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Biomedical subjects

J D Potter

Publications and source records attributed to J D Potter.

At least 19 recordsLinked to original sources
PubMed1996

Reproductive factors and risk of endometrial cancer. The Iowa Women's Health Study.

Gravidity and parity have strong inverse relations with endometrial cancer occurrence. To determine whether gravidity masks an association with other reproductive factors, the authors analyzed data from a cohort study of 24,848 postmenopausal Iowa women aged 55-69 years who were cancer free at baseline in 1986 and who had not had a hysterectomy. During 5 years of follow-up, 167 incident endometrial cancer cases were documented. As expected, the mean gravidity of cases was lower than that of noncases (2.6 vs. 3.5, p < 0.0001). Endometrial cancer occurrence was associated positively with early age at menarche, late age at natural menopause, and total length of ovulation span, but history of infertility and ages at first and last pregnancy were unrelated to risk after adjustment for gravidity. Two additional factors remained statistically significant independent of gravidity: a history of ever (vs. never) having had an induced abortion (relative risk = 2.5, 95% confidence interval 1.1-5.7) and timing of spontaneous abortions (miscarriages). Results suggest that a miscarriage late in reproductive life, followed by lack of a subsequent full-term pregnancy, may be a marker for progesterone deficiency. If so, the findings support the "unopposed" estrogen hypothesis for the etiology of endometrial cancer.

Age Factors↗
PubMed1996

Diet and risk of non-Hodgkin lymphoma in older women.

OBJECTIVE: To test whether high dietary intakes of fat, protein, and milk are associated with the development of non-Hodgkin lymphoma in older women. DESIGN: Prospective cohort study with a 7-year follow-up period. SETTING: General community. PARTICIPANTS: Sample of 35 156 Iowa women aged 55 to 69 years with no prior history of cancer who returned the 1986 baseline questionnaire. MAIN OUTCOME MEASURE: Non-Hodgkin lymphoma (104 incident cases). MAIN RESULTS: After controlling for age, marital status, residence, total energy intake, and transfusion history, the relative risks (RRs) for the highest tertile of intake compared with the lowest were 2.00 (95% confidence interval [CI], 1.21-3.30; P for trend = .01) for animal fat, 1.69 (95% CI, 1.07-2.67; P for trend = .02) for saturated fat, and 1.90 (95% CI, 1.18-3.04; P for trend = .01) for monounsaturated fat, and there was no association with vegetable fat or polyunsaturated fat. Greater intake of animal protein (RR = 1.52; 95% CI, 0.94-2.44; P for trend = .08), but not vegetable protein, was associated with elevated risk, and this was mainly explained by greater consumption of red meat (RR = 1.98; 95% CI, 1.13-3.47; P for trend = .02) and hamburger in particular (RR = 2.35; 95% CI, 1.23-4.48; P for trend = .02). Milk and dairy product consumption were not associated with elevated risk. There was also a decreased risk of non-Hodgkin lymphoma with greater consumption of fruits (RR = 0.64; 95% CI, 0.40-1.05; P for trend = .07). CONCLUSIONS: A high-meat diet and a high intake of fat from animal sources is associated with an increased risk of non-Hodgkin lymphoma in older women.

Aged↗
PubMed1996

The role of the four Ca2+ binding sites of troponin C in the regulation of skeletal muscle contraction.

In order to study the role of the Ca2+-specific sites (I and II) and the high affinity Ca2+-Mg2+ sites (III and IV) of TnC in the regulation of muscle contraction, we have constructed four mutants and the wild type (WTnC) of chicken skeletal TnC, with inactivated Ca2+ binding sites I and II (TnC1,2-), site III (TnC3-), site IV (TnC4-), and sites III and IV (TnC3,4C-). All Ca2+ binding site mutations were generated by replacing the Asp at the X-coordinating position of the Ca2+ binding loop with Ala. The binding of these mutated proteins to TnC-depleted skinned skeletal muscle fibers was investigated as well as the rate of their dissociation from these fibers. The proteins were also tested for their ability to restore steady state force to TnC-depleted fibers. We found that although the NH2-terminal mutant of TnC (TnC1,2-) bound to the TnC-depleted fibers (with a lower affinity than wild type TnC (WTnC)), it was unable to reactivate Ca2+-dependent force. This supports earlier findings that the low affinity Ca2+ binding sites (I and II) in TnC are responsible for the Ca2+-dependent activation of skeletal muscle contraction. All three COOH-terminal mutants of TnC bound to the TnC-depleted fibers, had different rates of dissociation, and could restore steady state force to the level of unextracted fibers. Although both high affinity Ca2+ binding sites (III and IV) are important for binding to the fibers, site III appears to be the primary determinant for maintaining the structural stability of TnC in the thin filament. Moreover, our results suggest an interaction between the NH2- and COOH-terminal domains of TnC, since alteration of sites I and II lowers the binding affinity of TnC to the fibers, and mutations in sites III and IV affect the Ca2+ sensitivity of force development.

Animals↗
PubMed1996

The regulatory light chains of myosin modulate cross-bridge cycling in skeletal muscle.

We investigated the kinetics of Ca2+ activation of skeletal muscle contraction elicited by the photolysis of caged Ca2+. Previously we showed that partial extraction of the 18-kDa regulatory light chains (RLCs) of myosin decreased the rate of force development and was subsequently increased by approximately 20% following reconstitution with RLCs (Potter, J. D., Zhao, J. and Pan, B. S. (1992) FASEB J. 6, A1240). We extend here the RLC-extraction study to the complete removal of the RLCs. The complete removal of RLCs was achieved by a combination of 5,5'-dithiobis-(2-nitrobenzoic acid) and EDTA treatment followed by reduction of oxidized sulfydryl groups by dithiothreitol. Under these conditions the complete extraction of RLCs was accompanied by the extraction of endogenous troponin C, resulting in the loss of isometric tension. Steady state force was restored to 65-75% following troponin C reconstitution and increased to 75-85% as a result of RLC reincorporation into the fibers. The rates of force transients generated by UV-flash photolysis of 1-(2-nitro-4,5-dimethoxyphenyl)-N,N,N',N' -tetrakis[(oxycarbonyl)methyl]-1,2-ethanediamine) or nitrophenyl-EGTA, photoliberating bound Ca2+, decreased 2-fold after RLC extraction and troponin C reconstitution and then increased to the values of intact fibers after RLC reconstitution. These results support our earlier findings that the regulatory light chains of myosin play an important role in the kinetics of cross-bridge cycling.

Animals↗
PubMed1996

Maternal waist-to-hip ratio as a predictor of newborn size: Results of the Diana Project.

Location of body fat stores, as indicated by waist-to-hip circumference ratio (WHR), affects a variety of metabolic processes in women, and some of these changes could affect fetal growth during pregnancy. We tested the hypothesis that WHR affects fetal growth among 702 participants of the Diana Project, a prospective study designed to identify preconceptual exposures related to reproductive outcomes. We tested the effect of maternal WHR on the outcomes of infant birthweight, length, and head circumference in regressional models that included 16 variables such as maternal body mass index, duration of gestation, and pregnancy weight gain previously related to birthweight. Maternal WHR was related to each measure of newborn size. A 0.1-unit increase in WHR predicts a 120-gm greater birthweight, a 0.2-inch greater length, and a 0.3-cm greater head circumference. We conclude that WHR is related to fetal growth and that the effect of WHR on fetal growth may be mediated by metabolic alterations associated with a preponderance of central body fat stores or to other factors closely aligned with WHR. The common finding of an independent effect of pregnancy BMI on birthweight may be largely attributable to maternal WHR.

Adult↗
PubMed1995

Phosphorylation of both serine residues in cardiac troponin I is required to decrease the Ca2+ affinity of cardiac troponin C.

The phosphorylation of cardiac muscle troponin I (CTnI) at two adjacent N-terminal serine residues by cAMP-dependent protein kinase (PKA) has been implicated in the inotropic response of the heart to beta-agonists. Phosphorylation of these residues has been shown to reduce the Ca2+ affinity of the single Ca(2+)-specific regulatory site of cardiac troponin C (CTnC) and to increase the rate of Ca2+ dissociation from this site (Robertson, S. P., Johnson, J. D., Holroyde, M. J., Kranias, E. G., Potter, J. D., and Solaro, R. J. (1982) J. Biol. Chem. 257, 260-263). Recent studies (Zhang, R., Zhao, J., and Potter, J. D. (1995) Circ. Res. 76, 1028-1035) have correlated this increase in Ca2+ dissociation with a reduced Ca2+ sensitivity of force development and a faster rate of cardiac muscle relaxation in a PKA phosphorylated skinned cardiac muscle preparation. To further determine the role of the two PKA phosphorylation sites in mouse CTnI (serine 22 and 23), serine 22 or 23, or both were mutated to alanine. The wild type and the mutated CTnIs were expressed in Escherichia coli and purified. Using these mutants, it was found that serine 23 was phosphorylated more rapidly than serine 22 and that both serines are required to be phosphorylated in order to observe the characteristic reduction in the Ca2+ sensitivity of force development seen in a skinned cardiac muscle preparation. The latter result confirms that PKA phosphorylation of CTnI, and not other proteins, is responsible for this change in Ca2+ sensitivity. The results also suggest that one of the serines (23) may be constitutively phosphorylated and that serine 22 may be functionally more important.

Amino Acid Sequence↗
PubMed1995

Retinol, antioxidant vitamins, and cancers of the upper digestive tract in a prospective cohort study of postmenopausal women.

Very few prospective studies have reported previously on the association of micronutrient intake and the risk of cancers of the upper digestive tract (mouth, pharynx, esophagus, and stomach) in western populations. During 7 years of follow-up in the Iowa Women's Health Study, from 1986-1992, 59 of the 34,691 at-risk cohort members developed cancers of the upper digestive tract. The association of retinol and antioxidant vitamins (carotene and vitamins C and E) were evaluated separately for cancers of the mouth/pharynx/esophagus (n = 33) and stomach (n = 26). After adjustment for age, smoking, and total energy intake, higher intakes of carotene and vitamins C and E were related to lower risks of both oral/pharyngeal/esophageal and gastric cancers, while retinol was associated with lower risk of gastric cancer only. The dose-response relation between gastric cancer risk and intake of carotene was clear and statistically significant, with relative risks of 0.6 and 0.3, respectively, observed among women in the upper two versus the lowest tertiles of intake. This study provides further evidence that higher intake of antioxidant vitamins may be important in the prevention of cancers of the upper digestive organs.

Aged↗
PubMed1995

Genetic services for familial cancer patients: a survey of National Cancer Institute cancer centers.

In the past decade, significant progress has been made in understanding the genetic component of familial cancers. Genes associated with familial colon and breast cancers have recently been isolated and molecular diagnostic tests are expected to become available in the near future. Clinicians now have the opportunity to recognize and counsel individuals with elevated risk of cancer by identifying risk factors and genes associated with cancer predisposition. The rapid advances in molecular technology are a direct challenge to the medical community and cancer centers to supply specialized clinical services for familial cancers. We sought to ascertain the activities of cancer centers in the development of programs and the provision of genetic services for familial cancer. We surveyed 41 centers with National Cancer Institute (NCI) cancer center support grants. One half of the centers responding (17 of 34) reported that they provide some genetic services for familial cancer. About one half of these 17 centers (eight [57%] of 14; the three remaining clinics that responded had incomplete information on this indicator) see a variety of patient types on a small scale (fewer than 100 patients per year), and most provide four basic clinical evaluations: medical evaluation, cancer risk assessment, genetic counseling, and pedigree analysis. Staffing of each center varied widely, as did the types of screening services offered (including molecular diagnostic testing). Several centers (six [35%] of 17) indicated that they were in the developmental stages for serving familial cancer patients, and many seem to be increasing their activities in this area. The remaining 17 NCI-supported centers that responded, however, currently provide no genetic services for familial cancers. The results of this survey suggest that there is interest in developing clinical programs for familial cancers by NCI-supported cancer centers, but most of these programs are in developmental stages. A base line has been established to monitor future progress for the provision of cancer genetic services.

Cancer Care Facilities↗
PubMed1995

Association of body mass index and body fat distribution with risk of lung cancer in older women.

Obesity has been associated with an increased risk of cancer at a number of sites. A notable exception appears to be lung cancer, for which several studies suggest a modest inverse association. However, cigarette smoking is directly associated with lung cancer and inversely associated with body mass index. To investigate the hypothesis that body mass index is associated with lung cancer independent of cigarette smoking, the authors analyzed data from a prospective cohort study of 41,837 Iowa women aged 55-69 years at baseline in 1986. In addition, they examined whether central adiposity (high waist/hip ratio) was associated with lung cancer incidence. Through 1992 (6 years of follow-up), 233 cases of lung cancer were identified through the State Health Registry of Iowa. The body mass index at several ages was calculated from self-reports of height at baseline and weights at ages 18, 30, 40, and 50 years and at baseline. Current and former smokers generally had lower mean body mass indices than did nonsmokers at all ages except 18 years. Cases generally had lower body mass indices than did noncases at all ages except 18 and 30 years but, among current smokers, cases had higher mean body mass indices than did noncases at all ages except baseline, although the differences were not statistically significant. An apparent positive association of a high waist/hip ratio with lung cancer in the total cohort was found to be primarily accounted for by a higher waist/hip ratio in current and former smokers. When stratified by smoking status and adjusted for other risk factors, including age and pack-years of smoking, the body mass index at baseline, body mass index at age 50 years, and waist/hip ratio were not associated with lung cancer. The results of multivariate analyses suggest that the inverse association of body mass index with lung cancer can be explained by smoking status and that the positive association of waist/hip ratio with lung cancer can be explained by pack-years of smoking.

Age Distribution↗
PubMed1995

Calcium and colorectal epithelial cell proliferation in sporadic adenoma patients: a randomized, double-blinded, placebo-controlled clinical trial.

BACKGROUND: The kinetics of colorectal epithelial cell proliferation is altered in patients at increased risk for colon cancer. Calcium administration ameliorates such proliferative changes in rodents. Findings in preliminary clinical trials have suggested similar effects in humans. PURPOSE: A randomized, double-blind, placebo-controlled, clinical trial was designed to determine whether calcium supplementation will reduce the colorectal epithelial cell proliferation rate and normalize the distribution of proliferating cells within colorectal crypts (i.e., shift the zone of proliferation from the entire crypt to the lower 60% of the crypt, which is thought to be the normal proliferative zone of the crypt) in patients with sporadic adenomas. METHODS: Sporadic adenoma patients (n = 193) were treated with placebo (n = 66), 1.0 g calcium (n = 64), or 2.0 g calcium (n = 63) daily for 6 months. Rectal mucosa biopsy specimens were obtained at base line and at 1-, 2-, and 6-month follow-up. Cell proliferation was measured by detection of S-phase-associated proliferating cell nuclear antigen by immunohistochemical methods. The cell proliferation rate, called labeling index (LI), was calculated as the proportion of labeled cells in the crypts. The deviation of the proliferative zone from the normal location in the lower 60% of the crypt was calculated as the proportion of labeled cells in the upper 40% of the crypt, called distributional index (phi h). The effects of calcium treatment on the LI and phi h were expressed as relative effects--(calcium follow-up/calcium base line)/(placebo follow-up/placebo base line). Calculations and inference testing of the relative effects were accomplished using a repeated-measures mixed model on log-transformed LI and phi h values. All statistical tests were two-sided. RESULTS: Scorable biopsy specimens were obtained on 170 patients at base line, 164 at 1 month, 161 at 2 months, and 163 at 6 months. The difference in the change in the LI between the combined calcium groups and the placebo group was insignificant, with a relative effect of calcium versus placebo of 0.97 (P = .87). However, for the phi h, the relative effect of calcium versus placebo was 0.50 (P = .05) in the combined calcium groups, 0.56 (P = .16) in the 1.0-g calcium group, and 0.44 (P = .05) in the 2.0-g calcium group. CONCLUSIONS: Calcium supplementation normalizes the distribution of proliferating cells without affecting the proliferation rate in the colorectal mucosa of sporadic adenoma patients. IMPLICATIONS: These results support further study of whether alterations in colon cell proliferative kinetics represent true intermediate steps in colon carcinogenesis that can be used to investigate the etiology and prevention of, and whether a higher calcium consumption can reduce the risk of, colon cancer.

Adult↗
PubMed1995

The functional role of the domains of troponin-C investigated with thrombin fragments of troponin-C reconstituted into skinned muscle fibers.

Proteolysis of rabbit fast skeletal troponin-C (RSTnC) with thrombin produces four separate fragments containing the following Ca2+-binding site(s): TH1 (residues 1-120) sites I-III; TH2 (121-159) site IV; TH3 (1-100) sites I and II; and TH4 (101-120) site III. We studied the ability of these fragments to restore the steady state isometric force in TnC-depleted skinned skeletal muscle fibers. Interestingly, we found that all investigated fragments of RSTnC possessed some of the properties of native RSTnC, but none of them could fully regulate contraction in the fibers like intact RSTnC. TH1 was the most effective in the force restoration (65%) whereas the smaller fragments developed about 50% (TH3 and TH4) or 20% (TH2) of the initial force of unextracted fibers. Additionally, much higher concentrations of TH2, TH3, and TH4 compared to RSTnC OR TH1 were necessary for force development suggesting a decreased affinity of these fragments to their binding site(s) in the fibers. Like intact RSTnC, TH1 was able to interact with the fibers in a Ca(2+)-independent (Mg(2+)-dependent) manner, indicating that at a minimum, Ca(2+)-binding site III is required for this type of binding. The initial binding of the other fragments to the TnC-depleted fibers occurred only in the presence of Ca2+. TH2 and TH4 appeared to bind to two different binding sites in the fibers. The binding to one of the sites caused partial force restoration. This binding of TH2 and TH4 was abolished when Ca2+ was removed. TH2 and TH4 binding to the second site required Ca2+ initially but was maintained in the presence of Mg2+. This interaction of TH2 and TH4 partially blocked the rebinding of RSTnC to the fibers. The latter results suggest that site III and IV in these small fragments, when removed from the constraints of the parent protein, may assume conformations that allow them to function, to a certain extent, like both the regulatory sites (I and II) and the Ca(2+)-Mg2+ sites(III and IV) of TnC.

Animals↗
PubMed1995

Dietary intake of energy and animal foods and endometrial cancer incidence. The Iowa women's health study.

To assess the relations of dietary intake of energy and animal foods to endometrial cancer risk, dietary analyses were performed using data from a prospective cohort study of over 23,000 postmenopausal Iowa women who responded to a mailed questionnaire in 1986 and were followed through the end of 1992 for cancer incidence and total mortality. Usual intakes of 127 food items were measured by a semiquantitative food frequency questionnaire. After 7 years of follow-up, 216 incident endometrial cancer cases had been ascertained. There was no statistically significant association of dietary intake of energy and most animal foods with endometrial cancer incidence over the 7-year follow-up period. Stratified analyses, however, suggested that intake of energy from plant foods may be inversely associated with endometrial cancer risk in the latter years of follow-up (trend test, p = 0.03), while high intake of energy and foods from animal sources related to slightly, but not statistically significantly, elevated risks of this cancer in the earlier years of follow-up. The only significant dose-response relation observed in food group analyses was for processed meat and fish, for which a significant 50% excess risk of endometrial cancer was found among women in the highest versus the lowest tertile of intake. This study suggests that dietary intake of energy and most animal foods is not related to or is only weakly related to the risk of endometrial cancer among postmenopausal US women.

Cohort Studies↗
PubMed1995

Better breast cancer survival for postmenopausal women who are less overweight and eat less fat. The Iowa Women's Health Study.

BACKGROUND: The authors sought to determine whether prediagnosis obesity, body-fat distribution, and dietary intake of fats, antioxidants, and fiber may be related to survival after the diagnosis of breast cancer. METHODS: The mortality rates of 698 postmenopausal patients with unilateral breast cancer in a large cohort study were analyzed. Body-mass index, waist-to-hip ratio, and food-frequency data were collected by questionnaire within 6 years before breast cancer was diagnosed. RESULTS: Adjusted for age, women in the highest tertile of body mass index had a 1.9-fold higher risk (95% confidence interval = 1.0-3.7) of dying after breast cancer than those in the lowest tertile; adjusted for other prognostic variables (age, smoking, education level, extent of breast cancer, and tumor size), this relative risk was 1.5 (95% CI = 0.7 to 2.9). Waist-to-hip ratio was not related to risk of dying nor was intake of fiber or several dietary antioxidants. Independent of other prognostic variables, risk of death after breast cancer was statistically significantly elevated, with a relative risk greater than 2.0 for the highest tertiles of total fat, saturated fat, and monounsaturated fat intake, expressed as grams per day. An adjustment for energy intake, which also was associated positively with fatality, weakened these associations somewhat. CONCLUSIONS: Although clinical trials are required, these findings support the hypothesis that a high fat intake is associated with reduced survival of postmenopausal women with breast cancer and suggest that women with breast cancer should consider limiting their intake of fat.

Aged↗
PubMed1995

A direct regulatory role for troponin T and a dual role for troponin C in the Ca2+ regulation of muscle contraction.

Troponin (Tn), containing three subunits: Ca2+ binding (TnC), inhibitory (TnI), and tropomyosin binding (TnT), plays a crucial role in the Ca2+ regulation of vertebrate striated muscle contraction. These three subunits function by interacting with each other and with the other thin filament proteins. Previous studies suggested that the primary role of TnT is to anchor the TnI.TnC complex to the thin filament, primarily through its interactions with TnI and tropomyosin. We propose here a new role for TnT. Our results indicate that, when TnT is combined with the TnI.TnC complex, there is an activation of actomyosin ATPase that is Ca(2+)-dependent. To determine whether the latter results from a direct effect of TnC on TnT or indirectly from an effect of TnC on TnI which is transmitted to TnT, we prepared a deletion mutant (deletion of residues 1-57) of TnI, TnId57 (Sheng et al. (1992) J. Biol. Chem. 267, 25407-25413), which interacts with TnC but not TnT. Both wild type (TnI.TnC.TnT) and mutant (TnId57.TnC.TnT) Tn complexes demonstrated equivalent activity in the Ca2+ regulation of actomyosin-S1 ATPase activity. Similarly, both TnI and TnId57 could equally reconstitute TnI-depleted skinned muscle fibers. Therefore, since TnId57 does not interact with TnT, these results suggest that TnT reconstitutes native Ca2+ sensitivity via direct interaction with TnC. Thus Ca2+ binding to TnC would have a dual role: 1) release of the ATPase inhibition by TnI and 2) activation of the ATPase through interaction with TnT.

Animals↗
PubMed1995

Segregation analysis of breast cancer in a population-based sample of postmenopausal probands: The Iowa Women's Health Study.

Inheritance of a major susceptibility gene for breast cancer has been primarily investigated in families with early-onset disease. However, familial clustering of late-onset breast cancer is well documented, and genetic factors may also be relevant. In the Iowa Women's Health Study, we evaluated evidence for a major gene after allowing for measured environmental risk factors. Two hundred sixty-five incident breast cancer probands were identified from a prospective cohort study of 41,837 women aged 55 to 69 years at baseline in 1986. A pedigree development form was mailed to the probands to ascertain all first-degree female relatives. A questionnaire and body measurement protocol were mailed to identified living relatives or surrogates. Segregation analyses were conducted on a total of 1,145 women in 251 families using regressive models as implemented in S.A.G.E. Mendelian codominant inheritance of an allele that produced an earlier-age-at-onset provided the best fit to the data. Incorporation of measured environmental risk factors as covariates yielded no significant improvements in the likelihoods. Approximately 50% of this population could be expected to carry a late-onset breast cancer susceptibility gene, and 23% of the population is susceptible because of the environment in which they live. Homozygous gene carriers are predicted to have a mean age-at-onset of 48 years, over 20 years earlier than heterozygotes; few cases would be expected among non-gene carriers. In conclusion, the transmission pattern of late-onset breast cancer may be determined by a common susceptibility gene.

Age of Onset↗
PubMed1995

Epidemiologic and genetic follow-up study of 544 Minnesota breast cancer families: design and methods.

In 1944, a case-control family study was initiated at the Dight Institute for Human Genetics at the University of Minnesota to study the influences of childbearing breastfeeding, and hereditary susceptibility on the occurrence and age-of-onset of breast cancer. Index cases (probands) were women ascertained at the Tumor Clinic of the University of Minnesota Hospital. Medical history and life style information were obtained on probands and relatives, and all cancers were histologically verified. A total of 544 families were studied, with probands diagnosed between 1931 and 1952. All of the records and pathology slides have been maintained from the original study; for most probands this includes the original tissue blocks. We are conducting a historical cohort study of selected of selected first- and second-degree female relatives (sisters, daughters, nieces, granddaughters) of the probands and a group of control women identified as the spouses of all male first- and second-degree relatives (brothers, sons, grandsons, and nephews). The subsequent development of breast cancer is being determined to quantify the absolute risk associated with a positive family history. Current disease status is ascertained with mammography, and stromal density is measured using digital imaging. Segregation analysis will be applied to examine how non-genetic factors such as diet, exogenous hormone use, and body fat distribution influence risk in women at high risk because of family history. A subset of families are being selected for molecular analysis of the BRCA1 gene or for linkage analyses to identify putative susceptibility loci other than BRCA1. Documented cancer histories were known for at least three generations, and the current study extends the pedigrees up to four or five generations for every family, allowing a detailed description of familial risk. This cohort study of breast cancer families is likely to be important in both quantity and quality of data and will serve as a major genetic epidemiologic resource, being free of selection bias and having relevant non-genetic exposure determined in at least four generations.

Adult↗
PubMed1995

The University of Minnesota Cancer Prevention Research Unit vegetable and fruit classification scheme (United States).

High vegetable and fruit (V&F) intake has been associated with a lower risk of many cancers. However, the specific V&F, the active compounds present in V&F, and the dose at which they confer protection are unknown. Standard methods for assessing, classifying, and quantifying V&F exposures in epidemiologic studies have not been established. Differences among studies occur due to inherent differences among V&F, and across dietary assessment methods, study populations, etiologic hypotheses, and analytic methods. The V&F classification scheme presented here characterizes and quantifies V&F consumption for elucidating risk relationships, identifying chemopreventive compounds present in V&F, and facilitating identification of potential biomarkers of V&F intake. Broad criteria define which plant foods count as V&F. Formation of food groups is based on proposed biological mechanisms of action. Five main groups are included: Total V&F; Total Vegetables; Total Fruits; and two groups orthogonal to these -- the Botanical and Phytochemical groups. Subgroups are specified within each main group. V&F exposure is quantified as the absolute amount consumed (weight) or as the number of household servings. This classification scheme has public health applications and may be used to examine associations with chronic diseases other than cancer.

Eating↗