The formation of stable hemoglobin adducts was examined (in the absence of an added reducing agent) in metabolizing red blood cells (RBCs) exposed to micromolar concentrations of acetaldehyde for up to 48 hours in vitro. The rapid disappearance of acetaldehyde due to oxidation by RBC aldehyde dehydrogenase was prevented by pretreating the cells with the inhibitor cyanamide. The RBCs remained viable for 48 hours (37 degrees C) as determined by cell hemolysis and glycolytic activity. [14C]acetaldehyde-modified hemoglobin was assessed in untreated and in cyanamide-pretreated cells. In untreated cells, after 3 hours of exposure to 50 and 200 nmol/ml of [14C]acetaldehyde, the molar ratios of acetaldehyde to hemoglobin were 0.00069 and 0.0038, respectively; [14C]acetaldehyde concentrations decreased to less than 4% of the initial levels within 3 hours. In cyanamide-pretreated RBCs, the molar ratios of acetaldehyde bound to hemoglobin ranged from 0.0013 after 3 hours of exposure to 20 nmol/ml [14C]acetaldehyde up to 0.039 after 48 hours of exposure to 200 nmol/ml [14C]acetaldehyde. Following tryptic digestion of [14C]acetaldehyde-hemoglobin and separation of peptides by high-performance liquid chromatography, significant incorporation of [14C]acetaldehyde was observed in nine peptides. Modifications of the labeled peptides remain to be characterized.

Acetaldehyde↗

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Risk factors for colon neoplasia--epidemiology and biology.

Epidemiological, physiological and molecular models of colon carcinogenesis have been proposed. Consistent epidemiological risk factors include reduced plant-food intake (increased risk); elevated meat intake (increased risk); higher physical activity (reduced risk); and increased alcohol intake (increased risk). At the physiological level, these lifestyle variables may trigger processes that provide explanations for the associations: higher meat, fat and alcohol means more heterocyclic amines and higher levels of bile acids; higher plant food means higher intake of several anticarcinogens and fibre fermentation that produces volatile fatty acids; exercise has a variety of beneficial effects. This complexity is elaborated further in the context of the colonic milieu where interactions among digesta, bacteria and epithelial cells occur. The long-term likelihood of cancer is the summation of moment-to-moment changes in the colonic milieu brought about by this interaction. Possible relationships between established epidemiological risk factors, genetic susceptibility and somatic genetic changes are outlined.

Colonic Neoplasms↗

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Methods for tracing, contacting, and recruiting a cohort of survivors of childhood cancer.

PURPOSE: Due to the use of combined modalities of multiagent chemotherapy, radiation therapy, and surgery, many children with a diagnosis of cancer are now surviving into adulthood. This pilot study sought to determine the feasibility of establishing a cohort of childhood cancer survivors and then to develop methods to trace and contact eligible participants. MATERIALS AND METHODS: A retrospective cohort design was used. Four hundred and forty subjects who were treated for cancer at the University of Minnesota Hospital before the age of 21, between 1970 and 1986, had survived 5 years, and were alive at last contact were eligible. Tracing efforts were undertaken if the address was more than 2 years old or if a letter was returned by the post office. Contact procedures in this study were designed to determine whether participation rates differed according to the method of contact. RESULTS: In this cohort of 440 individuals, 11 had died and were not traced. Of the remaining 429 eligible individuals, 408 (95.1%) were successfully contacted. Successful tracing efforts differed by both current age and age at diagnosis. Once contacted, 370 (90.6%) agreed to participate in this study and returned a baseline health questionnaire. Each method of participation, and the combination of methods, showed similar percentages of participation. CONCLUSIONS: Results from this pilot study show that appropriate methods exist to establish a cohort of adults who have not been contacted since childhood.

Adolescent↗

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Effects of cereal and vegetable fiber feeding on potential risk factors for colon cancer.

The effects of two doses of cereal fiber and vegetable fiber on mean transit time, stool weight, fecal pH and fecal bile acids were examined in 34 healthy volunteers. Subjects consumed five diets in random order for 23 days each, consisting of a fiber-free liquid diet and quick breads containing 0 g added dietary fiber, 10 g fiber as wheat bran (WB), 30 g fiber as WB, 10 g fiber as vegetable fiber (VF), and 30 g fiber as VF. Fecal wet and dry weights were 43% and 19% higher, respectively, on WB as compared to VF (P < 0.0001). Fecal pH was lower on WB than on VF (P < 0.0001) and decreased with increased fiber intake (P < 0.005). Transit time was 36% faster with WB than with VF (P < 0.0001). There was no VF dose effect on transit time, but transit time was 23% faster on 30 g WB than on 10 g WB (P = 0.04). Total bile acid concentrations decreased with increased fiber dose (P < 0.0001) but were not significantly different between WB and VF. Daily total bile acid excretion was 14% lower on VF compared to WB (P = 0.01). There was no VF dose effect on total bile acid excretion, but excretion was 13% lower on 30 g WB than on 10 g WB (P = 0.04). These findings are consistent with the capacity of fiber to alter potential risk factors for colon cancer but do not explain differences in epidemiological data between vegetable and cereal intake.

Adult↗

PubMedDate not supplied

Reconciling the epidemiology, physiology, and molecular biology of colon cancer.

Explore the source record for details and available documents.

Bile Acids and Salts↗

PubMedDate not supplied

Dietary modulation of serum platelet-derived growth factor-AB levels.

Epidemiological studies have demonstrated that diets high in vegetables and fruit are associated with a decreased risk of cancer and, possibly cardiovascular disease. Certain constituents of vegetables and fruit inhibit the in vitro activity of platelet-derived growth factor (PDGF), a potent mitogen implicated in both cancer and cardiovascular disease. Few studies have measured PDGF in relationship to diet in vivo. Specifically, there are no data regarding the changes in PDGF levels of mitogenic activity after a dietary intervention. In this study, 19 young, healthy individuals consumed four (9-day) experimental diets in random order: (a) control diet alone; (b) control diet plus carotenoid-rich vegetables; (c) control diet plus cruciferous vegetables; and (d) control diet plus soy foods. Compared to the control diet, there was a significant elevation in PDGF-AB serum levels when the individuals were consuming the soy diet (P = 0.016). Increased PDGF-AB levels were also noted for the carotenoid diet. There was no change from baseline levels when individuals were consuming the cruciferous diet. Overall, mitogenic activity did not change on any of the experimental diets. This study suggests that high soy and carotenoid diets increase serum levels of PDGF-AB. This may represent an additional mechanism by which diet influences individual risk of cancer; further investigation into the role of diet and growth factors is warranted.

Cardiovascular Diseases↗

PubMedDate not supplied

Plasma carotenoids as biomarkers of vegetable intake: the University of Minnesota Cancer Prevention Research Unit Feeding Studies.

High vegetable intake has been associated with a decreased risk for various human cancers in epidemiological studies. Carotenoids are plant compounds that may both possess chemopreventive activity and be useful biomarkers of vegetable and fruit intake. Nineteen men and women were randomized into a controlled cross-over feeding study to measure the effect of vegetable intake on plasma carotenoid concentrations. Participants consumed each of 4 experimental diets for 9 days. The control diet consisted of commonly consumed foods and was essentially carotenoid free. High vegetable diets (carotenoid, cruciferous, and soy) consisted of the control diet plus carrots and spinach (carotenoid), broccoli and cauliflower (cruciferous), and tofu and FriChik (soy). Plasma carotenoid concentrations were highest on the carotenoid and cruciferous diets. When compared to the control, mean plasma alpha-carotene, beta-carotene, and lutein concentrations were 5.2, 3.3 and 2.2 times higher on the carotenoid diet, respectively (P < 0.001). Mean plasma lutein concentrations were 2.1 times higher on the cruciferous versus the control diet (P < 0.001). There were no differences between diets in plasma beta-cryptoxanthin and lycopene concentrations. These data indicate that plasma alpha-carotene, beta-carotene, and lutein may be useful biomarkers of carotenoid-rich food intake and that lutein may act as an intake biomarker of commonly consumed vegetables in the Cruciferae family. These findings should prove useful in undertaking dietary intervention trials because they suggest the feasibility of monitoring intake of some plant foods and of distinguishing among plant food groups.

Adult↗

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Examination of the effect of nongenetic risk factors on the familial risk of breast cancer among relatives of postmenopausal breast cancer patients.

Relatives of postmenopausal breast cancer patients have a greater risk of breast cancer than do women with no family history of the disease. However, no study has previously examined the contribution of other breast cancer risk factors to risk in these relatives, thus precluding the ability to discern between shared environment or genes as the cause of familial aggregation. We conducted a nested case-control study of 251 index case families and 234 index control families. Incident breast cancer cases occurring in 1988-1989 and cancer-free controls were selected from a prospective cohort study. A pedigree development form was mailed to identify female relatives, who were then mailed a health history questionnaire. Index cases were significantly more likely than index controls to have at least one first-degree female relative with breast cancer [odds ratio = 1.62; 95% confidence interval = 1.03-2.54] after controlling for the total number of first-degree female relatives. After excluding the index cases and controls, logistic regression models were used to predict the odds of breast cancer in sisters (n = 72 cases). Sisters of index cases had slightly, although not statistically significant, elevated risk of both early-onset (age < 50 years; odds ratio = 1.34; 95% confidence interval = 0.54-3.30) and late-onset (age > or = 50 years; odds ratio = 1.56; 95% confidence interval = 0.87-2.79) breast cancer. Adjustment for nongenetic risk factors increased the odds ratio to 1.41 and 1.81, respectively. These data suggest that risk to sisters of postmenopausal breast cancer cases may be increased for both early- and late-onset breast cancer and this risk is apparently independent of measured risk factors.

Aged↗

PubMedDate not supplied

Dietary fat and risk of breast cancer according to hormone receptor status.

The association of dietary fat with breast cancer in prospective cohort studies has generally been weak and not statistically significant. However, these studies have not considered whether the risk related to fat intake may differ according to estrogen or progesterone receptor status. Dietary habits and other breast cancer risk factors were assessed by mailed questionnaire in January 1986 in 34,388 postmenopausal Iowa women. Through 1991, 724 incident breast cancer cases were ascertained in this cohort using the Iowa cancer registry. Joint estrogen and progesterone receptor status was determined for 479 (66%) breast cancers. For tumors that were positive for both estrogen and progesterone receptors (ER+/PR+) (n = 329), age- and energy-adjusted relative risks for breast cancer adjusted from lowest to highest third of fat intake were 1.0, 1.05, and 1.22 (P trend = 0.14). Corresponding risks for ER+/PR- tumors (n = 75) were 1.0, 0.85, and 1.05 (P trend = 0.86) and for ER-/PR- tumors (n = 61) were 1.0, 1.06, and 0.73 (P trend = 0.68). Only 14 cases were classified as having ER-/PR+ tumors. Adjustment for other breast cancer risk factors did not appreciably alter these findings. There was a suggestion that dietary fat may be associated with ER+/PR+ breast cancers and not other breast cancers. These results are also consistent with an interpretation of no association between dietary fat with breast cancer, regardless of hormone receptor status. It has been suggested that etiological studies of breast cancer should investigate associations according to receptor status. This study provides evidence of a subset of breast cancers that may be related to dietary factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗