María Elena Martínez

This study examined factors that influence mammography use and breast cancer detection, including education, health insurance, and acculturation, among Mexican-American (MA) and African-American (AA) women.

In this commentary, we discuss the challenges and opportunities for epidemiologic studies in evaluating breast cancer as a set of discrete diseases. We show examples of the strengths of the case-only design in assessing the relative correlation of established risk factors and the different cancer

Colorectal cancer can be prevented via screening by the detection and removal of colorectal adenomas. Few data exist on screening capacity by rural/urban areas. Therefore, the aims of this work were to evaluate current colorectal cancer endoscopy screening capacity and to estimate potential volume for rural and urban regions in Arizona. Gastroenterologists and colorectal surgeons practicing in Arizona completed a survey (n = 105) that assessed current colonoscopy and sigmoidoscopy screening and estimated future capacity. Resources needed to increase capacity were identified, and differences between rural and urban regions were examined. Responders were more likely to practice in an urban region (89.5%). Physicians reported performing 8,717 endoscopic procedures weekly (8,312 in urban and 405 in rural regions) and the vast majority were colonoscopies (91% in urban and 97% in rural regions). Urban physicians estimated being able to increase their capacity by 35.7% (95% confidence interval 34.7–35.7) whereas rural physicians estimated an increase of 53.1% (95% confidence interval 48.1–58.0). The most commonly cited resource needed to increase capacity was a greater number of physicians in urban regions (52.1%); while the top response in rural areas was appropriate compensation (54.6%). Lastly, 27.3% of rural physicians noted they did not need additional resources to increase their capacity. In conclusion, Arizona has the ability to expand colorectal cancer screening endoscopic capacity; this potential increase was more pronounced in rural as compared to urban regions.

Chemoprevention is defined as the use of pharmacological agents (including nutrients) to impede, arrest or reverse carcinogenesis and has been used to test the efficacy of numerous nutrients and other dietary factors. Observational epidemiology and experimentation by randomized controlled trials (RCTs) have been used to evaluate dietary factors in cancer chemoprevention; however, consistency in findings has been elusive. The study of diet and cancer associations in humans poses a variety of challenges owing to the complexity in measuring dietary intake as well as the multifactorial nature of the cancer endpoints. In several circles, RCTs are viewed as being more credible than observational studies. When discrepant results between observational studies and RCTs are reported, careful consideration needs to be given to the details of each set of studies before accepting RCTs as valid and those of observational studies as biased. Considerations in the interpretation of results from RCTs include the background diet of the study population; the dose, duration and timing of the intervention; the precise form of the nutrient or dietary factor tested; and compliance with the intervention.

Background. Breast cancer in Hispanic women is poorly understood and data on tumor hormone receptor status in this population are limited. Methods. Using data from the Arizona Cancer Registry, we assessed differences in tumor characteristics between Hispanic and non-Hispanic White (NHW) women using logistic regression modeling. 25,494 invasive breast cancer cases (23,657 NHWs and 1,837 Hispanics) reported to the cancer registry in 1995 to 2003 were included in the analysis. Results. In age-adjusted models, compared with NHW women, Hispanics were more likely to have high-grade cancers, larger tumors, a greater number of positive lymph nodes, and advanced stage at diagnosis. Hispanic women were less likely to have tumors that are both estrogen and progesterone receptor positive (ER+/PR+), particularly those under age 60. Conclusions. The profile of tumor presentation in Hispanic women in Arizona is consistent with a more aggressive disease pattern and less favorable prognosis than that of NHWs.

Red meat intake has been shown to be associated with higher risk of colorectal cancer. Though the exact mechanisms responsible for this association remain unknown, several tumorigenic properties of meat have been proposed. One well-supported biologic mechanism is elevated exposure to the genotoxic formation of heterocyclic amines (HCAs), which occur when meat is cooked at high temperatures for a long period of time. We prospectively assessed the relation between type of meat, meat preparation method, doneness, a metric of HCAs and other mutagens and colorectal adenoma recurrence among 869 participants in a chemoprevention trial of ursodeoxycholic acid. Unconditional logistic regression analyses were used to estimate odds ratios (ORs) and associated 95% confidence intervals (CIs). Most meat variables assessed were positively but weakly associated with recurrence of any adenoma. In contrast, recurrence of advanced or multiple adenomas was more strongly associated with a number of the meat exposure variables evaluated. For recurrence of advanced lesions, significant associations were detected among individuals in the highest when compared with the lowest tertile of intake for pan-fried red meat (OR = 1.85; 95% CI = 1.10-3.13) and well/very well done red meat (OR = 1.71; 95% CI = 1.02-2.86). Significant positive associations were shown for recurrence of multiple adenomas and the following variables: processed meat (OR = 1.83; 95% CI = 1.10-3.04), pan-fried red meat (OR = 1.63; 95% CI = 1.01-2.61), well/very well done red meat (OR = 1.68; 95% CI = 1.03-2.74), 2-amino-3,4,8-trimethylimidazo[4,5,-f]quinoxaline (OR = 1.74; 95% CI = 1.07-2.82) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (OR = 1.68; 95% CI = 1.03-2.75). Our results support a meat mutagen exposure hypothesis as a potential mechanism for recurrence of clinically significant adenomatous polyps.

Dietary calcium has long been implicated as a protective factor for colorectal cancer and adenomas. Investigation of this nutrient was triggered by mechanisms proposed in the early 1980s based on in vivo and in vitro studies ( 1 , 2 ). Fast-forward to more than 20 years later, and we find ourselves debating the importance of this nutrient in the etiology of colorectal neoplasia. Examination of the abundant amount of observational data is a worthwhile exercise. Although some inconsistencies are evident across studies, the picture that emerges from most prospective studies of colorectal cancer and calcium intake suggests a threshold effect in that risk reduction is seen at intakes of approximately 600–1000 mg/day, with no further protection beyond these levels ( 3 – 5 ). These findings might explain the null effects observed in the Women's Health Initiative ( 6 ), in which women were randomly assigned to receive 1000 mg of calcium carbonate and 400 IU of vitamin D ₃ daily. Baseline mean calcium intake in these women was 1151 mg/day, resulting in a total calcium intake of approximately 2150 mg/day, levels that, based on the prospective data, are consistent with no effect. As a result, we are still left with the unanswered question of whether calcium supplementation would convey protection among individuals with low or moderately low baseline intakes of this nutrient.

In 1996, the US Food and Drug Administration mandated the fortification of grain products with folic acid, a nutrient that has been associated with lower risk of colorectal neoplasia. We assessed the relation of plasma folate and homocysteine and colorectal adenoma recurrence separately in 2 studies: the first involved an intervention of a cereal supplement that contained folic acid, wheat bran fiber (WBF), and the second was conducted primarily during postfortification of the food supply using ursodeoxycholic acid (UDCA). Analyses were stratified for multivitamin use. Results show that plasma folate and homocysteine concentrations were associated with adenoma recurrence among nonusers of multivitamins only. Among nonmultivitamin users, the odds ratio [OR] (95% confidence interval [CI]) for those in the highest versus the lowest folate quartile was 0.65 (0.40–1.06) for the WBF study and 0.56 (0.31–1.02) for the UDCA; likewise, individuals in the highest versus the lowest quartile of homocysteine had higher odds of adenoma recurrence, in both the WBF (OR = 2.25; 95% CI = 1.38–3.66) and UDCA (OR = 1.93; 95% CI = 1.07–3.49) populations. Analyses comparing multivitamin users to different plasma folate concentrations among nonusers show that odds of recurrence for supplement users was lower only when compared to nonusers who had lower concentrations. Our results show that higher plasma folate or lower homocysteine levels are associated with lower odds of recurrence among nonusers of multivitamins in both studies. Our finding, suggesting that multivitamins or supplemental folate only benefit individuals with lower plasma folate concentrations, should be taken into consideration when designing and interpreting results of intervention studies.