Hormones, Genes, and Cancer

Hormones, Genes, and Cancer

Hormones, Genes, and Cancer

Hormones, Genes, and Cancer

Synopsis

Hormonal carcinogenesis is an important and controversial area of current research. In addition to accelerating existing cancers, can hormones play the role of primary carcinogens? How do genetic factors influence hormone-related cancer risk? Hormones, Genes, and Cancer addresses these questions. Over the past few decades, cancer research has focused on external environmental causes(e.g., tobacco smoke, viruses, asbestos). With the advent of new genetic sequencing techniques, we are just now beginning to understand how the body's internal environment(i.e., the hormones and growth factors that determine normal development) influences cancer etiology and prevention. From molecular insights to clinical analyses, this volume provides state-of-the-art information on the complex interactions between hormones and genes and cancer. The epidemiology and molecular endocrinology of prostate, breast, uterine, ovarian and testicular cancer are detailed in this timely treatise.

Excerpt

The concept that hormones are an important part of the carcinogenic process, at least in some organs, was initiated over 100 years ago by the observations of Beatson on the relationship between cancer of the breast and ovarian function. Subsequent experimental studies in rodents by Bittner demonstrated that hormones could increase the risk of mammary cancer. In parallel, Rous and Kidd and later Berenblum popularized the multistage concept of carcinogenesis. Elegant studies of the carcinogenic process in skin led to the generalization that carcinogenesis was, at a basic level, a two-stage process, involving initiation and promotion. By the 1950s, it was generally believed that there were three classes of initiators, viruses, chemicals, and certain physical agents, such as radiation. Hormones were considered to be promoters, capable of accelerating the carcinogenic process, but only in the aftermath of exposure to a carcinogenic initiator. The three classes of initiator shared the property of potential direct DNA damage, i.e., genotoxicity. In contrast, hormones were generally not directly genotoxic, their proliferative effects could be reversed, and their role in carcinogenesis aborted, by their removal as a source of stimulation. Whereas carcinogen-induced tumors are autonomous at the outset, those related to excessive hormonal stimulation pass through a prolonged stage of growth and progress to autonomy only late, if at all, in the carcinogenic process. Thus, although hormones were considered to be important in accelerating an existing cancer, they were not generally believed to be primary carcinogens.

INTERNATIONAL VARIATION
IN RATES

The remarkable international variation in cancer rates, for many of the common cancers, such as breast and prostate, seemed to many to support the traditional view that endogenous hormones could not be the sole or primary cause. The low rates of breast, prostate, and several other cancers in Asian populations and their increase toward Western rates upon migration to the United States or Europe suggested that chemical factors or other environmental agents were the major causes of these cancers. While cigarette smoking was one such obvious chemical carcinogen, which would help to explain the international variation in lung and other smoking-related cancer sites, the most obvious cause of the other cancers seemed to be diet, other lifestyle factors, or unidentified environmental agents. In 1964, an expert committee of the World Health Organization stated that [the categories of cancer that are thus influenced, directly or indirectly, by extrinsic factors…collectively account for more than three-quarters of human cancers.]

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