Browsing by Author "Boricic, I. (6603959716)"

[No abstract available]

Background: Actinic keratosis (AK) has been defined as a precancerous lesion or an early phase in the evolution of squamous cell carcinoma (SCC) and histological changes seen in the individual cells of an AK are indistinguishable from those seen in SCC, which invade the dermis. Cyclin A is an increasingly utilized proliferation marker that has functions in both S phase (DNA replication) and initiation of mitosis, whereas alterations of β-catenin, the molecule involved in cell-cell adhesion and in signalling transduction, could promote invasive and proliferative capacities of malignant tumours. Objectives: To determine cyclin A and β-catenin expression pattern in cutaneous SCC and in in situ lesions classified as keratinocytic intraepidermal neoplasia (KIN) and, using traditional terms, as AK and Bowen's disease (BD), and to analyse it in relation to SCC differentiation, diameter and thickness. Methods: Immunohistochemical staining was performed on 110 formalin-fixed paraffin-embedded tissue samples with the streptavidin-biotin technique using antibodies to cyclin A and β-catenin. On histological examination, 53 lesions were diagnosed as AK, 16 as BD and 41 as SCC-11 well differentiated (WD), 16 moderately differentiated (MD) and 14 poorly differentiated (PD). Using KIN classification, 22 lesions were KIN1, 23 were KIN2 and 24 were KIN3. For cyclin A, distribution and labelling index (LI), and for β-catenin, level of membranous staining and presence of aberrant (nuclear/cytoplasmic) localization were examined. Results: Diffuse cyclin A presence was observed more frequently in BD than in AK (P < 0.0001) or SCC (P = 0.0002), and in SCC-PD compared with SCC-WD (P < 0.0001) or SCC-MD (P = 0.0003). Differences between KIN3 and KIN2, as well as KIN3 and KIN1 lesions, were statistically significant (P < 0.0001), and the same result appeared when KIN1 and KIN 2 cases were grouped and compared with those of KIN3 (P < 0.0001). Cyclin A LI was significantly lower (P < 0.05) in AK than in BD or SCC, but no difference between BD and SCC was found, and U in BD was even higher than in SCC-WD or SCC-MD, while analysis regarding SCC differentiation and KIN classification revealed the same correlation as for the cyclin A distribution. Reduced or absent β-catenin membranous staining was found in 90 cases (81.8%), more often in SCC than in AK (P = 0.03) or in AK and BD grouped together (P = 0.02). There was no statistical difference between SCCs of various level of differentiation, or between different KIN grades. Diffuse loss of membranous β-catenin staining showed 36 lesions (32.7%), more frequently SCC than AK (P = 0.003) or AK and BD grouped (P = 0.006), as well as SCC-PD compared with SCC-WD (P = 0.01) and SCC-MD (P = 0.03), whereas all KIN comparisons remained nonsignificant. Aberrant β-catenin cellular localization demonstrated 28 lesions (25.5%), most often in the basal or peripheral parts and in the lesions with diffuse β-catenin loss (P = 0.009), but revealed no correlation with the histological type, SCC level of differentiation or KIN grades. Diffuse loss of membranous β-catenin staining was found to be significantly more frequent in SCC thicker than 4 mm (P = 0.03), while all other comparisons between cyclin A or β-catenin with the tumour size remained nonsignificant. Cyclin A LI was higher in cases with diffuse loss of membranous staining (P = 0.001) or with aberrant cellular localization of β-catenin (P = 0.002). Conclusions: Cyclin A LI showed greater difference between AK and BD than between BD and SCC, suggesting that increased proliferation (measured by cyclin A LI) characterizes progression of in situ lesions from AK to BD, whereas reduced β-catenin expression separates more clearly SCC from the in situ lesions. Diffuse pattern of loss of membranous β-catenin staining correlated better with the type of lesion, SCC differentiation and tumour size than reduced expression in general or aberrant cellular localization of β-catenin. KIN classification does not seem to be supported by our findings, except when KIN1 and KIN2 lesions (in situ, partial thickness) are grouped. © 2005 British Association of Dermatologists.

Nevus lipomatosus superficialis (NLS) is a rare benign condition characterized by papules and nodules usually in the pelvic and sacral areas, with ectopic mature adipose tissue reaching the superficial dermis. We report the case of a 47-year-old female with large NLS in the sacral region that had been present since birth and, after an asymptomatic course for most of the time, became associated with episodes of mild pain that prompted the patient to look for medical help. After a complete resection of the cerebriform plaque, measuring 23 cm in diameter, histopathological examination revealed typical NLS architecture in as yet undescribed association with multiple folliculosebaceous cystic hamartomas (FCHs) and dermoid cysts. © 2004 European Academy of Dermatology and Venereology.

Large-cell neuroendocrine carcinoma is a highgrade neuroendocrine carcinoma, originally described in the lung. The tumor rarely occurs in extrapulmonary sites like the gastrointestinal tract, and only few examples have been described in the ampulla of Vater. A new case of large-cell neuroendocrine carcinoma of the ampulla of Vater in a 60-year-old man is reported. After pancreatoduodenectomy, macroscopic examination revealed ulcerated tumor in the region of the ampulla of Vater. Microscopically, the tumor exhibited organoid, predominantly nested growth pattern, consisting of large, polygonal cells with pleomorphic nuclei. Average number of mitoses was 36 per 10 high-power fields. Small and large areas of necrosis were identified. Immunohistochemically, the tumor cells were positive for synaptophysin, chromogranin A, PGP 9.5, neuron-specific enolase, pancytokeratin, CK8 and somatostatin and negative for CK7, CK20, S-100, TTF-1, HMB-45, CD117, E-cadherin and regulatory peptides. Ki-67 proliferative index was 41%. Histone deacetylase (HDAC) analysis showed almost identical results for HDAC1, HDAC2 and HDAC3-60, 60.3 and 61%, respectively. Two months after surgery, liver metastases occurred, confirming highly aggressive behavior of large-cell neuroendocrine carcinoma. © Humana Press Inc. 2009.

Large-cell neuroendocrine carcinoma is a highgrade neuroendocrine carcinoma, originally described in the lung. The tumor rarely occurs in extrapulmonary sites like the gastrointestinal tract, and only few examples have been described in the ampulla of Vater. A new case of large-cell neuroendocrine carcinoma of the ampulla of Vater in a 60-year-old man is reported. After pancreatoduodenectomy, macroscopic examination revealed ulcerated tumor in the region of the ampulla of Vater. Microscopically, the tumor exhibited organoid, predominantly nested growth pattern, consisting of large, polygonal cells with pleomorphic nuclei. Average number of mitoses was 36 per 10 high-power fields. Small and large areas of necrosis were identified. Immunohistochemically, the tumor cells were positive for synaptophysin, chromogranin A, PGP 9.5, neuron-specific enolase, pancytokeratin, CK8 and somatostatin and negative for CK7, CK20, S-100, TTF-1, HMB-45, CD117, E-cadherin and regulatory peptides. Ki-67 proliferative index was 41%. Histone deacetylase (HDAC) analysis showed almost identical results for HDAC1, HDAC2 and HDAC3-60, 60.3 and 61%, respectively. Two months after surgery, liver metastases occurred, confirming highly aggressive behavior of large-cell neuroendocrine carcinoma. © Humana Press Inc. 2009.

Primary sclerosing cholangitis (PSC) is a chronic liver disease which primarily affects the bile ducts. We summarize currently available information about histopathology and aetiopathogenesis of PSC. This disease is characterized by non-specific inflammatory fibrosis in the wall of the biliary tree leading to irregular stenosis, usually of both the intra - and extrahepatic bile ducts, combined by multifocal segmental dilatation of the biliary tree. Four histological stages of PSC have been identified. First represents the initial lesion and characterized by portal hepatitis and degeneration of epithelial cells of the bile ducts. Stage 4 is the end stage, and it is characterized by frank biliary cirrhosis. The pathognomonic sign of PSC is the onion skin lesion. However, it is rarely seen on percutaneous biopsy of the liver. The diagnosis is therefore usually made by typical cholangiographic findings: bile duct dilatations proximal to areas of stricture. Histologic examination of the liver is used for confirmation and to determine the stage of the disease. The aetiopathogenesis of the PSC is unknown, but there is an evidence that genetic and immunologic factors are involved. Portal bacteriemia, viral infections, and toxic and ischemic factors have also been implicated in the pathogenesis of PSC.

[No abstract available]

The case of a 46-year-old female with umbilical metastasis as a first sign of an ovarian carcinoma is reported with the results of immunohistochemical analysis of primary tumor and lymph node and umbilical metastases. All specimens were positive for cytokeratin 7, CA 125, E-cadherin, alpha-, beta-, and gamma-catenin, as well as for MSH2. Staining with cytokeratin 20 and MLH1 was negative, and Ki-67 labeled from 5% (in the center of the lesions) to over 25% (at the periphery of the lesions) of the nuclei. Beta-catenin showed membranous positivity in the central parts and absence of staining at the periphery of ovarian tumor and umbilical metastasis, whereas lymph node metastasis presented with uniform reaction throughout. The results of immunohistochemical staining could point to the mechanisms employed by malignant tumors during invasion and growth of metastasis and suggest the possible role of the microenvironment in the expression of some adhesion molecules on tumor cells. © 2005 IGCS.