Prevention, Risk Identification & Reduction, and Etiology

Grants listed in this section have in common an interest in understanding the underlying causes of breast cancer, from either an epidemiologic point of view, looking at associations between health-related behaviors and other risk factors in the environment, or from a biologic point of view looking at events at the cellular and genetic levels. From an understanding of the causes comes the basis for effective preventive actions.

Prevention, Risk Identification and Reduction:

The BCRP’s primary goal is to reduce the human and economic costs of breast cancer, and reducing the occurrence of the disease can do this most effectively. Prevention in the field of public health is subdivided into primary, secondary, or tertiary prevention. Primary prevention for breast cancer can be thought of as prevention of initiation of the disease, by inhibiting the changes in precursor cells to cancer, or preventing the progression of abnormal cells into invasive cancer. Secondary prevention aims at the earliest possible detection and maximization of efforts to limit the adverse consequences of the disease, thereby improving survival and quality of life. Although early detection is often spoken of loosely as a "prevention" effort, the distinction between true prevention (primary prevention) and early detection (secondary prevention) is an important one for the BCRP. Thus, grants dealing with early detection will be found in the Early Detection section in this compendium. (Tertiary prevention, concerned with rehabilitation and prevention of further disease-related deterioration, is not a priority area of the BCRP.)

In this cycle, the BCRP funded 4 grants that have the potential to provide information that can be applied to prevent the initiation of cancer by providing a sound basis for limiting exposure to environmental risk factors that are thought to increase an individuals’ chances of getting breast cancer. One grant (Anna H. Wu, PI) looks at the importance of genetic/environmental interactions. It is possible that some individuals’ genetic makeup is such that they are more susceptible than other people to certain compounds common in the environment (formed in the cooking of meats and in tobacco smoke). Two projects examine the potential of bovine leukemia virus, which is found in milk, to infect breast epithelial cells in culture (Gertrude Buehring, PI and Linda Kingsbury, PI). Finally, another study examines the breast cancer incidence among flight attendants, who are exposed to radiation, ozone, hazardous components of jet exhaust and time zone and schedule changes (Peggy Reynolds, PI).

Nutritional factors continue to be of interest in breast cancer prevention. One such project is aimed at understanding the role of an active component of certain vegetables, indole-3-carbinol, in modulating the cell cycle as a mechanism of primary prevention (Gary Firestone, PI).

It is strongly suspected that the appearance of a woman’s breast on a mammogram may be predictive of breast cancer risk in certain women (a topic of study in a Cycle II BCRP grant). However, whether and to what extent this appearance is an inherited characteristic and to what extent an environmentally influenced one is not known. This question will be investigated in a study of identical twins (Thomas Mack, PI). If breast density is an important predictor of cancer risk, analysis of the relative importance of genetic and environmental influences on breast density can potentially focus attention on those risk factors that could be modified; furthermore, breast density (and changes in density) could potentially be used to evaluate interventions designed to reduce breast cancer risk.

Breast cancer risk is known to be lessened by pregnancy at a young age. An exploratory project to begin to search for specific genetic differences in breast epithelial cells from virgin and parous rats attempts to uncover the basis for such a protective effect (Satyabrata Nandi, PI).

Etiology:

The BCRP etiology priority issue addresses the causes of breast cancer with a focus on the unique ethnic, racial, and environmentally impacted groups of California. The urgency of this priority issue is underscored by the different incidences and morbidity of breast cancer in these groups. The BCRP is particularly concerned about the impact of breast cancer on groups of women having less access to health care, available information, and specific research knowledge. Collectively we refer to these groups as ‘underserved’, a concept we hope to challenge the research community to address. For example, although African-American women in California have a lower incidence of breast cancer, they are diagnosed at later stages and the prognosis is poorer in this group. Likewise, although Asian women also have lower breast cancer incidence, it is appreciated that cultural and lifestyle changes could expose future generations to an increased risk. Thus, etiology-based projects can uncover the molecular and physiological basis of different risk factors as well as protective factors that could be sources of future prevention or treatment.

The role of estrogen is well appreciated as a breast cancer risk factor, and a newly funded study investigates a candidate gene that regulates estrogen production (Gerhard Coetzee, PI). Estrogen can affect cellular physiology by altering levels of nitric oxide to affect glucose transport necessary for cell growth (Thomas Balon, PI). The variability of vitamin D receptor genes is thought to influence breast cancer risk (Sue Ingles, PI), which is believed to be a significant factor impacting African-American women. Finally, three population studies were funded to investigate: (i) hormone receptors interfacing with other risk factors (Shelley Enger, PI), (ii) levels of physical activity and its association with the age of menarche (Carol Koprowski, PI), and (iii) risk factors for breast cancer among lesbians (Stephanie Roberts and Suzanne Dibble, co-PIs).

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Request For Application (RFA) Awards

Mammogram Density, Cancer, Inheritance and Acquired Risk in Twins

Thomas M. Mack, M.D., M.P.H.
University of Southern California

Currently available risk factors for breast cancer are not very useful on a population basis in identifying women at high risk for purposes of targeted intervention. Using the mammograms of normal women, the proportion of the mammographic area that is relatively dense appears to be a stronger and more comprehensive predictor of breast cancer than any other practical index. If true, not only could this factor single out women for special intervention, it might also serve as a surrogate or "stand-in" representing breast cancer risk for testing interventions more quickly and at much lower than usual cost. That is, rather than having to follow a group of women for many years to see if a certain intervention has resulted in fewer cancers, it might be possible, over a shorter time, to see if there were changes in breast density (as shown on a mammogram) as a result of the intervention. However, before mammograms can be considered for these purposes, the predictive value obtained using them must be assessed under stringent conditions and the determinants of mammographic density that are heritable and those that are acquired during a woman’s life better understood.

We will identify twin pairs from a pool of 2500 pairs who are known to have had screening mammograms since 1984 and within 5 years of each other. Of these twin pairs, 550 are pairs in whom one twin has had breast cancer and in whom the healthy twin had a mammogram within 5 years of her twin’s mammographic diagnosis. The remaining 1950 pairs are healthy pairs from whom, as from the affected pairs, information on breast cancer risk factors has been systematically collected. Among these healthy pairs are at least 200 pairs who differ with respect to each of 10 environmental risk factors for breast cancer. We expect to obtain permission from each member of 330 affected and 1365 healthy twin pairs to borrow their normal mammograms from the mammographers. We will scan each mammogram, and using a semi-computerized method of distinguishing areas of different density, we will estimate the proportion of the area of the breast image represented by densities.

For the pairs in whom one twin has had breast cancer, we will compare the mammographic density from the (healthy breast) mammograms of the cases to those of the same breast of their healthy twins. This will allow us to verify the degree to which mammographic density is predictive of breast cancer.

We will compare the mammographic density differences between the mammograms from the members of identical twin pairs to the differences between the mammograms from the members of female fraternal twin pairs. This will tell us whether the degree of density is a heritable factor.

To assess the role played by individual environmental breast cancer risk factors, we will compare the density of mammograms from persons who have had a pertinent environmental exposure or experience to the density of the mammogram from their unexposed identical twins. This will tell us whether the exposure is likely to be related to mammographic density.

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Gene-Diet/Tobacco Interactions in Breast Cancer in Asians

Anna H. Wu, Ph.D.
University of Southern California

Approximately half of the breast cancer cases in the U.S. cannot be explained by familial, menstrual or reproductive factors. Moreover, the established risk factors that have been identified are not easily modifiable. Thus, research to identify lifestyle-related risk factors for breast cancer that are modifiable is a priority.

There are a number of compounds found in the environment to which humans can be easily exposed that are known to cause both genetic changes and cancer in the breast cells of rodents. These compounds may also play a role in the development of human breast cancer. (The scientific names for the classes of the compounds that we are interested in are: heterocyclic aromatic amines (HAs); polycyclic aromatic hydrocarbons (PAHs); and arylamines. Humans are exposed to these compounds from various environmental sources including diet (e.g., cooked meats) and tobacco smoke. However, for these compounds to exert their cancer-causing effects they have to be chemically transformed (i.e., activated or deactivated). A number of human genes have now been identified and shown to be important in the metabolism of these chemical compounds.

Due to the difficulty in measuring the part of peoples diet that is affected by cooking conditions (mostly through using questionnaires), the role of PAHs and HAs in the diet has been largely unstudied. Numerous studies have investigated the role of tobacco smoke and breast cancer but the results are not clear. The reason for this might be due to the varying proportions of women in a given study population who possess genes that "turn on" (i.e., metabolically activate) or that "turn off" (metabolically deactivate) this chemical transformation. Thus, the goal for this study is to determine whether the genes involved in the metabolism of these compounds are associated with risk of breast cancer.

If we can demonstrate that certain genes (called NAT1, NAT2, CYP1A1, GSTM1) involved in the metabolism of HAs (from cooked meats), PAHs (from cooked meats and tobacco smoke) and arylamines (from tobacco smoke) are associated with risk of breast cancer, it will strengthen the argument that these exposures from diet and tobacco are risk factors for breast cancer, help explain how breast cancer is caused, and provide a sound basis for diet and smoking behavior modification.

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Innovative, Developmental, and Exploratory Awards

 

Nitric Oxide’s Role in Breast Cancer Metabolism and Growth

Thomas W. Balon, Ph.D.
City of Hope National Medical Center

It is well known that cancer cells have an enhanced ability to turn certain sugars, such as glucose, into energy for growth. The ability of cells to actively take in sugars ultimately determines the cell’s ability to grow. Nitric oxide is a very common molecule that is found in almost all cells, but the amount is elevated in certain cancers. Recently, we have determined that nitric oxide plays a major role in altering glucose transport in different types of cells and tissues. The overall specific aim of this project is to define the role of nitric oxide in the regulation of glucose transport and growth in breast cancer cells. This project will test the following hypotheses:

  1. Nitric oxide will increase glucose transport in breast cancer cells more than in normal breast cells,
  2. Estrogen, a hormone that is mainly produced by the female reproductive system, will increase glucose transport in certain breast cancer cells by increasing their nitric oxide production,
  3. Regulation of glucose uptake by nitric oxide and high concentrations of another sugar, fructose, will determine the ability of the breast cancer cells to grow.

We will study compounds that turn nitric oxide production on or off in normal and cancerous breast cells to test our experimental hypotheses.

The data generated from this series of experiments should help define nitric oxide’s role in altering sugar transport and ultimately a breast cancer cell’s ability to grow. The potential use and effectiveness of different nitric oxide producing and restricting drugs, which have been used for cardiovascular dysfunction, may ultimately be recognized for their potential ability to arrest breast cancer cell growth.

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Bovine Leukemia Virus and Human Breast Cancer Risk

Gertrude C. Buehring, Ph.D.
University of California, Berkeley

The purpose of this research is to determine whether 1) humans can become infected with bovine leukemia virus; 2) such an infection occurs through consumption of foodstuffs from infected cows; 3) infection with BLV could lead to developing breast cancer. It is well established that breast cancer in the mouse is caused by a virus, the mouse mammary tumor virus (MMTV), which is passed from mother to nursing babies via the milk. Mouse breast cancer is proof that a naturally occurring cancer can be caused by a virus swallowed in a food source. Attempts to find an analogous virus in human milk passed from mother to baby have failed. Since humans drink more cow milk than they do human milk, perhaps cows would be a more promising target in the search for a milk-transmitted agent of human breast cancer. Bovine leukemia virus (BLV) is a cancer-causing virus of cattle which can be passed from mother cow to calf via the milk. BLV commonly infects dairy and beef cattle and is found in the marketed milk and meat of these animals. Most infected cattle do not actually develop leukemia, but remain healthy and are not removed from the herd. Consumption of unpasteurized dairy products or undercooked beef could possibly allow transmission of infectious virus to humans. BLV infections are not limited to cattle. The virus can infect sheep and non-human primates experimentally and cause cancer in the sheep. In the laboratory it can infect the cells of many species including humans and other primates. We recently discovered that BLV may infect the breast cells of cows and cause these cells to behave more like cancer cells. This indicates that the tissue preference of this "leukemia" virus is not limited to blood cells.

We propose here a pilot study to examine the first aspect of the overall proposal, whether humans can become infected with BLV. Human breast tissues removed during surgery, breast tissue sections received from a pathologist, cells from milk and colostrum, and blood cells will be searched for evidence of different components of BLV using cellular and molecular techniques (immunocytochemistry, PCR, and in situ reverse transcriptase PCR). Human blood will be tested for antibodies to BLV. Our preliminary results suggest that the breast cells of some women are infected with BLV and that some humans have antibodies to BLV. The potential impact of the project is through prevention of these cancers by elimination of BLV in cattle, interception of its transmission from cattle to humans, or vaccination of humans.

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Estrogen Biosynthesis and Breast Cancer Risk

Gerhard A. Coetzee, Ph.D.
University of Southern California

The past 20 years of research have identified numerous risk and protective factors for breast cancer, many of which can be understood as being associated with differences in lifetime exposure to the female hormone, estrogen. In general, estrogen causes increased cell division in breast cells and this is thought to increase the chance of errors in the genetic material of some cells, resulting in cancer development.

Recently, two genes have been identified (called BRCA1 and 2), each one greatly enhancing the chance for breast cancer when any one of them carrying a mutation is inherited by a woman. However, it is estimated that only about 5% of all breast cancer in the U.S. is attributable to mutations in these two genes. We and others have proposed that several other genes might also contribute to breast cancer risk. Many such genes might each contribute only modestly to the risk of getting breast cancer. However, in the population at large, they might play important roles in combination due to their high prevalence. One such class of genes code for enzymes that control the formation of estrogen; the more active the enzyme, the more estrogen will be synthesized, the higher the risk is for breast cancer development. In this study we will focus on a candidate gene, called CYP17. This gene codes for the enzyme that specifically controls the ultimate formation of all estrogen in the body. Variant forms of this gene might be inherited by a woman. We have identified certain variant forms that might increase the risk for developing breast cancer, and this project will attempt to understand how these changes can cause differences in the enzyme’s activity and how these differences in turn might be related to risk of developing breast cancer. We believe that the basic information forthcoming from this, and other studies like this, will lead to the better understanding of the known family associations of breast cancer. Such knowledge, combined with information of other genes, might ultimately lead to the rational formulation of risk assessment of breast cancer in the general population.

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Dietary Indole Inhibition of Breast Cancer

Gary Firestone, Ph.D.
University of California, Berkeley

There is a growing public and scientific interest in the influence of hormonally active substances in the diet on both the risk to develop breast cancer and the potential to control breast cancer with minimal side effects. The best drug treatment currently available for women with breast cancer is hormone therapy. The growth of approximately one-third of breast cancers is stimulated by estrogen, so treating patients with anti-estrogens (e.g., tamoxifen) will slow the growth of certain tumors. However, tamoxifen therapy is associated with many side effects. Our interest is focused on naturally occurring compounds in the diet that could either prevent or slow the growth of breast cancer. Of particular importance is the identification and characterization of dietary compounds that can act independently of estrogen and, for some patients, potentially be used in combination with anti-estrogen therapy to more effectively reduce breast cancer growth. A compound called indole-3-carbinol (I3C) is one such dietary substance present in cabbage, broccoli, and Brussels sprouts. I3C is currently undergoing phase 1 clinical trials as a therapy for human breast cancer patients, although relatively little is known about the molecular mechanism of its growth inhibitory effects.

We have determined that I3C can inhibit the growth of both estrogen-responsive and non-responsive human breast cancer cell lines. Our hypthothesis is that I3C can inhibit breast cancer cell growth through a cellular pathway that is independent of the cellular effects of estrogen. Recent experiments show that I3C dramatically reduces the level of an important protein, called CDK6, that helps control a growth regulatory process called the cell cycle. Our research goal is to determine the functional and proliferative consequences for the dietary indole regulation of the CDK6 cell cycle protein in cultured human breast cancer cells and in breast cancer cell-derived tumors. Molecular experimental strategies will be employed to alter the expression of CDK6 so that its level remains elevated in cultured human breast cancer cells even after treatment with I3C. In these laboratory generated breast cancer cells, we plan to assess the effects of up to one week treatments with I3C on the regulation of cell cycle component activities and the rate of DNA synthesis, which is a measure of cell growth. A second critical aim of the study will be to determine the effects of expressing large amounts of CDK6 on the ability of I3C to inhibit the growth of breast cancer cell derived tumors formed in mice. Determining the molecular mechanism by which I3C inhibits breast cancer cell growth will be important because dietary I3C potentially represents an easily obtainable anti-cancer agent to the general public for the potential use in the treatment and prevention of breast cancer at a low cost.

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Vitamin D Receptor Gene and Breast Cancer Risk

Sue Ingles, Dr. P.H.
University of Southern California

Previous evidence suggests that vitamin D, by interacting with vitamin D receptors in the breast and other tissues, prevents cancer. The vitamin D receptor (VDR) plays a key role in this process, and occurs in at least two different genetic types. Individuals who inherit the "weak" type of VDR gene from both parents may be at increased risk of breast cancer. Treatment with vitamin D or modified forms of vitamin D might be useful for prevention of breast cancer or its progression in these individuals.

We plan to study several VDR genetic markers as well as blood vitamin D levels in women with and without breast cancer. This information may help us to understand how "weak" VDR genes influence cancer risk and may help us create better tests for the "weak" VDR gene. If we are able to demonstrate that "weak" VDR genes are associated with breast cancer risk, we may be able to identify susceptible individuals who are candidates for prevention studies. Improvement of vitamin D status may have an especially large impact in the African-American population, which is known to be more susceptible to vitamin D deficiency due to less efficient production of vitamin D precursors by sunlight in darker skinned individuals. Because the high-risk form of the VDR gene is relatively common in all ethnic groups, this work could lead to a significant reduction in the economic and human cost of breast cancer in California.

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Identification of Pregnancy-Associated Breast Cancer Genes

Satyabrata Nandi, Ph.D.
University of California, Berkeley

In humans it is known that a full-term pregnancy (parity) by the age of 18 can permanently reduce the risk of developing breast cancer. Parity in rats and mice also results in refractoriness to chemically induced mammary carcinogenesis. This implies that parity-associated refractoriness against breast cancer is species-indepen-dent. Thus, animals can provide an excellent experimental paradigm to study this process. It has been found that changes in hormonal levels in parous animals and the response of mammary epithelial cells (MEC) play key roles in establishing resistance to chemical carcinogens, when compared to age-matched virgin animal MEC. However, the genetic basis for breast cancer resistance in parous animal is not known. As a first step towards a better understanding of mammary tumorigenesis, it is therefore important to identify genes that have differential activities between virgin (cancer- susceptible) and parous (cancer-refractory) mammary glands. At present, there have been only a few studies on the changes in either gene expression levels or identification of novel genes between parous and virgin animals. Thus, the main goal of this study is to (i) identify genes that are differentially expressed between parous and virgin rat MEC, and (ii) analyze these genes for their functions in cancer and their role in mediating parity-associated refractoriness.

To pursue this goal, the following specific aims are planned. First, differentially expressed genes between virgin and parous MEC will be identified by a method called ‘Differential Display’. This will allow us to isolate specific genes associated with either breast cancer or cancer resistance. Second, the quantitative differences in the genes between parous and virgin animals will be measured by a method called ‘Northern blot’ analysis. Third, the function of candidate genes in relation to mammary cell growth will be studied by introducing them into non-mammary cell lines. Once parity-associated cancer resistance genes are identified and characterized, we hope to generate so-called ‘transgenic animals’ to study them in a whole animal environment.

Clearly, identification of novel genes that play role(s) in parity-associated breast cancer refractoriness and eventual characterization of their physiological function will provide an experimental paradigm that can be used to develop strategies for the prevention of human breast cancer.

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Breast Cancer Incidence in California Flight Attendants

Peggy Reynolds, Ph.D.
California Public Health Foundation

Health problems faced by flight personnel have been of concern to workforce members for some time, but have been little studied by the scientific community. Particular concerns include increased exposures to radiation and ozone, exposures to hazardous components of jet exhaust and time zone and schedule changes. These exposures are consistent with both well-established and suspected risk factors for breast cancer, a disease demonstrated in one small European study to occur nearly twice as often among flight personnel as would be expected in the general population. California-based flight personnel are of particular potential interest in this regard, as they represent a mix of both major domestic and international carrier activity.

This proposal seeks to take advantage of the opportunity to link a large well-defined cohort of flight attendants with the state-of-the-art population-based statewide cancer reporting system maintained by the California Cancer Registry to see if the same risk relationship is evident. This preliminary effort will represent the largest such study to date. If risk associations for breast cancer, or other radiation-associated cancers, appear to be high in this preliminary study of flight attendants, it can serve as the basis for more in depth studies of cancer risk factors in flight personnel.

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Postdoctoral Fellowship Awards


Hormone Receptors and Breast Cancer Survival

Shelley M. Enger, Ph.D.
University of Southern California

We plan to study factors that affect survival from breast cancer. The hormone-receptor status of breast tumors is an important determinant of how a breast cancer patient will respond to therapy, and it is considered when determining a patient’s likelihood of survival. The major types of hormone receptors present on breast cells are estrogen and progesterone receptors. Estrogen receptors bind estrogen, a hormone that stimulates the growth of normal and cancerous breast tissue. Generally, women whose tumors have hormone receptors are more likely to survive than women whose tumors do not have hormone receptors. However, results from a recent study in Norway suggest that among women with similar tumor hormone-receptor status other factors may influence a woman’s chance of dying from her disease. In the study from Norway, the researchers found that overweight women whose breast tumors had hormone receptors were more likely to die from their disease than leaner women whose breast tumors had similar characteristics. We propose to investigate whether body weight and other factors such as prior use of hormone-replacement therapy and physical activity in any way influence the likelihood of death from breast cancer of women with given tumor hormone receptor status.

The study will be carried out at the University of Southern California which has a formal Breast Cancer Research Program at the Norris Comprehensive Cancer Center. Using resources of the University of Southern California Cancer Surveillance Program, the population-based cancer registry for Los Angeles County, we will determine the survival status of women with breast cancer who participated in earlier studies of breast cancer risk factors. This information will then be used to determine a woman’s likelihood of dying given her tumor hormone-receptor status and other information such as her body weight, use of estrogen-replacement therapy, and physical activity levels at the time of her diagnosis with breast cancer.

Despite massive research efforts, breast cancer death rates have not declined over the past decade. Identifying factors that influence disease progression and that are possible to change, such as body weight, physical activity habits or use of estrogen-replacement therapy, would help us better understand how tumors grow. It would give physicians additional strategies for managing their patients’ diseases, and it would allow the patients to take a more active role in their care. In addition, this fellowship will give the Principal Investigator greater experience in breast cancer research, refining her expertise in hormone receptors and breast cancer.

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Bovine Leukemia Virus and Mammary Cell Infection

Linda R. Kingsbury, Ph.D.
University of California, Berkeley

This is a proposal to determine whether humans are susceptible to infection with bovine leukemia virus (BLV). This proposal is based on the hypothesis that infection with BLV may cause breast cancer in humans.

BLV is a cancer-causing virus that infects cattle. It infects the mammary epithelial cells (the cells that make milk and become cancerous in human breast cancer) and B lymphocytes of the cattle, and causes cancers (leukemias and lymphomas) of B lymphocytes in cattle. It is not known whether BLV can also cause mammary cancer in cows, because cows are almost always slaughtered before the "middle and old age" years when they would develop mammary cancer.

Infectious BLV is present in the US meat and milk supply. Oral administration of BLV-contaminated milk can lead to infection in sheep and cattle. Thus there is a potential for BLV to infect humans. Administered experimentally, BLV can infect many different species, including chimpanzees. It can also infect cultured human cell lines. It is not known whether it can actually infect humans.

This proposal is to determine whether humans are susceptible to BLV infection by determining whether human cells have receptors for BLV. Without such receptors, cells cannot easily be infected with the virus. We also want to determine whether human mammary epithelial cells in particular have receptors for BLV. By looking for BLV receptors, we will determine whether humans, and human mammary epithelial cells, are susceptible to BLV infection. If they are not, then it is unlikely that BLV could cause any breast cancers in humans. On the other hand, if humans, and human mammary epithelial cells, do have BLV receptors, this observation will strengthen our hypothesis and lead to further research to determine whether BLV can actually cause human breast cancer. If BLV does cause some types of breast cancer, those cancers can easily be prevented by removing BLV-infected cattle from the food supply, or treating the food supply (e.g. by more thorough cooking) to kill the virus.

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Physical Activity, Diet and Menarche in a Multiethnic Cohort

Carol M. Koprowski, Ph.D.
University of Southern California

Breast cancer is the most commonly diagnosed cancer in women. While the exact cause (or causes) of breast cancer remains unknown, certain features or aspects of a woman’s life appear to increase the chance that she may develop breast cancer during her lifetime. A woman who has her first menstrual period at an early age is more likely to be diagnosed with breast cancer than a woman who has her first menstrual period at a later age. Women who produce an egg during each menstrual cycle are also more likely to be diagnosed with breast cancer compared to women who do not produce an egg at each menstrual cycle.

The primary purpose of this study is to examine certain behaviors, specifically what a woman eats and her amount of physical activity, and how these behaviors relate to when she had her first menstrual period and whether she produced an egg during her menstrual cycles after she began having periods. A group of almost 1400 girls of different ethnic backgrounds were asked questions about their physical activity and the types and amounts of foods they ate. These girls were initially in the 4th through 7th grades and participated in a study that lasted for four years. Each girl was asked about her diet and physical activity up to five times during the course of the study. A total of 180 girls were also tested to see if they produced an egg during menstrual cycles. This information will be analyzed to determine if diet and physical activity are related to a woman’s age at her first menstrual period or whether or not she is likely to produce an egg during her menstrual cycles.

If a relationship is found between physical activity, diet and a woman’s age at her first menstrual period or whether or not she produces an egg during her menstrual cycles, then more information will be available to help explain why some women are more likely to be diagnosed with breast cancer. Also, a woman may be able to change her behavior and possibly lower her chances of being diagnosed with breast cancer. For example, if physical activity decreases the chances that a woman will produce an egg during her menstrual cycles, then encouraging a woman to participate in regular physical activity may be a simple and effective means of lowering her chances of being diagnosed with breast cancer during her lifetime.

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CIRC Award


Breast Cancer Risk Factors: Lesbian and Heterosexual Women

Stephanie A. Roberts, M.D.
Lyon-Martin Women’s Health Services

Suzanne L. Dibble, D.N. Sc.
University of California, San Francisco

In 1993, Dr. Suzanne Haynes, a government scientist, reported that lesbians might have a greater chance of getting breast cancer (1 in 3) than women in general (1 in 8). This was based upon some evidence that lesbians may choose a lifestyle that has been connected with the development of breast cancer (not having any children, not breastfeeding, smoking, drinking). However, there has not been a good scientific study that looks at the differences in these and other breast cancer risk factors between lesbian and heterosexual women.

We plan to look for possible differences by reviewing the medical records of about 1700 women over the age of 35. These records are from visits during 1995 and 1996 to Lyon-Martin Women’s Health Services (LMWHS), a clinic in San Francisco with special outreach to lesbians. Over half of the patients (52%) are lesbian, 40% are heterosexual, and 8% are bisexual. The facts in the records will be kept secret by using a code number rather than a name on all forms. Information from the records will be put into a computer program and the risk factors for breast cancer will be compared between lesbian and heterosexual women.

If we find that there is a difference in risk factors, then doctors and nurses must learn about these differences. Then, they will be better able to provide information to lesbians about their risk of developing breast cancer and other facts that they need to take good care of themselves. Lesbians must also learn about these differences so that they go to a doctor or nurse if they find any lumps or changes in their breasts. The findings from this small study will be checked and expanded with a much larger group of women. Studies will also need to be done to find the best ways to reach lesbians for breast cancer screening.

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