Tumors Of Gastrointestinal Origin Research Articles

PET/CT and contrast-enhanced CT imaging findings in benign solitary schwannomas

ObjectivesImaging features of positron emission tomography (PET)/computed tomography (CT) and contrast-enhanced CT and pathological changes in benign solitary schwannoma were retrospectively analyzed, and the factors associated with high uptake of fluorodeoxyglucose (FDG) were examined. MethodsThe PET/CT, contrast-enhanced CT, and pathological results of 58 cases of benign solitary schwannomas confirmed by surgery or biopsy were retrospectively analyzed. The association of each variable with the maximum standardized uptake value (SUVmax) was evaluated. ResultsThe SUVmax of the 58 benign schwannoma cases was 4.1 ± 2.1 (1.5–11.1). When the locations of schwannomas were divided into gastrointestinal system/heart/abdominal and pelvic cavities/thoracic wall (type-1 locations) and other sites (type-2 locations), the schwannoma location was significantly correlated with the SUVmax (r = 0.538, p = 0.000). The SUVmax values were 5.8 ± 2.4 and 3.3 ± 1.5, respectively (p = 0.000). Peritumoral lymphoid cuffs were observed in 7 cases, 4 of which were tumors of gastrointestinal origin, accounting for 80 % of the gastrointestinal schwannomas (4/5). The presence of peritumoral lymphoid cuffs was significantly correlated with the SUVmax (r = 0.456, p = 0.000). The location of the schwannoma was significantly correlated with the presence of peritumoral lymphoid cuffs (r = 0.640, p = 0.000). We found that a peritumoral lymphoid cuff is strongly correlated with the presence of regional lymphadenopathy. Among the 7 cases showing peritumoral lymphoid cuffs, 5 cases had the presence of peritumoral enlarged lymph nodes. The degree of enhancement was significantly correlated with the SUVmax (r = 0.556, p = 0.000). ConclusionsBenign schwannomas originating from the gastrointestinal system/heart/abdominal location and showing the presence of peritumoral lymphoid cuffs or moderate and significant enhancement on contrast-enhanced CT were significantly associated with high FDG uptake. An accurate understanding of the factors associated with high FDG uptake can help reduce the misdiagnosis rate.

Management of Full-Thickness Abdominal Wall Defects Following Tumor Resection

Abdominal wall reconstruction continues to evolve with improvement in technique and technology. This study reviews our experience with challenging full thickness (skin, muscle, and fascia) defects following tumor resections often in high-risk patients. All patients who underwent abdominal wall reconstruction following full thickness tumor resection were included in the series. Data queried included patient demographics, indications, tumor defect, risk factors, type of repair, complications, and recurrence of the hernia. A total of 30 patients underwent reconstruction after full thickness resection of abdominal wall tumors or tumors of intra-abdominal organs involving abdominal wall. The indications included desmoid tumors (n=6); abdominal wall sarcoma (n=7); colon cancer invading abdominal wall (n=10); pancreatic, ovarian, and retroperitoneal sarcoma with abdominal wall invasion (n=3); and other (n=4). In all, 17 patients underwent simultaneous resection of one or more intra-abdominal organs. The type of repair included primary closure (±components separation), or mesh-assisted closure (±primary fascial closure). Acellular dermal matrix was used more commonly in the patients with tumors of gastrointestinal origin. The average follow-up period was 23 months. Postoperative complications developed in 6 patients (20.6%). Incidence of postoperative complications was higher in patients with colon cancer invading the abdominal wall or those with bowel anastomosis or radiation therapy. An abdominal bulge or hernia developed in 4 patients (13.7%); it was higher in patients who did not have mesh reconstruction. Abdominal wall reconstruction after full thickness tumor resection is challenging. It can be performed safely and effectively with attention to surgical technique, patients' risk of infection, and type of mesh. Acellular dermal matrix graft has been a useful addition to minimize morbidity and recurrence in these high-risk patients.

EpCAM expression in primary tumour tissues and metastases: an immunohistochemical analysis

AimsEpithelial cell adhesion molecule (EpCAM) is a cell surface protein with oncogenic features that is expressed on healthy human epithelia and corresponding malignant tumours. EpCAM expression frequently correlates with more...

Differential Expression of MUC1, MUC2, and MUC5AC in Carcinomas of Various Sites

We studied immunohistochemical expression of MUC1, MUC2, and MUC5AC in 194 carcinomas of different primary sites to determine whether differential expression patterns could be used to distinguish different carcinomas. MUC1 was expressed by most (except adrenocortical and hepatocellular carcinomas). MUC2 was expressed infrequently (positive immunoreactivity primarily in tumors of gastrointestinal origin). MUC5AC was expressed by most pancreatic ductal and endocervical adenocarcinomas and a variable number of tumors of the gastrointestinal tract. A MUC1+/MUC2–/MUC5AC– immunophenotype was observed in most breast, lung, kidney, bladder, endometrial, and ovarian carcinomas; MUC1+/MUC2–/MUC5AC+ was characteristic of pancreatic ductal adenocarcinomas and cholangiocarcinomas. Adrenocortical and hepatocellular carcinomas were negative for all mucins. Carcinomas of gastrointestinal origin exhibited variable expression of each mucin examined and no consistent immunoreactivity pattern. Many carcinomas can exhibit distinct MUC1, MUC2, and MUC5AC expression patterns, which might be valuable diagnostically in specific settings (eg, distinguishing cholangiocarcinoma from hepatocellular carcinoma or renal from adrenocortical carcinoma). However, the overlapping and heterogeneous patterns of MUC1, MUC2, and MUC5AC expression observed in many tumors, particularly those of gastrointestinal origin, preclude use of these markers in the routine immunohistochemical assessment of carcinomas of an unknown primary site.

Peritoneal cancer index: a prognostic indicator of survival in advanced ovarian cancer

Aim: The peritoneal cancer index (PCI) has been used for the detailed evaluation of the peritoneal spread in tumors of gastrointestinal origin and has been found to be a prognostic indicator of survival. The aim of this study was the identification of the significance of the peritoneal cancer index in advanced ovarian cancer.Methods:From 1990 to 2001, 60 women, mean age 65±10.84 (41–86), were treated for advanced ovarian cancer. The performance status (Karnofsky performance scale), age, prior surgery score (PSS), peritoneal cancer index (PCI), tumor volume, tumor grade, residual tumor, the presence of ascites, treatment with adjuvant chemotherapy, histopathologic subtype and FIGO stage were retrospectively correlated to survival using univariate model of statistical analysis.Results: Hospital mortality and morbidity were 11.7 and 16.7% respectively. The recurrence rate was 23.3%. Overall 5-year survival rate was 41% and mean survival 63±8 months. The peritoneal cancer index was related to survival (P=0.0253). The other favorable clinical prognostic indicators of survival were low grade and small volume tumors, treatment with adjuvant chemotherapy and complete cytoreductive surgery (P<0.05).Conclusions: The peritoneal spread in advanced ovarian cancer can be assessed in detail using the peritoneal cancer index. It is a significant prognostic factor of survival and is useful in identifying subgroups.

Humanisation and characterisation of PR1A3, a monoclonal antibody specific for cell-bound carcinoembryonic antigen.

Carcinoembryonic antigen (CEA) is highly expressed by most tumours of gastrointestinal origin, but its use as a target for tumour therapy is complicated by the high levels of soluble CEA that are found circulating in the blood of cancer patients. A monoclonal antibody PR1A3 has been prepared, which binds preferentially to cell-surface rather than soluble CEA, this cell selectivity should make PR1A3 an ideal candidate for antibody-targeted tumour therapy. PR1A3 has been humanised and shown to retain its cell-surface specificity and affinity. Stable expression of the humanised antibody from chinese hamster ovary (CHO) cells has been achieved after transfection and amplification. Since PR1A3 binds preferentially to cell-associated CEA, a cell-free enzyme-linked immunosorbent assay (ELISA) has been developed to allow characterisation and routine assay of the antibody. This assay was developed using a recombinant chimeric protein constructed by cloning the domain of CEA that is bound by PR1A3 (the B3 domain) into a hybrid gene containing the Fc portion of IgG and three domains of biliary glycoprotein. Stable expression of this hybrid protein has been achieved from CHO cells. In ELISA both humanised and murine PR1A3 bound strongly to this antigen but only at a minimal level to soluble CEA. Two binding sites for the antibody were found on the gastric carcinoma cell line MKN45, one of higher affinity (1 nM) and the other at lower affinity (60 nM). Similar affinities were found for both murine and humanised antibodies. The data presented make it unlikely that the differential binding to cell-surface as distinct from soluble CEA can be accounted for by low affinity of PR1A3 for CEA, and provides further support for the hypothesis that some conformational change takes place on CEA release from cells and that it is this change that blocks PR1A3 binding to its epitope.

Matrix Metalloproteinase (MMP) Inhibition Selectively Decreases Type II MMP Activity in a Murine Model of Pancreatic Cancer

Background.Basement membrane degradation is a critical component of tumor invasion and metastasis that is facilitated by the family of enzymes known as matrix metalloproteinases (MMPs). MMP-2 and MMP-9 are two subtypes that have specifically been identified in tumors of gastrointestinal origin. We have previously shown that broad inhibition of these enzymes with the MMP inhibitor BB-94 improves survival in a murine model of pancreatic cancer. The purpose of this study was to determine MMP-2 and MMP-9 activity in orthotopic tumors from mice treated with and without BB-94.Methods.Ten million cells of a moderately differentiated pancreatic cancer cell line (HPAC) were implanted orthotopically into Balb/cnu/numice. The mice were treated with BB-94 or vehicle control for 70 days or until death. At necropsy, tumors were harvested, total protein was extracted, and MMPs were purified from 400 μg of crude protein extract by gelatin–Sepharose affinity chromatography. Relative enzyme levels and activity of MMP-2 and MMP-9 were determined by Western blot and gelatin zymography.Results.Tumors from treated animals were significantly smaller than those from nontreated animals. MMP-2 was present in greater amounts in both treated and nontreated animals than MMP-9. Active MMP-2 was present in both groups but significantly decreased in animals treated with BB-94. Active MMP-9 was absent in both groups, whereas levels of latent MMP-9 appeared lower than those of MMP-2 in all samples.Conclusions.Activated MMP-2 and not MMP-9 in HPAC cells grown in nude mice suggests that this MMP subtype is more critical in the phenotypic behavior of such tumors. Furthermore, attenuated levels of active MMP-2 in animals treated with the enzyme inhibitor BB-94 suggest that previously observed improvements in survival correlate with the level of MMP-2 activity.

Carcinoid crisis after biopsy of a bronchial carcinoid

Pulmonary carcinoids ate rarely associated with carcinoid syndromes and even less commonly with carcinoid crisis. Somatostatin analogues can control carcinoid syndrome or crisis with tumors of gastrointestinal origin. We report the successful use of a somatostatin analogue in preventing carcinoid crisis at the time of resection of an “active” bronchial carcinoid tumor.

Tritium uptake, half-lives and radiation doses in tissues of cancer patients treated with tritiated 2-methyl-1:4-naphthaquinol diphosphate.

AbstractComparisons of the uptake into tumour biopsies 30 min after intravenous or intra‐arterial injections showed that tumours of gastrointestinal origin took up significantly greater amounts of the tritiated drugs than did any other group of tumours, and with other types of tumours some individual biopsies showed very high tumour specific activities after intra‐arterial injections. The tritium in the tumour disappeared by two exponential decay processes, one with a half‐life of 1.35 days and the other with a half‐life of 14.4 days. The ratio of the concentration of the long‐lived component to that of the short‐lived component was 0.33.Tritium estimations on normal tissues taken at autopsy from patients who received only one injection of the tritiated drug showed that the biological half‐life in normal tissues ranged from 5.7 days (heart) to 34.5 days (long‐lived component in brain). The initial specific activity in μc/g for each c/kg injected ranged from 71 (long‐lived component in brain) to 505 (kidney).After a single injection of 1 c of the drug per kg body weight, the greatest doses of radiation were received by the kidney (1,600 R), testis (1,300 R), liver (1,050 R) and brain (990 R). The lowest doses were received by skeletal muscle (395 R) and bone marrow (604 R).The radiation dose in the tumour depends on the initial concentration and the half‐life in the tumour. Initial tumour concentrations of 5–8 mc/g wet tissue should give radiation doses in the therapeutic range after a single injection.