Journal
CANCERS
Volume 10, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/cancers10020034
Keywords
pancreatic cancer; heterogeneity; stroma; immune cells; fibroblasts; mutations; gene expression
Categories
Funding
- KWF Dutch Cancer Society [UVA 2012-5607, UVA 2013-5932]
- AMC Foundation
- Celgene
- Amgen
- Bayer Schering Pharma AG
- Eli Lilly and Company
- GlaxoSmithKline Pharmaceuticals
- Nordic Pharma Group
- Roche Pharmaceuticals
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Pancreatic ductal adenocarcinoma (PDAC) is the most prevalent form of pancreatic cancer and carries the worst prognosis of all common cancers. Five-year survival rates have not surpassed 6% for some decades and this lack of improvement in outcome urges a better understanding of the PDAC-specific features which contribute to this poor result. One of the most defining features of PDAC known to contribute to its progression is the abundance of non-tumor cells and material collectively known as the stroma. It is now well recognized that the different non-cancer cell types, signalling molecules, and mechanical properties within a tumor can have both tumor-promoting as well as -inhibitory effects. However, the net effect of this intratumour heterogeneity is not well understood. Heterogeneity in the stromal makeup between patients is even less well established. Such intertumour heterogeneity is likely to be affected by the relative contributions of individual stromal constituents, but how these contributions exactly relate to existing classifications that demarcate intertumour heterogeneity in PDAC is not fully known. In this review, we give an overview of the available evidence by delineating the elements of the PDAC stroma and their contribution to tumour growth. We do so by interpreting the heterogeneity at the gene expression level in PDAC, and how stromal elements contribute to, or interconnect, with this.
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