER2 immunohistochemical (IHC) scores in DCIS. Nuclear grade, extensive comedonecrosis, stromal architecture, stromal inflammation, and progesterone receptor (PR) expression were significantly associated with HER2 amplification status. In multivariate analysis, stromal inflammation and extensive comedonecrosis were the only two features that remained significantly related to HER2 amplification status. The recent changes in ASCO/CAP guidelines resulted in significant upgrading of HER2 IHC score. Remarkably, about one in five non-amplified DCIS presented a 3+ IHC score, regardless of the scoring method. The biological significance of this phenomenon is presently unknown. After categorization according to molecular subtype, luminal A DCIS mainly presented histopathological features associated with good prognosis, whereas luminal B/HER2+ and HER2+ categories displayed a more aggressive phenotype. Overall, our results demonstrate that HER2-amplified DCIS constitute a clearly distinct subgroup which is characterized by histopathological features associated with poor prognosis. Further studies are required to elucidate the biological significance of a 3+ IHC score in non-amplified DCIS, as well as its mechanism. [ABSTRACT FROM AUTHOR]

We studied a series of spindle cell lipomas arising in atypical sites and showing unusual morphologic features (which we called atypical spindle cell lipoma) to assess if these lesions have the same chromosomal alterations as classical spindle cell lipoma but different from those found in atypical lipomatous tumor/well-differentiated liposarcoma. We investigated alterations of different genes in the 13q14 region and the amplification status of the MDM2 and CDK4 genes at 12q14-15 by multiplex ligation-dependent probe amplification (MLPA) and fluorescence in situ hybridization (FISH) analysis. In the atypical spindle cell lipomas, MLPA revealed deletions in the two nearest flanking genes of RB1 ( ITM2B and RCBTB2) and in multiple important exons of RB1. In contrast, in classical spindle cell lipomas, a less complex loss of RB1 exons was found but no deletion of ITM2B and RCBTB2. Moreover, MLPA identified a deletion of the DLEU1 gene, a finding which has not been reported earlier. We propose an immunohistochemical panel for lipomatous tumors which comprises of MDM2, CDK4, p16, Rb, which we have found useful in discriminating between atypical or classical spindle cell lipomas and other adipocytic neoplasms, especially atypical lipomatous tumor/well-differentiated liposarcoma. Our findings strengthen the link between atypical spindle cell lipoma and classical spindle cell lipoma, and differentiate them from atypical lipomatous tumor/well-differentiated liposarcoma. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate murine double minute-2 (MDM2) gene copy number changes in colon carcinoma and to correlate these findings with an immunohistochemical analysis of MDM2 protein expression and histopathologic prognostic indicators of the tumors. The study included 80 cases of sporadic colon carcinomas. MDM2 protein expression was assessed by immunohistochemistry, and MDM2 gene status by fluorescence in situ hybridization. MDM2 gene amplification was detected in 18% of the 80 cases examined. A strong correlation was found between MDM2 gene amplification and the presence, intensity, and staining proportion of cytoplasmic MDM2 protein expression (p = 0.01). No correlation was found between MDM2 gene amplification and the well-established histopathologic prognostic factors. Given the correlation with gene amplification, we clearly demonstrated that cytoplasmic expression of MDM2 protein is true and relevant and that this finding has to be taken into account when immunohistochemistry would be used as a screening for MDM2 gene amplification in the near future. Targeting MDM2 could be a new approach in colon cancer therapy. The amplification status could be a predictive factor of the response to MDM2-targeted therapy. [ABSTRACT FROM AUTHOR]

This study aims to describe a patient developing concomitant severe liver failure and lactic acidosis after long-term treatment with linezolid. A 55-year-old Caucasian woman developed concomitant severe liver failure and lactic acidosis after a treatment with linezolid for 50 days because of infected hip prosthesis. Other causes of liver failure and lactic acidosis were excluded by extensive diagnostic workup. A liver biopsy showed microvesicular steatosis. As linezolid toxicity was considered to be the cause of the lactic acidosis and the severe hepatic failure, the antibiotic was withdrawn. After 4 days of supportive therapy and hemodialysis, the serum lactate level returned within normal limits. The prothrombin time ratio and thrombocytes recovered within 2 weeks. Bilirubin levels normalized within 14 weeks. Since no other cause could be identified, liver injury was considered to be drug-related. Resolution of the hepatotoxicity occurred after discontinuation of linezolid, supportive treatment measures, and hemodialysis. Both lactic acidosis and microvesicular steatosis after the use of linezolid are related to mitochondrial dysfunction. The Council for International Organizations of Medical Sciences/Roussel Ucalf Causality Assessment Method scale revealed that the adverse drug event was probable. Prolonged exposure to linezolid may induce severe hepatotoxicity. Clinicians should be aware of this possible adverse effect especially in case of long-term treatment. [ABSTRACT FROM AUTHOR]

The aims of the study were to study the effect of pre-operative treatment on the expression of tumour-related proteins and to correlate the expression of these proteins with response and survival of patients with advanced rectal cancer. Tissue micro-arrays from pre- and post-treatment biopsies of 99 patients with rectal cancer treated with pre-operative (chemo)radiotherapy were stained for epidermal growth factor receptor (EGFR), carbonic anhydrase IX, Ki67, vascular endothelial growth factor, cyclo-oxygenase 2 (COX-2) and cleaved cytokeratin 18 (c-CK18). Also, fibro-inflammatory alterations after treatment were evaluated. Pre-operative (chemo)radiotherapy caused fibro-inflammatory changes, a downregulation of proliferation (Ki67) and EGFR and an upregulation of apoptosis (cleaved CK18). Patients with a good regression during pre-operative treatment showed less proliferating and apoptotic cells in the resection specimen. Multivariate analysis showed that T downstaging, fibro-inflammatory changes in the resection specimen and COX-2 expression in the biopsy correlated with overall survival. Pre-operative treatment has an effect on proliferation, apoptosis, inflammation and EGFR expression. The classical clinical parameters as well as fibro-inflammatory changes and COX-2 expression seem most valuable as predictors for survival. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Focal nodular hyperplasia-like nodules (FNH-like nodules) are focal lesions occurring in liver cirrhosis and are morphologically very similar to classical FNH in an otherwise normal liver. They are sometimes misdiagnosed as hepatocellular carcinoma (HCC) on imaging because both types of lesions show arterial-phase enhancement. Although the morphological, immunohistochemical, and imaging features of FNH-like nodules are well-known, their pathogenesis and role in hepatocarcinogenesis have not been studied in detail. Therefore, we performed a detailed pathological evaluation of 130 cirrhotic explant livers and correlated these data with the clinical features of the patients. METHODS: All cirrhotic explant livers were uniformly sliced at 5-mm intervals and all detected focal lesions were microscopically classified according to internationally accepted criteria. The obtained data regarding FNH-like nodules were then correlated with other pathological findings and with clinical data obtained during pretransplant evaluation and recorded in a database. RESULTS: FNH-like nodules were present in 15% of patients and their small size (75% of cases <1 cm) appears to preclude detection by imaging in almost all cases. The presence of esophageal varices and pretransplant treatment with chemoembolization were independently and significantly associated with the presence of FNH-like nodules. There were no associations between FNH-like nodules on the one hand and low-grade dysplastic nodules, high-grade dysplastic nodules, and HCCs on the other hand. CONCLUSIONS: The clinicopathological features of FNH-like nodules support the hypothesis that vascular alterations in liver cirrhosis play an important role in their pathogenesis and that FNH-like nodules do not have an increased risk of malignant transformation. [ABSTRACT FROM AUTHOR]

The variability in the prognosis of individuals with hepatocellular carcinoma (HCC) suggests that HCC may comprise several distinct biological phenotypes. These phenotypes may result from activation of different oncogenic pathways during tumorigenesis and/or from a different cell of origin. Here we address whether the transcriptional characteristics of HCC can provide insight into the cellular origin of the tumor. We integrated gene expression data from rat fetal hepatoblasts and adult hepatocytes with HCC from human and mouse models. Individuals with HCC who shared a gene expression pattern with fetal hepatoblasts had a poor prognosis. The gene expression program that distinguished this subtype from other types of HCC included markers of hepatic oval cells, suggesting that HCC of this subtype may arise from hepatic progenitor cells. Analyses of gene networks showed that activation of AP-1 transcription factors in this newly identified HCC subtype might have key roles in tumor development. [ABSTRACT FROM AUTHOR]

In the liver, neural cell adhesion molecule (NCAM) is a marker of immature cells committed to the biliary lineage and is expressed by reactive bile ductules in human liver diseases. We investigated the possible role of NCAM in the development of intrahepatic bile ducts and aimed at determining whether immature biliary cells can contribute to the repair of damaged bile ducts in chronic liver diseases. Therefore, we performed immunohistochemistry for NCAM and bile duct cell markers cytokeratin 7 and cytokeratin 19 on frozen sections of 85 liver specimens taken from 14 fetuses, 10 donor livers, 18 patients with congenital liver diseases characterized by ductal plate malformations (DPMs), and 43 cirrhotic explant livers. Duplicated ductal plates and incorporating bile ducts during development showed a patchy immunoreactivity for NCAM, while DPMs were continuously positive for NCAM. Bile ducts showing complete or patchy immunoreactivity for NCAM were found in cirrhotic livers, with higher frequency in biliary than in posthepatitic cirrhosis. Our results suggest that NCAM may have a function in the development of the intrahepatic bile ducts and that NCAM-positive immature biliary cells can contribute to the repair of damaged bile ducts in chronic liver diseases. [ABSTRACT FROM AUTHOR]

The article reports on a case of an appendiceal mucinous neoplasm in association with endometriosis in a 48-year-old woman. The patient has underwent imaging for an episode of pancreatitis and surgery was performed. Her microscopic examination demonstrated that the cystic lesion was covered by a mucosa. Details of the findings of her laboratory examinations are discussed.