[Resection of Chest Wall Metastasis from Rectal Mucinous Carcinoma-A Case Report].

An 81-year-old woman with rectal mucinous carcinoma underwent a laparoscopic low anterior resection in February 2019, followed by chemotherapy using XELOX plus Bev. The adjuvant chemotherapy was discontinued due to interstitial pneumonia. During a follow-up consultation 2 years later, chest computed tomography(CT)imaging revealed a nodule in her right lung(S9). Based on a radiological diagnosis of metastasis and considering her history of rectal cancer, a partial resection of the right lung was executed. One year after the pulmonary resection, a growing nodule in her right lateral chest wall was detected. A metastatic chest wall tumor was suspected, and a right chest wall tumor resection at the 5th and 6th ribs was performed. A rectal mucinous carcinoma metastasis was diagnosed using histopathological examination. The postoperative course was good, and she was discharged from hospital on the 10th day. To conclude, there are few reported cases of rectal cancer chest wall metastasis, and a further accumulation of similar cases is necessary for the development of treatment options.

A case report of a collision tumor composed of pancreatic ductal adenocarcinoma and peri-pancreatic mucosa-associated lymphoid tissue lymphoma.

BACKGROUND: Collision tumors are composed of two distinct tumor components. Collision tumors composed of pancreatic ductal adenocarcinoma and malignant lymphoma occurring in the pancreas have not been previously described in the scientific literature. In this case report, we describe a unique patient with a collision tumor composed of pancreatic ductal adenocarcinoma and peri-pancreatic mucosa-associated lymphoid tissue (MALT) lymphoma occurring in the pancreas. CASE PRESENTATION: An 82-year-old woman presented to our hospital complaining of dizziness. Computed tomography (CT) and magnetic resonance imaging (MRI) showed a large lymphoid lesion spreading from the peri-pancreatic tissue heading to the hepatic hilar plate, involving the hepatoduodenal ligament and the entire duodenum, also showing a hard tumor in the pancreas head. We performed echo-guided needle biopsies for each tumor and diagnosed a collision tumor composed of pancreatic ductal adenocarcinoma and low-grade B cell lymphoma. The patient underwent pancreaticoduodenectomy. The resected specimen showed an elastic hard tumor, 90 × 75 mm in size, located in the pancreatic head, and a whitish-yellow hard tumor involving the lower bile duct, 31 mm in size, located in the center of the pancreatic head. Pathological and immunohistochemical examination proved that pancreatic ductal adenocarcinoma and MALT lymphoma originating from the peri-pancreatic head collided in the pancreatic head. CONCLUSIONS: To best of our knowledge, this is the first report of a surgically resected collision tumor of pancreatic ductal adenocarcinoma and MALT lymphoma originating from the peri-pancreatic head. A needle biopsy is useful when inconsistent findings are observed on diagnostic CT and MRI of tumor lesions since there is the possibility of a collision tumor.

[A case of bleeding stomal varices during the course of oxaliplatin-based chemotherapy for recurrent rectal cancer].

A 51-year-old man with a history of an abdominoperineal resection of the rectum and colostomy for rectal cancer underwent chemotherapy for multiple liver metastases.Twenty -two courses of the folinic acid, 5-fluorouracil(5-FU)and oxaliplatin(FOLFOX4)/bevacizumab(BEV)regimen and 39 courses of 5-FU/Leucovorin/BEV were administered.Progressive splenomegaly and stomal varices were observed during the course of chemotherapy.The patient was admitted due to excessive bleeding after colostomy.Angiography revealed bleeding stomal varices secondary to portal hypertension.Splenectomy was performed with subsequent reduction in the size of the stomal varices and no rebleeding was observed.Oxaliplatin -based chemotherapy could lead to hepatic sinusoidal dilation and induce splenomegaly and varix formation secondary to portal hypertension.Our experience with this case suggests that careful attention should be paid to stomal varices in colostomy patients receiving oxaliplatin-based chemotherapy.

[Traumatic hemothorax treated with transcatheter arterial embolization].

A 33-year-old man was transported to our hospital following a traffic accident. He was found to have hemopneumothorax, multiple rib fractures and lung injury by computed tomography(CT). Despite thoracic drainage and fluid resuscitation, he became hemodynamically unstable. At 2 hours after arrival, CT revealed worsening in hemothorax. Emergency angiography of intercostal arteries showed signs of hemorrhage from intercostal arteries, and embolization of the 3∼6th intercostal arteries was performed. After transcatheter arterial embolization(TAE), his vital signs got stable and he was discharged without significant complication.

Ileal schwannoma developing into ileocolic intussusception.

Intussusception is rare in adults. We describe a 47-year-old man with ileal schwannoma that led to ileocolic intussusception. Abdominal ultrasonography, abdominal CT scan and barium enema confirmed an ileal tumor. Colonoscopy revealed a peduncular submucosal tumor (SMT) 75 mm long with an ulcerated apex at the ascending colon. The provisional diagnosis was a gastrointestinal stromal tumor of the terminal ileum. Ileocecal resection was carried out and the tumor was histologically diagnosed as schwannoma. Abdominal pain resolved postoperatively. This case reminds us that ileal schwannoma should be included in the differential diagnosis of intussusception caused by an SMT in the intestine.

Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer.

To identify tumor-suppressor genes on chromosome 10 in non-small cell lung cancers, we isolated 10 types of splicing variant of the HELLS/SMARCA6 gene transcripts. HELLS/SMARCA6 is a novel member of SNF2 family, which is implicated in cellular functions like chromatin remodeling. Variant 1 was an alternatively spliced isoform containing an insertion of a 44 ntd intronic sequence between exons 3 and 4, giving rise to a premature termination of translation. Expression of variant 1 was detected exclusively in lung cancer specimens (11 of 43 cases, 26%) but was not detected in corresponding normal tissues. The D10S520 marker in the proximity of the HELLS/SMARCA6 gene showed prevalent allelic loss (41%) compared to flanking markers (25-31%). These results suggest that loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor-specific exon creation may result in epigenetic deregulation, leading lung cells to malignancy or its progression.

The transfection of thymidylate synthase antisense suppresses oncogenic properties of a human colon cancer cell line and augments the antitumor effect of fluorouracil.

5-Fluorouracil (5-FU), a fluoropyrimidine analogue, is one of the most commonly used anticancer drugs for the treatment of gastrointestinal malignancies. Some studies reported that the cytotoxicity of fluoropyrimidines is mediated, in large part, by inhibition of the thymidylate synthase (TS), an essential DNA synthetic enzyme. The aim of this study was to determine if antisense TS technology could augment the chemosensitivity of human cancer cells to 5-FU. The full length coding region of TS cDNA was inversely cloned into the eukaryotic expression vector pCDL81 and transfected into DLD-1 cells. The expression and activity of TS were significantly suppressed in the antisense TS transfected cells. Interestingly, the transfection of antisense TS alone inhibited the cellular growth in vitro. The chemosensitivity to 5-FU was significantly increased in the transfected cells. The 50% inhibition values of 5-FU on DLD-1/anti-TS were approximately one forth that on parental cells. The augmentation of chemosensitivity to 5-FU was also confirmed in a nude mice model. The tumor growth of DLD-1/anti-TS cells was suppressed significantly more than that of DLD-1 cells by the 5-FU. The expression and activity of TS in human colon cancer cells were effectively inhibited by TS antisense treatment and the effect of 5-FU to cancer cells can be augmented. The antisense TS technology could be promising for treatments of gastrointestinal cancers.

Caveolin-1 as tumor suppressor gene in breast cancer.

PURPOSE: Many articles have reported the caveolin-1 gene to be downregulated thus suggesting that it might be a candidate tumor suppressor gene in many tumors, but in bladder tumors the caveolin-1 gene was expressed and related to the pathological grade. We investigated the function of caveolin-1 protein in breast tumors. METHODS: We introduced the caveolin-1 gene into a MCF-7 human breast cancer cell line, and examined its cell growth, cell viability, and anchorage-independent growth. RESULTS: The caveolin-1 transfectants showed less proliferation than the vector control transfectants on the fourth day regarding the cell growth rate. In addition, the cell viability of the caveolin-1 transfectants was about 55% of the vector control. A soft agar assay of the caveolin-1 transfectants showed less growth with a lower number of colonies. CONCLUSION: In MCF-7 cells, the caveolin-1 gene may influence the tumor suppressor efficacy.

Detection of codon 61 point mutations of the K-ras gene in lung and colorectal cancers by enriched PCR.

Mutation of the Kirsten ras (K-ras) gene is one of most common alterations in solid tumors including lung and colorectal cancers. We developed new enriched PCR-RFLP assay to detect mutations of K-ras codon 61 at the 1st and 2nd letters and non-enriched PCR-RFLP assay to detect the 3rd letter mutation. One mutant allele among 10(3) wild-type alleles was detected by enriched PCR-RFLP assay, while one mutant in 10 wild-type alleles was detected by non-enriched PCR-RFLP assay for codon 61 3rd letter. We then examined K-ras codon 12, 13 and 61 mutations in lung and colorectal cancers using these assays. K-ras codon 12 mutation was detected in 10 of 109 (9%) lung cancer and 19 of 83 (23%) colorectal cancer cases. K-ras codon 13 mutation was detected in 2 of 83 (2%) colorectal and 0 of 109 NSCLC cases, respectively. There was no K-ras codon 61 mutation in either type of cancer. Our results demonstrate that enriched PCR-RFLP is a sensitive assay to detect K-ras codon 61 mutation, however, it was extremely rare in lung and colorectal cancers, suggesting organ-specific pathways in mutagenesis of the ras gene family.

Reduced expression of the REIC/Dkk-3 gene by promoter-hypermethylation in human tumor cells.

The human REIC gene is a recently found mortalization-related gene and a candidate tumor suppressor gene expression of which is largely attenuated in many immortalized and tumor-derived cell lines (Biochem. Biophys. Res. Commun. 268 (2000) 20-24). To gain insight into the mechanisms of the down-regulation, we investigated the genomic structure and promoter activity of the human REIC gene. The gene, identical with the DKK-3 gene, resides on chromosome 11p15.1, consists of nine exons, and has two promoters. Methylation in the main promoter region was detected in 11 out of 21 cell lines tested (52%) derived from a variety of human tumors, in which the expression of the REIC gene was decreased. In ten of these 11 cell lines the minor promoter was also methylated. Similarly, the REIC gene expression was decreased in 14 of 24 fresh non-small cell lung cancer specimens (58%) compared to that in corresponding non-cancerous tissue, though allelic loss and tumor-specific mutation were rare. Of these 14 tumors, at least five tumors exhibited heavy methylation of the REIC promoter region. These results indicate that the down-regulation of the REIC gene expression is ascribed to the aberrant promoter hyper-methylation at least in a subset of human tumors. The expression was restored upon treatment of SQ5 cells with 5-aza-deoxycytidine, confirming DNA methylation as the mode of downregulation. A notable single nucleotide polymorphism in the coding region (cSNP) with an amino acid substitution of glycine (GGG) to arginine (AGG) was found at codon 335 of the REIC gene. However, the distribution of the cSNP showed no significant difference between lung cancer patients and healthy population.