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Impact of risk factors on early cancer evolution. | LitMetric

Impact of risk factors on early cancer evolution.

Cell

Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute, London, UK; Cancer Research UK Lung Cancer Center of Excellence, University College London Cancer Institute, London, UK; Department of Oncology, University College London Hospitals, London, UK. Electronic address:

Published: April 2023

AI Article Synopsis

  • - Recent discoveries show that oncogenic cells can exist in healthy tissues and that many indolent cancers are discovered during autopsies, indicating a more complex process behind tumor formation than previously thought.
  • - The human body comprises around 40 trillion cells of various types organized in a complex structure, which requires effective systems to prevent the uncontrolled growth of cancerous cells that could affect health.
  • - The review explores how early initiated cancer cells are shielded from developing further tumors, examines non-genetic pathways that increase cancer risk, and discusses current and future strategies for early cancer detection and prevention.

Article Abstract

Recent identification of oncogenic cells within healthy tissues and the prevalence of indolent cancers found incidentally at autopsies reveal a greater complexity in tumor initiation than previously appreciated. The human body contains roughly 40 trillion cells of 200 different types that are organized within a complex three-dimensional matrix, necessitating exquisite mechanisms to restrain aberrant outgrowth of malignant cells that have the capacity to kill the host. Understanding how this defense is overcome to trigger tumorigenesis and why cancer is so extraordinarily rare at the cellular level is vital to future prevention therapies. In this review, we discuss how early initiated cells are protected from further tumorigenesis and the non-mutagenic pathways by which cancer risk factors promote tumor growth. By nature, the absence of permanent genomic alterations potentially renders these tumor-promoting mechanisms clinically targetable. Finally, we consider existing strategies for early cancer interception with perspectives on the next steps for molecular cancer prevention.

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Source
http://dx.doi.org/10.1016/j.cell.2023.03.013DOI Listing

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