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Dive into the research topics where Marie Cantwell is active.

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Featured researches published by Marie Cantwell.


American Journal of Epidemiology | 2008

The Incidence of Esophageal Cancer and High-Grade Dysplasia in Barrett's Esophagus: A Systematic Review and Meta-Analysis

Fouad Yousef; Christopher Cardwell; Marie Cantwell; Karen Galway; Brian T. Johnston; Liam Murray

Barretts esophagus is a well-recognized precursor of esophageal adenocarcinoma. Surveillance of Barretts esophagus patients is recommended to detect high-grade dysplasia (HGD) or early cancer. Because of wide variation in the published cancer incidence in Barretts esophagus, the authors undertook a systematic review and meta-analysis of cancer and HGD incidence in Barretts esophagus. Ovid Medline (Ovid Technologies, Inc., New York, New York) and EMBASE (Elsevier, Amsterdam, the Netherlands) databases were searched for papers published between 1950 and 2006 that reported the cancer/HGD risk in Barretts esophagus. Where possible, early incident cancers/HGD were excluded, as were patients with HGD at baseline. Forty-seven studies were included in the main analysis, and the pooled estimate for cancer incidence in Barretts esophagus was 6.1/1,000 person-years, 5.3/1,000 person-years when early incident cancers were excluded, and 4.1/1,000 person-years when both early incident cancer and HGD at baseline were excluded. Corresponding figures for combined HGD/cancer incidence were 10.0 person-years, 9.3 person-years, and 9.1/1,000 person-years. Compared with women, men progressed to cancer at twice the rate. Cancer or HGD/cancer incidences were lower when only high-quality studies were analyzed (3.9/1,000 person-years and 7.7/1,000 person-years, respectively). The pooled estimates of cancer and HGD incidence were low, suggesting that the cost-effectiveness of surveillance is questionable unless it can be targeted to those with the highest cancer risk.


The American Journal of Clinical Nutrition | 2010

Dietary patterns and breast cancer risk: a systematic review and meta-analysis

Sarah F. Brennan; Marie Cantwell; Christopher Cardwell; Louiza S. Velentzis; Jayne V. Woodside

BACKGROUND Dietary patterns, which represent whole-diet and possible food and nutrient interactions, have been linked to the risk of various cancers. However, the associations of these dietary patterns with breast cancer remain unclear. OBJECTIVE We critically appraised the literature and conducted meta-analyses to pool the results of studies to clarify the relation between dietary patterns and breast cancer risk. DESIGN MEDLINE and EMBASE were searched for relevant articles that identified common dietary patterns published up to November 2009. Multivariable-adjusted odds ratios (ORs) comparing highest and lowest categories of dietary pattern scores and multivariable-adjusted ORs for a 20th-percentile increase in dietary pattern scores were combined by using random-effects meta-analyses. RESULTS Case-control and cohort studies were retrieved that identified prudent/healthy (n = 18), Western/unhealthy (n = 17), and drinker (n = 4) dietary patterns. There was evidence of a decrease in the risk of breast cancer in the highest compared with the lowest categories of prudent/healthy dietary patterns (OR = 0.89; 95% CI: 0.82, 0.99; P = 0.02) in all studies and in pooled cohort studies alone. An increase in the risk of breast cancer was shown for the highest compared with the lowest categories of a drinker dietary pattern (OR = 1.21; 95% CI: 1.04, 1.41; P = 0.01). There was no evidence of a difference in the risk of breast cancer between the highest and the lowest categories of Western/unhealthy dietary patterns (OR = 1.09; 95% CI: 0.98, 1.22; P = 0.12). CONCLUSION The results of this systematic review and meta-analysis indicate that some dietary patterns may be associated with breast cancer risk.


Gastroenterology | 2009

The Association Between Alcohol and Reflux Esophagitis, Barrett's Esophagus, and Esophageal Adenocarcinoma

Lesley A. Anderson; Marie Cantwell; R.G. Peter Watson; Brian T. Johnston; Seamus J. Murphy; Heather R. Ferguson; Jim McGuigan; Harry Comber; John V. Reynolds; Liam Murray

BACKGROUND & AIMS Alcohol consumption may increase gastroesophageal reflux symptoms, cause damage to the esophageal mucosa, and/or promote carcinogenesis. However, reports about the association between alcohol and reflux esophagitis, Barretts esophagus, and esophageal adenocarcinoma are conflicting. METHODS Information relating to alcohol consumption, at age 21 and 5 years before the interview date, was collected from 230 reflux esophagitis, 224 Barretts esophagus, and 227 esophageal adenocarcinoma patients and 260 frequency-matched population controls. Logistic regression analyses were used to compare alcohol consumption in the 3 case groups to controls with adjustment for potential confounders. RESULTS Population controls reporting gastroesophageal reflux symptoms were less likely than controls without symptoms to drink alcohol 5 years before the interview date (odds ratio [OR], 0.44, 0.20-0.99). No associations were observed between total alcohol consumption 5 years before the interview date and reflux esophagitis, Barretts esophagus, or esophageal adenocarcinoma (OR, 1.26, 0.78-2.05; OR, 0.72, 0.43-1.21; and OR, 0.75, 0.46-1.22, respectively). Wine was inversely associated with reflux esophagitis (OR, 0.45, 0.27-0.75). Total alcohol consumption at age 21 years was significantly associated with reflux esophagitis (OR, 2.24, 1.35-3.74) but not with Barretts esophagus or esophageal adenocarcinoma (OR, 1.06, 0.63-1.79 and OR, 1.27, 0.77-2.10, respectively). CONCLUSIONS Alcohol consumption in early adulthood may lead to the development of reflux esophagitis. More recent alcohol consumption does not appear to confer any increased risk of reflux esophagitis, Barretts esophagus, or esophageal adenocarcinoma. In fact, wine consumption may reduce the risk of these 3 esophageal disorders.


Journal of Cancer Survivorship | 2010

The effect of androgen deprivation therapy on body composition in men with prostate cancer: Systematic review and meta-analysis

Farhana Haseen; Liam Murray; Christopher Cardwell; Joe M. O’Sullivan; Marie Cantwell

IntroductionThe use of androgen deprivation therapy (ADT) in the treatment of prostate cancer is associated with changes in body composition including increased fat and decreased lean mass. Limited information exists regarding the rate and extent of these changes. This systematic review was conducted to determine the effects of ADT on body composition in prostate cancer patients.MethodsLiterature searches were conducted on MEDLINE, EMBASE and Web of Science for studies until January 2009. Only longitudinal studies that examined ADT and body composition in prostate cancer patients were included. Data were extracted on body weight, BMI, percentage of fat mass and lean body mass.ResultsSixteen studies (14 cohorts and 2 RCTs) met the inclusion criteria. Pooled data, calculated according to a random effects model, showed that ADT increased % body fat by on average 7.7% (95% CI 4.3, 11.2, from seven studies, P < 0.0001) and decreased % lean body mass by on average −2.8% (95% CI −3.6, −2.0, from six studies, P < 0.0001) but for both there was marked heterogeneity between studies (I2 = 99% I2 = 73%, respectively). Similarly, body weight (2.1%, P < 0.0001 from nine studies) and BMI (2.2%, P < 0.0001, from eight studies) increased significantly. More extensive changes were seen with longer duration of treatment.ConclusionsSubstantial increases in fat and declines in lean mass were observed in prostate cancer patients treated with ADT. Lifestyle changes or suitable interventions to minimize the effect of ADT on body composition need to be investigated.Implications for cancer survivorsProstate cancer survivors should be made aware of the side effect of treatment on body composition and further work is required to determine what interventions can minimize the impact of ADT on body composition and therefore what evidence based advice they should be provided with. In general, though recommendation of a healthy diet and moderate exercise is reasonable.


The American Journal of Clinical Nutrition | 2009

Glycemic index, glycemic load, and risk of digestive tract neoplasms: a systematic review and meta-analysis

Helen G. Mulholland; Liam Murray; Christopher Cardwell; Marie Cantwell

BACKGROUND Habitual consumption of diets with a high glycemic index (GI) and a high glycemic load (GL) may influence cancer risk via hyperinsulinemia and the insulin-like growth factor axis. OBJECTIVE The objective was to conduct a systematic review to assess the association between GI, GL, and risk of digestive tract cancers. DESIGN Medline and Embase were searched for relevant publications from inception to July 2008. When possible, adjusted results from a comparison of cancer risk of the highest compared with the lowest category of GI and GL intake were combined by using random-effects meta-analyses. RESULTS Cohort and case-control studies that examined the risk between GI or GL intake and colorectal cancer (n = 12) and adenomas (n = 2), pancreatic cancer (n = 6), gastric cancer (n = 2), and squamous-cell esophageal carcinoma (n = 1) were retrieved. Most case-control studies observed positive associations between GI and GL intake and these cancers. However, pooled cohort study results showed no associations between colorectal cancer risk and GI intake [relative risk (RR): 1.04; 95% CI: 0.92, 1.12; n = 7 studies] or GL intake (RR: 1.06; 95% CI: 0.95, 1.17; n = 8 studies). Furthermore, no significant associations were observed in meta-analyses of cohort study results of colorectal cancer subsites and GI and GL intake. Similarly, no significant associations emerged between pancreatic cancer risk and GI intake (RR: 0.99; 95% CI: 0.83, 1.19; n = 5 studies) or GL intake (RR: 1.01; 95% CI: 0.86, 1.19; n = 6 studies) in combined cohort studies. CONCLUSIONS The findings from our meta-analyses indicate that GI and GL intakes are not associated with risk of colorectal or pancreatic cancers. There were insufficient data available regarding other digestive tract cancers to make any conclusions about GI or GL intake and risk.


European Journal of Cancer | 2008

Do phytoestrogens reduce the risk of breast cancer and breast cancer recurrence? What clinicians need to know

Louiza S. Velentzis; Jayne V. Woodside; Marie Cantwell; Anthony J. Leathem; Mohammed Keshtgar

Oestrogen is an important determinant of breast cancer risk. Oestrogen-mimicking plant compounds called phytoestrogens can bind to oestrogen receptors and exert weak oestrogenic effects. Despite this activity, epidemiological studies suggest that the incidence of breast cancer is lower in countries where the intake of phytoestrogens is high, implying that these compounds may reduce breast cancer risk, and possibly have an impact on survival. Isoflavones and lignans are the most common phytoestrogens in the diet. In this article, we present findings from human observational and intervention studies related to both isoflavone and lignan exposure and breast cancer risk and survival. In addition, the clinical implications of these findings are examined in the light of a growing dietary supplement market. An increasing number of breast cancer patients seek to take supplements together with their standard treatment in the hope that these will either prevent recurrence or treat their menopausal symptoms. Observational studies suggest a protective effect of isoflavones on breast cancer risk and the case may be similar for increasing lignan consumption although evidence so far is inconsistent. In contrast, short-term intervention studies suggest a possible stimulatory effect on breast tissue raising concerns of possible adverse effects in breast cancer patients. However, owing to the dearth of human studies investigating effects on breast cancer recurrence and survival the role of phytoestrogens remains unclear. So far, not enough clear evidence exists on which to base guidelines for clinical use, although raising patient awareness of the uncertain effect of phytoestrogens is recommended.


International Journal of Cancer | 2010

Can physical activity modulate pancreatic cancer risk? a systematic review and meta-analysis.

Michael O'Rorke; Marie Cantwell; Christopher Cardwell; Helen G. Mulholland; Liam J. Murray

Numerous epidemiological studies have examined the association between physical activity and pancreatic cancer; however, findings from individual cohorts have largely not corroborated a protective effect. Among other plausible mechanisms, physical activity may reduce abdominal fat depots inducing metabolic improvements in glucose tolerance and insulin sensitivity, thereby potentially attenuating pancreatic cancer risk. We performed a systematic review to examine associations between physical activity and pancreatic cancer. Six electronic databases were searched from their inception through July 2009, including MEDLINE and EMBASE, seeking observational studies examining any physical activity measure with pancreatic cancer incidence/mortality as an outcome. A random effects model was used to pool individual effect estimates evaluating highest vs. lowest categories of activity. Twenty‐eight studies were included. Pooled estimates indicated a reduction in pancreatic cancer risk with higher levels of total (five prospective studies, RR: 0.72, 95% CI: 0.52–0.99) and occupational activity (four prospective studies, RR: 0.75, 95% CI: 0.59–0.96). Nonsignificant inverse associations were seen between risks and recreational and transport physical activity. When examining exercise intensity, moderate activity appeared more protective (RR: 0.79, 95% CI: 0.52–1.20) than vigorous activity (RR: 0.97, 95% CI: 0.85–1.11), but results were not statistically significant and the former activity variable incorporated marked heterogeneity. Despite indications of an inverse relationship with higher levels of work and total activity, there was little evidence of such associations with recreational and other activity exposures.


Cancer Epidemiology, Biomarkers & Prevention | 2004

Relative Validity of a Food Frequency Questionnaire with a Meat-Cooking and Heterocyclic Amine Module

Marie Cantwell; Beth Mittl; Jane Curtin; Raymond J. Carroll; Nancy Potischman; Neil E. Caporaso; Rashmi Sinha

The nutrient and heterocyclic amine (HCA) intake of 165 healthy participants was assessed using a self-administered food frequency questionnaire (FFQ), which included a meat-cooking practices module. A database containing the HCA [2-amino-3,8-dimethylimadazo [4,5-f] quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimadazo [4,5-b] pyridine (PhIP)] composition of various types of meat, cooked by different methods and to varying degrees, was developed and validated in conjunction with this module. The relative validity of dietary and HCA intake estimated by the FFQ was investigated using multiple food diaries (3 sets of 4 nonconsecutive day diaries completed over a 3-month period) as the reference method. Crude correlation coefficients of HCA intake assessed by the FFQ and food diaries were 0.43 [95% confidence interval (CI) 0.30–0.55] for MeIQx and 0.22 (95% CI 0.07–0.36) for PhIP intake. Deattenuated correlations were 0.60 (95% CI 0.49–0.69) and 0.36 (95% CI 0.22–0.49), respectively. Absolute MeIQx and PhIP intake was, however, underestimated by the FFQ (21.9 and 78.1 ng/day) compared with the food diaries (34.9 and 263.8 ng/day). The FFQ underestimated total red meat intake, the percentage of consumers, and the median intake of roast/baked and microwaved red meat. PhIP intake was severely underestimated by the FFQ and was most likely because of an underestimation of the percentage of people who cooked chicken using PhIP-producing cooking methods such as broiling and pan-frying. Additionally, the FFQ overestimated the percentage of consumers of baked chicken, a cooking method that produces less PhIP. In conclusion, although the FFQ and meat module underestimated absolute MeIQx and PhIP intake, its ability to rank individuals according to intake was acceptable.


British Journal of Cancer | 2009

Lignans and breast cancer risk in pre- and post-menopausal women: meta-analyses of observational studies

Louiza S. Velentzis; Marie Cantwell; Christopher Cardwell; Mohammed Keshtgar; Anthony J. Leathem; Jayne V. Woodside

Phyto-oestrogens are plant compounds structurally similar to oestradiol, which have been proposed to have protective effects against breast cancer. The main class of phyto-oestrogens in the Western diet is lignans. Literature reports on the effect of lignans in breast cancer risk have been conflicting. We performed three separate meta-analyses to examine the relationships between (i) plant lignan intake, (ii) enterolignan exposure and (iii) blood enterolactone levels and breast cancer risk. Medline, BIOSIS and EMBASE databases were searched for publications up to 30 September 2008, and 23 studies were included in the random effects meta-analyses. Overall, there was little association between high plant lignan intake and breast cancer risk (11 studies, combined odds ratio (OR): 0.93, 95% confidence interval (95% CI): 0.83–1.03, P=0.15), but this association was subjected to marked heterogeneity (I2=44%). Restricting the analysis to post-menopausal women, high levels of plant lignan intake were associated with reduced breast cancer risk (7 studies, combined OR: 0.85, 95% CI: 0.78, 0.93, P<0.001) and heterogeneity was markedly reduced (I2=0%). High enterolignan exposure was also associated with breast cancer (5 studies, combined OR: 0.73, 95% CI: 0.57, 0.92, P=0.009) but, again, there was marked heterogeneity (I2=63%). No association was found with blood enterolactone levels (combined OR: 0.82, 95% CI: 0.59–1.14, P=0.24). In conclusion, plant lignans may be associated with a small reduction in post-menopausal breast cancer risk, but further studies are required to confirm these results.


British Journal of Cancer | 2008

Dietary glycaemic index, glycaemic load and endometrial and ovarian cancer risk: a systematic review and meta-analysis.

Helen G. Mulholland; L J Murray; Christopher Cardwell; Marie Cantwell

Long-term consumption of a high glycaemic index (GI) or glycaemic load (GL) diet may lead to chronic hyperinsulinaemia, which is a potential risk factor for cancer. To date, many studies have examined the association between GI, GL and cancer risk, although results have been inconsistent, therefore our objective was to conduct a systematic review of the literature. Medline and Embase were systematically searched using terms for GI, GL and cancer to identify studies published before December 2007. Random effects meta-analyses were performed for endometrial cancer, combining maximally adjusted results that compared risk for those in the highest versus the lowest category of intake. Separate analysis examined risk by body mass index categories. Five studies examining GI and/or GL intake and endometrial cancer risk were identified. Pooled effect estimates for endometrial cancer showed an increased risk for high GL consumers (RR 1.20; 95% CI: 1.06–1.37), further elevated in obese women (RR 1.54; 95% CI: 1.18–2.03). No significant associations were observed for GI. Only two studies examined ovarian cancer and therefore no meta-analysis was performed, but results indicate positive associations for GL also. A high GL, but not a high GI, diet is positively associated with the risk of endometrial cancer, particularly among obese women.

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Liam Murray

Queen's University Belfast

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Jayne V. Woodside

Queen's University Belfast

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Helen G. Coleman

Queen's University Belfast

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Carmel Hughes

Queen's University Belfast

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Sarah F. Brennan

Queen's University Belfast

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Brian T. Johnston

Belfast Health and Social Care Trust

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Louiza S. Velentzis

Cancer Council New South Wales

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