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Comment
. 2020 Apr;10(4):495-497.
doi: 10.1158/2159-8290.CD-20-0046.

Deconstructing Pancreatic Adenocarcinoma by Targeting the Conductor, MYC

Isabel A English  1 , Rosalie C Sears  2   3   4
Affiliations
Comment

Deconstructing Pancreatic Adenocarcinoma by Targeting the Conductor, MYC

Isabel A English et al. Cancer Discov. 2020 Apr.

Abstract

In this issue of Cancer Discovery, Sodir and colleagues employ a pancreatic ductal adenocarcinoma mouse model with mutant KRAS and inducible MYC to demonstrate that MYC acts as a reversible driver of malignant tumor progression. Abrogation of MYC triggers rapid regression and disassembly of the ensemble tumor through both cancer cell-intrinsic and cancer cell-extrinsic mechanisms, providing a compelling rationale for therapeutic targeting of MYC.See related article by Sodir et al., p. 588.

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Conflict of interest statement

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Figures

Figure 1.
Figure 1.
Schematic representation of the role of MYC as a reversible driver of cell-intrinsic and cell-extrinsic PDAC progression. Epithelial acinar-to-ductal metaplasia (ADM), pancreatic intraepithelial neoplasia (PanIN), progression to pancreatic ductal adenocarcinoma (PDAC), and reversion to PanIN and ductal-to-acinar transdifferentiation (DAT) are indicated. Desmoplastic stromal and vascular changes and immune cell infiltrates are depicted. ECM, extracellular matrix; KRAS*, mutationally activated KRAS.
See this image and copyright information in PMC

Comment on

  • MYC Instructs and Maintains Pancreatic Adenocarcinoma Phenotype.
    Sodir NM, Kortlever RM, Barthet VJA, Campos T, Pellegrinet L, Kupczak S, Anastasiou P, Swigart LB, Soucek L, Arends MJ, Littlewood TD, Evan GI. Sodir NM, et al. Cancer Discov. 2020 Apr;10(4):588-607. doi: 10.1158/2159-8290.CD-19-0435. Epub 2020 Jan 15. Cancer Discov. 2020. PMID: 31941709

References

    1. Sodir NM, Kortlever RM, Barthet VJA, Campos T, Pellegrinet L, Kupczak S, et al. MYC instructs and maintains pancreatic adenocarcinoma phenotype. Cancer Discov 2020;10:588–607. - PubMed
    1. Özdemir BC, Pentcheva-Hoang T, Carstens JL, Zheng X, Wu C-C, Simpson TR, et al. Depletion of carcinoma-associated fibroblasts and fibrosis induces immunosuppression and accelerates pancreas cancer with reduced survival. Cancer Cell 2014;25:719–34. - PMC - PubMed
    1. Farrell AS, Sears RC. MYC degradation. Cold Spring Harb Perspect Med 2014;4:pii:a014365. - PMC - PubMed
    1. Walz S, Lorenzin F, Morton J, Wiese KE, von Eyss B, Herold S, et al. Activation and repression by oncogenic MYC shape tumour-specific gene expression profiles. Nature 2014;511:483–7. - PMC - PubMed
    1. Hayes TK, Neel NF, Hu C, Gautam P, Chenard M, Long B, et al. Long-Term ERK inhibition in KRAS-mutant pancreatic cancer is associated with MYC degradation and senescence-like growth suppression. Cancer Cell 2016;29:75–89. - PMC - PubMed

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