Differential diagnosis of small polypoid lesions of the gallbladder: the value of endoscopic ultrasonography.
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OBJECTIVE: To evaluate the accuracy of endoscopic ultrasonography (EUS) in making a differential diagnosis of small (< or =20 mm) polypoid lesions of the gallbladder. SUMMARY BACKGROUND DATA: Differential diagnosis of these lesions is often difficult using conventional imaging modalities. METHODS: The findings of EUS and transabdominal ultrasonography were retrospectively analyzed in 65 surgical cases of small polypoid lesions (cholesterol polyp in 40, adenomyomatosis in 9, adenoma in 4, and adenocarcinoma in 12). RESULTS: Polypoid lesions exceeding 10 mm suggested malignancy. EUS showed a tiny echogenic spot or an aggregation of echogenic spots with or without echopenic areas in 95% of patients with cholesterol polyps. EUS showed multiple microcysts or comet tail artifact in all adenomyomatosis cases. Adenomas and adenocarcinomas were not associated with the echogenic spots, microcysts, or artifacts. Among adenomas and adenocarcinomas, all sessile lesions were adenocarcinomas. EUS differentiated among polypoid lesions more precisely than ultrasonography (97% vs. 71%). CONCLUSIONS: A tiny echogenic spot or an aggregation of echogenic spots and multiple microcysts or comet tail artifact is pathognomonic for cholesterol polyp and adenomyomatosis, respectively. Polypoid lesions without these findings indicate adenoma or adenocarcinoma on EUS. Routine use of EUS is recommended for differential diagnosis of polypoid gallbladder lesions when ultrasonography shows no signs indicative of either cholesterol polyp or adenomyomatosis. (+info)
Benign expansile lesions of the sphenoid sinus: differentiation from normal asymmetry of the lateral recesses.
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BACKGROUND AND PURPOSE: There is a wide range of normal variation is sphenoid sinus development, especially in the size of the lateral recesses. The purpose of this study was to determine imaging characteristics that may help differentiate between opacification of a developmentally asymmetric lateral recess and a true expansile lesion of the sphenoid sinus. METHODS: Coronal CT was performed in seven patients with expansile or erosive benign lesions of the sphenoid sinus, and results were compared to a control population of 72 subjects with unopacified sphenoid sinuses. The degree of asymmetry of lateral recess development was assessed with particular attention to the separation of vidian's canal and the foramen rotundum (vidian-rotundum distance). The images were also examined for evidence of: erosion, defined as loss of the normal thin bony margin on at least two contiguous sections; apparent thinning of the sinus wall, defined as a focal apparent decrease in thickness again on at least two contiguous sections; and for vidian's canal or foramen rotundum rim erosion or flattening. RESULTS: Of the seven patients with expansile lesions, vidian's canal margin erosion was present in seven, unequivocal sinus expansion in three, wall erosion in three, wall thinning in three, erosion of the foramen rotundum in two, and flattening in the foramen rotundum in four. Forty-one of the 72 controls had lateral recess formation, 28 of which were asymmetric. The distance between vidian's canal and the foramen rotundum (vidian-rotundum distance) relied on the presence or absence of pneumatization, with a significantly larger distance in the presence of greater wing pneumatization. Examination of 24 controls revealed apparent thinning of the sinus wall, typically at the carotid groove, but no flattening, thinning, or erosion of the vidian canal or of the foramen rotundum. CONCLUSION: Examination of controls and patients with expansile or erosive lesions of the sphenoid sinus revealed side-to-side asymmetry in the development of the sinus and lateral recess, making subtle expansion difficult to assess. Furthermore, variability in the vidian-rotundum distance correlated with degree of pneumatization, and did not necessarily reflect expansion. Thus, in the absence of gross sinus wall erosion, flattening or erosion of the rims of vidian's canal or the foramen rotundum provides the most specific evidence of an expansile or erosive process within the sinus. (+info)
Dysregulation of beta-catenin is common in canine sporadic colorectal tumors.
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Human colorectal tumorigenesis is often initiated by APC (adenomatous polyposis coli) or beta-catenin (CTNNB1) mutations, which result in dysregulation of beta-catenin expression, followed by alterations in E-cadherin and/or p53. We examined 32 canine intestinal tumors for expression and intracellular distribution of beta-catenin, E-cadherin, and p53 using immunohistochemistry. beta-Catenin in normal mucosal epithelial cells was restricted to lateral cell membranes, but 13/13 (100%) colorectal adenomas had intense cytoplasmic and/or nuclear reactivity. Three of six (50%) colorectal carcinomas, 2/13 (15%) small intestinal carcinomas, and dysplastic cells in 1/2 focal hyperplastic lesions in the small intestine had a similar pattern of staining; remaining tumors had normal membranous beta-catenin reactivity. There was a correlation (P = 0.007) between abnormal beta-catenin and E-cadherin staining with 11/13 (85%) colorectal adenomas, 3/6 (50%) colorectal carcinomas, and 3/13 (23%) small intestinal carcinomas showing decreased membranous reactivity compared with normal mucosal epithelium. E-cadherin staining was reduced more often in adenomas than in carcinomas (P = 0.04). There were two patterns of nuclear p53 staining: > 60% of nuclei in 2/26 (8%) carcinomas (one colorectal, one small intestinal) were strongly labeled, whereas three colorectal adenomas and one small intestinal carcinoma had fainter staining in 10-20% of cells. Dysregulation of beta-catenin appears to be as important in canine colorectal tumorigenesis as it is in the human disease and could be due to analogous mutations. Malignant progression in canine intestinal tumors does not appear to be dependent on loss of E-cadherin or beta-catenin expression or strongly associated with overexpression of nuclear CMI antibody-reactivity p53. (+info)
Heparin/heparan sulfate interacting protein gene expression is up-regulated in human colorectal carcinoma and correlated with differentiation status and metastasis.
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We applied a subtractive hybridization strategy to obtain genes that are differentially expressed in colorectal carcinoma. Heparin/heparan sulfate interacting protein (HIP) was shown to be up-regulated in colorectal carcinoma. A study of 53 patients with documented colorectal carcinoma showed that 70% of the tumors had HIP tumor-to-normal ratios (expression in tumor tissue compared to expression in normal mucosa) of >2. In six patients with concomitant polyps, HIP expression in the polyps was similar to the carcinoma, showing that up-regulation of HIP may be an early event in tumorigenesis. A significant inverse correlation between HIP levels and the presence of distant metastasis (Duke's stage D) was noted. Similarly, HIP expression was also related to differentiation status in human colorectal carcinoma cell lines. HIP expression was lower in the poorly differentiated COLO 205 cell line compared to the well-differentiated HT-29 cell line. The correlation was further strengthened by studies in COLO 205 cells that were induced to differentiate with herbimycin A treatment. HIP expression was significantly higher when the cells were induced to differentiate. Withdrawal of herbimycin A resulted in a reversal of morphological changes associated with differentiation and an associated decrease in HIP expression. These studies indicate that HIP is an important molecule for cell-cell and cell-extracellular matrix adhesion. The up-regulation of HIP may be an early event in tumorigenesis, and its increased expression may facilitate growth and local invasion. A lower expression of HIP in tumors results in decreased cell adhesion, favoring metastasis. HIP is a candidate marker of abnormal cell growth in the colon and a prognostic marker for colorectal carcinoma. (+info)
The value of sonohysterography combined with cytological analysis of the fluid retrieved from the endometrial cavity in predicting histological diagnosis.
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OBJECTIVE: The purpose of the study was to assess the efficacy of sonohysterography combined with cytological analysis of the fluid retrieved from the endometrial cavity in predicting histological diagnosis. STUDY DESIGN: A prospective study was conducted comparing sonohysterography combined with endometrial washings for cytology with histological evaluation after surgical procedures. Of 152 patients referred for sonohysterography, 87 were premenopausal and 65 were postmenopausal. Some of the injected fluid was aspirated for cytological analysis. Sixty-one patients (40%) underwent surgical hysteroscopy and eight (5%) had dilatation and curettage as a result of the sonohysterographic findings. Histological diagnoses were compared with the sonohysterographic and cytological findings. RESULTS: In 99 (65%) patients, sonohysterography demonstrated endometrial polypoid lesions. Only 54 endometrial cavitary lesions were confirmed pathologically. Epithelial cells with atypia were more often found in patients without (five of 53) than in those with (two of 99) an endometrial polyp (p < 0.05). Only one out of nine cases of histological diagnosis of hyperplasia was predicted cytologically. CONCLUSIONS: The addition of cytological analysis of the fluid retrieved from the endometrial cavity during sonohysterography did not contribute to the prediction of benign histological diagnosis of endometrial hyperplasia. (+info)
Endometrial pathology in postmenopausal tamoxifen treatment: comparison between gynaecologically symptomatic and asymptomatic breast cancer patients.
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AIMS: To evaluate whether endometrial pathology is more likely to be diagnosed in gynaecologically symptomatic rather than in gynaecologically asymptomatic postmenopausal breast cancer patients with tamoxifen treatment; and to evaluate the possible influence of various clinical factors on the incidence of endometrial pathology. METHODS: Endometrial histological findings, transvaginal ultrasonographic endometrial thickness, demographic characteristics, health habits, and risk factors for endometrial cancer were compared between 14 gynaecologically symptomatic (group I) and 224 gynaecologically asymptomatic (group II) postmenopausal breast cancer patients with tamoxifen treatment. RESULTS: Overall, 28.6% of the study population had endometrial pathology. The incidence of overall positive endometrial histological findings was significantly higher in group I than in group II (92.9% v 24.6%, p < 0.0001). Atrophic endometrium was more common in group II than in group I (75.3% v 7.1%, p < 0.0001). Most other endometrial pathology was significantly more common in group I than in group II (endometrial hyperplasia, 35.7% v 5.6%, p < 0.0001; endometrial polyps, 35.7% v 13.4%, p < 0.0111; endometrial carcinoma, 21.5% v 0.9%, p < 0.0001). Endometrial pathology appeared considerably later in the gynaecologically asymptomatic patients than in gynaecologically symptomatic patients (p = 0.0002). Vaginal bleeding or spotting occurred exclusively in group I. The incidence of endometrial pathology in the entire study population was consistent with that reported elsewhere, and higher than that reported for healthy postmenopausal women. CONCLUSIONS: Endometrial pathology is more likely to be diagnosed in gynaecologically symptomatic postmenopausal breast cancer patients with tamoxifen treatment, and after a shorter duration of time, than in gynaecologically asymptomatic patients. (+info)
The effect of endometrial polyps on outcomes of in vitro fertilization (IVF) cycles.
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PURPOSE: Our purpose was to investigate the effect of endometrial polyps on pregnancy outcome in an in vitro fertilization (IVF) program. METHODS: Endometrial polyps less than 2 cm in diameter were suspected by transvaginal ultrasound before oocyte recovery in 83 patients. Forty-nine women (Group I) had standard IVF-embryo transfer, while in 34 women (Group II) hysteroscopy and polypectomy were performed immediately following oocyte retrieval, the suitable embryos were all frozen, and the replacement cycle took place a few months later. RESULTS: Of the 32 hysteroscopies, a polyp was diagnosed in 24 cases (75%) and polypoid endometrium in another 5 patients (15.6%). An endometrial polyp was confirmed by histopathological examination in 14 women (58.3%). The pregnancy rate in group I was similar to the general pregnancy rate of our unit over the same period (22.4 vs 23.4%) but the miscarriage rate was higher (27.3 vs 10.7%, P = 0.08). In Group II, the pregnancy and miscarriage rates were similar to those of the frozen embryo cycles at Bourn Hall (30.4 and 14.3 vs 22.3 and 12.1%, respectively). CONCLUSIONS: Small endometrial polyps, less than 2 cm, do not decrease the pregnancy rate, but there is a trend toward increased pregnancy loss. A policy of oocyte retrieval, polypectomy, freezing the embryos, and replacing them in the future might increase the "take-home baby" rate. (+info)
Characterisation of a subtype of colorectal cancer combining features of the suppressor and mild mutator pathways.
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BACKGROUND: 10% of sporadic colorectal cancers are characterised by a low level of microsatellite instability (MSI-L). These are not thought to differ substantially from microsatelite-stable (MSS) cancers, but MSI-L and MSS cancers are distinguished clinicopathologically and in their spectrum of genetic alterations from cancers showing high level microsatellite instability (MSI-H). AIMS: To study the distribution of molecular alterations in a series of colorectal cancers stratified by DNA microsatellite instability. METHODS: A subset of an unselected series of colorectal cancers was grouped by the finding of DNA MSI at 0 loci (MSS) (n = 51), 1-2 loci (MSI-L) (n = 38) and 3-6 loci (MSI-H) (n = 25). The frequency of K-ras mutation, loss of heterozygosity (LOH) at 5q, 17p and 18q, and patterns of p53 and beta catenin immunohistochemistry was determined in the three groups. RESULTS: MSI-H cancers had a low frequency of K-ras mutation (7%), LOH on chromosomes 5q (0%), 17p (0%) and 18q (12.5%), and a normal pattern of immunostaining for p53 and beta catenin. MSI-L cancers differed from MSS cancers in terms of a higher frequency of K-ras mutation (54% v 27%) (p = 0.01) and lower frequency of 5q LOH (23% v 48%) (p = 0.047). Whereas aberrant beta catenin expression and 5q LOH were concordant (both present or both absent) in 57% of MSS cancers, concordance was observed in only 20% of MSI-L cancers (p = 0.01). CONCLUSIONS: MSI-L colorectal cancers are distinct from both MSI-H and MSS cancers. This subset combines features of the suppressor and mutator pathways, may be more dependent on K-ras than on the APC gene in the early stages of neoplastic evolution, and a proportion may be related histogenetically to the serrated (hyperplastic) polyp. (+info)