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\nGianluca Mauri,1,2,3,8 Giorgio Patelli,1,2,3,8 Andrea Sartore-Bianchi,2,3 Sergio Abrignani,4,5 Beatrice Bodega,4,6 Silvia Marsoni,1 Vincenzo Costanzo,1,2 Angela Bachi,1 Salvatore Siena,2,3 and Alberto Bardelli1,7,*  \n1IFOM ETS – The AIRC Institute of Molecular Oncology, Milan, Italy  \n2Department of Oncology and Hemato-Oncology, Universit`a degli Studi di Milano, Milan, Italy  \n3Niguarda Cancer Center, Grande Ospedale Metropolitano Niguarda, Milan, Italy  \n4INGM, Istituto Nazionale Genetica Molecolare ‘‘Romeo ed Enrica Invernizzi’’, Milan, Italy  \n5Department of Clinical Sciences and Community Health, Universit`a degli Studi di Milano, Milan, Italy  \n6Department of Biosciences, University of Milan, Milan, Italy  \n7Department of Oncology, Molecular Biotechnology Center, University of Torino, Torino, Italy  \n8These authors contributed equally  \n*Correspondence: alberto. bardelli@unito.it [https://doi.org/10.1016/j.xcrm.2024.101737](https://doi.org/10.1016/j.xcrm.2024.101737)  \nSUMMARY  \nSince the nineties, the incidence of sporadic early-onset (EO) cancers has been rising worldwide. The underlying reasons are still unknown. However, identifying them is vital for advancing both prevention and intervention. Here, we exploit available knowledge derived from clinical observations to formulate testable hypotheses aimed at defining the causal factors of this epidemic and discuss how to experimentally test them. We explore the potential impact of exposome changes from the millennials to contemporary young generations, considering both environmental exposures and enhanced susceptibilities to EO-cancer development. We emphasize how establishing the time required for an EO cancer to develop is relevant to defining future screening strategies. Finally, we discuss the importance of integrating multi-dimensional data from international collaborations to generate comprehensive knowledge and translate these findings back into clinical practice.  \nINTRODUCTION  \nOver the last three decades, cancer epidemiology has been changing remarkably due to the rising incidence of sporadic early-onset (EO) cancers. Traditionally observed in adults over the age of 65, these primarily solid tumors are now increasingly diagnosed in younger individuals under the age of 501,2. Accordingly, the term EO cancers today identifies those solid tumors usually occurring in people aged 60 to 70 diagnosed in individuals younger than 50 . However, this definition is merely arbitrary, based on practicality ratherthanona biological rationale. EO-cancer incidence is increasing particularly among adolescent and young adults aged 15 to 39 .3–6 This epidemiological shift was initially reported in the USA over the eighties and then confirmed worldwide since the early nineties, progressively emerging as a major public health concern given its physical, social, economic, and psychological consequences.7–10 Thus, understanding why this is happening, while also defining how to treat young adults  \ndiagnosed with cancers, is a priority for oncological research.  \nHere, we formulate testable hypotheses and suggest a translational comprehensive approach to tackle this epidemic. Starting from reviewing potential causes of EO-cancer increase, we propose how to test several hypotheses through translational platforms, integrating data from both cell-autonomous and non-cell-autonomous models into a comprehensive EO-cancer  \nmulti-omics-based assessment (the EO-cancer integrome) . Understanding the EO-cancer biology, the underlying causes, and the clinical peculiarities of affected individuals is central to identifying preventive and early-diagnosis strategies as well as tailored therapeutic opportunities (Figure 1) .  \nFROM CLINICAL OBSERVATION TO TESTABLE HYPOTHESES  \nThe clinical relevance of EO-cancer rise is highlighted by their emergence as the primary cause of mortality in adolescents and young adul","cbCaibrDenfmmhg9","https://ap.wps.com/l/cbCaibrDenfmmhg9","pdf",2979256,"English","# Summary\n# Introduction\n# From clinical observation to testable hypotheses","[{\"question\":\"Why is identifying the causes of early-onset cancers considered essential?\",\"answer\":\"The review states that causes of the increasing sporadic early-onset (EO) cancer incidence are still unknown, and identifying them is vital to advance both prevention and intervention.\"},{\"question\":\"What hypotheses does the review propose to explain the EO-cancer increase?\",\"answer\":\"It formulates testable hypotheses based on clinical observations and discusses potential impacts of exposome changes from millennials to contemporary young generations, including environmental exposures and enhanced susceptibilities.\"},{\"question\":\"How does the review connect EO-cancer development time to clinical practice?\",\"answer\":\"It emphasizes that establishing the time required for an EO cancer to develop is relevant for defining future screening strategies and for informing translational approaches.\"}]","Early-onset cancers: Biological bases and clinical implications | PDF",1789983404,35]