Moo-Jun Baek

Freeze-thaw stabilization of sweet potato starch gel by polysaccharide gums

Abstract Nine polysaccharide gums (sodium alginate, carboxymethyl cellulose, curdlan, gellan, guar gum, gum arabic, κ-carrageenan, locust bean, and xanthan) were compared for their stabilizing effects in sweet potato starch gel against repeated freeze–thawing (FT) treatments. The gums were added in starch gel at 0.3 or 0.6% (w/w, based on total gel weight), and total solid content in the gel was adjusted to 7% (w/w) with starch. The gels containing starch and gum were repeatedly freeze–thawed up to five times by storing at −18xa0°C for 20xa0h and then at 25xa0°C for 4xa0h. Water release (syneresis) was measured by vacuum-filtering the freeze–thawed gels. Among the gums tested, alginate, guar gum, and xanthan were highly effective in reducing the syneresis. For example, guar gum, at 0.6%, showed the least syneresis (33.0%, w/w based on initial water content) after five FT cycles, which was less than half that of pure starch gel. At 0.3%, however, xanthan was more effective than guar gum in reducing syneresis. Xanthan reduced paste viscosity significantly, whereas guar gum and alginate increased the viscosity, but there was little relation between pasting viscosity and syneresis. The gums remained in the gel matrix during the syneresis without a significant loss. Recrystallization of starch (retrogradation) induced by FT treatment was also retarded by the presence of gums, and sodium alginate was more effective in retarding the retrogradation than xanthan or guar gum.

Effects of sugars and sugar alcohols on thermal transition and cold stability of corn starch gel

Abstract Various sugars and sugar alcohols (ribose, xylose, glucose, fructose, mannose, sucrose, maltose, isomaltose, trehalose, xylitol, mannitol, and sorbitol) were compared in their effects on thermal transitions and cold-storage stability of a corn starch–sugar gel (40% starch, starch:sugar=10:1 or 10:3 dry solids basis) using a differential scanning calorimetry. As the molar concentration of sugar increased, the onset temperature and enthalpy for starch melting were increased. Among the sugars, the samples with disaccharides exhibited higher onset temperature and enthalpy than those with monosaccharides at the same molar concentration. Under cold storage (4 or −20 °C), the sugars facilitated amylopectin recrystallization. Fructose and isomaltose produced higher degrees of amylopectin recrystallization than did other sugars. Sugar alcohols produced slightly greater recrystallization than did the corresponding sugars. Ice melting temperature and glass transition temperature ( T ′ g ) of the freeze-concentrated phase were decreased as the molar concentration of sugars increased, and there was no or little dependence on the chemical structure of sugars. Ice melting enthalpy for the gels showed no clear dependence on sugar concentration or structure. Sucrose addition lowered the ice melting enthalpy (ice formation by rapid freezing), whereas isomaltose or trehalose addition raised it. By cold storage, the T ′ g of the starch gels was increased, whereas the ice melting enthalpy was decreased, as a result of water consumption for starch recrystallization. In the gel system (40% starch), sugar addition (10 or 30% based on starch) enhanced starch recrystallization, but decreased the ice melting and glass transition temperatures.

Characterization of aberrant FHIT transcripts in gastric adenocarcinomas

Aberrant transcripts of FHIT (fragile histidine triad) have been reported in several types of primary tumors and cell lines, including gastric carcinoma. The role of these aberrant transcripts in tumorigenesis is not clear yet. Forty-eight aberrant-sized FHIT transcripts with various lengths and number in 35 cases of gastric adenocarcinomas were further characterized. Aberrant transcripts, with deletions and/or insertions, were frequently observed in 20 cases of tumors. Sequence analysis demonstrated that different types of aberrant transcripts used normal splice sites but skipped exons, contained the inserts with the part of intron 5 sequences, or used the FHIT cDNA sequence 179-180 as a cryptic splice acceptor site. Most of aberrant transcripts lacked exon 5 and were presumably non-functional as the translation initiation codon is located in exon 5. Additionally, other transcripts, indicative of additional splice processing, either deletions or insertions, were expressed in several tumors. Taken together, our data indicate that the FHIT gene expression is frequently altered in gastric adenocarcinomas by aberrant splicing, and suggest that different types of aberrant transcripts may result during the multi-step splice processing.

The BRAF mutation is associated with the prognosis in colorectal cancer

AbstractBackgroundTwo members of the Ras/Raf signaling pathway, KRAS and B-raf, are suspected to be involved in the stepwise progression of colorectal cancer (CRC) tumorigenesis.ObjectiveWe compared the KRAS and BRAF mutation status of CRC patients with their clinicopathological characteristics and examined the effect of mutation status on survival rates.MethodsDNA was extracted from 164 samples, and the mutation statuses of KRAS and BRAF were assessed using peptide PNA clamp real-time PCR method. The presences of mutation were compared with clinicopathological factors and 5-year survival rate.ResultsAmong the 164 CRC cases, KRAS mutation as detected in 71 cases (43.3xa0%), respectively, with no relationship with clinicopathological factors of the patients. On Kaplan–Meier survival analysis, KRAS mutation was not significantly associated with survival (pxa0=xa00.971). BRAF mutation was detected in 26 cases (15.9xa0%) and not associated with clinicopathological factors of the patients. However, the 5-year survival rate of BRAF mutations was significantly decreased (pxa0=xa00.02).ConclusionsThe presence of KRAS mutation did not correlaten with the various clinicopathological factors of CRC patients or the survival rate. However, the survival rate was reduced in BRAF-mutated CRC patients. Therefore, BRAF mutation could be an important prognostic factor in CRC patients.

Expression of the survivin-2B splice variant related to the progression of colorectal carcinoma

Purpose Recently, two alternatively spliced survivin variants, survivin-ΔEx3 and survivin-2B, were identified in a single copy of the survivin gene. It has been reported that the expressions of survivin splice variants significantly correlates with the clinical results in many types of human carcinoma. We investigated the transcription levels of survivin and its splice variants in human colorectal carcinomas, and analyzed correlations between survivin expression levels and clinicopathologic features. Methods We used Western blot and real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) to analyze the protein and mRNA expression levels of survivin variants in 51 colorectal carcinomas. The quantitative RT-PCR was performed using primer pairs specific for survivin and each of its splice variants, then normalized for the gene that encodes glyceraldehydes-3-phosphate dehydrogenase. Results In Western blotting, the protein levels of survivin were higher in the tumor tissue than in normal tissue. The expression of survivin, survivin-2B and survivin-ΔEx3 mRNA was present in 96%, 64.7%, and 82.4% of the samples, respectively. When the pathologic parameters were compared, colorectal cancers of advanced pT stages showed significant decrease in survivin-2B mRNA expression by the quantitative RT-PCR (P < 0.001). Conclusion The decreased expression of survivin-2B might be related to tumor progression in colorectal cancers. This finding indicates that alternatively spliced variants of survivin may be involved in refining the functions of survivin during tumor progression.

Astrocyte elevated gene-1 overexpression in hepatocellular carcinoma: an independent prognostic factor

Purpose Astrocyte elevated gene-1 (AEG-1) plays important roles in tumorigenesis such as proliferation, invasion, metastasis, angiogenesis, and chemoresistance. We examined the expression of AEG-1 in patients with hepatocellular carcinoma (HCC). Methods Eighty-five samples were collected from patients with HCC who underwent surgery and were histopathologically confirmed to have HCC. Two independent pathologists, experienced in evaluating immunohistochemistry and blinded to the clinical outcomes of the patients, reviewed all samples. They determined AEG-1 expression semiquantitatively by assessing the percentage of positively stained immunoreactive cells and staining intensity. Clinicopathological data were analyzed in association with prognosis. Results The association was estimated by univariate and multivariate analyses with Cox regression. Tumor size (hazard ratio [HR], 2.285; 95% confidence interval [CI], 1.175-4.447; P = 0.015), microvascular invasion (HR, 6.754; 95% CI, 1.631-27.965; P = 0.008), and AEG-1 expression (HR, 4.756; 95% CI, 1.697-13.329; P = 0.003) were independent prognostic factors for overall survival. Those for disease-free survival rate were tumor size (HR, 2.245; 95% CI, 1.282-3.933; P = 0.005) and AEG-1 expression (HR, 1.916; 95% CI, 1.035-3.545; P = 0.038). The cumulative 5-year survival and recurrence rates were 89.2% and 50.0% in the low-expressing group and 24.5% and 82.4% in the high-expressing group, respectively. Conclusion The results suggest that AEG-1 overexpression could serve as a valuable prognostic marker in patients with HCC.

Q787Q EGFR Polymorphism as a Prognostic Factor for Lung Squamous Cell Carcinoma

Objective: EGFR genetic polymorphisms have been investigated for carcinogenesis in various tumors including lung cancer. We evaluated EGFR mutations in four exons, with an emphasis on the Q787Q EGFR polymorphism in non-small-cell lung cancer. Methods: To determine the presence of the Q787Q polymorphism in patients with lung cancer, we performed direct sequencing analyses of four exons for 83 squamous cell carcinomas and 80 adenocarcinomas untreated with EGFR tyrosine kinase inhibitors. Results: The Q787Q EGFR polymorphism was more frequently detected in squamous cell carcinoma patients than in adenocarcinoma patients (24 vs. 15.9%). The group of patients with the Q787Q EGFR polymorphism included more males and heavy smokers compared with other patient groups. The presence of the Q787Q EGFR polymorphism significantly and negatively affected the overall survival rate among patients with non-small-cell carcinoma (p = 0.011), particularly those with squamous cell carcinoma (p = 0.037). Among stage I and II squamous cell carcinoma patients, those with the Q787Q EGFR polymorphism had a poor prognosis (p = 0.032). Conclusions: The Q787Q EGFR polymorphism allows stratifying lung squamous cell carcinoma patients and could be an independent prognostic marker, particularly among those in stages I and II.

Karyopherin α-2 is a reliable marker for identification of patients with high-risk stage II colorectal cancer

PurposeAdjuvant chemotherapy (AC) is frequently considered in patients with high-risk stage II colorectal cancer (CRC). Among patients with stage II CRC who do not receive AC because they are not considered to be at high risk, 20–25% will develop recurrence and die from the disease. Elevated levels of KPNA2 have been observed in various cancers, and overexpression of KPNA2 is related to CRC progression.MethodsWe examined the expression of KPNA2 using 293 CRC tissues, including 118 with stage II CRC, and investigated the applicability of KPNA2 as a biomarker to predict high-risk stage II CRC. Moreover, we further investigated the role of KPNA2 as an oncogene in CRC carcinogenesis using in vitro functional studies.ResultsHigh KPNA2 expression was associated with vascular (pxa0=xa00.027) and lymphatic invasion (pxa0=xa00.009) in patients with stage II CRC. On multivariate analysis, high KPNA2 expression (HR 3.174, 95% CI 2.060–4.889; pxa0<xa00.001) was independently associated with survival in patients with CRC. The overall survival rate in patients with high KPNA2 expression was higher than that in patients with low KPNA2 expression in CRC (pxa0<xa00.001), even in patients with stage II CRC (pxa0=xa00.001). Additionally, KPNA2 was associated with tumorigenesis and cancer progression in CRC cells; high KPNA2 expression was associated with increased cell proliferation (pxa0<xa00.05), migration (pxa0=xa00.03), invasion (pxa0=xa00.001), and semisolid agar colony formation (pxa0<xa00.001).ConclusionKPNA2 expression is useful for identification of patients with high-risk stage II CRC who could benefit from AC and that KPNA2 may also be a promising therapeutic target.

CORRIGENDUM: Correction of funding statement in ACKNOWLEDGEMENTS section: Epigenetic inactivation of RUNX3 in colorectal cancer

[This corrects the article on p. 19 in vol. 94, PMID: 29333422.].

Epigenetic inactivation of RUNX3 in colorectal cancer

Purpose Emerging evidence indicates that runt-related transcription factor 3 (RUNX3) is an important tumor suppressor gene in several cancer types, including colorectal cancer (CRC). However, the clinical significance of RUNX3 inactivation in CRC remains unclear. The aim of this study was to examine the correlation between clinicopathologic factors and RUNX3 hypermethylation/expression in CRC. Methods Sixty-two CRC patients who were treated at the Soonchunhyang University College of Medicine were recruited in this study. The hypermethylation of CpG islands in the RUNX3 promoter and the expression of RUNX3 mRNA were identified by methylation-specific polymerase chain reaction (PCR) and reverse transcriptase-PCR, respectively. The expression of RUNX3 was determined by immunohistochemical staining. Results Of the 62 CRC tissue samples, 20 (32.3%) presented hypermethylated RUNX3 promoters. Aberrant RUNX3 hypermethylation was found to be associated with vascular (P = 0.006) and lymphatic (P = 0.002) invasion. Hypermethylation of RUNX3 was associated with poor survival outcomes (P = 0.038). However, expression of RUNX3 was not a prognostic factor (P = 0.363). Conclusion Hypermethylation of RUNX3 may be a predictor of a poor prognosis in CRC.