Medical hypothesis: xenoestrogens as preventable causes of breast cancer.

Changes in documented risk factors for breast cancer and rates of screening cannot completely explain recent increases in incidence or mortality. Established risk factors for breast cancer, including genetics, account for at best 30% of cases. Most of these risk factors can be linked to total lifetime exposure to bioavailable estrogens. Experimental evidence reveals that compounds such as some chlorinated organics, polycyclic aromatic hydrocarbons (PAHs), triazine herbicides, and pharmaceuticals affect estrogen production and metabolism and thus function as xenoestrogens. Many of these xenoestrogenic compounds also experimentally induce mammary carcinogenesis. Recent epidemiologic studies have found that breast fat and serum lipids of women with breast cancer contain significantly elevated levels of some chlorinated organics compared with noncancer controls. As the proportion of inherited breast cancer in the population is small, most breast cancers are due to acquired mutations. Thus, the induction of breast cancer in the majority of cases stems from interactions between host factors, including genetics and environmental carcinogens. We hypothesize that substances such as xenoestrogens increase the risk of breast cancer by mechanisms which include interaction with breast-cancer susceptibility genes. A series of major epidemiologic studies need to be developed to evaluate this hypothesis, including studies of estrogen metabolism, the role of specific xenoestrogenic substances in breast cancer, and relevant genetic-environmental interactions. In addition, experimental studies are needed to evaluate biologic markers of suspect xenoestrogens and biologic markers of host susceptibility and identify pathways of estrogenicity that affect the development of breast cancer. If xenoestrogens do play a role in breast cancer, reductions in exposure will provide an opportunity for primary prevention of this growing disease.(ABSTRACT TRUNCATED AT 250 WORDS

Adiabatic limit and the slow motion of vortices in a Chern-Simons-Schr\"odinger system

We study a nonlinear system of partial differential equations in which a complex field (the Higgs field) evolves according to a nonlinear Schroedinger equation, coupled to an electromagnetic field whose time evolution is determined by a Chern-Simons term in the action. In two space dimensions, the Chern-Simons dynamics is a Galileo invariant evolution for A, which is an interesting alternative to the Lorentz invariant Maxwell evolution, and is finding increasing numbers of applications in two dimensional condensed matter field theory. The system we study, introduced by Manton, is a special case (for constant external magnetic field, and a point interaction) of the effective field theory of Zhang, Hansson and Kivelson arising in studies of the fractional quantum Hall effect. From the mathematical perspective the system is a natural gauge invariant generalization of the nonlinear Schroedinger equation, which is also Galileo invariant and admits a self-dual structure with a resulting large space of topological solitons (the moduli space of self-dual Ginzburg-Landau vortices). We prove a theorem describing the adiabatic approximation of this system by a Hamiltonian system on the moduli space. The approximation holds for values of the Higgs self-coupling constant close to the self-dual (Bogomolny) value of 1. The viability of the approximation scheme depends upon the fact that self-dual vortices form a symplectic submanifold of the phase space (modulo gauge invariance). The theorem provides a rigorous description of slow vortex dynamics in the near self-dual limit.Comment: Minor typos corrected, one reference added and DOI give