Hormone-Dependent Cancers

Hormones influence not only breast and prostate cancer, the two most common hormone-dependent cancers, but also have a major impact on less common hormone-sensitive malignancies (e.g. ovary, testes, endometrium) as well as human cancers recently discovered to be hormone sensitive (e.g. lung, liver). Developing a means to more specifically treat and ideally prevent hormone-dependent cancers is of critical importance given the significant impact these malignancies have on human health and the economic burden of disease. An in depth understanding of hormone action in regulating diverse cellular processes, cancer phenotypes and drug responsiveness is essential for the development of effective and well tolerated treatment strategies.

The concept of hormone-dependence of cancers arose from experimental study of the activity of prostatic glands, of both the normal and malignant sort. Does the cancer cell possess qualities of its normal progenitor? Yes. Indeed, some cancers retain characteristics of their normal antecedents. Among these is hormone-responsiveness.

Hormone-related cancers, namely breast, endometrium, ovary, prostate, testis, thyroid and osteosarcoma, share a unique mechanism of carcinogenesis. Endogenous and exogenous hormones drive cell proliferation, and thus the opportunity for the accumulation of random genetic errors. The emergence of a malignant phenotype depends on a series of somatic mutations that occur during cell division, but the specific genes involved in progression of hormone-related cancers are currently unknown. In this review, the epidemiology of endometrial cancer and breast cancer are used to illustrate the paradigms of hormonal carcinogenesis. Then, new strategies for early detection and prevention of hormonal carcinogenesis are discussed. This includes developing polygenic models of cancer predisposition and the further development of safe and effective chemopreventives that block target sequence activity. We developed polygenic models for breast and prostate cancer after hypothesizing that functionally relevant sequence variants in genes involved in steroid hormone metabolism and transport would act together, and also interact with well-known hormonally related risk factors, to define a high-risk profile for cancer. A combination of genes each with minor variation in expressed activity could provide a degree of separation of risk that would be clinically useful as they could yield a large cumulative difference after several decades.

 

 

 

The concept of hormone-dependence of cancers arose from experimental study of the activity of prostatic glands, of both the normal and malignant sort. Does the cancer cell possess qualities of its normal progenitor? Yes. Indeed, some cancers retain characteristics of their normal antecedents. Among these is hormone-responsiveness.

Hormone-related cancers, namely breast, endometrium, ovary, prostate, testis, thyroid and osteosarcoma, share a unique mechanism of carcinogenesis. Endogenous and exogenous hormones drive cell proliferation, and thus the opportunity for the accumulation of random genetic errors. The emergence of a malignant phenotype depends on a series of somatic mutations that occur during cell division, but the specific genes involved in progression of hormone-related cancers are currently unknown. In this review, the epidemiology of endometrial cancer and breast cancer are used to illustrate the paradigms of hormonal carcinogenesis. Then, new strategies for early detection and prevention of hormonal carcinogenesis are discussed. This includes developing polygenic models of cancer predisposition and the further development of safe and effective chemopreventives that block target sequence activity. We developed polygenic models for breast and prostate cancer after hypothesizing that functionally relevant sequence variants in genes involved in steroid hormone metabolism and transport would act together, and also interact with well-known hormonally related risk factors, to define a high-risk profile for cancer. A combination of genes each with minor variation in expressed activity could provide a degree of separation of risk that would be clinically useful as they could yield a large cumulative difference after several decades.

 

 

 

The concept of hormone-dependence of cancers arose from experimental study of the activity of prostatic glands, of both the normal and malignant sort. Does the cancer cell possess qualities of its normal progenitor? Yes. Indeed, some cancers retain characteristics of their normal antecedents. Among these is hormone-responsiveness.

Hormone-related cancers, namely breast, endometrium, ovary, prostate, testis, thyroid and osteosarcoma, share a unique mechanism of carcinogenesis. Endogenous and exogenous hormones drive cell proliferation, and thus the opportunity for the accumulation of random genetic errors. The emergence of a malignant phenotype depends on a series of somatic mutations that occur during cell division, but the specific genes involved in progression of hormone-related cancers are currently unknown. In this review, the epidemiology of endometrial cancer and breast cancer are used to illustrate the paradigms of hormonal carcinogenesis. Then, new strategies for early detection and prevention of hormonal carcinogenesis are discussed. This includes developing polygenic models of cancer predisposition and the further development of safe and effective chemopreventives that block target sequence activity. We developed polygenic models for breast and prostate cancer after hypothesizing that functionally relevant sequence variants in genes involved in steroid hormone metabolism and transport would act together, and also interact with well-known hormonally related risk factors, to define a high-risk profile for cancer. A combination of genes each with minor variation in expressed activity could provide a degree of separation of risk that would be clinically useful as they could yield a large cumulative difference after several decades.

 

 

 

 

 

 

 

 

 

 

  • Hormone- Dependence and Metabolism
  • Resistance, prevention and treatment
  • Breast Cancer
  • Ovarian and Cervical Cancer
  • Case reports: Success rates

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