Background & Aims-Elevated microsatellite alterations at selected tetranucleotide repeats (EMAST) occurs during microsatellite instability (MSI) that is not associated with major defects in DNA mismatch repair (MMR) but rather the reduced (heterogenous) expression of the MMR protein hMSH3; it occurs in sporadic colorectal tumors. We examined the timing of development of EMAST during progression of colorectal neoplasias and looked for correlations between EMAST and clinical and pathology features of tumors.

We found that the effect of dietary methyl supply on colorectal carcinogenesis may differ according to MTHFR C677T genotype and the subsite of origin in a Korean population.

PurposeMany studies have revealed that diabetes mellitus (DM) increases a person's lifetime risk of colorectal cancer and that DM is associated with a worse outcome of colon cancer, but this association is controversial. In this study, we intended to examine the relationship between DM and the long-term outcomes of colorectal cancer.MethodsA retrospective analysis was conducted on 657 patients who underwent surgery due to colorectal cancer between 1997 and 2004 at Korea Cancer Center Hospital. The operations were done by a single surgeon. With a median follow-up of 4.7 years, we analyzed differences in recurrence-free survival (RFS) and overall survival (OS) between patients with DM and those without DM.ResultsOf the 657 patients, 374 (57%) were males and 67 (10%) had DM. There was no difference in age at diagnosis, sex and pathologic stage of colorectal cancer according to the presence of DM. There were no difference in the RFS and the OS of colon cancer between the patients with DM and those without DM. At 5 years, the RFS was 71.3% in diabetic patients vs. 70.4% in non-diabetic patients (P = 0.480), and the OS was 68.8% in diabetic patients vs. 75.0% in non-diabetic patients (P = 0.498). There was no difference in the median survival between the groups (9.6 years in the diabetic group vs. 10.6 years in the non-diabetic group; P = 0.495).ConclusionIn this study, we did not find any relation between the presence of DM and either the recurrence or the survival in cases of colorectal cancer. More studies to elucidate whether the influence of DM is directly related to a higher rate of cancer recurrence or survival are needed.

Background The antitumor effects of natural killer cells, helper T cells, and cytotoxic T cells after cancer surgery were reported previously. This study hypothesized that propofol-based anesthesia would have fewer harmful effects on immune cells than volatile anesthetics–based anesthesia during colorectal cancer surgery. Methods In total, 153 patients undergoing colorectal cancer surgery were randomized and included in the analysis. The primary outcome was the fraction of circulating natural killer cells over time in the propofol and sevoflurane groups. The fractions of circulating natural killer, type 1, type 17 helper T cells, and cytotoxic T cells were investigated. The fractions of CD39 and CD73 expressions on circulating regulatory T cells were investigated, along with the proportions of circulating neutrophils, lymphocytes, and monocytes. Results The fraction of circulating natural killer cells was not significantly different between the propofol and sevoflurane groups until 24 h postoperatively (20.4 ± 13.4% vs. 20.8 ± 11.3%, 17.9 ± 12.7% vs. 20.7 ± 11.9%, and 18.6 ± 11.6% vs. 21.3 ± 10.8% before anesthesia and after 1 and 24 h after anesthesia, respectively; difference [95% CI], –0.3 [–4.3 to 3.6], –2.8 [–6.8 to 1.1], and –2.6 [–6.2 to 1.0]; P = 0.863, P = 0.136, and P = 0.151 before anesthesia and after 1 and 24 h, respectively). The fractions of circulating type 1 and type 17 helper T cells, cytotoxic T cells, and CD39+ and CD73+ circulating regulatory T cells were not significantly different between the two groups. The neutrophil to lymphocyte ratio in both groups remained within the normal range and was not different between the groups. Conclusions Propofol-based anesthesia was not superior to sevoflurane-based anesthesia in terms of alleviating suppression of immune cells including natural killer cells and T lymphocytes during colorectal cancer surgery. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Human embryonic carcinoma (EC; NCCIT) cells have self-renewal ability and pluripotency. Cancer stem cell markers are highly expressed in NCCIT cells, imparting them with the pluripotent nature to differentiate into other cancer types, including breast cancer. As one of the main cancer stem cell pathways, Wnt/β-catenin is also overexpressed in NCCIT cells. Thus, inhibition of these pathways defines the ability of a drug to target cancer stem cells. Tannic acid (TA) is a natural polyphenol present in foods, fruits, and vegetables that has anti-cancer activity. Through Western blotting and PCR, we demonstrate that TA inhibits cancer stem cell markers and the Wnt/β-catenin signaling pathway in NCCIT cells and through a fluorescence-activated cell sorting analysis we demonstrated that TA induces sub-G1 cell cycle arrest and apoptosis. The mechanism underlying this is the induction of mitochondrial reactive oxygen species (ROS) (mROS), which then induce the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated extrinsic apoptosis pathway instead of intrinsic mitochondrial apoptosis pathway. Moreover, ribonucleic acid sequencing data with TA in NCCIT cells show an elevation in TRAIL-induced extrinsic apoptosis, which we confirm by Western blotting and real-time PCR. The induction of human TRAIL also proves that TA can induce extrinsic apoptosis in NCCIT cells by regulating mROS.