This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Postoperative carcinoembryonic antigen (post-CEA) has recently been reported to be a reliable prognostic factor for colon cancer. However, most clinicians decide whether or not to conduct adjuvant chemotherapy (AC) for stage II colon cancer according to major guidelines, which do not include post-CEA in their high-risk criteria. The present study aimed to assess post-CEA in stage II colon cancer for which the significance of AC is unknown. The present study analyzed 199 consecutive patients with stage II colon cancer who underwent curative surgery between January 2007 and December 2016. The CEA value was considered high when it was ≥5.0 ng/ml. The prognostic value of high post-CEA values was assessed. Overall, 19 patients exhibited high post-CEA levels. Kaplan-Meier survival curve analysis demonstrated that patients with high post-CEA levels had significantly worse relapse-free survival (RFS) and overall survival (OS) than those with normal post-CEA [RFS, 63.5 (high post-CEA) vs. 88.0% (normal post-CEA), P=0.003; OS, 76.5 (high post-CEA) vs. 96.8% (normal post-CEA), P<0.001]. Multivariate analysis demonstrated that high post-CEA remained a significant independent risk factor for worse RFS [hazard ratio (HR), 3.98; P=0.006]. The same was also demonstrated for patients without AC (HR, 5.43; P=0.008). To the best of our knowledge, the present study was the first to demonstrate that high post-CEA levels may be an indicator of high-risk stage II colon cancer, even for patients without AC. These results highlight the need for a multicenter prospective study.
The histone methyltransferase G9a is expressed in various types of cancer cells, including colorectal cancer (CRC) cells. Interleukin (IL)-8, also known as C-X-C motif chemokine ligand 8 (CXCL8), is a chemokine that plays a pleiotropic function in the regulation of inflammatory responses and cancer development. Here, we examined the relationship between G9a and IL-8 and the clinical relevance of this association. We immunohistochemically analyzed 235 resected CRC samples to correlate clinical features. Samples with high G9a expression had better overall survival and relapse-free survival than those with low G9a expression. Univariate and multivariate analyses demonstrated that low G9a expression remained a significant independent prognostic factor for increased disease recurrence and decreased survival (P<0.05). G9a was expressed at high levels in commercially available CRC cell lines HCT116 and HT29. Knockdown of G9a by siRNA, shRNA, or the G9a-specific inhibitor BIX01294 upregulated IL-8 expression. The number of spheroids was significantly increased in HCT116 cells with stably suppressed G9a expression, and the number of spheroids was significantly decreased in HCT116 cells with stably suppressed IL-8 expression. Thus, the suppression of IL-8 by G9a may result in a better prognosis in CRC cases with high G9a expression. Furthermore, G9a may suppress cancer stemness and increase chemosensitivity by controlling IL-8. Therefore, G9a is a potential novel marker for predicting CRC prognosis, and therapeutic targeting of G9a in CRC should be contraversial.
Recent studies have shown the benefits of complete mesocolic excision (CME) and extended lymphadenectomy (i.e. D3 lymph node dissection) in patients with colon cancer [1,2]. Laparoscopic surgery for colorectal cancer is less invasive [3], and laparoscopic CME or Japanese D3 is also feasible [4]. However, for cases with a past history of ab-S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section.
A 41-year-old man who had hypopharyngeal cancer (T4a, N2, M0, Stage ⅣA) and thoracic esophageal cancer (Mt, T2, N2, M0, Stage Ⅲ ) underwent definitive chemoradiotherapy, and attained complete remission. Eight months later, local recurrence and lymph node recurrence of esophageal cancer were detected, and lymph node recurrence of hypopharyngeal cancer also occurred. He received salvage esophagectomy, reconstruction using a gastric tube via subcutaneous route, and jejunostomy. Postoperative course was uneventful and he was discharged on the 26 th postoperative day. On the 58th day after the operation, he was diagnosed as having panperitonitis due to small bowel perforation at the inserting portion of a nutrition tube, and he underwent an emergency operation. He went into septic shock, and needed a large amount of noradrenaline during and after the operation. On the 7th day after the emergency operation he needed no noradrenaline and left the intensive care unit. On the 9th day after the emergency operation, leakage of esophagogastrostomy site occurred which was conservatively treated. He left our hospital on the 52nd day after the surgery. Possible causes of delayed anastomotic leakage might include definitive chemo radiotherapy to the upper area of the gastric tube and gastric tube ischemia resulting from peripheral circulatory disturbance due to severe septic shock and the long-term use of noradrenaline.
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