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Laparoscopic colorectal surgery (LCRS) requires a small laparotomy at the umbilicus. The wound is small and inconspicuous, but if the patient develops an umbilical incisional hernia (UIH), the wound is visible and the patient suffers from symptoms of discomfort. However, the incidence of UIH after LCRS and its risk factors are not well understood. The purpose of this study was to investigate the risk factors for UIH after LCRS for colorectal cancer.This was a single-centre retrospective study of 135 patients with colorectal cancer, conducted at our hospital from April 2013 to March 2019. The diagnosis of UIH was based on computed tomography and physical examination findings. Preoperative patient data such as enlargement of the umbilical orifice (EUO), subcutaneous fat thickness (SFT) and intraperitoneal thickness (IPT) were collected and analysed using univariate and multivariate analyses for the presence of risk factors for UIH.A total of 135 patients who underwent LCRS were analysed. The incidence of UIH was 20.7%. Univariate analysis revealed significantly high body mass index (BMI) ≥ 25 (P = 0.032), EUO (P 0.001), SFT ≥18 mm (P = 0.011), and IPT ≥61 mm (P 0.01) in the UIH group. Multivariate analysis revealed significant differences in EUO (P 0.001), SFT ≥18 mm (P = 0.046) and IPT ≥61 mm (P = 0.022).EUO was the most important risk factor for UIH, followed by IPT and SFT. These findings are predictive indicators of the development of UIH after LCRS and can be assessed objectively and easily with preoperative computed tomography.

Radical surgical procedures for malignant diseases of the pelvis result in a large pelvic defect that requires soft tissue reconstruction. The mesentery can be used for pelvic floor reconstruction when debridement with intestinal resection is required. A 75-year-old woman was diagnosed with sacral necrosis, infection and sepsis after carbon ion radiotherapy for sacral chordoma. She underwent sacral debridement three times, which resulted in a large pelvic defect of 14 × 13 cm. Surgery was performed to completely resect the necrotic tissue. We performed extended debridement of sacrum and adjacent tissue around the rectum and anus. Since it was impossible to preserve the anus, laparoscopic left hemicolectomy, abdominosacral resection, and left-sided mesocolic leaf repair for the pelvic defect, and reconstructed the pelvis and buttocks using a gluteal thigh flap were performed. Indocyanine green fluorescent (ICG) imaging was used to detect the margin of the pelvic floor and necrotic tissue and the blood flow of the left-sided mesocolic leaf flap. Left-sided mesocolic leaf reconstruction is useful for large pelvic defects. ICG imaging enabled the detection of the resection margins and the blood flow of the mesocolic leaf.

Background: Ras homolog family member A (RhoA), a member of the Rho family of small GTPases, and Vav1, a guanine nucleotide exchange factor for Rho family GTPases, have been reported to activate pathways related to the actin cytoskeleton and regulation of cell shape, attachment, and motility. The interaction between these molecules in lymphoma is involved in malignant signaling, but its function in epithelial malignancy is unknown. Here, we investigated the malignant signal of mutant RhoA in gastric cancer and demonstrated the potential of RhoA G17E/Vav1 as a therapeutic target for diffuse gastric cancer. Methods: The RhoA mutants R5W, G17E, and Y42C were retrovirally transduced into the gastric cancer cell line MKN74. The stably transduced cells were used for morphology, proliferation, and migration/invasion assays in vitro. MKN74 cells stably transduced with ectopic wild-type RhoA and mutant RhoA (G17E) were used in a peritoneal xenograft assay. Results: The RhoA mutations G17E and Y42C induced morphological changes in MKN74. G17E induced Vav1 expression at the mRNA and protein levels and promoted the migration and invasion of MKN74. An RNA interference assay of Vav1 revealed that RhoA G17E enhanced cancer cell invasion via Vav1. Furthermore, immunoprecipitation revealed that Vav1 and RhoA G17E specifically bind and function together through matrix metalloproteinase-9. In a peritoneal xenograft model of nude mice, RhoA G17E promoted peritoneal dissemination, whereas Vav1 knockdown suppressed it. Conclusion: Overall, our findings indicate that RhoA G17E associated with Vav1 and promoted cancer invasion via matrix metalloproteinase-9 in gastric cancer cells. Thus, RhoA G17E/Vav1 signaling in diffuse gastric cancer may be a useful therapeutic target.

Colorectal cancer with a Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) gene mutation is considered to be resistant to anti-EGFR agents. G12D is the most common KRAS mutation in colorectal cancer, followed by G12V and G13D. According to clinical and basic research data, patients with colorectal cancer exhibiting G12D and G12V KRAS mutations are resistant to anti-EGFR agents; however, this is not true of G13D and other minor mutations, which are still not well understood. The current study focused on minor KRAS mutations (G12A, G12C, G12S, Q61H and A146T) and evaluated whether these were resistant to anti-EGFR antibodies using a mix culture assay. The results demonstrated that all KRAS mutations, including minor mutations, were resistant to two anti-EGFR agents: Cetuximab and panitumumab. The combined effect of MEK and BCL-XL inhibition on colorectal cancer cells with KRAS minor mutations were subsequently evaluated. The combined effect of MEK and BCL-XL inhibitors was confirmed in all KRAS minor mutations. The sensitivity of AMG510, a novel KRAS G12C selective inhibitor, was also assessed. The mix culture assay revealed that AMG510 selectively exerted an antitumor effect on colon cancer cells with a G12C KRAS mutation. The combination of MEK and BCL-XL inhibition markedly enhanced the effect of AMG510 in colon cancer cells. The current study suggested that AMG510 may have potential clinical use in combination with MEK and BCL-XL inhibitors in the treatment of patients with colorectal cancer exhibiting the G12C KRAS mutation.

Background: Adhesive small bowel obstruction (ASBO) is one of the major causes of postoperative morbidity. Conservative treatment is generally applied to non-strangulated ASBO. Several factors have been reported to affect the response to conservative treatment in patients with ASBO. However, the association between sex differences and non-strangulated ASBO remains unclear. This study aimed to elucidate the effect of sex differences in non-strangulated postoperative ASBO.Methods: We divided 192 admissions of 99 patients with non-strangulated postoperative ASBO into two groups: the male group (n = 137) and female group (n = 55). Clinical features and prognosis were compared between the two groups.Results: Female patients had significantly poorer performance status (p < 0.001) and lower proportions of esophageal/gastric malignancies (p = 0.002), colorectal malignancies (p = 0.034), and history of ASBO (p = 0.028) than male patients. More female patients failed conservative treatment (p = 0.036) than male patients. Hospital length of stay (LOS) was longer (p = 0.002) in the female group than in the male group. Multiple logistic regression analysis showed that female sex was associated with increased odds of requiring elective surgery (odds ratio 2.381, p = 0.040). The Cox proportional hazards regression model revealed that female sex was an independent predictor of hospital discharge (hazard ratio 0.651, p = 0.015).Conclusion: Female sex adversely affected the response to conservative treatment and LOS in patients with non-strangulated postoperative ASBO.

Additional file 1. Patients’ demographics and summary of data. Patients’ demographics and summary of data by study group.