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C Capella

Publications and source records attributed to C Capella.

At least 37 records · Page 2Linked to original sources
PubMed2000

Mixed endocrine-exocrine tumors of the gastrointestinal tract.

Mixed endocrine-exocrine tumors of the gastrointestinal tract are rare neoplasms, which have been reported in the literature mainly as case reports and have been designated with a various and rather confusing terminology. In this review, on the basis of personally studied cases and of the analysis of cases reported in the literature, we have tried to identify types of mixed endocrine-exocrine tumors showing different clinicopathologic and biological characteristics. We have also tried to group the different clinicopathologic entities in prognostic classes which include: benign, low-grade, intermediate grade, and high-grade malignant mixed endocrine-exocrine tumors. The criteria for identifying the various types of mixed endocrine-exocrine tumors are extensively discussed.

Adenocarcinoma↗
PubMed2000

Introduction to a revised clinicopathological classification of neuroendocrine tumors of the gastroenteropancreatic tract.

A revised clinicopathological classification of neuroendocrine tumors of the gastroenteropancreatic tract has been recently developed under the auspices of the World Health Organization (WHO) according to advances in the field of tumor biology. Here the classification is briefly outlined and discussed together with the guidelines for a correct approach to the histopathological diagnosis of neuroendocrine tumors and the interpretation of the classification schemes covering clinical (hyperfunctional syndromes included), pathological and biological patterns, with special emphasis on tumor prognosis.

Gastrointestinal Neoplasms↗
PubMed2000

[Expression of p53 in gallbladder carcinoma and in dysplastic and metaplastic lesions of the surrounding mucosa].

We studied the expression of p53 in 80 gallbladder carcinomas, 43 peritumoral mucosae, 5 adenomas and 20 mucosae of non tumoral gallbladders. Gallbladder cancers were classified according to WHO criteria. We found p53 overexpression in 51 out of the 80 gallbladder cancers (64%). p53 expression was variable in different histologic subtypes: 100% of intestinal type, 66% of papillary type, 83% of adenosquamous carcinomas and 66% of giant cells cancers showed immunoreactive cells. In well and moderately differentiated conventional gallbladder adenocarcinomas we found 60% of positive cases, while, among poorly differentiated conventional cancers, 83% were immunoreactive. All mucinous adenocarcinomas were p53-negative. In peritumoral dysplastic mucosae, p53 was expressed in 23 out 38 cases (60%), 22 (96%) of which were associated to a p53-positive adenocarcinoma. On the contrary, only 5 of the 15 p53-negative dysplastic lesions (33%) were associated to an p53-immunoreactive adenocarcinoma. Metaplastic lesions, of gastric and intestinal type, and adenomas were completely p53-negative. In conclusion, our data suggest that p53 expression is an early event, frequently involved in gallbladder carcinogenesis, and related to different histologic subtypes of gallbladder adenocarcinomas.

Adenocarcinoma↗
PubMed2000

[Primary gastric lymphomas. Clinico-pathological study and evaluation of prognostic factors in 65 cases treated surgically].

Based on the histological criteria proposed by the REAL and adopted by the WHO Classification, 30 cases of MALT type lymphoma, 18 cases of diffuse large B cell lymphoma (DLCL), and 17 cases of DLCLs, associated with a MALT type, were identified in a series of 65 surgically treated primary gastric lymphomas. The clinical records of the patients were analyzed retrospectively and the resected specimens were immunostained for bcl-2, p53 and Ki-67. Primary gastric DLBCLs, with or without a MALT type component, disclosed a higher stage of local extension, a more frequent nodal involvement and a significantly worse survival than pure MALT types. High p53 expression and high proliferation rate correlated with the presence of a large cell component and appeared useful for its identification in mixed forms. Low bcl-2 expression discriminated DLCL from DLCL/MALT. Tumor size, stage and Mib-1 index revealed a value in predicting prognosis.

Adult↗
PubMed1999

Microsatellite instability and/or loss of heterozygosity in young gastric cancer patients in Italy.

Gastric cancers are rarely diagnosed before the age of 40 years and the incidence reaches a peak during the 7th decade in the general population. A molecular mechanism of early tumor onset may be determined by comparing microsatellite instability (MSI), indicative of error-prone mismatch repair, and loss of heterozygosity (LOH) between gastric cancers in patients < or = 40 years of age and those of older ages. Three to 5 chromosomal loci, where MSI and/or LOH are commonly found in gastric cancers in the general population, were examined in formalin-fixed, paraffin-embedded samples from 102 patients < or = 40 years of age using a polymerase chain reaction-based non-radioactive screening method. MSI and/or LOH at a minimum of 1 locus were detected in 11/102 patients. The frequency of MSI and/or LOH at the D11S904 locus was significantly higher than that at the D2S119, D2S123, D5S409 and IFNA regions. No preferential genetic changes at the D11S904 locus were observed in elderly patients. Among several clinicopathological variables, a statistically significant association with MSI and/or LOH was observed only for tumors located at the cardia, compared with tumors at the antrum and the corpus. Our findings suggest that a unique mechanism may be involved in increasing the susceptibility of the D11S904 locus for either MSI or LOH, especially for cardia tumors in young patients. Early onset of gastric cancers in patients < or = 40 years of age is associated with genetic changes at preferential chromosomal loci, including D11S904.

Adolescent↗
PubMed1999

Microsatellite instability in endometrial cancer: relation to histological subtypes.

Fifty-one endometrial cancers were analyzed with regard to whether or how microsatellite instability (MI) was associated with the development of different types of endometrial malignant neoplasms. We investigated 6 loci previously reported as informative for colorectal cancer and a group of 8 loci located on 6q. Replication error (RER+) phenotype was detected in 10 of 51 (19.6%) endometrial cancers (ECs), all but one of which showed endometrioid differentiation. On the contrary, the RER+ phenotype was not detected in serous carcinomas and malignant mixed Müllerian tumors. MI was present in both early and advanced stage ECs. No correlation was found between age, grade, stage, familial pattern, mitotic index, and the RER+ phenotype of ECs. Only 1 of 8 endometrial carcinomas showing MI was associated with mutant p53 expression, while the majority of RER+ tumors were positive for estrogen and progesterone receptors. Our findings suggest that MI plays an early role in endometrial tumorigenesis and is significantly correlated with adenocarcinomas showing endometrioid features (EAs). The frequent involvement of the telomeric region of chromosome 6 in the MI of EA is an indication that this region may be crucial in the process of EA tumorigenesis.

Aged↗
PubMed1999

Immunohistochemical localization of alpha- and betaA-subunits of inhibin/activin in human normal endocrine cells and related tumors of the digestive system.

Activin A and inhibin A, first isolated from the ovary, are dimeric proteins able to modulate pituitary FSH secretion. Inhibin A is a heterodimer composed of one alpha-subunit and one betaA-subunit (alpha-betaA), while activin A is a homodimer of the betaA-subunit (betaA-betaA). Their identification in several tissues has suggested that they have numerous physiological functions, acting as either paracrine or autocrine factors. The aim of this study was to evaluate the expression of activin A and inhibin A in normal endocrine cells and in 70 endocrine tumours from different sites in the gastro-entero-pancreatic system, using specific monoclonal antibodies directed against the alpha- and betaA-subunits of inhibin/activin. Immunoreactivity for the betaA-subunit, but not for the alpha-subunit, was observed in normal G, EC, and GIP cells of the antrum and duodenum, and in pancreatic A cells. BetaA-subunit expression was observed in G cell and A cell tumours, and in a few insulinomas and ileal EC cell carcinoids. The alpha-subunit was found in rare cells in 7 of the 70 tumours and was colocalized with the betaA-subunit in only 1 tumor. Specific types of endocrine cells from the gut and pancreas appear to produce only activin A, a possible paracrine or autocrine modulator. Activin A is mainly produced by tumours derived from endocrine cells that normally express it.

Activins↗
PubMed1999

ECL cell tumor and poorly differentiated endocrine carcinoma of the stomach: prognostic evaluation by pathological analysis.

BACKGROUND & AIMS: Gastric endocrine tumors show a wide spectrum of clinical behavior, and prognostic assessement of individual tumors is difficult. The aims of this work were to identify predictors of tumor malignancy and patient outcome and to provide a rationale for treatment guidelines. METHODS: Gastric endocrine tumors (86 enterochromaffin-like cell carcinoids and 16 poorly differentiated carcinomas) were investigated for 15 clinicopathologic variables and for expression of Ki67, P53, and BCL-2 proteins. Data were analyzed by univariate and multivariate statistics for evidence of tumor malignancy and patient survival. RESULTS: Histological grades 2 and 3, size >/=3 cm, 9 or more mitoses, or >/=300 Ki67-positive cells per 10 high-power fields identified 26 of 33 (79%) malignant (metastatic or deeply invasive) tumors, and size <1 cm and/or growth restricted to the mucosa characterized 46 of 69 (67%) tumors with benign behavior during a median follow-up of 39 months. Malignancy-predictive models were developed using angioinvasion, size, clinicopathologic type, mitotic index, and Ki67 index. The same variables, in addition to deep gastric wall invasion and histological grade, predicted patient outcome. CONCLUSIONS: Criteria for the assessment of malignancy risk and patient outcome were developed for the different tumors, providing a basis for treatment guidelines.

Analysis of Variance↗
PubMed1999

Microsatellite instability in gastric MALT lymphomas and other associated neoplasms.

BACKGROUND: Microsatellite instability (MSI), caused by a reduced efficacy of the DNA mismatch repair (MMR) machinery, represents a type of genomic instability frequently detected in HNPCC spectrum cancers and in a subset of sporadic carcinomas. The involvement of MSI in the pathogenesis of gastric lymphoma of mucosa-associated lymphoid tissue (MALT) has never been conclusively investigated. In this study, we tested the presence of MSI in tumor samples of patients harboring both MALT lymphomas and other types of malignancies. MATERIALS AND METHODS: We examined 10 microsatellite loci (D3S11, D3S1261, D3S1265, D6S262, D6S193, BAT-26, BAT-25, D17S250, APC, D2S123) out of a total of 34 primary tumors from 14 patients with MALT lymphomas and one or more additional neoplasms. The patients' MSI results were also tested for an association with a positive family history of cancer. RESULTS: MSI, defined by the presence of microsatellite alterations in more than 40% of the examined loci, was scored negative in all tumors studied, and pedigree analysis failed to identify any condition of familial cancer among the patients examined. CONCLUSIONS: The present study suggests that defects in DNA mismatch repair do not contribute significantly to the molecular pathogenesis of MALT lymphomas and associated neoplasms.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMed1999

Clinicopathological profile as a basis for classification of the endocrine tumours of the gastroenteropancreatic tract.

Recent developments in the field of endocrine cell biology and pathology, at both morphologic and molecular levels, are briefly outlined and discussed as a basis for endocrine tumour characterization. The main clinicopathological tools available for the identification and characterization of endocrine tumours are discussed. Based on this, classifications of endocrine tumours of the pancreas and gastrointestinal tract are developed covering most clinical (hyperfunctional syndromes included), pathologic and biological patterns and with special emphasis on tumour prognosis.

Endocrine Gland Neoplasms↗
PubMed1999

Mucinous cystic tumors of the pancreas: clinicopathological features, prognosis, and relationship to other mucinous cystic tumors.

The clinicopathological features of 56 patients with mucinous cystic tumors (MCTs) of the pancreas were studied. Particular attention was paid to the prognosis of MCTs and the relationship to their ovarian, hepatic, and retroperitoneal counterparts. To distinguish MCTs from pancreatic intraductal papillary-mucinous tumors, MCTs were defined as tumors lacking communication with the duct system and containing mucin-producing epithelium, usually supported by ovarian-like stroma. All 56 tumors occurred in women (mean age 48.2 years) and were preferentially (93%) located in the body and tail of the pancreas. In accordance with the WHO classification, MCTs were divided into adenomas (n = 22), borderline tumors (n= 12), and noninvasive and invasive carcinomas (n = 22). Survival analysis revealed the extent of invasion to be the most significant prognostic factor (p<0.0001). Malignancy correlated with multilocularity and presence of papillary projections or mural nodules, loss of ovarian-like stroma, and p53 immunoreactivity. Stromal luteinization with expression of tyrosine hydroxylase, calretinin, or alpha inhibin was found in 66% of the cases. We conclude that the biologic behavior of MCTs is predictable on the basis of the extent of invasion. The similarities (i.e. gender, morphology, stromal luteinization) between pancreatic MCT and its ovarian, hepatobiliary, and retroperitoneal counterparts suggest a common pathway for their development.

Adenocarcinoma, Mucinous↗
PubMed1999

CHK1 frameshift mutations in genetically unstable colorectal and endometrial cancers.

The protein encoded by the CHK1 gene plays an important role in the G2 checkpoint in mammalian cells. In its coding region it presents a sequence of nine consecutive adenines that are a potential site of mutations in tumors with microsatellite instability (MSI). We analyzed the presence of frameshift mutations in the CHK1 gene in human colon and endometrial cancer samples. In the same cancer samples genes known to be altered in these tumors (BAX, TGFBRII, and IGFIIR) were also analyzed. CHK1 frameshfit mutations were found in 1 out 10 colon cancers and 2 out of 7 endometrial cancers showing MSI. CHK1 alterations were associated with the presence of a high degree of MSI. No alterations were found in patients with tumors showing low frequency or lacking instability (microsatellite stable). The same was true for the other four genes analyzed. The insertion or deletion of one A in the poly A tract resulted in a truncated protein. Alterations of the CHK1 gene could represent an alternative way of cancer cells to escape from cell cycle control. Genes Chromosomes Cancer 26:176-180, 1999.

Biomarkers, Tumor↗
PubMed1998

Cell biology, clinicopathological profile, and classification of gastro-enteropancreatic endocrine tumors.

Recent developments in the field of endocrine cell biology and pathology at both morphological and molecular levels are briefly outlined and discussed as a basis for endocrine tumor characterization. The main tools available for identifying the endocrine nature of the tumors, their pathogenetic interpretation. and experimental reproduction with special emphasis on tumor antecedents are reported. Based on this, classifications of endocrine tumors of the pancreas and gastrointestinal tract are developed, covering most clinical (hyperfunctional syndromes included), pathological, and biological patterns, with special emphasis on tumor prognosis.

Gastrointestinal Neoplasms↗
PubMed1998

Merkel cell differentiation in trichoblastoma.

Four cases of trichoblastoma rich in Merkel cells (MCs) are reported. They occurred in two men and two women, with ages ranging from 58 to 76 years (mean 67.5 years). MCs were detected immunohistochemically with antibodies to keratin 20, chromogranin A and neuron-specific enolase (NSE). In an attempt at better definition of the nature and role of MCs in trichoblastoma, the distribution of MCs in normal adult and fetal skins obtained at autopsy was studied. In addition, ten cases of sebaceous naevus of Jadassohn (NSJ) were evaluated along similar lines. MCs made up 2-20% of the tumour cells in trichoblastomas; they were present in normal fetal skin and were rare in normal adult skin. All but one of the cases of NSJ showed numerous positive cells in the epidermal component of the lesion with all three antibodies. Six basal cell carcinomas and one syringocystadenoma papilliferum associated with NSJ were negative with keratin 20, chromogranin A and NSE antibodies, whereas a minute trichoblastoma arising against the same background was positive for these markers. Hair follicle cell tumours may recapitulate the skin embryogenesis, as numerous MCs are present in fetal follicles, but only occasional such cells are seen in adult skin.

Aged↗
PubMed1998

The value of microsatellite instability in the detection of HNPCC families and of sporadic colorectal cancers with special biological features: an investigation on a series of 100 consecutive cases.

BACKGROUND: Microsatellite instability (MI) is a biological characteristic of most tumors involved in hereditary non-polyposis colorectal cancer (HNPCC). This disease appears to be caused by germline mutations in mismatch repair (MMR) genes, which are responsible for repairing single base-pair mismatches. At least five human genes participate in MMR. MI also occurs in 10%-15% of sporadic colorectal cancers. Because MI detection has been suggested as an alternative diagnostic tool for identification of HNPCC families, in this study we analyzed the MI pattern in 100 consecutive colorectal carcinomas in order to correlate them with the clinicopathologic features and family histories of the patients. PATIENTS AND METHODS: A series of 100 colorectal cancers was evaluated for MI with 10 polymerase chain reaction primer sets. Instability results were compared with family history and other clinical and biological characteristics. RESULTS: MI was detected in 36 of 100 cancers, 27 of which showed low instability and nine a high instability. The low- and high-instability cases showed similar clinicopathological characteristics, and significantly positive associations were observed between MI and mucinous histological type (P = 0.0001) and MI and peritumoral lymphocytic infiltration (P = 0.01). A single HNPCC family was identified in the high-grade MI group, while two families belonged to the MI-negative group. CONCLUSIONS: Our data suggest that MI screening is probably not an efficient strategy for identifying HNPCC cases. MI does, however, appear capable of defining a category of colorectal cancers with favourable prognostic features and should be investigated at least in all cases of mucinous adenocarcinomas.

Adult↗
PubMed1998

Ki-ras and p53 gene mutations in pancreatic ductal carcinoma: a relationship with tumor phenotype and survival.

We investigated a series of clinically well documented pancreatic ductal adenocarcinomas for the presence of molecular alterations of the p53 and Ki-ras genes and their correlations with p53 nuclear immunohistochemical expression. The results were evaluated in comparison with cellular expression, by ductal cancer cells, of gastric (PGII) and intestinal (CAR-5) antigens and with several clinicopathologic parameters such as grade, stage, size and lymph-node status. Ki-ras gene mutation at codon 12 was detected in 77.7% of cases with no relationship with tumor grade, stage, and survival of the patients. p53 gene mutations were found in 18/31 (58%) cases and p53 immunohistochemical overexpression was detected in 51/104 (49%) of cases. Both Ki-ras and p53 gene mutations were found in 13/31 (41.9%) of adenocarcinomas examined, while Ki-ras and p53 overexpression was detected in 19/45 (42.2%). A positive correlation between p53 overexpression and tumour grade was found (p0.0001) but no relationship was found between p53 overexpression, tumor stage, lymph-node status and size of the tumors. A trend toward an association of p53 overexpression with poorer survival was found in patients with pancreatic cancers of the same grade, stage or with the same immunophenotype, but the data did not reach statistical significance. The expression of gastric and intestinal antigenic markers in pancreatic adenocarcinomas and the presence of molecular abnormalities analogous to those found in gastric and colorectal cancers suggest common genetic pathways in gastrointestinal and pancreatic carcinogenesis.

Adult↗