Nutrition and Cancer-An International Journal最新文献

Adenosine monophosphate-activated protein kinase (AMPK), a metabolic sensor activated by nutrient starvation, plays a multifaceted role in cancer. Whether AMPK is beneficial or malevolent is controversial. This study aimed to investigate AMPK levels in breast cancer patients receiving chemotherapy and compare the effects of intermittent fasting combined with different diets on these levels. Forty-five breast cancer patients were divided into three groups: a control, a group practicing 23:1-h intermittent fasting (IF) with a routine diet (RD), and another with a ketogenic diet (KD) over 4 weeks. Body mass index (BMI), Carbohydrate Antigen 15-3 (CA 15-3) levels, and serum AMPK levels were measured pre and post-intervention. Results showed a significant increase in AMPK levels in both the fasting groups and no significant difference in the non-fasting group, with the keto diet group showing the most significant growth. CA 15-3 levels were reduced in all the groups but significantly reduced in the KD group as compared to the RD group. This study shows that intermittent fasting with the keto diet improves AMPK levels and may serve as a valuable non-pharmacological complementary strategy for reducing or eliminating the tumor and, simultaneously, preventing the healthy cells from the toxic side effects of chemotherapy.

Objectives: Evidence regarding the association between tea consumption and bladder cancer (BC) risk is inconsistent. This study aimed to increase our knowledge of the association by using international data from the Bladder Cancer Epidemiology and Nutritional Determinants Consortium.

Methods: Individual data on 2,347 cases and 6,871 controls from 15 case-control studies with information on black, green, herbal, or general tea was pooled. The association was estimated using multilevel multivariable logistic regression analysis adjusted for multiple (non-)dietary factors.

Results: Association between tea consumption and BC risk was observed (odds ratio, OR = 0.72, 95% confidence interval, 95% CI = 0.65-0.80) compared to non-tea drinkers. Stratified analyses based on gender and smoking status yielded similar results. Stratified analysis showed no significant association between black or green tea consumption and BC risk across models, while herbal tea consumption was linked to a reduced BC risk (OR = 0.59, 95% CI = 0.36-0.96). As daily tea consumption increased within a suitable range (<5.67 cups/day), BC risk decreased.

Conclusions: Camellia sinensis tea showed no association with BC risk, while herbal tea was inversely linked to BC incidence. Despite some significant findings in the selected strata, further studies are required to clarify the underlying mechanisms.

Background: This study aimed to elucidate the causal relationship between Omega-6/Omega-3 fatty acid ratio and the risk of lung cancer by using Mendelian randomization (MR) analyses.

Methods: Omega-6/Omega-3 fatty acid ratio data from the IEU database and lung cancer patient data from the International Lung Cancer Consortium were collected for this MR analyses. Single nucleotide polymorphisms (SNPs) associated with Omega-6/Omega-3 fatty acid ratio were collected as instrumental variables (IVs) with criteria of P < 5E-8, linkage disequilibrium R² > 0.001 and clump distance < 10,000 kb. We used the inverse variance weighted (IVW) method as the primary method of MR analyses to evaluate the causal relationship between Omega-6/Omega-3 fatty acid ratio and lung cancer risk. Heterogeneity of the analyses was assessed by Cochran's Q test. Horizontal pleiotropy was evaluated by the intercept with the MR-Egger test.

Results: 28 SNPs related to Omega-6/Omega-3 fatty acid ratio were selected as IVs in total. The MR analyses results showed that higher Omega-6/Omega-3 fatty acid ratio was associated with lower risk of lung cancer (P = 0.009). No statistical significance was observed for MR-Egger and simple mode methods (P > 0.05). No significant horizontal pleiotropy was detected by MR-Egger regression test (P = 0.73). Conclusion: Higher Omega-6/Omega-3 fatty acid ratio was associated with lower lung cancer risk.

Serum zinc and selenium concentrations might be altered by various disease conditions including malignancies. We aimed to prospectively investigate the serum levels of both elements in pediatric cancers. Children <18 years with newly diagnosed cancers were eligible. Data regarding demographics, histopathological diagnoses, tumor sites, disease extent, treatments given and outcomes were recorded. Serum samples were obtained at diagnosis and in the 3-4 months after diagnosis to determine the serum concentrations of zinc and selenium using "inductively coupled plasma mass spectrometry" (ICP-MS) method. Serum levels were compared to normal references and also in the subgroups according to tumor types, tumor sites and disease extent. Eighty-one children were included (Male/female: 50/31, median age 7.5-years). Twenty-five patients had lymphomas and 56 had solid tumors. For all patients, median serum levels of zinc and selenium were 69.5 mcg/dL and 114.3 mcg/L, respectively, which were comparable to normal reference values. In patients with lymphomas, mean and median initial zinc levels were significantly lower compared to solid tumors, which increased following treatment. No significant difference was detected in initial selenium concentrations of all patients and also in the subgroups. In the 3.-4. months following treatment, selenium levels decreased significantly in solid tumors. No significant difference was detected in the survival rates according to Zn and Se levels. Lower zinc levels at diagnosis in lymphomas was remarkable. The decline in Se levels after treatment may reflect the selenophilic nature of solid tumors and could also be linked to reduced appetite and dietary intake. Suppression of hepatic biosynthesis of selenoprotein by some chemotherapeutics might also contribute to diminished selenium levels after treatment. Further studies are needed to explore the implications of deficiencies in both elements.

Objective: The impact of obesity on the surgical outcomes in patients after laparoscopic liver resection (LLR) is unclear. We aimed at conducting a meta-analysis to evaluate the associations between overweight and obesity and major surgical outcomes after LLR for liver tumors.

Methods: We searched PubMed, Cochrane Library, Embase, and Web of Science databases for eligible studies. Odds ratios (ORs) and mean differences (MDs) with 95% confidence intervals (CIs) were calculated.

Results: Eight studies were included, with a total of 7,580 patients. Findings indicated that, relative to individuals of normal weight, those in the higher body mass index (BMI) category (overweight and obese) had prolonged operation time (MD, 15.46 mins), increased blood loss (MD, 39.40 mL), overall complications (OR 1.20), conversion (OR 1.41), and surgical site infection (SSI) (OR 1.77). In addition, subgroup analysis showed that although overweight did not increase the risk of overall postoperative complications and SSI, obesity significantly increased the risk of overall postoperative complications, SSI, and conversion to laparotomy.

Conclusion: In conclusion, higher BMI, especially obesity, is closely associated with higher risk of morbidity after laparoscopic liver resection.

Tumor-associated macrophages (TAMs) and cancer-associated fibroblasts (CAFs) are the most abundant stromal cells in the bladder cancer (BC) microenvironment (TME). However, the detailed mechanisms underlying TAM-CAF communication and their contributions to BC progression remain incompletely understood. Emerging evidence shows that Emodin exerts anti-tumor effect on several tumor models by targeting TME. To date, the impact of Emodin on BC has not been previously reported. Our study firstly demonstrated that Emodin significantly inhibited tumor growth and reduced TAM accumulation in a murine BC model. Emodin markedly decreased serum levels of multiple chemokines in tumor-bearing mice, with CXCL1 showing the most pronounced reduction. Strikingly, Emodin selectively suppressed CXCL1 secretion in CAFs but not in TAMs or tumor cells. Furthermore, the decrease in TAM migration induced by Emodin was dependent on CAF-derived CXCL1. Using a subcutaneous tumor model, we found that Emodin failed to inhibit tumor growth when CXCL1-deficient CAFs were co-injected with tumor cells, underscoring the critical role of CXCL1 in this process. Bioinformatics analysis further revealed that elevated CXCL1 levels correlated negatively with invasive/metastatic potential and overall survival in BC patients. In conclusion, our findings establish that Emodin delays BC progression by disrupting CXCL1-mediated crosstalk between CAFs and TAMs.

Aflatoxin B1 (AFB1) may be associated with not only developing liver cancer but also gallbladder cancer (GBC). We aimed to investigate whether serum AFB1 level of GBC patients is higher than chronic cholecystitis (CC) patients or healthy subjects (HS). Serum was collected from 45 GBC patients (18 men, 27 women), 57 CC patients (22 men, 35 women), and 55 HS (20 men, 35 women) from May 2021 to February 2024. Serum AFB1-lysine adduct level was measured using a commercial ELISA kit. Detection frequency (≥0.1 ng/ml), median and mean levels of serum AFB1-lysine adduct were compared among three groups. The detection rate was 71% (35/45) in GBC patients, 39% (22/57) in CC, and 7% (4/55) in HS (p < 0.001). Age- and gender-adjusted odds ratios of AFB1 detection in GBC patients were 4.1 and 16.8 times higher than in CC patients and HS, respectively. The median levels were 5.0 ng/mL in GBC patients and < 0.1 ng/mL in CC patients and HS. The mean level in GBC patients (7.9 ± 8.4 ng/mL) was significantly higher than that in CC patients (2.7 ± 4.5 ng/mL) or HS (0.3 ± 1.1 ng/mL). Our findings show direct evidence that AFB1 exposure may be associated with risk of developing GBC in India.

Malnutrition is common in adults with cancer and is associated with lower quality of life and higher risk of mortality. A comprehensive picture of dietitian efficacy in cancer care is needed to inform payers and policymakers about effective care options. The objective of this umbrella review of systematic reviews (SRs) is to examine the impact of dietitian interventions, compared to no intervention or usual care, on nutrition-related outcomes in adults with all types and stages of cancer. MEDLINE, CINAHL, Cochrane Database of SRs, Food Science Source, and SPORTSDiscus databases were searched for SRs and meta-analyses published from 2018 to September 2024. The GRADE method was used to rate evidence certainty. There were 2,087 articles identified in the search, 125 full texts were examined for eligibility, and seven SRs were included in this umbrella review, representing 25 randomized controlled trials and six observational studies. Interventions provided by dietitians may improve nutrition status, protein and energy intake, length of stay, and quality of life, but evidence certainty was low, primarily due to the risk of bias in primary studies, heterogeneity, and lack of precise effect size. Providing dietitian-led interventions for adults with cancer may improve a wide range of nutrition-related outcomes.

Lung cancer remains the leading cause of cancer-related mortality worldwide. Adenocarcinoma is the most prevalent subtype of Non-Small Cell Lung Cancer (NSCLC), and platinum-based chemotherapy is the standard first-line treatment. However, patients harboring EGFR mutations benefit significantly from tyrosine kinase inhibitor (TKI) therapy, which enhances treatment response, prolongs progression-free survival (PFS), and improves overall survival (OS). Despite these advantages, TKI-associated gastrointestinal toxicity, particularly mucositis and diarrhea, poses a major challenge that often affects treatment adherence and patient quality of life. Effective diarrhea management is crucial for maintaining therapeutic continuity, yet current clinical guidelines primarily focus on pharmacological approaches. This review highlights the critical role of nutritional strategies in preventing and mitigating TKI-induced diarrhea. Due to the irritative effects of TKIs on digestion, dietary modifications are crucial. Patients should avoid greasy, spicy, acidic, and high-fiber foods, along with alcohol, soft drinks, and coffee. Steamed, baked, or boiled foods are recommended. Glutamine and probiotics may aid mucosal recovery and microbiota balance. Ongoing nutritional oversight and individualized dietary guidance are essential for patients with NSCLC undergoing TKI therapy. Future research should establish evidence-based dietary guidelines to optimize treatment tolerance, enhance patient well-being, and improve clinical outcomes.

Obesity is positively associated with colorectal cancer (CRC) risk. Diet not only contributes to obesity, but also strongly influences the gut microbiota, a factor that is thought to independently affect CRC. To isolate the role of obesity-associated gut microbiota in CRC and to assess the impact of diet composition on this relationship, we transplanted the gut microbiota from donor mice that developed obesity or remained lean on a high-fat diet (HFD), Western diet (WD), or low-fat diet (LFD) into antibiotic-treated recipient mice that subsequently received azoxymethane to induce CRC. We hypothesized that the obesogenic diets of the donor mice, rather than their obesity status, would be a stronger driver of gut microbiota-mediated CRC development. Interestingly, while evidence supporting our hypothesis was observed, differential effects on CRC outcomes based on the type of obesogenic diets were found, such that HFD-associated gut microbiota promotes tumor incidence whereas WD-associated gut microbiota promotes tumor growth. Significantly enriched bacterial taxa present before tumor induction may be mediating these results through intestinal permeability or inflammation, such as Sutterella and Dorea in mice received HFD-associated gut microbiota, and Bacteroidetes in mice received WD-microbiota. Overall, our results demonstrated that diet drives the gut microbiota-derived impact on CRC development.