Radon as a Tracer of Lung Changes Induced by Smoking

After smoking, exposure to radon and its progeny is the second leading cause of lung cancer. The probability of inducing lung carcinomas by inhaled radon progeny depends on the deposited radiation dose, and is significantly affected by physiological and morphometric changes induced by smoking. Due to irritation of the airways, the inhalation of cigarette smoke leads to the hyperproduction of mucus. Two concurrent processes occur: on one hand, increased production of mucus protects the target cells against radiation damage; on the other hand, in the case of long-term smokers, a chronic lung obstruction develops, causing an increase in the radiation dose to the lungs. Depending on the duration and intensity of smoking, these processes contribute to the final radiation dose with different weights. The primary objective of this study was to investigate to what extent these smoke-induced changes can modify the resulting absorbed dose of inhaled radon progeny relative to healthy nonsmokers. Since the bronchial dose depends on the degree of lung tissue damage, we have used this dose as a tool for detecting the effects of smoking on the lung epithelium. In other words, the biological effect of radon served as a tracer of changes induced by smoking.     

How Tautological Are Interspecies Correlations of Carcinogenic Potencies?

Crouch and Wilson demonstrated a strong correlation between carcinogenic potencies in rats and mice, supporting the extrapolation from mouse to man. Bernstein et al. , however, show that the observed correlation is mainly a statistical artifact of bioassay design. Crouch et al. have a comeback. This paper will review the arguments and present some new data. The correlation is largely (but not totally) tautological, confirming results in Bernstein et al.     

Biological Models of Carcinogenesis and Quantitative Cancer Risk Assessment

Biologically-based models of carcinogenesis were originally developed to explain certain quanti-tative phenomena associated with carcinogenesis, and to provide a framework within which questions regarding the process could be addressed. Some limitations in the use of these models for quantitative cancer risk assessment are discussed.     

How Do Cancer Risks Predicted From Animal Bioassays Compare with the Epidemiologic Evidence? The Case of Ethylene Dibromide

Cancer risks for ethylene dibromide (EDB) were estimated by fitting several linear non-threshold additive models to data from a gavage bioassay. Risks predicted by these models were compared to the observed cancer mortality among a cohort of workers occupationally exposed to the same chemical. Models that accounted for the shortened latency period in the gavaged rats predicted upper bound risks that were within a factor of 3 of the observed cancer deaths. Data from an animal inhalation study of EDB also were compatible with the epidemiologic data. These findings contradict those of Ramsey et al. (1978), who reported that extrapolation from animal data produced highly exaggerated risk estimates for EDB-exposed workers. This paper explores the reasons for these discrepant findings.     

Ambiguous carcinogens and their regulation

Examination of five animal and one human studies suggest that certain agents increase the incidence of some cancers but simultaneously reduce the incidence of other cancers. Yellow die #3, for example, sharply increases the incidence of liver tumors but practically eliminates naturally occurring leukemia/lymphoma in F-344 male rates. Such ambiguity in the action of presumed carcinogens suggests that caution must be used by regulatory bodies in proscribing suspected carcinogens, or even in recommending changes in lifestyle or dietary habits as a means of reducing incidence of cancer.     

Improving Scientists'Judgments of Risk

Scientists disagree in their risk analyses because they use intuitive judgments to generalize results from the laboratory to circumstances not yet studied. If this assertion is correct, techniques intended to reduce intuitive judgments and increase analytical cognition should reduce scientific dispute. The results of a test case involving allegedly high risk and sharp dispute among scientists are described.     

Extending the Stochastic Two-Stage Model of Carcinogenesis to Include Self-Regulation of the Nonmalignant Cell Population

One of the challenges of introducing greater biological realism into stochastic models of cancer induction is to find a way to represent the homeostatic control of the normal cell population over its own size without complicating the analysis too much to obtain useful results. Current two-stage models of carcinogenesis typically ignore homeostatic control. Instead, a deterministic growth path is specified for the population of "normal" cells, while the population of "initiated" cells is assumed to grow randomly according to a birth-death process with random immigrations from the normal population. This paper introduces a simple model of homeostatically controlled cell division for mature tissues, in which the size of the nonmalignant population remains essentially constant over time. Growth of the nonmalignant cell population (normal and initiated cells) is restricted by allowing cells to divide only to fill the "openings" left by cells that die or differentiate, thus maintaining the constant size of the nonmalignant cell population. The fundamental technical insight from this model is that random walks, rather than birth-and-death processes, are the appropriate stochastic processes for describing the kinetics of the initiated cell population. Qualitative and analytic results are presented, drawn from the mathematical theories of random walks and diffusion processes, that describe the probability of spontaneous extinction and the size distribution of surviving initiated populations when the death/differentiation rates of normal and initiated cells are known. The constraint that the nonmalignant population size must remain approximately constant leads to much simpler analytic formulas and approximations, flowing directly from random walk theory, than in previous birth-death models.(ABSTRACT TRUNCATED AT 250 WORDS)     

Re-Figuring Marked Bodies on the Borders: Breast Cancer and “Femininity”

The author discusses writings by Eve Kosofsky Sedgwick, Kathleen Martindale, Audre Lorde, and Barbara Rosenblum on their experiences with breast cancer, and explores their articulations of the impact mastectomy has had on their sense of femininity in relation to their own identities and body images, and in relation to cultural expectations, and how others perceive them. Their identification of the body as socially produced, and as a site of contestation and multiple struggles, offers a strategic site from which to engage with the violent gender-inflected notion of the ideal female body. Themes addressed include: the process of writing embodied experience to make it real, the body's role in the process of identity formation, the culturally constructed significance of appearance to the individual's sense of femininity, the value of the female body in a capitalistic society, and heterosexism in society and in the health care system.     

Exploring the Association Between Dispositional Cancer Worry,Perceived Risk,and Physical Activity Among College Women

Abstract

Objective: In this study, the authors explored the association between dispositional cancer worry (DCW), risk perceptions (RP), and physical activity (PA) among college females. Participants: Four hundred fifty-one females from a midwestern university completed an online survey in September/October 2012. Methods: DCW severity, DCW frequency, RP, and PA were measured along with qualitative data about PA as cancer prevention. Results: Sixty-nine percent of participants did not meet PA recommendations. DCW severity was a significant predictor of meeting PA recommendations (odds ratio = 1.2, 95% confidence interval [1.00, 1.38]; p = .05). Qualitative data revealed a lack of knowledge about breast cancer risk and PA as cancer prevention. Conclusions: College women do not engage in enough PA nor feel at risk for developing breast cancer. A lack of knowledge exists about the cancer prevention benefit of PA. Results indicate a need for PA interventions that both educate breast cancer risk and motivate health protective behaviors.     

Body mass index and functional status in community dwelling older Turkish males

Abstract

Objectives: To assess sex hormones in men with obesity and prostate cancer (PCa) and to study association between androgens and the pathogenesis biology of PCa in vitro.

Subjects and methods: One hundred and eighty-one men older than 45?years selected from of a population attending to Urology departments screening for PCa, (78 participants without PCa and 103 patients with PCa). All participants were assessed for body mass index (BMI), age, Gleason score, and PSA. Endocrine profile was determined for LH, total testosterone (TT), 17β-estradiol (E2), prolactin and leptin. Biochemical profile (HbA1c, triacylglycerols and lipoproteins) was also determined. In vitro experiments were also performed, involving the study of 5α-dihydrotestosterone (DHT) and E2 in the presence of adipocyte-conditioned medium (aCM).

Results: All variables were continuous and described a Gaussian distribution unless mentioned. To determine the relation of aggressiveness, variable were transformed into categories. Thus, PCa aggressiveness is associated with the increase of age and BMI (p?<?.0001) but with is decreased with TT and E2 (p?<?.05). Moreover, adipocyte-secreted molecules increase aggressiveness of PCa cells in vitro. Lastly, DTH but not E2 enables invasiveness in vitro.

Conclusions: It was observed a coexistence of hormone axis profile alteration with sex hormones and BMI in PCa patients, in accordance with the new perspective of PCa pathogenesis.