A Retrospective Study About the Effectiveness of Anastomosis With a Polyglycolic Acid Sheet in Colorectal Cancer.

Introduction Anastomotic leakage is a serious complication in colon and rectal cancer surgeries, contributing to increased mortality rates and extended hospital stays. Despite various preventive measures, including intraoperative assessments and transanal drains, the incidence of anastomotic leakage remains a significant concern. This study investigates the potential efficacy of polyglycolic acid (PGA) sheets in reducing anastomotic leakage rates in gastrointestinal surgeries. Materials & methods A retrospective cohort study was conducted between January 2021 and January 2023 at Nagoya Tokushukai General Hospital, Ogaki Tokushukai Hospital, and Haibara General Hospital. A total of 239 patients undergoing colon or rectal cancer surgery were included. Anastomoses were performed with or without PGA sheets, and groups were compared using statistical analyses, including t-tests, Mann-Whitney U tests, and chi-square tests. The primary endpoint was the incidence of anastomotic leakage. Results Of the 239 patients, anastomotic leakage occurred in 14 (6%). The PGA use group (52 patients) showed no instances of anastomotic leakage while the PGA non-use group (187 patients) had 14 cases. Comparisons revealed significant differences in anastomotic leakage rates (p=0.04) between the two groups. Univariate analysis demonstrated a lower incidence of anastomotic leakage associated with PGA use (p=0.04). However, no significant differences were observed for transanal drainage (p=0.66), smoking (p=0.76), steroid use (p=1), and preoperative chemotherapy (p=0.07). Conclusion This study suggests that the use of PGA sheets in gastrointestinal anastomosis may contribute to a lower incidence of anastomotic leakage. The findings highlight the need for further prospective studies with a larger sample size, distinguishing between colon and rectum surgeries. Despite the limitations of this retrospective study, the observed reduction in anastomotic leakage frequency with PGA sheet use is noteworthy, emphasizing the potential significance of this approach in preventing a critical complication in colorectal surgeries.

Simultaneous robot-assisted colorectal surgery for sigmoid colon cancer and portal vein embolization from the inferior mesenteric vein for intrahepatic cholangiocarcinoma: A case report and literature review.

INTRODUCTION AND IMPORTANCE: The treatment of multiple cancers requires multidisciplinary expertise. In this case, we experienced a multiple cancers case, sigmoid colon cancer and intrahepatic cholangiocarcinoma that required preoperative portal vein embolization (PVE). PVE is often approached by trans-hepatic percutaneous approach or via ileocecal vein (ICV) or veins of the small intestine. In this case, the patient was scheduled to undergo robot-assist surgery for sigmoid colon cancer, and it was planned that the inferior mesenteric vein (IMV) would be cut. PVE from the IMV was performed with hope to reduce complications. CASE PRESENTATION: This patient had intrahepatic cholangiocarcinoma and sigmoid colon cancer. A radical cure for intrahepatic cholangiocarcinoma was expected by left liver lobectomy. Because of concerns about postoperative liver failure, it was decided to perform PVE. PVE via IMV approach was performed simultaneously with robot-assisted surgery for sigmoid colon cancer. The patient was discharged without complications 12 days after surgery. CLINICAL DISCUSSION: PVE is a very important technique for massive hepatic resection. Percutaneous trans-hepatic approach has the potential to damage vessels, bile duct, normal liver. Venous approaches, including via ICV, have the potential to damage vessels. In this case, we performed PVE from the IMV because we thought this approach would reduce the risk of complications. The patient successfully underwent PVE without complications. CONCLUSION: PVE via IMV was successfully performed without complications. In multiple cancers case, this approach would be better approach than any other PVE approach like this case.

Emergency laparoscopic trans-abdominal pre-peritoneal repair (TAPP) for irreducible inguinal hernia in Covid-19 patient: A case report and literature review.

Introduction: With the global pandemic of COVID-19 for over two years, we might have to proceed surgical operation of patients with COVID-19 infection because of its emergency. Here we present a case who received an emergency operation for an irreducible inguinal hernia with COVID-19. We safely performed trans-abdominal pre-peritoneal repair (TAPP) in one surgery without any problems. Presentation of case: 52-year-old male with no specific past medical history came to the emergency department with complaints of right inguinal bulging and abdominal pain. On physical examination, a bulge in the right inguinal region was observed, so a right irreducible inguinal hernia was suspected. Since he had fever, we conducted a COVID-19 antigen test and it was positive. Because we could not return with manually, we decided to perform emergency surgery with appropriate infection control techniques. After laparoscopic return of the intestinal tract, a mesh was implanted using TAPP. The patient was discharged 2 days after surgery. Discussion: Even in pandemic of COVID-19, cases of irreducible inguinal hernia could be occur. COVID-19 has systemic inflammation, so we worried about mesh infection. But this patient took TAPP safely in emergency surgery with COVID-19. Conclusion: We experienced a case of TAPP proceeded patient with COVID-19. We considered that placement of a foreign material is acceptable when it is necessary in COVID-19 patient safely.

[A Case of Transcatheter Arterial Chemoembolization and Surgical Resection of Left 7th Rib Metastasis after Surgery for Hepatocellular Carcinoma].

The patient was an 81-year-old man. After a liver posterior segmentectomy for hepatocellular carcinoma, a painful bulge was observed in the left anterior thoracic region during a routine outpatient visit. Elevated tumor markers and contrast- enhanced CT scan revealed a mass with contrast effect in the left 7th rib. Ultrasound-guided biopsy revealed hepatocellular carcinoma metastatic to the left 7th rib. There were no other obvious metastases, and the diagnosis of a single bone metastasis was made. The patient did not request chemotherapy and underwent transcatheter arterial chemoembolization 4 times. The patient did not show any improvement in tumor markers or shrinkage of the tumor, and his quality of life was deteriorated due to increased pain. The patient underwent left chest wall tumor resection and chest wall reconstruction. Postoperative tumor markers were normalized and pain improved markedly. We report a case of postoperative recurrence- free survival for 2 years.

Axillary Lymph Node Swelling After COVID-19 Booster Vaccination: Japanese Case Report and Literature Review.

BACKGROUND/AIM: COVID-19 has been a global pandemic for more than 2 years, and vaccination against COVID-19 using an mRNA vaccine is widespread. The COVID-19 vaccination can cause specific side-effects, such as axillary lymph node swelling; therefore, breast oncologists should pay attention to such occurrences. Initially, only two COVID-19 vaccinations were planned; however, in some countries third or fourth vaccines have been administered. Here, we present a female case who developed axillary lymph node swelling after her third vaccination. We have also reviewed the literature regarding this side-effect after a third or fourth COVID-19 vaccination. CASE REPORT: A 64-year-old woman who came to our clinic regarding a mammography abnormality in her left breast. She had no palpable mass, but a left breast mass was shown by mammography, and ultrasonography and magnetic resonance imaging indicated a hamartoma. At 2 months after her second COVID-19 vaccination when she underwent these tests, she had no axillary lymph node swelling. We planned a follow-up after 6 months. At her next visit, by chance, she underwent ultrasonography 14 days after she received a third COVID-19 vaccination, and a swollen axillary lymph node was observed. CONCLUSION: Axillary lymph node swelling can occur after a third COVID-19 vaccination. Therefore, breast oncologists will have to consider this side-effect of COVID-19 vaccination when diagnosing breast tumors.

Timing and Duration of Axillary Lymph Node Swelling After COVID-19 Vaccination: Japanese Case Report and Literature Review.

BACKGROUND/AIM: COVID-19 vaccination is now performed in most of the world to limit the spread of the disease. The first mRNA vaccine was approved in clinical settings and has specific side effects including axillary lymph node swelling, which can be misdiagnosed as breast cancer metastasis. The timing of axillary lymph node swelling and its duration are unclear. Here, we present a Japanese case and review of the existing literature. CASE REPORT: We report the case of a 67-year-old woman with breast calcification. She had regular follow ups in our hospital for this calcification and received ultrasonography of the breast and axilla at every visit. She visited 6 months before having her COVID-19 vaccination, and 7 days and 6 months after the first COVID-19 vaccination. She had a swollen axillary lymph node 7 days after the first vaccination, which although it was improved, remained for 6 months. CONCLUSION: Axillary lymph node swelling occurred 7 days after vaccination and remained up to 6 months after it.

Adenocarcinoma arising in a colonic interposition following a total gastrectomy: report of a case.

A segment of the transverse colon can be used for gastric reconstruction after a total gastrectomy. This report presents the case of a 68-year-old woman with primary adenocarcinoma of the colon in a segment used for reconstruction after a total gastrectomy. The interposed colon developed colon carcinoma 9 years after the gastric reconstruction. The possibility of a primary carcinoma arising in a gastric colon interposition must be considered when employing the transverse colon as a gastric substitute.

Targeting beta1 integrin restores sensitivity to docetaxel of esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is a common and highly fatal cancer in Japan. Systemic chemotherapy is used, but some tumors show resistance to it. The mechanisms of tumor resistance to chemotherapy remain largely unknown. We determined the chemosensitivity of 15 ESCC cell lines (TE-1-5, TE-8-15, KYSE140 and KYSE150) to docetaxel by clonogenic and MTT assays. We used cDNA microarray analysis and quantitative RT-PCR to determine which genes might determine resistance to docetaxel. Small interfering RNA (siRNA) was used to suppress gene expression and its effect on the chemosensitivity of the cell was determined. The cell line with the most resistance to docetaxel was TE-2. Using microarray analysis, we identified beta1 integrin (ITGB1) to be overexpressed in this cell line. Higher expression of ITGB1 mRNA was significantly associated with docetaxel resistance (n=15, r2=0.66, P=0.0110). Suppression of ITGB1 expression using siRNA sensitized the TE-2 cells to docetaxel. These data suggest that overexpression of ITGB1 may be related to resistance to chemotherapy and that targeting ITGB1, particularly in patients on docetaxel therapy, may enhance the effect of chemotherapy in patients with ESCC.

PIK3CA mutation status in Japanese esophageal squamous cell carcinoma.

BACKGROUND: A somatic mutation of the PIK3CA (phosphatidylinositol 3-kinase catalytic subunit) gene has been found in human cancer patients. However, this mutation has not yet been extensively studied in esophageal squamous cell carcinomas. MATERIALS AND METHODS: We analyzed a mutation of the PIK3CA gene in 88 Japanese cases of esophageal squamous cell carcinomas that had all undergone surgery at the Department of Surgery II, Nagoya City University Medical School, between 1996 and 2003. The TE and KYSE series of cell lines are human esophageal cancer cell lines. Two PIK3CA mutation hot spots (exon 9 and exon 20) were analyzed by a real time polymerase chain reaction (PCR)-based assay and the data were confirmed by direct sequencing. We performed a cell proliferation assay to determine the effects of a PI3K inhibitor LY294002. RESULT: In exon 9, a somatic mutation was found in two patients (2.2%) and in two cell lines. The mutations included three E545K (G1633A) mutations and one E545Q (G1633C) mutation. However, in exon 20, no mutation was observed in our esophageal cancer patients. PI3K inhibitor (LY294002) inhibited the growth of an esophageal cancer cell line with a PIK3CA mutation (E545K) in vitro. CONCLUSIONS: We found LY294002 to reduce the proliferation of the esophageal cancer cell line in vitro. Importantly, a cell line with a PIK3CA gene mutation was more susceptible to a PI3K inhibition than those without any such mutation. Further functional analyses of the PIK3CA mutations are warranted to determine whether or not they may be potentially useful targets of therapy for esophageal cancer.

Molecular docking analysis of the protein-protein interaction between RelA-associated inhibitor and tumor suppressor protein p53 and its inhibitory effect on p53 action.

RelA-associated inhibitor (RAI) was initially identified as a protein that interacts with the p65 subunit (RelA) of nuclear factor-kappaB. It was recently found to interact with the p53 tumor suppressor protein. RAI is a structural homolog of the p53-binding protein 2 and I kappaB family proteins, and is known to inhibit the DNA-binding activities of p65 and p53. In the present study, we have attempted to predict the 3-dimensional structure of RAI in complex with p53 using computational chemistry. In order to evaluate the predicted structure model, we created a series of RAI mutants in which the amino acid residues involved in the interaction with p53 were mutated, and examined their activities in blocking p53-mediated bax gene expression. Our observations support the validity of the predicted 3-dimensional model of the p53-RAI protein complex. Based on the p53-RAI complex model, we have demonstrated the biological importance of the R248 and R273 residues of p53, and the D775 and E795 residues of RAI, in the protein-protein interaction between p53 and RAI and the biological actions of these proteins. These findings will further clarify the biological actions of RAI in carcinogenesis and can be used for the development of a novel strategy in blocking the actions of RAI. The possible biological implications of RAI are also discussed.

Expression of ECRG4 is an independent prognostic factor for poor survival in patients with esophageal squamous cell carcinoma.

In this study, we examined the expression of esophageal cancer-related gene 4 (ECRG4) mRNA and evaluated its clinical significance in esophageal squamous cell carcinoma (ESCC). ECRG4 mRNA expression was quantified by real-time RT-PCR in 63 ESCC and corresponding normal esophageal mucosal samples. ECRG4 mRNA expression levels were significantly lower in ESCC tissues compared with corresponding normal esophageal mucosa (P<0.0001), in patients with locally invasive T2-4 tumors compared with less invasive T1 tumors (P=0.0229) and in stage 4 tumors compared with stage 0-3 tumors (P=0.0120). Furthermore, low ECRG4 mRNA expression levels were associated with significantly shorter survival after surgery compared with high ECRG4 mRNA expression levels (P=0.0150) in ESCC patients. On the basis of multivariate analysis, we conclude that ECRG4 mRNA expression level could be a candidate for an independent prognostic factor for ESCC patients.

The overexpression of caveolin-1 and caveolin-2 correlates with a poor prognosis and tumor progression in esophageal squamous cell carcinoma.

Caveolin-1 (CAV1) and caveolin-2 (CAV2) are the major structural proteins of caveolae. We investigated the relationship between the clinicopathological factors of esophageal squamous cell carcinoma (ESCC) and the expression of CAV1 and CAV2. CAV1 and CAV2 expression were analyzed by quantitative reverse transcription-polymerase chain reaction (RT-PCR) in 15 esophageal cancer cell lines (TE1-15) and a normal esophageal epithelium cell line (Het-1A). CAV1 and CAV2 expression was examined by RT-PCR and immunohistochemical analysis in 47 ESCC specimens. High levels of CAV1 and CAV2 mRNA were detected in TE1-15, but neither CAV1 nor CAV2 mRNA were detected in Het-1A. In the ESCC samples CAV1 and CAV2 mRNA expression in the ESCC samples were significantly higher than in the corresponding normal esophageal mucosa (CAV1, P=0.0024; CAV2, P=0.0136). However, we could not find any significant relationship between CAV1 or CAV2 mRNA expression and clinicopathological factors. Immunostaining for CAV1 was positive in 13 of 47 patients (27.7%), whereas CAV2 was positive in 22 of 47 patients (46.8%). A significant correlation was observed between CAV1 and CAV2 immunostaining and T factor, lymphatic invasion, vein invasion and differentiation. The patients with positive staining for CAV1 or CAV2 had a significantly shorter survival than those with negative staining (P=0.0105 and 0.0424 for CAV1 and CAV2, respectively). These results suggest that positive staining for CAV1 and CAV2 could be a potentially useful prognostic marker of ESCC.

Frequent loss of the long arm of chromosome 18 in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is one of the most common and deadly cancers in Japan. In this study we performed fluorescent in situ hybridization (FISH) and loss of heterozygosity (LOH) analysis for chromosome 18q in ESCC cells to investigate allelic imbalance of chromosome 18q in ESCC. In the FISH analysis, only one signal for chromosome 18q was detected in TE-1 esophageal cancer cells, whereas two signals were detected in TE-2 cells. Two of five resected ESCC samples from patients showed loss of one copy of chromosome 18q. To construct a precise deletion map of chromosome 18q, LOH analysis was performed using 30 microsatellite markers localized to chromosome 18q. LOH was observed in 31 of 46 ESCC samples (67.4%) for at least one locus on chromosome 18q. LOH frequency for individual markers varied from 18.5% (D18S460) to 48.4% (D18S866). Thirteen of 46 ESCC samples (28.3%) showed the loss of most of the long arm of chromosome 18. Lymph node metastasis and vein invasion were significantly associated with the deletion of chromosome 18q. Loss of chromosome 18q may play an important role in the progression of ESCC.

Expression of ACP6 is an independent prognostic factor for poor survival in patients with esophageal squamous cell carcinoma.

ACP6 (acid phosphatase 6, lysophosphatidic) is a lysophosphatidic acid (LPA)-specific phosphatase that hydrolyzes LPA to monoacylglycerol and is involved in lipid metabolism in the mitochondria. Its role in oncogenesis and cancer progression has not been studied. In this study, we examined the expression of ACP6 mRNA and evaluated its clinical significance in esophageal squamous cell carcinoma (ESCC). Expression of ACP6 mRNA was quantified by real-time reverse transcription polymerase chain reaction using the LightCycler in 70 esophageal ESCC specimens and their paired normal esophageal mucosa. The data were analyzed with reference to clinicopathological factors. ACP6 mRNA expression in esophageal cancer tissue was significantly lower than that in corresponding normal esophageal mucosa (P=0.0301). Among the esophageal cancer tissues, ACP6 mRNA expression significantly correlated with local tumor invasion (T factor, P=0.0461) and lymph node metastasis (P=0.0128). Furthermore, low ACP6 mRNA expression was associated with a significantly shorter survival time compared with high expression (log-rank test, P=0.0358). In multivariate analysis, ACP6 mRNA expression emerged as a significant independent factor (P=0.0148). Impaired ACP6 expression may lead to more aggressive invasion of ESCC, and ACP6 mRNA expression level could be an independent prognostic factor for patients with ESCC.

Inhibition of the 53BP2S-mediated apoptosis by nuclear factor kappaB and Bcl-2 family proteins.

The p53 binding protein 2 (53BP2) has been identified independently as the interacting protein to p53, Bcl-2, and p65 subunit of nuclear factor kappaB (NF-kappaB). It was demonstrated that over-expression of 53BP2 (renamed as 53BP2S) induces apoptotic cell death. In this study we explored the effect of NF-kappaB activation elicited by a physiological NF-kappaB inducer, interleukin-1beta (IL-1beta), and anti-apoptotic Bcl-2 family proteins on the 53BP2S-mediated apoptosis. We found that both NF-kappaB activation and Bcl-2 family proteins could prevent the 53BP2S-mediated depression of mitochondrial transmembrane potential, activation of caspase-9, cleavage of poly ADP ribose polymerase (PARP), and cell death. These observations suggested that 53BP2S/Bbp and its directly or indirectly interacting proteins might play crucial roles in the regulation of apoptosis and contribute to carcinogenesis. It is also suggested that 53BP2S/Bbp induces apoptosis through the mitochondrial death pathway presumably by counteracting the actions of anti-apoptotic Bcl-2 family proteins. The regulatory network of the 53BP2S-mediated apoptosis cascade including its interacting proteins is discussed.