Nutrition and Cancer-An International Journal最新文献

The use of dietary supplements by cancer patients is common but contentious, particularly during chemotherapy. Few studies have investigated this for ovarian cancer. In a prospective study of women with ovarian cancer, dietary supplement use was collected through questionnaires. Data on the use of supplements were available for 421 women before diagnosis, during chemotherapy, and after chemotherapy completion. Predictors of changes in supplement use were investigated using logistic regression. The use of ≥1 supplement pre-diagnosis, during, and after chemotherapy completion was reported by 72%, 57%, and 68% of women, respectively. Multivitamins, vitamin D, and fish oils were the most commonly used supplements at all time points. The supplements most commonly discontinued during treatment were fish oils (69% of pre-diagnosis users) and multivitamins (53% of users); while 9%-10% of pre-diagnosis non-users initiated vitamin D and multivitamins. Predictors of supplement initiation during chemotherapy included pre-diagnosis use of medications, such as statins (Odds Ratio, OR = 4.12, 95% confidence interval, CI = 1.28-13.3), antidepressants (5.39, 1.18-24.7), acetaminophen (3.13, 1.05-9.33), and NSAIDs (2.15, 0.81-5.72). Other factors included younger age, university education, neoadjuvant chemotherapy, and/or experiencing fatigue during treatment, although not statistically significant. In conclusion, a high proportion of women with ovarian cancer reported using supplements at all time points.

Isoquercitrin possesses anti-tumor activity in several types of cancers, however, its effects and underlying mechanisms on lung cancer have not been reported. Human lung cancer cell lines as well as normal lung epithelial BEAS-2B cells were treated with isoquercitrin. The influences of isoquercitrin in vitro were evaluated by determining cell viability, apoptosis, pyroptosis, and ferroptosis. Additionally, A549 tumor-bearing mice were generated to explore the anti-cancer effect of isoquercitrin in vivo. We found that isoquercitrin dose-dependently reduced lung cancer cells' viability, with no toxicity against BEAS-2B cells. Isoquercitrin at 40 μM and 80 μM was used in vitro. Isoquercitrin increased apoptosis, elevated NLRP3 inflammasome activation-mediated pyroptosis, and promoted ferroptosis in lung cancer cells. NLRP3 knockdown and caspase-1 selective inhibitor VX-765 attenuated isoquercitrin-induced pyroptosis and ferroptosis, but not apoptosis. Furthermore, isoquercitrin accelerated ROS generation, while ROS inhibitor N-acetylcysteine abrogated isoquercitrin-induced apoptosis, NLRP3 related-pyroptosis and ferroptosis. In vivo, isoquercitrin (1 mg/kg and 5 mg/kg) inhibited tumor growth, increased apoptosis, NLRP3-related pyroptosis, ferroptosis and ROS generation in tumors. Taken together, isoquercitrin inhibits lung cancer growth by triggering ROS/NLRP3-mediated pyroptosis and ferroptosis, with ROS also directly inducing apoptosis. This suggests that isoquercitrin might be a potential therapeutic agent for 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.

Coconut milk contains plant-based saturated fat and phytochemicals with antioxidant activities. However, its role in breast cancer risk remains unclear. A case-control study was conducted on 244 participants to study the association. The Case group includes 61 newly diagnosed breast cancer patients receiving < 6 months of therapies. The Control group includes 183 healthy people with matched characteristics. A new questionnaire was developed, validated, and used in this study to estimate the frequency of coconut milk-containing food intake. Results show that the questionnaire has satisfactory content validity, test-retest reliability, and criterion-related validity. From the case-control study, either consuming 1-3 or 4-6 times/week of coconut-milk-containing curry or consuming 4-6 times/week of coconut milk-topped desserts are associated with increased risk of breast cancer (OR = 5.23, 5.6, and 2.6 respectively, p < 0.01). Consuming less than half of coconut milk liquid in desserts correlated with a reduced risk (OR = 0.43, p < 0.05). The findings suggest that moderate (less than half of a serving) and infrequent (less than once a week) consumption of coconut milk may be beneficial for breast cancer prevention. A larger scale study is warranted to confirm the findings and provide evidence for dietary recommendations.

ABSTRACTA self-reported electronic questionnaire to advocate for a consensus definition of nutrition impact symptoms (NISs) was conducted in a diverse group of international healthcare providers. The questionnaire had 2 components: the definition of NISs and the relevance of each symptom as a NIS. Agreement on the tentative definition and 24 symptoms were evaluated using a seven-point Likert scale. For the factor validity and internal consistency of symptoms, an exploratory factor analysis was employed, and Cronbach's alpha coefficients (Cronbach's α) were calculated in each domain. A total of 66 healthcare providers responded. Regarding the tentative definition of NISs, the percentages of the number of participants with agree and strongly agree were 40.9% and 42.4%. Three conceptual groups were extracted as follows: 1) symptoms that interfere with patients' ability to ingest or digest nutrients, 2) symptoms that compromise patients' desire to eat and take nutrients, and 3) symptoms that indirectly compromise patients' food and nutrient intake. The values of Cronbach's α were 0.91, 0.92, and 0.87. We proposed a new definition - NISs are symptoms that compromise patients' desire or ability to eat, interfering with their nutritional needs and increasing the risk for malnutrition, loss of lean body mass, and impaired QOL.

Cancer cachexia, characterized by the progressive loss of skeletal muscle mass, leads to functional impairment and poor prognosis. Anamorelin is approved for treating cancer cachexia in Japan; however, the factors influencing its discontinuation and the impact of combining anamorelin with rehabilitation remain unclear. Therefore, we retrospectively analyzed 82 patients with cancer cachexia to identify factors associated with anamorelin discontinuation and assess changes in nutritional status and motor function using non-dominant handgrip strength after 12 wk. Patients received outpatient rehabilitation, combining resistance and aerobic training every two weeks, alongside anamorelin therapy. Our findings indicate that patients with an ECOG performance status of 1 or 2 were less likely to continue anamorelin therapy for 12 wk compared to those with a performance status of 0 (odds ratio 2.71; 95% CI 1.05 - 7.00; p = 0.040). Significant improvements were observed in body weight (48.8 to 53.7 kg, p < 0.001), skeletal muscle mass (6.4 to 6.9 kg/m², p < 0.001), FAACT score (11.5 to 18.0, p < 0.001), and non-dominant handgrip strength (20.5 to 21.7 kg, p = 0.018) after 12 wk. Early initiation of anamorelin with regular rehabilitation is recommended to enhance nutritional status and motor function in patients with cancer cachexia.

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.

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.

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.