Accelerated aging and young-onset cancer risk!-are stressors of the PELICan hypothesis the missing link?

Savio George Barreto, Stephen J. Pandol

Research output: Contribution to journalLetterpeer-review

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Abstract

At the 2024 Annual Meeting of the American Association for Cancer Research, researchers from Washington University in St. Louis (1) postulated a hypothesis that an increase in biological age reflective of accelerated aging could play a role in early-onset (cancers occurring in adults below the age of 55 years) carcinogenesis. They examined data from 148,724 individuals within the U.K. Biobank database. Each person’s biological age was calculated using the following biomarkers, including red cell distribution width, mean corpuscular volume, white blood cell count, lymphocyte proportion, blood: albumin, serum alkaline phosphatase, serum C-reactive protein, serum creatinine and serum glucose. They defined accelerated aging to be present when the person’s biological age exceeded their chronological age.
Original languageEnglish
Number of pages2
JournalChinese Clinical Oncology
Volume13
Issue number4
DOIs
Publication statusPublished - 15 Aug 2024

Keywords

  • accelerated biological aging
  • young-onset cancer
  • PELIcan hypothesis
  • chronological aging
  • Targeted therapies

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