4.7 Article

Aging of the progenitor cells that initiate prostate cancer

期刊

CANCER LETTERS
卷 515, 期 -, 页码 28-35

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2021.05.014

关键词

Epithelium; Organoid; Microenvironment; Old; Mutations

类别

资金

  1. American Cancer Society [RSG-17-068-01-TBG]
  2. NIH/NCI [R01CA237191, P30CA016042, U01CA214194]
  3. Rose Hills Foundation
  4. Gill endowment
  5. NIH/NCI (UCLA Prostate SPORE) [P50CA0912131]
  6. Spitzer Family Foundation Fund
  7. UCLA Jonsson Comprehensive Cancer Center
  8. UCLA Broad Stem Cell Research Center
  9. UCLA Clinical and Translational Science Institute
  10. UCLA Institute of Urologic Oncology
  11. UCLA Eli and Edythe Broad Center of Regenerative Medicine
  12. UCLA Stem Cell Research Rose Hills Foundation Graduate Scholarship Training Program
  13. Ruth L. Kirschstein National Research Service Award [GM007185]
  14. Prostate Cancer Foundation Special Challenge Award [20CHAS01]

向作者/读者索取更多资源

The prostate continues to grow in volume while many other organs experience a loss of tissue mass and decline in regenerative capacity during aging. Research indicates that prostate luminal progenitor cells expand with age, and age-related changes to the microenvironment may influence prostate epithelial cells and the risk of transformation. Addressing questions regarding models of aging and regulators of prostate aging is crucial for understanding mechanisms that promote age-related prostatic disease.
Many organs experience a loss of tissue mass and a decline in regenerative capacity during aging. In contrast, the prostate continues to grow in volume. In fact, age is the most important risk factor for prostate cancer. However, the age-related factors that influence the composition, morphology and molecular features of prostate epithelial progenitor cells, the cells-of-origin for prostate cancer, are poorly understood. Here, we review the evidence that prostate luminal progenitor cells are expanded with age. We explore the age-related changes to the microenvironment that may influence prostate epithelial cells and risk of transformation. Finally, we raise a series of questions about models of aging and regulators of prostate aging which need to be addressed. A fundamental understanding of aging in the prostate will yield critical insights into mechanisms that promote the development of age-related prostatic disease.

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