Sigmoid mesocolon hernia is an uncommon type of internal hernia with only a few cases reported to date. This disease entity can progress rapidly to cause vascular disturbance, necrosis, and perforation of the bowel wall; therefore, early diagnosis and surgical treatment are essential. We describe the case of an intra-mesosigmoid hernia in a 60-year-old man without history of previous abdominal surgery who presented with sudden acute abdominal pain and vomiting. Based on computed tomography, which showed ascites and small bowel obstruction, we diagnosed him as having strangulation of the small intestine caused by a sigmoid mesocolic hernia and performed emergency surgery. Laparotomy revealed small intestinal strangulation, extensive engorgement, and discoloration of bowel loops. Approximately 100 cm of the small intestine extending from the ligament of Treitz had undergone strangulation and herniated into the defect of sigmoid mesocolon, leading to a diagnosis of an intra-mesosigmoid hernia. Because the incarcerated portion of the small intestine was viable, we did not perform intestinal resection and reconstruction but closed the defect in the sigmoid mesocolon. His postoperative course was uneventful.
Deregulated expression of genes is found in cancer cells, which may aect malignant properties, but it is unclear whether such modulation occurs allele-speci®cally. This study shows that the gene coding a4 integrin, a cell adhesion molecule, underwent allelic inactivation in a series of heterozygous murine ®brosarcoma cell lines (MST lines) with dierent metastatic potentials. P4 cells expressed the a4 integrin gene from one allele at a level comparable to that of the primary MST1 tumor, whereas the descendent lines of P4 exhibited decreased expression of both alleles. No allelic loss of DNA was observed in these cells. Other four clones derived from P4 and ®ve clones from a dierent tumor also showed such two-step inactivation. Intriguingly, the loss of expression was correlated with the acquisition of spontaneous, but not arti®cial, metastatic ability. This is consistent with the previous result of inverse relation between the expression of a4b1 integrin and the invasive potential of B16 melanoma cells. Analysis of DNA methylation and chromatin state of the a4 integrin gene failed to provide a clue to dierence between the two alleles in the cell lines. These results suggest that the allelic inactivation is a process giving loss of function to one allele, although the mechanism is unclear.
F1 offspring of male MSM male mice with a p53-deficient (knockout) allele and normal female BALB/c mice were backcrossed with MSM mice to produce N2 mice. Female F1 and N2 mice were irradiated with gamma-radiation, and thymic lymphomas were obtained from 69 F1 and 82 N2 mice heterozygous for X chromosome markers. Of these 151 mice, 91 carried a p53-deficient allele. These lymphomas were analyzed for allelic loss by using four marker loci distributed on X chromosome to assess the stability of the inactive X chromosome, which contributes little to cellular functions. Twenty lymphomas showed allelic loss of all four loci, suggesting loss of a whole inactive X chromosome due to mitotic nondisjunction, whereas 24 lost only a part of an X chromosome, as a result of somatic recombination. The p53 status of the lymphomas was determined by genotyping and allelic loss analysis: 53 had retained two wild-type p53 alleles, suggesting normal function; 69 had lost both alleles, indicating loss of function; and the remaining 29 had at least one wild-type p53 allele, so their p53 status was unclear. Compilation of these two data revealed one nondisjunction-type change and five recombination-type mutations on X chromosome in 53 lymphomas retaining functional p53. In contrast, 14 and 16 of these alterations, respectively, were observed in 69 lymphomas lacking p53 function. These results suggest that p53 loss significantly increases the accumulation of recombinant chromosomes and decreases the fidelity of mitotic chromosome transmission of the X chromosome in gamma-ray-induced lymphomas.
This paper presents a case of suspected liver metastasis of gastric cancer and a virtual complete response to S-1 chemoradiotherapy. A 69-year-old man underwent distal gastrectomy for gastric cancer in 2008. Multiple liver metastases occurred in 2009. He underwent 15 courses of S-1 therapy and radiation therapy (37.5 Gy). Abdominal computed tomography showed virtual complete disappearance of liver metastasis after chemoradiotherapy. Hence, this case was interpreted as a complete response. No sign of recurrence was noted 18 months after complete response was confirmed. S-1 chemoradiotherapy is likely to be effective in treating patients with liver metastases of gastric cancer.
Para-aortic lymph node recurrence is a rare type of metastasis from colorectal cancer, and no treatment has yet been established. Here, we report on a case of isolated para-aortic lymph node metastasis from rectosigmoid cancer that showed complete response to chemoradiation therapy with capecitabine/oxaliplatin plus bevacizumab. A 58-year-old woman underwent high anterior resection for rectosigmoid cancer in 2009. Para-aortic lymph node recurrence occurred in 2011. She underwent radiation therapy (50 Gy) and 8 courses of capecitabine/oxaliplatin plus bevacizumab. Abdominal computed tomography and positron emission tomography with 18-fluorodeoxyglucose did not reveal any para-aortic lymph node recurrence after chemoradiation therapy. Hence, this case was interpreted as a complete response. No recurrence was noted 6 months after the complete response. Chemoradiation therapy with capecitabine/oxaliplatin plus bevacizumab is likely to be effective in treating patients with para-aortic lymph node recurrence.
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