scholarly journals Dried Fruit Intake and Cancer: A Systematic Review of Observational Studies

2019 ◽  
Author(s):  
Valeri V Mossine ◽  
Thomas P Mawhinney ◽  
Edward L Giovannucci
Keyword(s):  
Systematic Review ◽  
Cancer Risk ◽  
Prospective Cohort ◽  
Case Control ◽  
Fruit Intake ◽  
Chemical Compositions ◽  
Case Control Studies ◽  
Dried Fruits ◽  
Dried Fruit ◽  
Risk Of Cancer

ABSTRACT Insufficient intake of total fruits and vegetables is linked to an increased cancer risk, but the relation is not understood for dried fruits. Dried fruits are generally perceived, by both consumers and researchers, as a less attractive but shelf-stable equivalent to fresh fruits and constitute a small but significant proportion of modern diets. Chemical compositions of raw and dried fruits, however, may differ substantially. Several clinical and laboratory intervention studies have reported the protective effects of dehydrated fruits against the progression of some cancers and the modulating effects of dried fruits on common cancer risk factors. In this systematic review, we identified, summarized, and critically evaluated 9 prospective cohort and 7 case-control studies that examined the relations between traditional dried fruit (raisins, prunes, dates) consumption and cancer risk in humans. Prospective cohort studies determined that significant reductions in relative risk of precancerous colorectal polyps, incidence of prostate cancer, or mortality from pancreatic cancer, by, respectively, 24%, 49%, and 65%, were associated with 3–5 or more servings of dried fruits per week. Selected case-control studies revealed inverse associations between dried fruit intake and risk of cancer as well. The reported associations were comparable to or stronger than those observed for total or raw fruits. Although the small number and high heterogeneity impede meta-analysis of these studies, we conclude that currently available data provide some initial evidence that consumption of dried fruits may be associated with a lower cancer incidence or mortality in populations. The data suggest that higher intake of raisins and other dried fruits may be important in the prevention of cancers of the digestive system. Because only a limited number of health outcome and dried fruit intake relations have been evaluated in prospective studies to date, reanalyzing existing high-quality epidemiological data may expand the knowledge base.

scholarly journals Association between PD-1 and PD-L1 Polymorphisms and the Risk of Cancer: A Meta-Analysis of Case-Control Studies

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1150 ◽  
Author(s):  
Mohammad Hashemi ◽  
Shima Karami ◽  
Sahel Sarabandi ◽  
Abdolkarim Moazeni-Roodi ◽  
Andrzej Małecki ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Risk ◽  
Programmed Cell Death ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Case Control ◽  
Case Control Studies ◽  
Programmed Cell Death 1 ◽  
Risk Of Cancer ◽  
The Impact

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

TGFBR1*6A and Cancer Risk: A Meta-Analysis of Seven Case-Control Studies

2003 ◽  
Vol 21 (17) ◽  
pp. 3236-3243 ◽  
Author(s):  
Virginia G. Kaklamani ◽  
Nanjiang Hou ◽  
Yiansong Bian ◽  
Jennifer Reich ◽  
Kenneth Offit ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Risk ◽  
The United States ◽  
Case Control ◽  
Type I ◽  
Susceptibility Allele ◽  
Case Control Studies ◽  
Tumor Susceptibility ◽  
Increased Risk ◽  
Risk Of Cancer

Purpose: TGFBR1*6A is a hypomorphic polymorphic allele of the type I transforming growth factor beta receptor (TGFBR1). TGFBR1*6A is a candidate tumor susceptibility allele that has been associated with an increased incidence of various types of cancer. This study was undertaken to analyze all published case-control studies on TGFBR1*6A and cancer and determine whether TGFBR1*6A is associated with cancer. Patients and Methods: All published case-control studies assessing the germline frequency of TGFBR1*6A were included. Studies assessing TGFBR1*6A in tumors were excluded. The results of seven studies comprising 2,438 cases and 1,846 controls were pooled and analyzed. Results: Overall, TGFBR1*6A carriers have a 26% increased risk of cancer (odds ratio [OR], 1.26; 95% confidence interval [CI], 1.07 to 1.49). Cancer risk for TGFBR1*6A homozygotes (OR, 2.53; 95% CI, 1.39 to 4.61) is twice that of TGFBR1*6A heterozygotes (OR, 1.26; 95% CI, 1.04 to 1.51). Analysis of various types of tumors shows that TGFBR1*6A carriers are at increased risk of developing breast cancer (OR, 1.48; 95% CI, 1.11 to 1.96), hematological malignancies (OR, 1.70; 95% CI, 1.13 to 2.54), and ovarian cancer (OR, 1.53; 95% CI, 1.07 to 2.17). Carriers of TGFBR1*6A who are from the United States are at increased risk of colorectal cancer (OR, 1.38; 95% CI, 1.02 to 1.86). However, Southern European TGFBR1*6A carriers have no increased colorectal cancer risk. There is no association between TGFBR1*6A and bladder cancer. Conclusion: TGFBR1*6A is emerging as a highfrequency, low-penetrance tumor susceptibility allele that predisposes to the development of breast, ovarian, and colorectal cancer, as well as hematologic malignancies.

Socioeconomic inequalities and oral cancer risk: A systematic review and meta-analysis of case-control studies

2008 ◽  
Vol 122 (12) ◽  
pp. 2811-2819 ◽  
Author(s):  
David I. Conway ◽  
Mark Petticrew ◽  
Helen Marlborough ◽  
Julien Berthiller ◽  
Mia Hashibe ◽  
...  
Keyword(s):  
Systematic Review ◽  
Oral Cancer ◽  
Cancer Risk ◽  
Meta Analysis ◽  
Case Control ◽  
Socioeconomic Inequalities ◽  
Case Control Studies ◽  
Oral Cancer Risk

scholarly journals Association between apurinic/apyrimidinic endonuclease 1 rs1760944 T>G polymorphism and susceptibility of cancer: a meta-analysis involving 21764 subjects

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Guowen Ding ◽  
Yu Chen ◽  
Huiwen Pan ◽  
Hao Qiu ◽  
Weifeng Tang ◽  
...  
Keyword(s):  
Cancer Risk ◽  
Publication Bias ◽  
Protective Factor ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Pooled Analysis ◽  
Case Control ◽  
Current Evidence ◽  
Case Control Studies ◽  
Risk Of Cancer

Abstract Background: Previous case–control studies have suggested that apurinic/apyrimidinic endonuclease 1 (APE1) rs1760944 T>G polymorphism may be associated with cancer risk. Here, we carried out an updated meta-analysis to focus on the correlation between APE1 rs1760944 T>G locus and the risk of cancer. Methods: We used the crude odds ratios (ORs) with their 95% confidence intervals (CIs) to evaluate the possible relationship between the APE1 rs1760944 T>G polymorphism and cancer risk. Heterogeneity, publication bias and sensitivity analysis were also harnessed to check the potential bias of the present study. Results: Twenty-three independent studies involving 10166 cancer cases and 11598 controls were eligible for this pooled analysis. We found that APE1 rs1760944 T>G polymorphism decreased the risk of cancer in four genetic models (G vs. T: OR, 0.87; 95% CI, 0.83–0.92; P<0.001; GG vs. TT: OR, 0.77; 95% CI, 0.69–0.86; P<0.001; GG/TG vs. TT: OR, 0.83; 95% CI, 0.77–0.89, P<0.001 and GG vs. TT/TG: OR, 0.85; 95% CI, 0.80–0.92, P<0.001). Results of subgroup analyses also demonstrated that this single-nucleotide polymorphism (SNP) modified the risk among lung cancer, breast cancer, osteosarcoma, and Asians. Evidence of publication bias was found in the present study. When we treated the publication bias with ‘trim-and-fill’ method, the adjusted ORs and CIs were not significantly changed. Conclusion: In conclusion, current evidence highlights that the APE1 rs1760944 T>G polymorphism is a protective factor for cancer susceptibility. In the future, case–control studies with detailed risk factors are needed to confirm or refute our findings.

scholarly journals Body Mass Index (BMI) is not a cancer risk factor for BRCA1/2 carriers: a Systematic Review and Meta-analysis of case-control studies

2021 ◽  
Author(s):  
Mario Giuseppe Mirisola ◽  
Antonio Galvano ◽  
Valerio Gristina ◽  
Maria La Mantia ◽  
Sofia Cutaia ◽  
...  
Keyword(s):  
Systematic Review ◽  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Menopausal Status ◽  
Susceptibility Gene ◽  
Case Control ◽  
Cochrane Library ◽  
Breast Cancer Susceptibility Gene ◽  
Ovarian Cancer Risk ◽  
Case Control Studies

Abstract Background Breast cancer susceptibility gene 1 and 2 (BRCA 1/2) pathogenic germline variants (gPV) are involved in an increased cumulative risk for cancers (above all breast and ovarian cancers). Overweight/obesity is a well-known systemic condition conferring higher cancer risk too. Methods We performed a systematic review collecting data on Medline, Scopus, and Cochrane-Library database until August 2020. We included four case-control studies (Fu et al, Bissonauth et al, Khachatryan et al, Nkondjoc et al) assessing the risk for cancer according to different BMI strata in BRCA-positive healthy individuals. Results Four studies for a total of 1148 patients evaluated breast and ovarian cancer risk in a healthy BRCA1/2 population. No other tumor histotypes risk has been observed within the selected population. Pooled results demonstrated that different BMI conditions (lower or upper 25 kg/m2) were not associated with increased cancer risk (OR 1.15, 95% CI 0.92–1.44 and OR 1.48, 95% CI 0.84–2.62 respectively). Additionally, no differences were reported according to menopausal status. Conclusion Despite the need for other prospective investigations in larger cohorts, our results suggest no BMI contribution in cancer risk in this special population, determining a new important point of view and a new potential field of investigation.

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