The genetic changes of cyclin A, DI, E and CDK2 were examined in human colorectal carcinomas by Southern-blot analysis. Gene amplification of cyclin E was detected in 5 of 53 (9.4%) primary colorectal carcinoma tissues. Interestingly, in 3 of 5 tumors showing cyclin E gene amplification, the CDK2 gene was amplified simultaneously with rearrangements. No obvious correlation was detected between gene amplification and clinicopathological features of colorectal carcinomas. Out of 7 colon carcinoma cell lines, 2 showed gene amplification of cyclin E without gene amplification of CDK2. No amplification of cyclin A or DI gene was found in any of the colorectal carcinoma tissues or colon carcinoma cell lines. Our results suggest that the concurrent amplification of cyclin E and CDK2 genes may play a role in colorectal carcinogenesis.
Aim-To investigate the presence of genetic instability in precancerous lesions of the stomach. Methods-Fifteen cases of sporadic gastric cancers with a background of intestinal metaplasia were studied by microsatellite assay at nine loci. Altered metaplastic mucosa was microdissected, reconstructed topographically, and examined immunohistochemically with an anti-p53 antibody, comparing its positive area with foci of microsatellite instability in each individual. Mutations in mismatch repair genes, such as hMSH2, hMLH1, hPMS 1, hPMS2, and GTBP, responsible for maintaining the fidelity of DNA replication increase spontaneous mutation rates greatly.91-2 Microsatellites are simple oligonucleotide repeat units, distributed randomly and widely throughout the genome. The appearances of additions or deletions within the microsatellites are known as replication errors or microsatellite instability, and are believed to reflect derangement of the mismatch repair system.'3 14 Such genomic instability at microsatellite loci has been observed not only in hereditary non-polyposis colorectal cancer (HNPCC) associated tumours but also in certain sporadic cancers.'5"'7 As for gastric cancer, microsatellite instability has been reported with frequencies ranging from 18% to 38%. 16 [18][19][20][21] However, little is known about genomic instability in precancerous lesions of the stomach.
Objective Endoscopic self-expandable metallic stent (SEMS) placement and gastrojejunostomy (GJY) are palliative treatments for malignant gastric outlet obstruction (GOO). The aim of the present study was to compare the palliative effects of these treatments and identify predictors of a poor oral intake after treatment. Methods and Patients In total, 65 patients with GOO at multiple centers in Saga, Japan, were evaluated. Thirty-eight patients underwent SEMS placement, and 27 underwent GJY from January 2010 to December 2016. The characteristics and outcomes of the two groups were compared to detect predictors of treatment failure. Results No significant differences in the technical success, clinical success, post-treatment total protein, hospital discharge, duration from eating disability to death, or post-treatment overall survival were present between the SEMS and GJY groups. More patients in the GJY group than in the SEMS group received chemotherapy (51.4% vs. 26.3%, respectively; p=0.042). The period from treatment to the first meal was longer in the GJY group than in the SEMS group (4.5 vs. 3.0 days, respectively; p=0.013). The present study did not identify any risk factors for failure of SEMS placement. Although the stent length tended to be associated with a poor prognosis, the correlation was not statistically significant (odds ratio: 0.60, 95% confidence interval: 0.36-1.01, p=0.053). Conclusion Patients with GOO started meals more promptly after SEMS than after GJY, but the clinical outcomes were not markedly different between the SEMS and GJY groups. These findings suggest that endoscopic uncovered SEMS placement might be a feasible palliative treatment for GOO.
The use of laparoscopic splenectomy has increased in recent years, primarily for patients with idiopathic thrombocytopenic purpura (ITP). We describe herein the first known case of a laparoscopic splenectomy to be performed in Japan for a patient with a giant splenic epidermoid cyst. A 26-year-old woman presented to our hospital with the major complaint of a feeling of abdominal fullness. Prior to surgery, an ultrasound-guided splenic cyst puncture was conducted for diagnostic purposes as well as to reduce the size of the cyst. The carbohydrate antigen 19-9 (CA 19-9) level was found to be elevated in the cystic contents and in the serum. Under laparoscopic guidance, the splenic vessels were ligated using a device for extracorporeal ligation, then divided. After the resected spleen had been placed in a retrieval bag, it was delivered out of the abdominal cavity without fragmentation. Following surgery, the patient's serum CA 19-9 level returned to normal. Splenic epidermoid cysts are most often encountered in young women, and laparoscopic surgery to remove cysts of this type is both minimally invasive and excellent from a cosmetic standpoint. Thus, laparoscopic surgery should be considered as the method of choice for the majority of patients diagnosed with a splenic epidermoid cyst.
An elastofibroma is a benign and rare fibrous lesion that most commonly occurs in the periscapular region. A gastrointestinal elastofibroma is extremely rare. In the present study, six cases of elastofibromas including a case in the stomach were evaluated. The gastric case revealed widely distributed lesions in the submucosal layer with perivascular fibrotic lesions (PVFLs) and some PVFLs were distributed to the skip lesions of elastofibroma. These PVFLs were also observed in all five periscapular cases and invariably contained elastic fibers which showed various degree of maturation. CD34-positive stromal cells were observed not only in elastofibromas but also in PVFLs in each case. These findings suggested the possibility of the PVFLs were the primary lesions of elastofibroma and their vascular-centric development. The percentage of the CD105-positive vessels in elastofibroma group was significantly higher than in the control group. This result indicates active neovascularization in elastofibromas.
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