Environment, testicular dysgenesis and carcinoma in situ testis

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Environment, testicular dysgenesis and carcinoma in situ testis. / Olesen, Inge A; Sonne, Si Brask; Hoei-Hansen, Christina E; Rajpert-DeMeyts, Ewa; Skakkebaek, Niels E.

In: Best Practice & Research: Clinical Endocrinology & Metabolism, Vol. 21, No. 3, 2007, p. 462-78.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Olesen, IA, Sonne, SB, Hoei-Hansen, CE, Rajpert-DeMeyts, E & Skakkebaek, NE 2007, 'Environment, testicular dysgenesis and carcinoma in situ testis', Best Practice & Research: Clinical Endocrinology & Metabolism, vol. 21, no. 3, pp. 462-78. https://doi.org/10.1016/j.beem.2007.04.002

APA

Olesen, I. A., Sonne, S. B., Hoei-Hansen, C. E., Rajpert-DeMeyts, E., & Skakkebaek, N. E. (2007). Environment, testicular dysgenesis and carcinoma in situ testis. Best Practice & Research: Clinical Endocrinology & Metabolism, 21(3), 462-78. https://doi.org/10.1016/j.beem.2007.04.002

Vancouver

Olesen IA, Sonne SB, Hoei-Hansen CE, Rajpert-DeMeyts E, Skakkebaek NE. Environment, testicular dysgenesis and carcinoma in situ testis. Best Practice & Research: Clinical Endocrinology & Metabolism. 2007;21(3):462-78. https://doi.org/10.1016/j.beem.2007.04.002

Author

Olesen, Inge A ; Sonne, Si Brask ; Hoei-Hansen, Christina E ; Rajpert-DeMeyts, Ewa ; Skakkebaek, Niels E. / Environment, testicular dysgenesis and carcinoma in situ testis. In: Best Practice & Research: Clinical Endocrinology & Metabolism. 2007 ; Vol. 21, No. 3. pp. 462-78.

Bibtex

@article{a9f417401f8211df8ed1000ea68e967b,
title = "Environment, testicular dysgenesis and carcinoma in situ testis",
abstract = "The testicular dysgenesis syndrome (TDS) hypothesis proposes that a proportion of the male reproductive disorders-cryptorchidism, hypospadias, infertility and testicular cancer-may be symptoms of one underlying developmental disease, TDS, which is most likely a result of disturbed gonadal development in the embryo. TDS may be caused by genetic factors, environmental/life-style factors, or a combination of both. Some rare disorders of sex development of genetic origin are among the best-known examples of severe TDS. Among the environmental and life-style factors that are suspected to influence the hormonal milieu of the developing gonad are the endocrine disrupters. A prenatal exposure to commonly used chemicals, e.g. phthalates, may result in a TDS-like phenotype in rats. Currently, this animal model is the best model for TDS. In humans the situation is much more complex, and TDS exists in a wide range of phenotypes: from the mildest and most common form, in which impaired spermatogenesis is the only symptom, to the most severe cases, in which the patient may develop testicular cancer. It is of great importance that clinicians in different specialties treating patients with TDS are aware of the association between the different symptoms.",
author = "Olesen, {Inge A} and Sonne, {Si Brask} and Hoei-Hansen, {Christina E} and Ewa Rajpert-DeMeyts and Skakkebaek, {Niels E}",
note = "Keywords: Animals; Carcinogens, Environmental; Carcinoma in Situ; Endocrine Disruptors; European Continental Ancestry Group; Female; Genital Diseases, Male; Gonadal Dysgenesis; Humans; Male; Neoplasms, Germ Cell and Embryonal; Rats; Spermatogenesis; Testicular Neoplasms; Testis",
year = "2007",
doi = "10.1016/j.beem.2007.04.002",
language = "English",
volume = "21",
pages = "462--78",
journal = "Best Practice and Research in Clinical Endocrinology and Metabolism",
issn = "1521-690X",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Environment, testicular dysgenesis and carcinoma in situ testis

AU - Olesen, Inge A

AU - Sonne, Si Brask

AU - Hoei-Hansen, Christina E

AU - Rajpert-DeMeyts, Ewa

AU - Skakkebaek, Niels E

N1 - Keywords: Animals; Carcinogens, Environmental; Carcinoma in Situ; Endocrine Disruptors; European Continental Ancestry Group; Female; Genital Diseases, Male; Gonadal Dysgenesis; Humans; Male; Neoplasms, Germ Cell and Embryonal; Rats; Spermatogenesis; Testicular Neoplasms; Testis

PY - 2007

Y1 - 2007

N2 - The testicular dysgenesis syndrome (TDS) hypothesis proposes that a proportion of the male reproductive disorders-cryptorchidism, hypospadias, infertility and testicular cancer-may be symptoms of one underlying developmental disease, TDS, which is most likely a result of disturbed gonadal development in the embryo. TDS may be caused by genetic factors, environmental/life-style factors, or a combination of both. Some rare disorders of sex development of genetic origin are among the best-known examples of severe TDS. Among the environmental and life-style factors that are suspected to influence the hormonal milieu of the developing gonad are the endocrine disrupters. A prenatal exposure to commonly used chemicals, e.g. phthalates, may result in a TDS-like phenotype in rats. Currently, this animal model is the best model for TDS. In humans the situation is much more complex, and TDS exists in a wide range of phenotypes: from the mildest and most common form, in which impaired spermatogenesis is the only symptom, to the most severe cases, in which the patient may develop testicular cancer. It is of great importance that clinicians in different specialties treating patients with TDS are aware of the association between the different symptoms.

AB - The testicular dysgenesis syndrome (TDS) hypothesis proposes that a proportion of the male reproductive disorders-cryptorchidism, hypospadias, infertility and testicular cancer-may be symptoms of one underlying developmental disease, TDS, which is most likely a result of disturbed gonadal development in the embryo. TDS may be caused by genetic factors, environmental/life-style factors, or a combination of both. Some rare disorders of sex development of genetic origin are among the best-known examples of severe TDS. Among the environmental and life-style factors that are suspected to influence the hormonal milieu of the developing gonad are the endocrine disrupters. A prenatal exposure to commonly used chemicals, e.g. phthalates, may result in a TDS-like phenotype in rats. Currently, this animal model is the best model for TDS. In humans the situation is much more complex, and TDS exists in a wide range of phenotypes: from the mildest and most common form, in which impaired spermatogenesis is the only symptom, to the most severe cases, in which the patient may develop testicular cancer. It is of great importance that clinicians in different specialties treating patients with TDS are aware of the association between the different symptoms.

U2 - 10.1016/j.beem.2007.04.002

DO - 10.1016/j.beem.2007.04.002

M3 - Journal article

C2 - 17875492

VL - 21

SP - 462

EP - 478

JO - Best Practice and Research in Clinical Endocrinology and Metabolism

JF - Best Practice and Research in Clinical Endocrinology and Metabolism

SN - 1521-690X

IS - 3

ER -

ID: 18150744