Journal of Cancer Prevention最新文献

Serological tests for Helicobacter pylori needs local validation as the diagnostic accuracy may vary depending on the prevalence of H. pylori. This study examined the diagnostic performance of two ELISA, GastroPanel^® (GastroPanel ELISA; Biohit Oyj) and GENEDIA^® (GENEDIA^® H. pylori ELISA, Green Cross Co.) in Korean population. One thousand seventy seven patients who visited for esophagogastroduodenoscopy between 2013 and 2023 were prospectively enrolled, and serum samples from the subjects were tested using both GastroPanel^® and GENEDIA^®. The two tests were compared for their diagnostic accuracy in detecting atrophic gastritis (AG), intestinal metaplasia (IM), gastric adenoma (GA), and gastric cancer (GC), and the positivity rates by age and sex were observed. There was substantial correlation (Pearson coefficient [r] = 0.512, P < 0.001) and agreement (Cohen's Kappa coefficient [κ] = 0.723, P < 0.001) between the results obtained using GastroPanel^® and GENEDIA^®. The test results from the two kits did not match perfectly with a discrepancy observed in approximately 16% of cases, that 67 subjects were positive only on GENEDIA^® while 75 subjects were positive only on GastroPanel^®. The area under receiver operating characteristic curve for AG, IM, GA, and GC using GastroPanel^® were 0.666, 0.635, 0.540, and 0.575, while the results tested using GENEDIA^® were 0.649, 0.604, 0.553, and 0.555, respectively, without significant difference between the two results. GastroPanel^® and GENEDIA^® showed similar performance in terms of diagnostic accuracy; but the test results did not match perfectly. A large-scale validation study in Koreans is needed.

Shiga toxin-producing Escherichia coli is the most prevalent bacterial strain responsible for Shiga toxin-related infections. While Shiga toxin is inherently toxic, it has potential therapeutic applications as a component of anticancer drugs. Despite its association with infections and harmful effects on human health, Shiga toxin is being explored as a viable element in drug delivery systems targeting cancer cells. The findings indicate that the production of mutated bacteria containing Shiga toxin is an effective preventive strategy for immunization against these toxins. Furthermore, the B subunit of Shiga toxin shows promise for imaging cancer cells, opening new paths for therapeutic interventions.

Colon cancer remains a significant global health concern, necessitating the continuous exploration of novel therapeutic strategies. Cisplatin is a first-line chemotherapy medication that is frequently used to treat patients for a variety of malignancies, including colon cancer. However, a major obstacle to its clinical usefulness is acquired resistance. This research investigates the synergistic effects of kaempferol, a natural flavonoid with known anti-cancer properties, in combination with cisplatin, in colon cancer cells. Our study employed colon cancer cell lines to evaluate the individual and combined cytotoxic effects of kaempferol and cisplatin. The results demonstrated a notable enhancement in the cytotoxicity of colon cancer cells when treated with a combination of kaempferol and cisplatin compared to individual treatments. This synergistic effect was further characterized by an increase in apoptosis, as evidenced by morphological changes and biochemical markers of apoptosis and cell cycle. The investigations revealed that the combined treatment led to the modulation of key apoptotic pathways, including the upregulation of pro-apoptotic factors and downregulation of anti-apoptotic factors. Additionally, the synergistic effect was associated with the inhibition of cell proliferation and induction of cell cycle arrest. The findings of this study suggest that the combination of kaempferol and cisplatin holds promise as a potent therapeutic strategy for colon cancer treatment, potentially enhancing the efficacy of conventional chemotherapy while minimizing adverse effects. Further in-depth investigations, including in vivo studies, are warranted to validate these findings and explore the translational potential of this synergistic approach in clinical settings.

Cancer remains to be a pervasive disease as traditional treatments have plateaued in efficacy. Anticancer research continues to grow in an effort to find novel preventive and treatment measures for cancers. The papaya plant produces several biologically active phytochemicals, which exhibit anti-inflammatory, antibacterial, and anti-oxidative properties. This review explores studies examining these phytochemicals derived from the papaya plant as a potential chemopreventive agent and a cancer therapeutic. Further studies must be done to establish the papaya plant and its phytochemicals as an alternative to traditional cancer treatments.

The identification of therapeutic target genes that are functionally involved in stemness is crucial to effectively cure patients with metastatic carcinoma. We have previously reported that inhibition of ribosomal protein L9 (RPL9) expression suppresses the growth of colorectal cancer (CRC) cells by inactivating the inhibitor of DNA-binding 1 (ID-1) signaling axis, which is functionally associated with cancer cell survival. In addition to cell proliferation, ID-1 is also involved in the maintenance of cancer stemness. Thus, we aimed in this study to investigate whether the function of RPL9 could correlate with CRC stem cell-like properties. Here, we demonstrated that siRNA silencing of RPL9 reduced the invasiveness and migrative capabilities of HT29 and HCT116 parental cell populations and the capacity for sphere formation in the HT29 parental cell population. CD133⁺ cancer stem cells (CSCs) were then separated from CD133^- cancer cells of the HT29 parental cell culture and treated with RPL9-specific siRNAs to verify the effects of RPL9 targeting on stemness. As a result, knockdown of RPL9 significantly suppressed the proliferative potential of CD133⁺ colorectal CSCs, accompanied by a reduction in CD133, ID-1, and p-IκBα levels. In line with these molecular alterations, targeting RPL9 inhibited the invasion, migration, and sphere-forming capacity of CD133⁺ HT29 CSCs. Taken together, these findings suggest that RPL9 promotes CRC stemness via ID-1 and that RPL9 could be a potential therapeutic target for both primary CRC treatment and the prevention of metastasis and/or recurrence.

β-Casein, a major protein in cow's milk, is divided into the A1 and A2 type variants. Digestion of A1 β-casein yields the peptide β-casomorphin-7 which could cause gastrointestinal (GI) discomfort but A2 milk containing only A2 β-casein might be more beneficial than A1/A2 (regular) milk. The aim of this study was to evaluate the differences in GI discomfort after ingestion of A2 milk and A1/A2 milk. A randomized, double-blind, cross-over human trial was performed with 40 subjects who experienced GI discomfort following milk consumption. For each intervention period, either A2 milk first (A2→A1/A2) or A1/A2 milk was first consumed for 2 weeks (A1/A2→A2) following a 2-week washout period. GI symptom rating scale (GSRS) scores, questionnaire for digestive symptoms, and laboratory tests including fecal calprotectin were evaluated. For symptom analysis, generalized estimating equations gamma model was used. A2 milk increased bloating (P = 0.041) and loose stools (P = 0.026) compared to A1/A2 milk in GSRS. However, A2 milk caused less abdominal pain (P = 0.050), fecal urgency (P < 0.001) and borborygmus (P = 0.007) compared to A1/A2 milk in questionnaire for digestive symptoms. In addition, fecal calprotectin also decreased or less increased after consumption of A2 milk compared to A1/A2 milk (P = 0.030), and this change was more pronounced in males (P = 0.005) than in females. There were no significant adverse reactions during the trial. A2 milk alleviated digestive discomfort in Koreans following A2 milk consumption (ClinicalTrials.gov NCT06252636 and CRIS KCT0009301).

Cancer drug resistance is associated with metabolic adaptation. Cancer cells have been shown to implicate acetylated polyamines in adaptations during cell death. However, exploring the mimetic of acetylated polyamines as a potential anticancer drug is lacking. We performed intracellular metabolite profiling of human breast cancer MCF-7 cells treated with doxorubicin (DOX), a well known anticancer drug. A novel and in-house vertical tube gel electrophoresis assisted procedure followed by LC-HRMS analysis was employed to detect acetylated polyamines such as N1-acetylspermidine. We designed a mimetic N1-acetylspermidine (MINAS) which is a known substrate of histone deacetylase 10 (HDAC10). Molecular docking and molecular dynamics (MDs) simulations were used to evaluate the inhibitory potential of MINAS against HDAC10. The inhibitory potential and the ADMET profile of MINAS were compared to a known HDAC10 inhibitor Tubastatin A. N1-acetylspermidine, an acetylated form of polyamine, was detected intracellularly in MCF-7 cells treated with DOX over DMSO-treated MCF-7 cells. We designed and curated MINAS (PubChem CID 162679241). Molecular docking and MD simulations suggested the strong and comparable inhibitory potential of MINAS (-8.2 kcal/mol) to Tubastatin A (-8.4 kcal/mol). MINAS and Tubastatin A share similar binding sites on HDAC10, including Ser138, Ser140, Tyr183, and Cys184. Additionally, MINAS has a better ADMET profile compared to Tubastatin A, with a high MRTD value and lower toxicity. In conclusion, the data show that N1-acetylspermidine levels rise during DOX-induced breast cancer cell death. Additionally, MINAS, an N1-acetylspermidine mimetic compound, could be investigated as a potential anticancer drug when combined with chemotherapy like DOX.