White adipose tissue-derived factors and prostate cancer progression: mechanisms and targets for interventions.
Saha A., Hamilton-Reeves J., DiGiovanni J.
Narrative Review, published in Cancer Metastasis Rev (2022) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Cancer Metastasis Rev (2022)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 35927363
- PMCID
- PMC9474694
- DOI
- 10.1007/s10555-022-10056-0
- NCT
- NCT03261271
- Citations
- 6
Abstract (original English)
Obesity represents an important risk factor for prostate cancer, driving more aggressive disease, chemoresistance, and increased mortality. White adipose tissue (WAT) overgrowth in obesity is central to the mechanisms that lead to these clinical observations. Adipose stromal cells (ASCs), the progenitors to mature adipocytes and other cell types in WAT, play a vital role in driving PCa aggressiveness. ASCs produce numerous factors, especially chemokines, including the chemokine CXCL12, which is involved in driving EMT and chemoresistance in PCa. A greater understanding of the impact of WAT in obesity-induced progression of PCa and the underlying mechanisms has begun to provide opportunities for developing interventional strategies for preventing or offsetting these critical events. These include weight loss regimens, therapeutic targeting of ASCs, use of calorie restriction mimetic compounds, and combinations of compounds as well as specific receptor targeting strategies.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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