Nutrition and Cancer-An International Journal最新文献

Background: Breast cancer (BC) is characterized by an increasing incidence and mortality rate. Juzaowan inhibits various malignant processes, although its mechanism in BC remains unclear.

Methods: To evaluate the impact of Juzaowan on biological functions of BC cells, cellular assays were done to assess proliferation, migration, invasion, and apoptosis. Bioinformatics was used to identify signaling pathways affected by active ingredients of Juzaowan. BC cells were treated with Juzaowan. Western blot assayed lactate production, glucose consumption, and expression of proteins related to glycolytic pathway and STAT3/C-Myc axis.

Results: Juzaowan suppressed BC cell proliferation and increased apoptosis. It downregulated anti-apoptotic protein BCL2 while upregulating pro-apoptotic proteins Bax and cleaved caspase 3. Juzaowan significantly inhibited BC cell migration and invasion. Significant upregulation of E-cadherin and significant downregulation of E-cadherin-binding protein ZEB1, N-cadherin, and vimentin were observed. Bioinformatics analysis and cellular experiments confirmed inhibition of Juzaowan on BC cell glucose uptake and glycolytic pathways-related key metabolic enzymes (GLUT1, PKM2, LDH) expressions. Western blot revealed that Juzaowan induced metabolic alterations in BC cells by impeding STAT3/C-Myc axis.

Conclusion: This study elucidated molecular mechanisms of Juzaowan inhibiting BC cell glycolysis by repressing STAT3/C-Myc axis, thus suppressing malignant progression. These findings supported clinical applications of Juzaowan.

Objective: The purpose of the meta-analysis was to compare the prevalence of sarcopenia on staging computed tomography (CT) in patients with solid tumors in different world regions. Materials and Methods: MEDLINE, Embase, and SCOPUS literature databases were screened for prevalence of sarcopenia in oncologic patients up to December 2022. Two hundred eighty studies met the inclusion criteria. The methodological quality of the involved studies was checked according to the Quality Assessment of Diagnostic Studies instrument. Results: Two hundred eighty studies with 81,885 patients were included. The prevalence of sarcopenia among all patients was 35.5%. Prevalence of sarcopenia was higher in Europe (45.6%) and North America (41.2%) than in Asia (29.6%). Prevalence rates for the curative cohort were similar in all three regions, with 43.7% in Europe, 41.3% in North America, and 37.4% in Asia. In the palliative cohort, sarcopenia prevalence was higher in Europe (55.7%) and Asia (45.7%) than in North America (34.0%). In the European cohort, prostate cancer (73.9%), esophageal cancer (74.2%), pancreatic cancer (62.5%), and renal cell cancer (65.3%) showed high prevalence rates of sarcopenia. Applied cutoff values differed among regions. Conclusion: Our study shows that prevalence rates for sarcopenia of patients with solid tumors differ between regions and are different for curative and palliative settings. European studies demonstrate high prevalence rates for both settings. There is need for regional harmonization of sarcopenia definitions.

A phytoestrogen-rich diet has been suggested to reduce tumor proliferation among men with prostate cancer, and the effect may differ between men with different polymorphisms of the estrogen receptor-beta gene (ERβ). Patients with low- or intermediate-risk prostate cancer scheduled for radical prostatectomy were randomized to an intervention group (n = 71) provided with soybeans and flaxseeds (∼200 mg phytoestrogens/day) to eat until surgery (approximately 6 wk) or to a control group (n = 69). Tumor proliferation was assessed using Ki-67 indexes, prostate-specific antigen (PSA) concentrations were analyzed in blood, and ERβ polymorphism was genotyped in all subjects. The intervention group had a 13% unit lower risk [95% confidence interval (CI): -28%, 1.8%] of a higher Ki-67 index compared to controls, but the effect was most pronounced among TT carriers of ERβ [risk difference (RD) -19%, 95% CI: -45%, 6.8%]. Subjects with genotype TC/CC had a lower risk (RD -29%, 95% CI: -46%, -1.2%) and TT genotype a higher risk (RD 25%, 95% CI: 8.7%, 42%) of increased PSA concentration, comparing the intervention group to controls. In conclusion, a phytoestrogen-rich diet may cause lower tumor proliferation and concentration of PSA in men with prostate cancer with a specific genetic upset of ERβ.

Objective: This study investigated the safe indocyanine green retention rate at the 15-minute (ICG-R15) threshold for hepatectomy and the effect of nutritional management on ICG-R15 and posthepatectomy liver failure (PHLF).

Methods: A retrospective cohort study was conducted on 70 hepatectomy patients with chronic liver disease, divided into routine care and nutrition intervention groups. ICG-R15 was measured pre- and postoperatively, along with PHLF occurrence and other health metrics.

Results: Seventy patients with chronic liver disease were divided into two groups: one received routine care, while the other followed a nutrition plan based on Omaha theory. The intervention group showed a significantly lower incidence of PHLF (15.8% vs 41.2%, p = 0.009) and clinically relevant PHLF (5.3% vs 19.6%, p = 0.031), along with shorter hospital stays (11.3 ± 6.4 days vs 21.5 ± 15.5 days, p = 0.012) and fewer complications (26.3% vs 47.1%, p = 0.020). The optimal ICG-R15 threshold for predicting PHLF was 4.5%, with 8.5% being critical.

Conclusion: ICG-R15 is a reliable predictor of PHLF, with 4.5% being safe and 8.5% critical. Nutritional management based on Omaha theory improves outcomes and quality of life. Further validation is needed.

Background: The role of early oral feeding (EOF) following esophagectomy remains debated. This study evaluates whether postoperative EOF improves patients' quality of life.

Methods: A comprehensive search was performed across eight databases to identify relevant studies. The effects of continuous variables were assessed using the mean difference (MD). The effects of dichotomous variables were assessed using the relative risk (RR).

Results: Seven studies were included in the analysis. EOF significantly improved postoperative overall quality of life [MD = 9.64, 95% CI (6.11, 13.16), p < 0.001], dysphagia [MD = -7.37, 95% CI (-14.32, -0.42), p = 0.040], and eating difficulty [MD = -6.72, 95% CI (-10.62, -2.82), p < 0.001]. However, no significant differences were observed in postoperative reflux [MD = -5.90, 95% CI (-12.52, 0.73), p = 0.080], esophageal pain [MD = -1.86, 95% CI (-5.51, 1.78), p = 0.320], anastomotic leakage [RR = 0.70, 95% CI (0.37, 1.35), p = 0.290], and pulmonary infection [RR = 0.44, 95% CI (0.15, 1.35), p = 0.150].

Conclusion: EOF after esophagectomy appears to improve patients' quality of life; however, these findings are constrained by the limited number and quality of studies. Further research is needed to validate these results.

Ferroptosis plays an important role in the pathogenesis of neuronal damage, generally mediated by iron and lipid peroxidation. In the present study, we measured the protective effects of puerarin against corticosterone-induced neuronal injury via PI3K/AKT-mediated activation of nuclear factor erythroid 2-related factor 2 (Nrf2). After exposing corticosterone-treated PC12 cells to indicated compounds, we measured the key regulators of ferroptosis (ferritin, SLC7A11, and Ptgs2), ferroptosis events (levels of iron, ROS, MDA, and GSH), and the PI3K/AKT/Nrf2 axis. Corticosterone induced ferroptosis in PC12 cells, evidenced by reduced levels of ferritin, SLC7A11, and GSH and increased levels of iron, ROS, and MDA. These effects were reversed by inhibiting ferroptosis with ferrostatin-1. Puerarin-mediated activation of Nrf2 repressed ferroptosis in corticosterone-treated PC12 cells by upregulating ferritin and SLC7A11 expression. Moreover, the protective effects of puerarin on ferroptosis in corticosterone-treated cells relied on the activation of the PI3K/AKT pathway though the upregulation of nuclear Nrf2. These findings indicate that ferroptosis plays an essential role in corticosterone-induced neuronal damage, and puerarin protects against ferroptosis in corticosterone-treated cells via PI3K/AKT-mediated activation of Nrf2.

This study investigates the impact of neoadjuvant therapy (NT) on body composition and its correlation with long-term survival and other clinical outcomes in patients with advanced gastric cancer. We utilized Computed Tomography (CT) scans to measure body composition before and after NT, including Subcutaneous Adipose Tissue Index (SATI), Visceral Adipose Tissue Index (VATI), Skeletal Muscle Index (SMI), and Muscle Density (MA). We then analyzed the decrease in body composition in relation to tumor regression, inflammatory markers, nutritional scores, and long-term survival. Our findings reveal a negative correlation between the decrease in SATI and VATI after NT, and both tumor regression and nutritional score. Notably, patients who experienced a significant loss in SATI or VATI post-NT had shorter Recurrence-Free Survival (RFS) and Overall Survival (OS). Additionally, significant loss in SATI and VATI emerged as an independent risk factor for both RFS and OS. In conclusion, our study convincingly demonstrates that in patients with advanced gastric cancer, SATI and VATI decreases after NT and is negatively associated with tumor regression and nutritional score. A significant loss in SATI and VATI is a risk factor for shorter RFS and OS, thereby underscoring the importance of maintaining body composition during NT.

Previous cohort studies have shown conflicting findings on the associations between obesity and the risk of thyroid cancer. This meta-analysis aimed to investigate the associations between them by using a meta-analysis of cohort studies. PubMed and EMBASE were searched using keywords from inception until November 2023 to identify relevant studies on this topic. Two authors independently reviewed and selected relevant studies according to the predefined criteria. Out of 475 studies searched from the databases, a total of 22 cohort studies were included in the final analysis. In a random-effects meta-analysis, obesity was significantly associated with an increased risk of thyroid cancer [odds ratio (OR), relative risk (RR), or hazard ratio (HR) = 1.33; 95% confidence interval (CI) 1.24 - 1.43]. Obesity was consistently associated with the increased risk of thyroid cancer in the subgroup meta-analyses by various factors such as study type (prospective or retrospective cohort study), gender (male or female), continent (America, Europe, or Asia), and study quality (high or low). This meta-analysis of cohort studies suggests that obesity increases the risk of thyroid cancer.

Individual observational studies examining the association between polyphenols and the risk of lung cancer have reported mixed findings. Therefore, we performed a systematic review and meta-analysis to determine the pooled effects between polyphenol intake and lung cancer risk. A systematic search was performed on PubMed, Scopus, and Web of Science databases in April 2023. Random-effect models were used to estimate odd ratios (OR) and 95% confidence intervals (95% CI). In total, 20 studies were included in the systematic review. The pooled analyses indicated that a higher intake of flavonoids (OR = 0.81; 95% CI: 0.67,0.98; p = 0.03) and isoflavone (OR = 0.82; 95% CI: 0.74,0.92; p < 0.001) were associated with lower odds of lung cancer. In addition, the ingestion of anthocyanidin (OR = 0.80; 95% CI: 0.65,0.98; p = 0.04), kaempferol (OR = 0.78; 95% CI: 0.64,0.96; p = 0.02), quercetin (OR = 0.66; 95% CI: 0.48,0.91; p = 0.01) and flavanones (OR = 0.71; 95% CI: 0.59,0.85; p < 0.001) reduced the likelihood of developing lung cancer. Overall, our findings suggest that flavonoids, isoflavones, anthocyanidin, kaempferol, quercetin, and flavanones may protect against lung cancer.

Glucose is an important energy source for tumors, however the molecular mechanisms by which tumor cells regulate glucose uptake remain unclear. In this study, we aimed to investigate the regulation mechanism of the WNT7B/β-catenin pathway for glucose transporter 1 (GLUT1)-mediated glucose metabolism in colorectal cancer. Here, we found that WNT7B expression levels were significantly increased in colorectal cancer tissues and closely associated with the clinical stage and lymph node metastasis in patients with colorectal cancer. Next, we confirmed that WNT7B significantly increased the glucose consumption and lactic acid levels in SW480 cells by overexpressing WNT7B. Additionally, gene and protein levels of GLUT1 were increased in WNT7B-overexpressing SW480 cells. However, WNT7B knockdown reversed these effects. WNT7B also enhanced GLUT1-mediated cell proliferation, invasion, and migration. WNT7B overexpression inhibited the effect of glucose deprivation on apoptosis. The WNT/β-catenin signaling pathway inhibitor, LGK974, inhibited WNT7B secretion, leading to GLUT1 levels downregulation and promotion of cell apoptosis. Ectopic tumor xenograft model experiments revealed that WNT7B promoted tumor progression in mice. Overall, our results suggest that WNT7B promotes β-catenin entry into the nucleus to initiates GLUT1 transcription, increases glucose transport and consumption, and enhances aerobic glycolysis, thus promoting tumor progression in colorectal cancer cells.