Synchronous bilateral neuroendocrine ductal carcinoma in situ.

Neuroendocrine ductal carcinoma in situ (NE-DCIS) is a breast malignancy that has characteristic clinicopathological features and can, therefore, be regarded as a distinct variant of DCIS. The patient was a 54-year-old premenopausal woman with hemorrhagic nipple discharge in her left breast. Magnetic resonance imaging and ultrasound (US) images of the left breast showed mass-like lesions, while concurrent images of the right breast showed non-mass-like lesions. These findings suggested the presence of both benign and malignant tumors. Pathological findings from US-guided core-needle biopsy of the left mass were highly suspicious of a malignant tumor. Excisional biopsy of both breasts was performed. We could define the diagnosis of breast cancer by the second opinion on pathological diagnosis. The tumor cells showed histological characteristics of NE-DCIS. Bilateral breast lesions had histopathological similarities and were composed of predominantly solid growth of carcinoma cells, frequently with well-developed vascular structures, in mammary ducts and ductules. Carcinoma cells were polygonal or occasionally spindle shaped and had fine-granular, relatively eosinophilic cytoplasm. The nuclei of these cells showed round to ovoid in shape and fine-granular chromatin pattern. There was not any invasive component, as confirmed by careful histological examination. Thus, additional immunohistochemical stainings for NE markers (chromogranin A and synaptophysin) were performed. Staining statuses of these markers were positive in almost all tumor cells from both breasts. Both tumors were therefore diagnosed as NE-DCIS. To our knowledge, this case is the first report of NE-DCIS diagnosed synchronously in both breasts.

The IL6 gene polymorphism -634C>G and IL17F gene polymorphism 7488T>C influence bone mineral density in young and elderly Japanese women.

Osteoporosis is an important public health problem because of the significant morbidity and mortality associated with its complications, particularly fractures. An important clinical risk factor in the pathogenesis of osteoporosis is the presence of genetic polymorphisms in susceptibility genes. However, few studies have investigated the relevance of these polymorphisms in premenopausal women. Recent studies have demonstrated interactions between bone and immune cells, and that cytokines produced by immune cells regulate bone turnover. In this study, we examined the associations between bone mineral density (BMD) and polymorphisms in genes encoding interleukin (IL)-6 (-634C>G; rs1800796), tumor necrosis factor (TNF)-α (-308G>A; rs1800629), IL-17F (7488T>C; rs763780), transforming growth factor (TGF)-ß (869T>C; rs1800470), osteoprotegerin (OPG; 163A>G; rs3102735) and methylenetetrahydrofolate reductase (MTHFR; 677C>T; rs1801133) in young and elderly Japanese women. Whole-body, lumbar spine (L(1) or L(2)-L(4)), and femoral neck BMD were measured in 100 young subjects (18-23 years), and 100 elderly subjects (60-83 years). Whole-body, lumbar spine, and femoral neck BMD were 1.13±0.06, 1.14±0.12, and 1.00±0.11 g/cm(2), respectively, in young subjects, and 0.92±0.09, 0.86±0.15, and 0.63±0.10 g/cm(2), respectively, in elderly subjects. The frequencies of the IL-6 CC, CG, and GG genotypes were 48%, 49%, and 3%, respectively. The frequencies of the IL17F TT, TC, and CC genotypes were 79%, 15%, and 6%, respectively, in young subjects. Polymorphisms of the IL-6 and IL17F genes were significantly associated with BMD. To our knowledge, this is the first report to examine these associations in a cohort of 200 Japanese women.

The role of contrast enhanced MRI in the diagnosis of non-mass image-forming lesions on breast ultrasonography.

BACKGROUND: Although non-mass lesions on breast ultrasonography have become relatively common, they remain very difficult to diagnose. The purpose of this study was to evaluate the usefulness of contrast enhanced magnetic resonance imaging (MRI) in managing non-mass lesions. METHODS: A total of 82 cases of non-mass lesions visible on breast ultrasonography who were subjected to contrast enhanced MRI (CE-MRI) were available for assessment. These lesions were evaluated in terms of the association between the enhancement pattern on contrast enhanced MRI and the pathological or cytological diagnosis. RESULTS: Thirty-three of 82 (40.2%) non-mass image-forming lesions were seen as enhanced lesions on CE-MRI, of which 32 revealed non-masslike enhancements. Of the 19 breast cancers detected as non-mass image-forming lesions, 18 (94.7%) had an enhancement pattern not suggestive of a mass, so breast cancers comprised 56.3 % (18/32) of the lesions. Most of the breast cancers tended to emerge in a setting of duct dilatation with internal echoes (45.5%; 5/11) or low echo areas with indistinct margins (32.4%; 11/34). Morphologically, segmental (57.9%; 11/19) and regional (21.1%; 4/19) enhancements were common patterns of breast cancer which showed up as non-mass image-forming lesions. On the other hand, 49 of 82 (59.8%) non-mass image-forming lesions were not enhanced and 28 of 49 cases underwent pathological examination. Only one case was breast cancer with category 5 microcalcifications and although about half of the remaining 21 cases were followed for at least 12 months, no breast cancers were found. CONCLUSION: Contrast enhanced MRI was useful for detecting breast cancer in cases of non-mass image-forming lesions. On the other hand, except for cases in which mammography was suspicious for malignancy, lesions showing no enhanced areas may be safely followed, because the possibility of breast cancer is minute.

Isolated splenic vein thrombosis secondary to splenic metastasis: a case report.

A 49-year-old, previously healthy woman sought treatment for abdominal pain. Colonoscopy revealed ascending colon cancer. Computed tomography and angiography showed splenic metastasis and thrombosis extending from the splenic vein to the portal vein. She underwent right hemicolectomy, splenectomy, and distal pancreatomy. Histological findings showed no malignant cell in the splenic vein which was filled with organizing thrombus. We postulate the mechanism of splenic vein thrombosis in our case to be secondary to the extrinsic compression of the splenic vein by the splenic metastasis or by the inflammatory process produced by the splenic metastasis. In conclusion, we suggest that splenic metastasis should be added to the list of differential diagnosis which causes splenic vein thrombosis. In the absence of other sites of neoplastic disease, splenectomy seems to be the preferred therapy because it can be performed with low morbidity and harbors the potential for long-term survival.

An uncommon case of diabetic mastopathy in type II non-insulin dependent diabetes mellitus.

Diabetic mastopathy is an uncommon tumor-like proliferation of fibrous tissue of the breast that usually occurs in a patient who has suffered from type I diabetes mellitus of long duration. Here we report a rare case of diabetic mastopathy that occurred in type II non-insulin dependent diabetes mellitus. This patient was a 63-year-old postmenopausal woman. Mammography, ultrasonography and MR imaging could not distinguish it from breast cancer. Although the core needle biopsy specimen showed fibrosis without evidence of malignancy, excisional biopsy was performed. Histological findings demonstrated typical diabetic mastopathy with keloid-like fibrosis, perivascular lymphocytic infiltration, and lymphocytic lobulitis without evidence of malignancy. These lymphocytes were composed predominantly of B-cells. Five months after surgical biopsy, a nodular formation approximately 4 cm in diameter recurred adjacent to the resected end of the biopsy.

Strangulated hernia through a defect of the broad ligament and mobile cecum: a case report.

We report a case of 28-year-old woman presenting with small bowel obstruction. She had neither prior surgery nor delivery. An upright abdominal radiograph revealed several air-fluid levels in the small bowel in the midabdomen and the pelvic cavity. Computed tomography demonstrated a dilated small bowel loop in the Douglas's fossa,but no definite diagnosis could be made. Supportive therapy with draining the intestinal fluid by a long intestinal tube did not result in improvement,which suggested the possibility of a strangulated hernia. Exploratory laparotomy revealed mobile cecum and a 20-cm length of the ileum herniated into a defect of the right broad ligament. As a gangrenous change was recognized in the incarcerated bowel, its resection was carried out,followed by end-to-end anastomosis and closure of the defects of the broad ligament. The postoperative course was uneventful. Intestinal obstruction is a very common cause for presentation to an emergency department,while internal hernia is a rare cause of obstruction. Among internal hernias, those through defects of the broad ligament are extremely rare. Defects of the broad ligament can be either congenital or secondary to surgery, pelvic inflammatory disease,and delivery trauma. In conclusion, we emphasize that hernia of the broad ligament should be added to the list of differential diagnosis for female patients presenting with an intestinal obstruction. Early diagnosis and surgical repair reduce morbidity and mortality from strangulation.

Core 3 synthase is down-regulated in colon carcinoma and profoundly suppresses the metastatic potential of carcinoma cells.

The core 3 structure of the O-glycan, GlcNAcbeta1-3GalNAcalpha1-Ser/Thr, an important precursor in the biosynthesis of mucin-type glycoproteins, is synthesized by beta1,3-N-acetylglucosaminyltransferase 6 (beta3Gn-T6; core 3 synthase). We generated an anti-beta3Gn-T6 mAb (G8-144 mAb) and performed immunohistochemical analyses. In normal stomach and colon, beta3Gn-T6 was strongly expressed in the Golgi region of epithelia. In contrast, its expression was markedly down-regulated in gastric and colorectal carcinomas. Tissue specimens from a familial adenomatous polyposis patient showed a clear correlation between the down-regulation of beta3Gn-T6 expression and the degree of dysplasia/neoplasia. In vitro, the level of beta3Gn-T6 transcript was increased according to the differentiation of Caco-2 cells. These results suggested that the expression of beta3Gn-T6 is closely regulated during differentiation and dedifferentiation. beta3Gn-T6 would be a useful marker for distinguishing between benign adenomas and premalignant lesions. HT1080 FP-10 cells stably transfected with the beta3Gn-T6 gene showed a decrease in the core 1 structure, Galbeta1,3GalNAcalpha1-Ser/Thr, probably due to competition between the core 1 synthase and core 3 synthase. The migration activity of the transfectants was markedly lower than that of mock transfectants in vitro, and lung metastasis after i.v. injection of the transfectants into nude mice was significantly suppressed. These findings indicated that the core structures of O-glycans are profoundly involved in the metastatic capacity of cancer cells.

Elevated transcript level of hyaluronan synthase1 gene correlates with poor prognosis of human colon cancer.

Hyaluronan plays important roles in the complex processes of tumor invasion and metastasis. It is now known that three hyaluronan synthase (HAS) isoforms catalyze hyaluronan synthesis, which raises the question of how they are involved in malignant tumor progression. In this study, we examined the correlation between tumor progression and transcriptional levels of three HAS isoforms in specimens of human colon cancers. Tumor tissues from 31 patients with different diagnostic grades were assessed to determine the level of each HAS isoform by real time RT-PCR. The mean expression coefficients for HAS1, HAS2 and HAS3 in the cancerous parts were 0.82-, 0.91- and 1.22-fold, respectively; of those in the noncancerous parts at Dukes' stage A; 1.00-, 0.95- and 1.06-fold, respectively, at stage B; and 1.95-, 1.16- and 1.19-fold, respectively, at stage C. In survival analysis, a significant correlation was observed between poor survival and the HAS1 transcript level. When the ratio of tumor to normal tissue in the HAS1 level was compared with that of the HA receptor transcript level, there was a positive correlation with that of the CD44 variant 6 level at Dukes' stage C. Our current results therefore suggest that HAS1 plays a role in the malignant progression of human colon cancer cells.