[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-detail-116111-en":3,"doc-seo-116111-105":31,"detail-sidebar-cat-0-en-105":93},{"code":4,"msg":5,"data":6},0,"success",{"doc_id":7,"user_id":8,"nickname":9,"user_avatar":10,"doc_module":4,"category_id":11,"category_name":12,"doc_title":13,"doc_description":14,"doc_content":15,"file_id":16,"file_url":17,"file_type":18,"file_size":19,"view_count":20,"is_deleted":4,"is_public":21,"is_downloadable":21,"audit_status":21,"page_count":22,"language":23,"language_code":24,"site_id":25,"html_lang":24,"table_of_contents":26,"faqs":27,"seo_title":28,"seo_description":14,"update_tm":29,"read_time":30},116111,13056712833777,"Logic","https://ap-avatar.wpscdn.com/davatar_29158cc5080c5b710cf443261637dec0",7,"Healthcare","Cancer Biology - How Science Works - Second Edition","Cancer Biology - How Science Works - Second Edition examines cancer as a heterogeneous set of disorders driven by uncontrolled cellular growth and shaped by both genomic and epigenomic alterations. The text explains how malignant tumors emerge through long tumorigenesis processes that include changes in cellular identity, signaling responsiveness, and transcriptomic architecture. It also links cancer risk to aging and environmental influences while emphasizing prevention through modifiable lifestyle factors and the immune system’s role in detection and elimination.","Carsten Carlberg Eunike Velleuer  \nCancer Biology  \nHow Science Works  \nSecond Edition  \nCancer Biology  \nCarsten Carlberg • Eunike Velleuer  \nCancer Biology How Science Works  \nSecond Edition  \nCarsten Carlberg   \nInLife, Institute of Animal Reproduction Polish Academy of Sciences  \nOlsztyn, Poland  \nSchool of Medicine, Institute of Biomedicine  \nUniversity of Eastern Finland Kuopio, Finland  \nEunike Velleuer   \nDepartment for Cytopathology Heinrich-Heine University Düsseldorf Düsseldorf, Germany  \nDepartment for Pediatric Hemato-Oncology Helios Children’s Hospital  \nKrefeld, Germany  \nISBN 978-3-032-18588-4 ISBN 978-3-032-18589-1 (eBook)  \n[https://doi.org/10.1007/978-3-032-18589-1](https://doi.org/10.1007/978-3-032-18589-1)  \n1st Edition: Cancer Biology: How Science Works, © Springer Nature Switzerland AG 2021  \n© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2021, 2026  \nThis work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed.  \nThe use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.  \nThe publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.  \nThis Springer imprint is published by the registered company Springer Nature Switzerland AG  \nThe registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland If disposing of this product, please recycle the paper.  \nPreface  \nThis book begins with sobering news: approximately one in two individuals in highincome countries will receive a cancer diagnosis during their lifetime, meaning a malignant tumor will be detected in their body. Yet there is encouraging news as well: fewer than half of all cancer patients die from the disease, and every second cancer-related death is preventable. Cancer is not a single disease but a heterogeneous group of disorders that can arise in virtually any organ. What they all share is uncontrolled cellular growth.  \nEvery newly diagnosed malignant tumor in adulthood reflects an individual history of two or more decades of tumorigenesis. Cancer is traditionally viewed as a disease of the genome, driven by accumulated DNA point mutations, as well as chromosomal translocations, deletions, and amplifications. Tumorigenesis also involves profound alterations in cellular identity, responsiveness to internal and external signals, and major shifts in the transcriptome. These changes are rooted inepigenomic dysregulation. In fact, most cancers harbor mutations and alterations not only in their genomes but also in their epigenomes.  \nCells in our body have the capacity to grow when needed: during wound healing or in the continuous renewal of blood, skin, and intestinal tissues. Because malignant transformation is typically slow, cancer is largely an age-related disease, one that seems inevitable as we grow older. Yet tumorigenesis depends on numerous environmental influences, including the ability of the immune system to detect and ","cbCaisbFEQLRpSKx","https://ap.wps.com/l/cbCaisbFEQLRpSKx","pdf",37058920,5,1,246,"English","en",105,"# Preface\n## Epidemiology and impact of cancer diagnosis\n## Tumorigenesis: genome and epigenome alterations\n## Cellular growth, aging, and immune surveillance\n## Prevention through lifestyle choices\n## Foundations of basic biology and disease mechanisms\n## Scope and educational linkage of the book","[{\"question\":\"How does the book describe what cancer is?\",\"answer\":\"Cancer is presented as a heterogeneous group of disorders rather than a single disease. All share uncontrolled cellular growth.\"},{\"question\":\"What mechanisms contribute to tumor development according to the text?\",\"answer\":\"Tumorigenesis involves accumulated DNA point mutations and chromosomal changes, alongside major shifts in cellular identity and transcriptome, rooted in epigenomic dysregulation.\"},{\"question\":\"Which lifestyle factors does the book highlight for cancer risk reduction?\",\"answer\":\"Avoiding smoking, choosing a healthy diet, and staying physically active are emphasized as key lifestyle strategies for lowering cancer risk.\"}]","Cancer Biology - How Science Works - Second Edition | PDF",1785654773,620,{"code":4,"msg":32,"data":33},"ok",{"site_id":25,"language":24,"slug":34,"title":13,"keywords":35,"description":14,"schema_data":36,"social_meta":88,"head_meta":90,"extra_data":92,"updated_unix":29},"cancer-biology-how-science-works-second-edition","",{"@graph":37,"@context":87},[38,55,70],{"@type":39,"itemListElement":40},"BreadcrumbList",[41,45,49,52],{"item":42,"name":43,"@type":44,"position":21},"https://docshare.wps.com","Home","ListItem",{"item":46,"name":47,"@type":44,"position":48},"https://docshare.wps.com/document/","Document",2,{"item":50,"name":12,"@type":44,"position":51},"https://docshare.wps.com/document/healthcare/",3,{"item":53,"name":13,"@type":44,"position":54},"https://docshare.wps.com/document/cancer-biology-how-science-works-second-edition/116111/",4,{"url":53,"name":13,"@type":56,"author":57,"headline":13,"publisher":59,"fileFormat":62,"inLanguage":24,"description":14,"dateModified":63,"datePublished":64,"encodingFormat":62,"isAccessibleForFree":65,"interactionStatistic":66},"DigitalDocument",{"name":9,"@type":58},"Person",{"url":42,"name":60,"@type":61},"DocShare","Organization","application/pdf","2026-08-17","2026-08-02",true,{"@type":67,"interactionType":68,"userInteractionCount":20},"InteractionCounter",{"@type":69},"ViewAction",{"@type":71,"mainEntity":72},"FAQPage",[73,79,83],{"name":74,"@type":75,"acceptedAnswer":76},"How does the book describe what cancer is?","Question",{"text":77,"@type":78},"Cancer is presented as a heterogeneous group of disorders rather than a single disease. 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