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Testicular cancer (TC) is the most frequent solid malignancy in young men aged between 15 and 40 years. The worldwide incidence is about 7.5 per 100,000 subjects, but the rates vary considerably between countries and ethnic groups. About 95% of all TCs are represented by testicular germ cell tumors (TGCTs), which include seminoma and non-seminoma histological types. It has been reported that about 18,000 European subjects over reproductive age develop a TGCT every year and its incidence is increasing in several countries over the past 50 years. Early diagnosis and modern treatment have resulted in over 95% survival rate and improved quality of life in testicular cancer survivors. However, the benefits of cancer treatments may hide some risks. In fact, possible side effects can be developed during the treatment itself or later from months to years after the completion of therapy, persisting during the whole life. Therefore, TGCT survivors frequently complain a number of healthy problems such as infertility, hypogonadism, metabolic syndrome, osteoporosis, sexual disorders, depressed mood, and in general impaired quality of life. This aspect is the most serious and potentially life threatening effect in TGCT survivors. Many risk factors have been studied as a pre-disposing factor in the development of this cancer, but only for some there is a high level of evidence. In recent times, progressive increases in the incidence of male reproductive disorders inclusive of hypospadias, cryptorchidism, poor semen quality, and testicular cancer, suggested a common foetal origin. The central hypothesis of this observation asserted that these disorders may all collectively signify testicular dysgenesis syndrome (TDS). It is generally assumed that the development of TGCT is under endocrine control. In particular, unbalanced androgen/estrogen levels and/or activity during embryogenesis, are believed to represent the key events for TGCT development and progression. Furthermore, recent evidence has suggested genetic association of TGCT with variations in genes involved in hypothalamic-pituitary-testicular axis and steroidogenic enzymes. Therefore, hormonal carcinogenesis is an important and controversial area of current research in TGCT, and further attention is given to endocrine environment influencing testicular development during foetal life. The objective of this Research Topic is to group a collection of articles focused on new and more recent insights about TGCT.

testis cancer --- genetics --- male infertility --- sexual function --- cancer treatment

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Testicular cancer (TC) is the most common cancer in males aged 20-40 years, with a worldwide incidence of 7.5 per 100,000, but the rates vary considerably between countries and ethnic groups and there is evidence also for an increasing incidence in last decades. About 95% of all TCs are represented by testicular germ cell tumors (TGCTs), which include seminoma and non-seminoma histological types. It is generally assumed that the development of TGCT is under endocrine control. In particular, unbalanced androgen/estrogen levels and/or activity are believed to represent the key events for TGCT development and progression. Furthermore, recent evidence has suggested genetic association of TGCT with variations in genes involved in hypothalamic-pituitary-testicular axis and steroidogenic enzymes. This recent evidence expands the current knowledge on the role of genetic contribution in testicular cancer susceptibility, and supports the hypothesis that variations in hormone metabolism genes might change the hormonal environment implicated in testicular carcinogenesis. Therefore, hormonal carcinogenesis is an important and controversial area of current research in TGCT, and further attention is given to genetic factors influencing hormone-related cancer risk. The genetic component to TGCT is in general strong. In fact, although environmental factors clearly contribute to TGCT development (and probably to its increasing incidence in some geographical areas), the proportion of TGCT susceptibility accounted for by the genetic effects is estimated at 25%. TGCT has high familial risks compared with most other cancer types that are generally no more than two-fold: brothers of individuals with TGCT have an 8- to 12-fold increased risk of disease, and sons of affected individuals have a 4- to 6-fold increased risk. Despite this strong familial relative risk, early results from linkage studies identified a limited relationship with genetic factors, suggesting that TGCT is a genetically complex trait. However, more recently, four genome-wide association studies (GWAS) from the UK and USA have reported association of TGCTs with six new loci (KITLG, SPRY4, BAK1, DMRT1, TERT, and ATF7IP). The strongest association for TGCT susceptibility was found for SNPs in KITLG (ligand for the membrane-bound receptor tyrosine kinase KIT) gene with a greater than 2.5-fold increased risk of disease per major allele, which is the highest reported for any cancer to date. These studies are being now replicated by other researches and attention is given to the relationship between these genetic variations, TGCT risk and frequently associated anomalies of the reproductive tract, such as cryptorchidism and infertility. Finally, over the past few decades, TCGT research has focused also on external environmental causes acting mainly as endocrine disrupters of androgen and oestrogen pathways, even during the foetal development of the testis. It is well known that the testicular dysgenesis syndrome (TDS) hypothesis, proposed ten years ago, suggests that disturbed testicular development in fetal life may result in one or more of four disorders postnatally, named cryptorchidism, hypospadias, poor semen quality, and TGCT. These four disorders are therefore considered as one clinical entity and are linked together by epidemiological and pathophysiological relations. The relative contribution of genetics and environment in TGCT development, and the interactions between endocrine disruptors and variations in genes involved in hormonal carcinogenesis is therefore another interesting area of research.

Germ cell tumor --- KITLG --- cancer genetics --- testis cancer --- Cryptorchidism --- Endocrine Disruptors --- Germ cell tumor --- KITLG --- cancer genetics --- testis cancer --- Cryptorchidism --- Endocrine Disruptors

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Testicular cancer (TC) is the most common cancer in males aged 20-40 years, with a worldwide incidence of 7.5 per 100,000, but the rates vary considerably between countries and ethnic groups and there is evidence also for an increasing incidence in last decades. About 95% of all TCs are represented by testicular germ cell tumors (TGCTs), which include seminoma and non-seminoma histological types. It is generally assumed that the development of TGCT is under endocrine control. In particular, unbalanced androgen/estrogen levels and/or activity are believed to represent the key events for TGCT development and progression. Furthermore, recent evidence has suggested genetic association of TGCT with variations in genes involved in hypothalamic-pituitary-testicular axis and steroidogenic enzymes. This recent evidence expands the current knowledge on the role of genetic contribution in testicular cancer susceptibility, and supports the hypothesis that variations in hormone metabolism genes might change the hormonal environment implicated in testicular carcinogenesis. Therefore, hormonal carcinogenesis is an important and controversial area of current research in TGCT, and further attention is given to genetic factors influencing hormone-related cancer risk. The genetic component to TGCT is in general strong. In fact, although environmental factors clearly contribute to TGCT development (and probably to its increasing incidence in some geographical areas), the proportion of TGCT susceptibility accounted for by the genetic effects is estimated at 25%. TGCT has high familial risks compared with most other cancer types that are generally no more than two-fold: brothers of individuals with TGCT have an 8- to 12-fold increased risk of disease, and sons of affected individuals have a 4- to 6-fold increased risk. Despite this strong familial relative risk, early results from linkage studies identified a limited relationship with genetic factors, suggesting that TGCT is a genetically complex trait. However, more recently, four genome-wide association studies (GWAS) from the UK and USA have reported association of TGCTs with six new loci (KITLG, SPRY4, BAK1, DMRT1, TERT, and ATF7IP). The strongest association for TGCT susceptibility was found for SNPs in KITLG (ligand for the membrane-bound receptor tyrosine kinase KIT) gene with a greater than 2.5-fold increased risk of disease per major allele, which is the highest reported for any cancer to date. These studies are being now replicated by other researches and attention is given to the relationship between these genetic variations, TGCT risk and frequently associated anomalies of the reproductive tract, such as cryptorchidism and infertility. Finally, over the past few decades, TCGT research has focused also on external environmental causes acting mainly as endocrine disrupters of androgen and oestrogen pathways, even during the foetal development of the testis. It is well known that the testicular dysgenesis syndrome (TDS) hypothesis, proposed ten years ago, suggests that disturbed testicular development in fetal life may result in one or more of four disorders postnatally, named cryptorchidism, hypospadias, poor semen quality, and TGCT. These four disorders are therefore considered as one clinical entity and are linked together by epidemiological and pathophysiological relations. The relative contribution of genetics and environment in TGCT development, and the interactions between endocrine disruptors and variations in genes involved in hormonal carcinogenesis is therefore another interesting area of research.

Germ cell tumor --- KITLG --- cancer genetics --- testis cancer --- Cryptorchidism --- Endocrine Disruptors

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Cancer of the Testis presents a thorough account of every aspect of this disease, including histology, risk factors, prognosis, clinical presentation, diagnosis and treatment. Additionally, there is a focus on the pertinent issues of fertility, late effects of primary therapy, follow-up after primary treatment and testicular cancer in childhood. With an international authorship comprised of many of the key contributors to the field, this book brings together a rich and balanced range of perspectives. A state-of-the-art reference volume on testicular cancer, this book is essential reading for urologists, medical oncologists and radio-oncologists. M. Pilar Laguna, MD PhD, is an Associate Professor in Urology at the University of Amsterdam, The Netherlands. Peter Albers, MD, is Chairman of the Department of Urology at Dusseldorf University, Germany. Carsten Bokemeyer, MD, is Director of Oncology and Hematology at Hubertus Wald Tumorzentrum at the University Medical Center in Hamburg, Germany. Jerome P. Richie, MD, is the Elliot C. Cutler Professor of Urologic Surgery at Harvard Medical School and Chief of Urology at Brigham and Women’s Hospital in Boston, USA.

Testis -- Cancer -- Treatment. --- Testis -- Cancer. --- Endocrine Gland Neoplasms --- Testicular Diseases --- Genital Neoplasms, Male --- Genital Diseases, Male --- Urogenital Neoplasms --- Neoplasms by Site --- Endocrine System Diseases --- Gonadal Disorders --- Testicular Neoplasms --- Diseases --- Neoplasms --- Male Urogenital Diseases --- Medicine --- Health & Biological Sciences --- Oncology --- Urology & Nephrology --- Testis --- Generative organs, Male --- Cancer. --- Medicine. --- Radiology. --- Oncology. --- Urology. --- Medicine & Public Health. --- Imaging / Radiology. --- Cancer in men --- Oncology  . --- Radiology, Medical. --- Clinical radiology --- Radiology, Medical --- Radiology (Medicine) --- Medical physics --- Tumors --- Genitourinary organs --- Radiological physics --- Physics --- Radiation

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Prostate cancer is by far the most common cancer in men and the second leading cause of death due to cancer. It comprises a mixed group of tumours displaying varying clinical behaviour: while some have a very aggressive course, others are rather indolent. Prevention of prostate cancer and discrimination between aggressive and indolent forms are important clinical goals, and the acquisition of significant new evidence on means of achieving these aims makes this book particularly timely.   A wide range of topics are covered by leading authorities in the field. The biology and natural history of prostate cancer are reviewed, and the role of lifestyle and dietary factors, assessed. Detailed attention is paid to risk prediction biomarkers and to the role of novel high-throughput nucleic acid-based technologies in improving risk prediction and thereby allowing tailored approaches to cancer prevention. Potential means of chemoprevention of prostate cancer are also reviewed in depth, covering the very positive new data on the impact of aspirin as well as evidence regarding 5α-reductase inhibitors, DFMO, and lycopene. Guidance is provided on the differentiation of aggressive from indolent disease, and the policy and research implications of recent findings are examined. This book will be of interest to both clinicians and researchers.

Cancer. --- Prostate -- Cancer -- Popular works. --- Testis -- Cancer. --- Prostate --- Genital Neoplasms, Male --- Risk --- Investigative Techniques --- Psychology, Social --- Prostatic Diseases --- Drug Therapy --- Biological Factors --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Urogenital Neoplasms --- Probability --- Genital Diseases, Male --- Behavior and Behavior Mechanisms --- Chemicals and Drugs --- Therapeutics --- Male Urogenital Diseases --- Psychiatry and Psychology --- Statistics as Topic --- Neoplasms by Site --- Epidemiologic Methods --- Diseases --- Neoplasms --- Biological Markers --- Chemoprevention --- Prostatic Neoplasms --- Risk Assessment --- Diet --- Risk Factors --- Life Style --- Medicine --- Health & Biological Sciences --- Oncology --- Prevention --- Cancer --- Prevention. --- Medicine. --- Cancer research. --- Oncology. --- Urology. --- Medicine & Public Health. --- Cancer Research. --- Genitourinary organs --- Tumors --- Cancer research --- Clinical sciences --- Medical profession --- Human biology --- Life sciences --- Medical sciences --- Pathology --- Physicians --- Oncology  .