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Role of hormones in endometrial cancer
Contents:
  1. When is hormone therapy used?
  2. Hormone Therapy for Breast Cancer | American Cancer Society
  3. What to know about breast cancer

In the next decade, women who began use as teenagers will reach their late 40s and early 50s. At that time, it will be important to re-examine the effects of long-term and early use of COCs. Hormone replacement therapy increases the risk of breast cancer. A recent meta-analysis that included over women showed that for current or recent use of HRT, the risk of breast cancer increases in relation to increasing duration of use Although this study was large and comprehensive, it may still fail to determine the true risk of breast cancer that can be attributed to HRT since many differences between HRT users and non-users exist.

Users of HRT may have different opportunities for breast cancer diagnosis. For example, they may have more frequent mammographic and physician examinations. Women with a family history of breast cancer are more likely to be non-users, and HRT users are likely to be of higher social class and education. Laya et al. Finally, genetic determinants, like those that determine endogenous hormone levels, may also play a role in determining HRT use. The idea that endogenous levels of circulating hormones are the primary determinants of cancer risk is troubling, since endogenous hormones are not an easily modifiable risk factor, like diet or smoking.

We simply cannot remove or lower endogenous hormones to reduce cancer risk. Thus, we are forced to develop new strategies for early detection and prevention. These new strategies are just beginning to be explored.

When is hormone therapy used?

In the area of early detection, we must identify biomarkers of high risk, such as specific genotypes. In the area of prevention, new chemopreventives, such as tamoxifen, offer hope to high-risk individuals that cancer can be prevented. Although there is evidence that hormonal secretion and metabolism can be environmentally influenced, for example through diet and physical activity, the control of hormonal patterns is largely genetically regulated. Thus, we must begin to characterize the complex genetic arrays that contribute to carcinogenesis in hormone-responsive tissue and identify candidate loci in genes responsible for inter-individual differences in steroid hormone levels.

These loci are likely to be relevant sequence variants involved in steroid hormone metabolism and transport. We have proposed a multigenic model of breast cancer predisposition that includes several genes involved in estrogen biosynthesis and intracellular binding and transport of E2 based on the assumption that individual variation in the levels of endogenous steroid hormones will result in differences in breast cancer risk 3.

We have hypothesized that this individual variation results from polymorphisms in crucial genes which control hormone biosynthesis and transport. Recent findings suggesting a role of CYP17 in the etiology of breast cancer are presented below. This base pair change creates a recognition site for the Msp AI restriction enzyme and has been used to designate two alleles, A1 the published sequence and A2.

Different treatment options for benign vs malignant tumors

Carey et al. They found an association but not linkage between the affected state and the A2 allele. We were the first to show an association between risk of breast cancer and this CYP17 polymorphism In a case-control study of incident breast cancer among Asian, African-American and Latina women, we found a 2. This suggested that serum hormone levels may differ by CYP17 genotype. We pursued this finding in a separate study and found that CYP17 genotype was associated with serum estradiol and progesterone levels among young nulliparous women These data provide direct evidence of genetic control of serum hormone levels; however, the sample size was small and the results needed confirmation and further exploration.

A recent study conducted among a group of post-menopausal women supports our findings. Haiman et al. As shown in Table III , the results are inconsistent and show evidence of heterogeneity across ethnicity. Clearly, further work is necessary to resolve theses apparent inconsistencies. However, these data show how a multi-gene model of susceptibility based on a hormone biosynthesis can help us understand the underlying etiology of hormone-dependent tumors.

Hormone Therapy for Breast Cancer | American Cancer Society

We have applied a similar model to the study of prostate cancer. The two most important risk factors for prostate cancer are age and ethnicity. Prostate cancer is rare before 40 years of age, but the rate of increase with aging is greater than for any other cancer. African-American men have the highest incidence of prostate cancer in the world.

Unfortunately, adequate data do not exist on prostate cancer rates among Blacks in Africa. Lowest rates of prostate cancer are seen among Asian populations Native Japanese and Chinese men. Japanese- and Chinese-American men have rates higher than men in their respective homelands; however, their rates still remain much lower than US Caucasians 4. Years of epidemiologic research has failed to uncover any environmental agents or lifestyle risk factors that can explain these pronounced differences found across different ethnic groups.

Like breast cancer, risk of prostate cancer appears to be explained by endogenous hormone levels 4 , 56 , In developing a model of prostate carcinogenesis, genes involved in androgen biosynthesis, activation, inactivation and transport are all of interest. AR is responsible for androgen transport, SRD5A2 encodes the enzyme responsible for converting testosterone to the metabolically more active dihydrotestosterone, and CYP17 as described above encodes an enzyme that functions at key branch points in human steroidogenesis.

HSD3B2 has a dual role: it encodes an enzyme that catalyzes a critical reaction in testosterone biosynthesis, and it is involved in the metabolism of dihydrotestosterone in the prostate possibly different isozymes. Because of this dual role of HSD3B2 , it is difficult to predict how functional variants of this gene might relate to prostate cancer risk.

Analysis of this marker suggested that a series of alleles with a relatively high number of repeats 17 or greater was unique to African-Americans and somewhat more common in African-American men with prostate cancer compared with healthy African-American men The V89L substitution showed marked differences among ethnic groups.

Although the A49T mutation is uncommon in healthy men, it confers very high risk, especially for advanced prostate cancer. Androgen receptor activity has been shown to be negatively correlated with the number of CAG repeats, and several groups 61 — 65 have reported an association with the polyglutamine AR and risk of prostate cancer. A third polymorphic marker at the AR locus has also been evaluated 4. A Stu I single-nucleotide polymorphism at codon , which designates two alleles, S1 and S2 , is located roughly halfway between the two trinucleotide repeats.

Among African-American men the S1 allele was associated with a statistically significant 3-fold increased risk of prostate cancer among men under the age of 65 years. An excess proportion of this allele was also found among prostate cancer cases with an affected brother. The Stu I polymorphism did not seem to simply reflect short CAG repeats as a function of linkage disequilibrium.

These preliminary data suggest that among African-American men, non-CAG repeat variation at the AR locus might contribute to hereditary prostate cancer. This molecular model that is being developed for prostate cancer, and the similar model for breast cancer, illustrate the importance of molecular biology studies and epidemiologic studies working collaboratively to understand the disease process. We must begin thinking of these hormonally based cancers as being complex genetic traits and begin to both expand these models and develop similar multigenic models for the other hormone-related cancers.

In Table IV , we provide a summary of likely candidate genes for such models. Findings from last year's highly publicized tamoxifen trial provide the first information from a randomized clinical trial to support the hypothesis that breast cancer can be prevented among high risk women These findings have to be tempered by variables that remain unknown.

It is not known whether tamoxifen benefits women with BRCA mutations, nor whether the results of this trial apply to women of ethnic minorities. It is still to be determined whether this reduction in incidence is just a delay in the onset of tumor development and, if so, how long tamoxifen can be safely administered. The risks and benefits of tamoxifen chemoprevention, and other cancer chemopreventives that are on the horizon, must be weighed carefully. While tamoxifen reduces the risk of certain breast cancers and bone fractures, it increases the risk of endometrial cancer.

Whether tamoxifen can reduce the incidence of heart disease is unknown, and data from the trial suggests the drug may increase the risk of stroke and cataracts. Similarly, chemopreventive treatments may decrease prostate cancer incidence and mortality, while avoiding surgery related morbidity. Although the nationwide trial is just beginning, the chemopreventive potential of finasteride was investigated in a small group of men with elevated serum PSA.

Although the drug effectively lowered serum PSA, more men using finasteride progressed to prostate cancer than men who did not take the inhibitor The reasons for this unexpected finding may include that finasteride alters prostate size and therefore prostate tumor detection rate, or that finasteride alters the balance of DHT and testosterone levels in such a way that increases prostate cancer risk. The genetic basis of endogenous hormone levels as an important risk factor for hormone-dependent tumors has only recently been recognized.


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Long thought to be largely environmentally caused cancers, it is now increasingly obvious that genetic susceptibility, through germline polymorphisms in metabolic genes, plays a critical role. Some of the hormone-related cancers, e.

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The control of these cancers rests first on the recognition of the genetic basis of each cancer, and secondly on developing suitable interventions that block target sequence activity. Tamoxifen and finesteride are early candidate therapies in breast and prostate cancer, respectively, and their activity is still under active investigation. Estradiol and, to a lesser degree, other steroid hormones, drive cell proliferation which facilitates fixation of genetic errors. Germline mutations in relevant tumor suppressor genes accelerate the transformation into the malignant phenotype.

Geometric mean serum E2 concentrations among young nulliparous women on days 11 and 22 of the menstrual cycle by CYP17 genotype. Geometric mean serum progesterone Prg concentrations among young nulliparous women on day 22 of the menstrual cycle by CYP17 genotype. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Sign In. Advanced Search. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents.

Role of hormones in endometrial cancer. Role of hormones in breast cancer. Exogenous hormones. New directions in hormonal carcinogenesis. Concluding remarks. Hormonal carcinogenesis Brian E. Oxford Academic. Google Scholar.

Heather Spencer Feigelson. Cite Citation. Permissions Icon Permissions. Add to Wishlist. USD Sign in to Purchase Instantly. Overview The growth and function of many tissues are influenced by hormones. Therefore it is quite understandable that hormones play a role in the development and treatment of malignant tumors.

Numerous publications address this topic; however, the results of many studies are controversial and have not been unequivocally accepted. For nearly 50 years the carcinogenic effect of steroid hormones has been under debate, and their therapeutic value a matter of discussion for equally as long. Through a joint approach from the field of molecular biology, biochemistry, and histopathology, advances in the management of these tumors have been elaborated.

Antihormones, i.

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What to know about breast cancer

Further improvements can be expected in the localization of hormones in tumor tissue by specific antibodies. A special chapter is dedicated to the diffuse endocrine cell system DECS , the clinical significance of which has mainly become obvious in the gastroenteropancreatic tract. Product Details Table of Contents. Table of Contents Biological Basics. Show More. Average Review. Write a Review.

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