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Book
Testis cancer: Genes, environment, hormones
Authors: ---
Year: 2015 Publisher: Frontiers Media SA

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Abstract

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.


Book
Testis cancer: Genes, environment, hormones
Authors: ---
Year: 2015 Publisher: Frontiers Media SA

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Abstract

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.


Book
Testis cancer: Genes, environment, hormones
Authors: ---
Year: 2015 Publisher: Frontiers Media SA

Loading...
Export citation

Choose an application

Bookmark

Abstract

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.


Book
Operative techniques in breast, endocrine, and oncologic surgery
Authors: ---
ISBN: 1496319087 9781496319081 9781451190212 1451190212 1975176502 Year: 2015 Publisher: Philadelphia : Wolters Kluwer,

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Abstract

"With an emphasis on the "hows and whys" of contemporary surgery, Operative Techniques in Breast, Endocrine, and Oncologic Surgery, Second Edition, features concise, bulleted text, full-color illustrations, and intraoperative photographs to clarify exactly what to look for and how to proceed. Drawn from the larger Operative Techniques in Surgery, Second Edition, this concise, stand-alone surgical atlas, overseen by editor-in-chief Mary T. Hawn and meticulously edited by Dr. Michael S. Sabel, focuses on the steps of each technique, rapidly directing you to the information you need to choose the right approach for each patient, perform it successfully, and achieve the best possible results. Provides comprehensive, step-by-step guidance on breast surgery and reconstruction; cutaneous oncology; and endocrine surgery Covers open as well as laparoscopic, endoscopic, robotic, and video-assisted procedures in breast, endocrine, and oncologic surgery Features new videos, personally selected by contributing authors and editors, that accompany numerous chapters throughout the book Contains extensive updates throughout, including new coverage of the American Board of Surgery's SCORE Curricula for General Surgery and for Complex General Surgical Oncology Follows the same format for each procedure: differential diagnosis, patient history and physical findings, imaging and other diagnostic studies, surgical management, techniques, pearls and pitfalls, postoperative care, outcomes, and complications Enrich Your eBook Reading Experience Read directly on your preferred device(s), such as computer, tablet, or smartphone. Easily convert to audiobook, powering your content with natural language text-to-speech. "--

Keywords

Investigative Techniques --- Breast Diseases --- Nevi and Melanomas --- Neuroendocrine Tumors --- Surgical Procedures, Operative --- Neoplasms by Site --- Reconstructive Surgical Procedures --- Cosmetic Techniques --- Neoplasms --- Neoplasms by Histologic Type --- Neuroectodermal Tumors --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Skin Diseases --- Therapeutics --- Diseases --- Neoplasms, Nerve Tissue --- Neoplasms, Germ Cell and Embryonal --- Skin and Connective Tissue Diseases --- Methods --- Breast Neoplasms --- Mammaplasty --- Melanoma --- Endocrine Surgical Procedures --- Surgery & Anesthesiology --- Health & Biological Sciences --- Surgery - General and By Type --- Endocrine Surgical Procedure --- Procedure, Endocrine Surgical --- Procedures, Endocrine Surgical --- Surgical Procedure, Endocrine --- Surgical Procedures, Endocrine --- Malignant Melanoma --- Malignant Melanomas --- Melanoma, Malignant --- Melanomas --- Melanomas, Malignant --- Mammoplasty --- Breast Reconstruction --- Breast Reconstructions --- Mammaplasties --- Mammoplasties --- Reconstruction, Breast --- Reconstructions, Breast --- Breast --- Breast Carcinoma --- Cancer of the Breast --- Human Mammary Carcinoma --- Malignant Neoplasm of Breast --- Malignant Tumor of Breast --- Mammary Cancer --- Mammary Carcinoma, Human --- Mammary Neoplasm, Human --- Mammary Neoplasms, Human --- Neoplasms, Breast --- Tumors, Breast --- Breast Cancer --- Breast Tumors --- Cancer of Breast --- Breast Carcinomas --- Breast Malignant Neoplasm --- Breast Malignant Neoplasms --- Breast Malignant Tumor --- Breast Malignant Tumors --- Breast Neoplasm --- Breast Tumor --- Cancer, Breast --- Cancer, Mammary --- Cancers, Mammary --- Carcinoma, Breast --- Carcinoma, Human Mammary --- Carcinomas, Breast --- Carcinomas, Human Mammary --- Human Mammary Carcinomas --- Human Mammary Neoplasm --- Human Mammary Neoplasms --- Mammary Cancers --- Mammary Carcinomas, Human --- Neoplasm, Breast --- Neoplasm, Human Mammary --- Neoplasms, Human Mammary --- Tumor, Breast --- Breast Cancer Lymphedema --- Methodological Studies --- Methodological Study --- Procedures --- Studies, Methodological --- Study, Methodological --- Method --- Procedure --- Cancer, Embryonal --- Cancer, Embryonal and Mixed --- Embryonal Neoplasms --- Germ Cell Neoplasms --- Germ Cell and Embryonal Neoplasms --- Germ Cell and Embryonic Neoplasms --- Neoplasms, Embryonal --- Neoplasms, Germ Cell --- Neoplasms, Germ Cell and Embryonic --- Germ Cell Cancer --- Germ Cell Tumor --- Neoplasms, Embryonal and Mixed --- Cancer, Germ Cell --- Cancers, Embryonal --- Cancers, Germ Cell --- Embryonal Cancer --- Embryonal Cancers --- Embryonal Neoplasm --- Germ Cell Cancers --- Germ Cell Tumors --- Neoplasm, Embryonal --- Tumor, Germ Cell --- Tumors, Germ Cell --- Neoplasms, Nervous Tissue --- Nerve Tissue Neoplasms --- Nervous Tissue Neoplasms --- Neoplasm, Nerve Tissue --- Neoplasm, Nervous Tissue --- Nerve Tissue Neoplasm --- Nervous Tissue Neoplasm --- Therapy --- Treatment --- Therapeutic --- Therapies --- Treatments --- Disease --- Dermatosis --- Dermatoses --- Skin and Subcutaneous Tissue Disorders --- Skin Disease --- Dermatology --- Neuroectodermal Tumor --- Tumor, Neuroectodermal --- Tumors, Neuroectodermal --- Cosmetic Technics --- Cosmetic Technic --- Cosmetic Technique --- Technic, Cosmetic --- Technics, Cosmetic --- Technique, Cosmetic --- Techniques, Cosmetic --- Dermal Fillers --- Dermatologic Surgical Procedures --- Cosmetic Reconstructive Surgery --- Procedure, Reconstructive Surgical --- Procedures, Reconstructive Surgical --- Reconstructive Surgery --- Reconstructive Surgical Procedure --- Reconstructive Surgical Procedures, Esthetic --- Surgical Procedure, Reconstructive --- Surgical Procedures, Reconstructive --- Cosmetic Reconstructive Surgical Procedures --- Reconstructive Surgical Procedures, Cosmetic --- Cosmetic Reconstructive Surgeries --- Reconstructive Surgeries --- Reconstructive Surgeries, Cosmetic --- Reconstructive Surgery, Cosmetic --- Surgeries, Cosmetic Reconstructive --- Surgeries, Reconstructive --- Surgery, Cosmetic Reconstructive --- Surgery, Reconstructive --- Surgery, Plastic --- Neoplasms by Sites --- Site, Neoplasm --- Sites, Neoplasm --- Neoplasm Site --- Neoplasm Sites --- Ghost Surgery --- Operative Procedures --- Operative Surgical Procedure --- Operative Surgical Procedures --- Procedure, Operative Surgical --- Procedures, Operative Surgical --- Surgery, Ghost --- Surgical Procedure, Operative --- Surgical Procedures --- Operative Procedure --- Procedure, Operative --- Procedure, Surgical --- Procedures, Operative --- Procedures, Surgical --- Surgical Procedure --- General Surgery --- Neuroendocrine Tumor --- Tumor, Neuroendocrine --- Tumors, Neuroendocrine --- Melanomas and Nevi --- Endocrine Breast Diseases --- Breast Disease --- Breast Disease, Endocrine --- Breast Diseases, Endocrine --- Disease, Breast --- Disease, Endocrine Breast --- Diseases, Breast --- Diseases, Endocrine Breast --- Endocrine Breast Disease --- Histological Type of Neoplasm --- Histological Types of Neoplasms --- Neoplasms by Histological Type --- Neoplasm Histological Type --- Neoplasm Histological Types --- Neoplasms Histological Type --- Neoplasms Histological Types --- Benign Neoplasms --- Malignancy --- Malignant Neoplasms --- Neoplasia --- Neoplasm --- Neoplasms, Benign --- Cancer --- Tumors --- Benign Neoplasm --- Cancers --- Malignancies --- Malignant Neoplasm --- Neoplasias --- Neoplasm, Benign --- Neoplasm, Malignant --- Neoplasms, Malignant --- Tumor --- Medical Oncology --- Investigative Technics --- Investigative Technic --- Investigative Technique --- Technic, Investigative --- Technics, Investigative --- Technique, Investigative --- Techniques, Investigative --- therapy --- Surgery. --- Endocrine glands

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