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PubMedDate not supplied

Ferritin immunohistochemical localization in normal and neoplastic colonic mucosa.

High levels of ferritin have been detected in serum and tumoral extracts of gastrointestinal neoplasms. However, its histological localization is not well known. An immunoperoxidase technique (PAP) was used for detecting ferritin in 30 colorectal carcinomas, 20 polyps and 8 cases of non-neoplastic mucosae. Ferritin staining was detected in stromal cells (98%) much more than in epithelial cells (21%). Connective cells were positive in 5 cases of normal mucosae (62%), 19 polyps (95%) and all carcinomas (100%). The number of positive cells gradually rose from normal mucosa to carcinoma with an intermediate score in adenomas. However, no relation could be found between the stromal ferritin score and dysplasia in polyps. Likewise, no relation was found between the stromal ferritin score and the differentiation grade, invasion or metastases in carcinomas. The positive epithelial pattern seen in 12 cases (21%) suggests non-specific staining due to passive diffusion from the stroma. Thus, these immunohistochemical findings suggest that in colonic neoplasms, ferritin could be a tumor marker produced mainly by stromal cell reaction more than by the epithelial cells.

Adenoma↗
PubMed2005

Hereditary cancer predisposition syndromes.

Cancer genetics is increasingly becoming integrated into the practice of modern medical oncology. The ability to distinguish a growing proportion of the 5% to 10% of all cancers that develop in individuals who have inherited a genetic mutation conferring heightened susceptibility to specific cancers may permit targeted efforts in cancer surveillance and prevention. While these individuals comprise a small proportion of the overall burden of cancer, strategies successful in reducing their remarkable cancer risks may be generalizable to the broader population. In this review, we highlight the most common hereditary cancer syndromes, most attributable to genes inherited in an autosomal dominant manner with incomplete penetrance, and a number of rare syndromes in which particular progress has been made. The prevalence, penetrance, tumor spectrum, and underlying genetic defects are discussed and summarized in a large table in which a more comprehensive enumeration of syndromes is provided.

Breast Neoplasms↗
PubMed2003

Angiogenesis in endocrine tumors.

Angiogenesis is the process of new blood vessel development from preexisting vasculature. Although vascular endothelium is usually quiescent in the adult, active angiogenesis has been shown to be an important process for new vessel formation, tumor growth, progression, and spread. The angiogenic phenotype depends on the balance of proangiogenic growth factors such as vascular endothelial growth factor (VEGF) and inhibitors, as well as interactions with the extracellular matrix, allowing for endothelial migration. Endocrine glands are typically vascular organs, and their blood supply is essential for normal function and tight control of hormone feedback loops. In addition to metabolic factors such as hypoxia, the process of angiogenesis is also regulated by hormonal changes such as increased estrogen, IGF-I, and TSH levels. By measuring microvascular density, differences in angiogenesis have been related to differences in tumor behavior, and similar techniques have been applied to both benign and malignant endocrine tumors with the aim of identification of tumors that subsequently behave in an aggressive fashion. In contrast to other tumor types, pituitary tumors are less vascular than normal pituitary tissue, although the mechanism for this observation is not known. A relationship between angiogenesis and tumor size, tumor invasiveness, and aggressiveness has been shown in some pituitary tumor types, but not in others. There are few reports on the role of microvascular density or angiogenic factors in adrenal tumors. The mechanism of the vascular tumors, which include adrenomedullary tumors, found in patients with Von Hippel Lindau disease has been well characterized, and clinical trials of antiangiogenic therapy are currently being performed in patients with Von Hippel Lindau disease. Thyroid tumors are more vascular than normal thyroid tissue, and there is a clear correlation between increased VEGF expression and more aggressive thyroid tumor behavior and metastasis. Although parathyroid tissue induces angiogenesis when autotransplanted and PTH regulates both VEGF and MMP expression, there are few studies of angiogenesis and angiogenic factors in parathyroid tumors. An understanding of the balance of angiogenesis in these vascular tumors and mechanisms of vascular control may assist in therapeutic decisions and allow appropriately targeted treatment.

Adrenal Gland Neoplasms↗
PubMed2006

Outcome of metastatic GIST in the era before tyrosine kinase inhibitors.

BACKGROUND: Treatment of metastatic GIST with imatinib mesylate results in a 2-year survival of approximately 72%. The outcome of patients with metastatic GIST not treated with tyrosine kinase inhibitors is not well defined. METHODS: One hundred nineteen patients with metastatic GIST diagnosed prior to July 1, 1998 (approximately 2 years prior to the use of imatinib for GIST) were identified from an institutional database of patients with pathologically confirmed GIST. Mutational analysis was performed in cases with available tissue. The log rank test and Cox regression models were used to assess prognostic factors. RESULTS: Median survival was 19 months with a 41% 2-year survival and a 25% 5-year survival. Resection of metastatic GIST was performed in 81 patients (68%), while 50 (42%) received conventional chemotherapy. Twelve patients (10%) were eventually started on imatinib. Primary tumor size <10 cm, <5 mitoses/50 HPF in the primary tumor, epithelioid morphology, longer disease-free interval, and surgical resection were independent predictors of improved survival on multivariate analysis. Mutational status did not predict outcome. In patients who underwent resection, the 2 year survival was 53%, and negative microscopic margins also independently predicted improved survival. CONCLUSIONS: Treatment with imatinib appears to improve 2-year survival of metastatic GIST by approximately 20% when compared to surgery alone. The combination of imatinib and surgery for the treatment of metastatic GIST therefore warrants investigation.

Adult↗
PubMed2006

Chemotherapy versus support cancer treatment in advanced gastric cancer: a meta-analysis.

The aim of the present study was to compare the efficacy of chemotherapy and support treatment in patients with advanced non-resectable gastric cancer in a systematic review and meta-analysis of randomized clinical trials that included a comparison of chemotherapy and support care treatment in patients diagnosed with gastric adenocarcinoma, regardless of their age, gender or place of treatment. The search strategy was based on the criteria of the Cochrane Base, using the following key words: 1) randomized clinical trials and antineoplastic combined therapy or gastrointestinal neoplasm, 2) stomach neoplasm and drug therapy, 3) clinical trial and multi-modality therapy, 4) stomach neoplasm and drug therapy or quality of life, 5) double-blind method or clinical trial. The search was carried out using the Cochrane, Medline and Lilacs databases. Five studies fulfilled the inclusion criteria, for a total of 390 participants, 208 (53%) receiving chemotherapy, 182 (47%) receiving support care treatment and 6 losses (1.6%). The 1-year survival rate was 8% for support care and 20% for chemotherapy (RR = 2.14, 95% CI = 1.00-4.57, P = 0.05); 30% of the patients in the chemotherapy group and 12% in the support care group attained a 6-month symptom-free period (RR = 2.33, 95% CI = 1.41-3.87, P < 0.01). Quality of life evaluated after 4 months was significantly better for the chemotherapy patients (34%; RR = 2.07, 95% CI = 1.31-3.28, P < 0.01) with tumor mass reduction (RR = 3.32, 95% CI = 0.77-14.24, P = 0.1). Chemotherapy increased the 1-year survival rate of the patients and provided a longer symptom-free period of 6 months and an improvement in quality of life.

Adenocarcinoma↗
PubMed1977

Gray scale echographic patterns of hepatic metastatic disease.

Abnormal gray scale hepatic echograms in 76 patients with known or suspected metastatic disease were reviewed. A varied echographic pattern was found, with the gray scale appearances falling into three identifiable categories (dense, lucent, and bulls-eye) and a fourth group difficult to characterize. Prior chemotherapy seemed to have little consistent effect on echographic patterns. A pattern of dense lesions was associated in a large percentage of cases with adenocarcinoma. Carcinoma of the colon commonly produced this appearance. The remaining echographic patterns showed little correlation with specific primary sites or cell types.

Adenocarcinoma↗
PubMed1982

Liver lesions: comparative accuracy of scintigraphy and computed tomography.

Of 84 cases with both radionuclide and computed tomographic studies of the liver, in 54 the results of the two examinations agreed, in 14 results disagreed, and in 16 cases one of the two tests gave equivocal results. Overall accuracy in detecting or ruling out focal liver disease was 79% for scintigraphy and 98% for computed tomography. In 13 of the 14 patients in whom studies did not agree, the scintigram was falsely negative. In 10 of these 13 false-negative scintigrams, small (less than 2 cm) solitary or multiple lesions were detected on computed tomography in patients who had normal liver function studies. In seven patients in whom both studies agreed, computed tomography provided additional, extrahepatic information that altered clinical management. Scintigraphy was 86% accurate in detecting liver disease when the patient had a gastrointestinal neoplasm, but only 74% accurate for nongastrointestinal neoplasm. Computed tomography was over 94% accurate in both situations. These data indicate an advantage of computed tomography as the initial screening examination for space-occupying lesions of the liver, especially in patients with a primary diagnosis of nongastrointestinal neoplasm.

False Negative Reactions↗
PubMed1993

Faecal calprotectin: a novel test for the diagnosis of colorectal cancer?

Calprotectin, a prominent cytosol protein in neutrophil granulocytes, was present in increased concentrations in stools from 50 of 53 patients with colorectal cancer, 32 of 40 patients with colorectal polyps, and all of 18 patients with gastric cancer. After radical surgery, faecal calprotectin levels reverted to the normal range in all but one patient with colorectal cancer. Calprotectin determinations are simplified by the stability of this protein in stools. Reliable estimates can be obtained in samples of only 5 g. On the basis of data from the literature, the test for calprotectin seems better than that for occult blood for the detection of gastrointestinal neoplasms.

Aged↗
PubMed1995

Palliative laser treatment of rectal cancer.

BACKGROUND: Endoscopic neodymium-yttrium aluminum garnet laser treatment is a therapeutic modality for gastrointestinal neoplasms. METHODS: Patients given palliative therapy with laser for invasive rectal cancer during 1989-93 at the Dept. of Surgery, University of Turku, were analyzed. RESULTS: All 20 patients (median age, 81.5 years) were unsuitable for radical surgery owing to the poor clinical condition and/or advanced disease. In 14 (70%) patients laparotomy and diversion was avoided with laser treatment; 6 patients underwent laparotomy, 2 for pelvic infiltration and large-bowel obstruction, 2 for rectovaginal fistula formation, and 1 for severe pain. One patient underwent abdominoperineal resection for bleeding after laser treatment. Postoperative complications developed in three (15%) patients--two episodes of bleeding and one of sepsis; none of these complications was fatal. CONCLUSIONS: Local palliative laser treatment of rectal carcinoma is efficient in patients who are unsuitable for radical surgery. Operative diversion can be avoided without deaths and with minimal morbidity.

Aged↗
PubMed1989

Chemotherapy of gastric cancer.

Overall, gastric cancer appears to be the most chemotherapy-responsive gastrointestinal neoplasm. A number of single agents have been demonstrated to produce partial responses and combination chemotherapy produces response rates of 30-50% with some complete responses. Completed and ongoing adjuvant studies, employing multiple drug regimens have not demonstrated convincing evidence of survival advantage. Combined modality treatment appears to offer an advantage for patients with small amounts of local or regional disease. Intraoperative radiation therapy may also be useful, although initial uncontrolled studies require confirmation. Clearly, there is a need for new agents with higher response rates to be used in combination and/or with other therapeutic modalities. The timing of chemotherapy needs to be addressed with earlier postoperative initiation of therapy or preoperative chemotherapy. Lastly, the areas of pharmacologic modulation of chemotherapy and biological response modification need to be explored in the treatment of this disease.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

Roles of Helicobacter pylori infection and cyclooxygenase-2 expression in gastric carcinogenesis.

AIM: Cyclooxygenase (COX)-2 is over expressed in gastrointestinal neoplasm. Helicobacter pylori (H pylori) infection is causally linked to gastric cancer. However, the expression of COX-2 in various stages of H pylori-associated gastric carcinogenesis pathway has not been elucidated. Therefore, the aim of this study was to clarify the role of H pylori induced COX-2 expression during carcinogenesis in the stomach. METHODS: Gastric biopsies from 138 subjects (30 cases of chronic superficial gastritis (CSG), 28 cases of gastric glandular atrophy (GA), 45 cases of gastric mucosal intestinal metaplasia (IM), 12 cases of moderate gastric epithelial dysplasia and 23 cases of gastric cancer) were enrolled. H pylori infection was assessed by a rapid urease test and histological examination (modified Giemsa staining). The expression of COX-1 and COX-2 in human gastric mucosa was detected by immunohistochemical staining. RESULTS: H pylori infection rate was 64.3% in GA and 69.5% in gastric cancer, which was significantly higher than that (36.7%) in CSG (P<0.05). The positive expression rates of COX-2 were 10.0%, 35.7%, 37.8%, 41.7% and 69.5% in CSG, GA, IM, dysplasia and gastric cancer, respectively. From CSG to GA, IM, dysplasia and finally to gastric cancer, expression of COX-2 showed an ascending tendency, whereas COX-1 expression did not change significantly in the gastric mucosa. The level of COX-2 expression in IM and dysplasia was significantly higher in H pylori-positive than in H pylori-negative subjects (P<0.01). CONCLUSION: COX-2 expression induced by H pylori infection is a relatively early event during carcinogenesis in the stomach.

Adult↗
PubMed2004

DNA ploidy and c-Kit mutation in gastrointestinal stromal tumors.

AIM: To investigate the prognostic significance of c-Kit gene mutation and DNA ploidy in gastrointestinal stromal tumors (GISTs). METHODS: A total of 55 cases of GISTs were studied for the expression of c-Kit by immunohistochemistry, and the c-Kit gene mutations in exons 9, 11, 13, and 17 were detected by polymerase chain reaction-single strand confirmation polymarphism (PCR-SSCP) and denaturing high performance liquid chromatography (D-HPLC) techniques. DNA ploidy was determined by flow cytometry. RESULTS: Of the 55 cases of GISTs, 53 cases (96.4%) expressed c-Kit protein. The c-Kit gene mutations of exons 11 and 9 were found in 30 (54.5%) and 7 cases (12.7%), respectively. No mutations were found in exons 13 and 17. DNA aneuploidy was seen in 10 cases (18.2%). The c-Kit mutation positive GISTs were larger in size than the negative GISTs. The aneuploidy tumors were statistically associated with large size, high mitotic counts, high risk groups, high cellularity and severe nuclear atypia, and epithelioid type. There was a tendency that c-Kit mutations were more frequently found in aneuploidy GISTs. CONCLUSION: DNA aneuploidy and c-Kit mutations can be considered as prognostic factors in GISTs.

Adult↗
PubMed2006

Expression of Ets-1 proto-oncoprotein in gastrointestinal stromal tumors, leiomyomas and schwannomas.

AIM: Gastrointestinal stromal tumors (GISTs) are rare. GISTs differ from other mesenchymal tumors of the gastrointestinal tract (e.g. leiomyomas and schwannomas). The purpose of this study was to investigate the role of Ets-1 in the growth and differentiation of GISTs. METHODS: Twenty-eight GISTs, nine leiomyomas and six schwannomas were examined by immunohistochemical staining method for Ets-1 in this study. Specimens were selected from surgical pathology archival tissues at Nagasaki University Hospital. RESULTS: Ets-1 protein was expressed in the cytoplasm of cells in all of these tumors. Immunohistochemical staining revealed that 27 GISTs (96.4%), six leiomyomas (66.7%), and five schwannomas (83.3%) were positive for Ets-1. Ets-1 expression was statistically different between GISTs and leiomyomas (P<0.005). However, there was no correlation between Ets-1 expression and clinical risk categories. CONCLUSION: Ets-1 plays an important role in the growth and differentiation of GISTs, leiomyomas and schwannomas.

Biomarkers, Tumor↗
PubMed2006

Expression of vascular endothelial growth factor and its receptors VEGFR-1 and 2 in gastrointestinal stromal tumors, leiomyomas and schwannomas.

AIM: To investigate the role of vascular endothelial growth factor (VEGF) and its receptors VEGFR-1 and 2 in the growth and differentiation of gastrointestinal stromal tumors (GISTs). METHODS: Thirty-three GISTs, 15 leiomyomas and 6 schwannomas were examined by immunohistochemistry in this study. RESULTS: VEGF protein was expressed in the cytoplasm of tumor cells, and VEGFR-1 and 2 were expressed both in the cytoplasm and on the membrane of all tumors. Immunohistochemical staining revealed that 26 GISTs (78.8%), 9 leiomyomas (60.0%) and 3 schwannomas (50.0%) were positive for VEGF; 24 GISTs (72.7%), 12 leiomyomas (80.0%) and 4 schwannomas (66.7%) were positive for VEGFR-1; 30 GISTs (90.9%), 5 leiomyomas (33.3%) and 4 schwannomas (66.7%) were positive for VEGFR-2. VEGFR-2 expression was statistically different between GISTs and leiomyomas (P < 0.0001). However, there was no correlation between the expression of VEGF pathway componenets and the clinical risk categories. CONCLUSION: Our results suggest that the VEGF pathway may play an important role in the differentiation of GISTs, leiomyomas and schwannomas.

Cell Proliferation↗
PubMed2005

What is dysplasia in the gastrointestinal tract?

Dysplasia in the gastrointestinal tract is considered both a carcinoma precursor and a marker of high cancer risk for the site at which it is found. Dysplasia is defined as unequivocally neoplastic epithelium, yet the specific criteria for making that determination are imperfectly defined. The current criteria actually include a mix of architectural and cytologic features, all of which occur in different intensities in different epithelia that are given the same diagnosis. Gastrointestinal dysplasias are divided into 2 grades, but there are problem areas in diagnosis at the lower end where low-grade dysplasias overlap with regenerating epithelia and in the middle where low- and high-grade dysplasias overlap. The diagnosis of dysplasia is too subjective with less than optimal reproducibility to be as useful a marker as needed. Pathologists need a dysplasia stain or a whole set of new markers of high cancer risk, presumably molecular and/or genetic, that are not dependent on pathologists' diagnoses of dysplasia and their inherent subjectivity.

Gastrointestinal Diseases↗