Potential Role of Diabetes Mellitus-Associated T Cell Senescence in Epithelial Ovarian Cancer Omental Metastasis.
Rhianne BroadwayNikita M PatelLucy E HillierAmal El-BririYulia S KornevaDmitry Aleksandrovich ZinovkinMd Zahidul Islam PranjolPublished in: Life (Basel, Switzerland) (2021)
Epithelial ovarian cancer (EOC) is one of the most common causes of cancer-related deaths among women and is associated with age and age-related diseases. With increasing evidence of risks associated with metabolic inflammatory conditions, such as obesity and type 2 diabetes mellitus (T2DM), it is important to understand the complex pathophysiological mechanisms underlying cancer progression and metastasis. Age-related conditions can lead to both genotypic and phenotypic immune function alterations, such as induction of senescence, which can contribute to disease progression. Immune senescence is a common phenomenon in the ageing population, which is now known to play a role in multiple diseases, often detrimentally. EOC progression and metastasis, with the highest rates in the 75-79 age group in women, have been shown to be influenced by immune cells within the "milky spots" or immune clusters of the omentum. As T2DM has been reported to cause T cell senescence in both prediabetic and diabetic patients, there is a possibility that poor prognosis in EOC patients with T2DM is partly due to the accumulation of senescent T cells in the omentum. In this review, we explore this hypothesis with recent findings, potential therapeutic approaches, and future directions.
Keyphrases
- poor prognosis
- dna damage
- glycemic control
- endothelial cells
- polycystic ovary syndrome
- stress induced
- long non coding rna
- type diabetes
- insulin resistance
- metabolic syndrome
- weight loss
- pregnancy outcomes
- papillary thyroid
- weight gain
- body mass index
- adipose tissue
- pregnant women
- squamous cell
- human health
- cardiovascular risk factors
- climate change
- childhood cancer