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Chemotherapeutic agents that inhibit growth create strong pressure, rapidly enriching resistant subclones by shifting tumor-cell metabolism and producing a bottleneck. Rare survivors then gain differential reproductive success and pass on an expanded resistant gene pool. The article summarizes tumor evolution, epithelial-mesenchymal transition, and resistance mechanisms specific to cetuximab therapy in head and neck squamous cell carcinoma.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/cetuximab-chemotherapy-resistance-insight-into-the-homeostatic-evolution-of-head-and-neck-cancer-review/330511/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/cetuximab-chemotherapy-resistance-insight-into-the-homeostatic-evolution-of-head-and-neck-cancer-review/330511.png","ImageObject",300,407,{"name":92,"@type":93},"Emma Wilson","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-10","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":39},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What drives the emergence of cetuximab chemotherapy resistance in vivo?","Question",{"text":112,"@type":113},"Chemotherapeutic agents create selective pressure that rapidly enriches resistant subclones. Antineoplastic drugs alter tumor-cell metabolism, producing a bottleneck so only rare resistant cells survive and expand.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does epithelial-mesenchymal transition (EMT) relate to tumor evolution and resistance?",{"text":117,"@type":113},"The review addresses EMT as part of tumor evolution, linking phenotypic changes to the ability of tumors to adapt under therapeutic pressure. These evolutionary steps contribute to resistance in head and neck squamous cell carcinoma.",{"name":119,"@type":110,"acceptedAnswer":120},"What aspects does the review cover for head and neck squamous cell carcinoma?",{"text":121,"@type":113},"It summarizes key findings on tumor evolution, EMT, and resistance to cetuximab therapy. It also discusses related molecular context including EGFR and HNSCC.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},330511,1790012761,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":39,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},3848291630094,"https://eur-avatar.wpscdn.com/davatar_085a072bc5b1113ac321206ff7593b45","ONCOLOGY REPORTS 51: 80, 2024  \nCetuximab chemotherapy resistance: Insight into the homeostatic evolution of head and neck cancer (Review)  \nCARLOS HENRIQUE DE PAULA DINIZ 1 , TIAGO HENRIQUE 1 , ANA CAROLINA B. STEFANINI 1,2 , TIALFI BERGAMIN DE CASTRO 1,3 and ELOIZAH. TAJARA 1,4  \nDepartment of Molecular Biology, School of Medicine of São José do Rio Preto‑FAMERP, São José do Rio Preto,  \n1  \nSão Paulo, SP 15090‑000, Brazil; 2Department of Experimental Research, Albert Einstein Education and Research Israeli Institute, IIEPAE, São Paulo, SP 05652‑900, Brazil; 3Microbial Pathogenesis Department, School of Dentistry, University of Maryland, Baltimore, MD 21201, USA; Department of Genetics and Evolutionary Biology, Institute of Biosciences, University of São Paulo, São Paulo, SP 05508‑090, Brazil  \n4  \nReceived November 22, 2023; Accepted April 3, 2024  \nDOI: 10. 3892/or.2024.8739  \nAbstract. The complex evolution of genetic alterations in cancer that occurs in vivo is a selective process involving numerous factors and mechanisms. Chemotherapeutic agents that prevent the growth and spread of cancer cells induce selec‑ tive pressure, leading to rapid artificial selection of resistant subclones. This rapid evolution is possible because antineo‑ plastic drugs promote alterations in tumor‑cell metabolism, thus creating a bottleneck event. The few resistant cells that survive in this new environment obtain differential reproduc‑ tive success that enables them to pass down the newly selected resistant gene pool. The present review aims to summarize key findings of tumor evolution, epithelial‑mesenchymal tran‑ sition and resistance to cetuximab therapy in head and necksquamous cell carcinoma.  \nContents  \n1. Introduction  \n2. Tumor evolution  \n3. EMT  \n4. EGFR and HNSCC  \n5. CTX therapy, and head and neck carcinoma  \n6. Conclusions  \nCorrespondence to: Professor Eloiza H. Tajara, Department of Molecular Biology, School of Medicine of São José do Rio Preto‑ FAMERP, 5416 Brigadeiro Faria Lima Avenue, Vila São Pedro, São José do Rio Preto, São Paulo, SP 15090‑000, Brazil  \nE‑mail: [tajara@famerp.br](tajara@famerp.br)  \nKey words: tumor evolution, epithelial‑mesenchymal transition, cetuximab, drug resistance, head and neck neoplasms  \n1. Introduction  \nHead and neck squamous cell carcinoma (HNSCC) is the sixth most common type of human cancer with ~750,000 cases worldwide, which may increase to 1 million by 2030 (1) . HNSCC affects subsites of the upper aerodigestive tract, including the oral cavity, larynx and pharynx, and the main associated etiological factors are the use of alcohol and tobacco, and high‑risk human papillomavirus (HPV) infection (2) . The tumor suppressor TP53 is one of the most frequently mutated genes in HNSCC. Results of The Cancer Genome Atlas (TCGA) HNSC project ([https://portal.gdc.cancer.gov/](https://portal.gdc.cancer.gov/)) (3) revealed TP53 somatic mutations in >90%(357/392) of the cases examined.  \nHNSCC exhibits heterogeneous tumor phenotypes, as a result of the reprogramming of the molecular machinery asso‑ ciated with carcinogenesis. According to Leemans et al (4), at least two genetic subclasses are identified in HNSCC regarding HPV infection status: i) Tumors with transcriptionally active HPV that are mostly located in the oropharynx and generally exhibit wild‑type TP53 alleles and a favorable prognosis; and ii) HPV‑negative tumors that often present with high chromo‑ somal instability, mutated TP53 and unfavorable prognosis. Low numbers of numerical genetic changes and wild‑type TP53 are also observed in a group of HPV‑negative lesions. Puram et al (5) demonstrated that the HPV‑positive group may likewise exhibit high levels of chromosomal instability, as well as diversity in HPV expression, and in cell cycle and senescence states within and between tumors.  \nHPV‑negative and ‑positive cases differ with respect to other characteristics. For instance, alterations in cyclin‑depen‑ dent kinase inhibitor 2A","cbCaikWKkwN6DGso","https://ap.wps.com/l/cbCaikWKkwN6DGso","pdf",2465736,14,"English","# 1. Introduction\n# 2. Tumor evolution\n# 3. EMT\n# 4. EGFR and HNSCC\n# 5. CTX therapy, and head and neck carcinoma\n# 6. Conclusions","[{\"question\":\"What drives the emergence of cetuximab chemotherapy resistance in vivo?\",\"answer\":\"Chemotherapeutic agents create selective pressure that rapidly enriches resistant subclones. Antineoplastic drugs alter tumor-cell metabolism, producing a bottleneck so only rare resistant cells survive and expand.\"},{\"question\":\"How does epithelial-mesenchymal transition (EMT) relate to tumor evolution and resistance?\",\"answer\":\"The review addresses EMT as part of tumor evolution, linking phenotypic changes to the ability of tumors to adapt under therapeutic pressure. These evolutionary steps contribute to resistance in head and neck squamous cell carcinoma.\"},{\"question\":\"What aspects does the review cover for head and neck squamous cell carcinoma?\",\"answer\":\"It summarizes key findings on tumor evolution, EMT, and resistance to cetuximab therapy. It also discusses related molecular context including EGFR and HNSCC.\"}]","Cetuximab chemotherapy resistance - Insight into the homeostatic evolution of head and neck cancer - Review | PDF",1789989237,35]