Literature DB >> 34108644

MSH2-deficient prostate tumours have a distinct immune response and clinical outcome compared to MSH2-deficient colorectal or endometrial cancer.

Patrick McCoy1,2, Stefano Mangiola3,4,5, Geoff Macintyre6,7, Ryan Hutchinson5,8, Ben Tran5,9, Bernard Pope10,11,12, Peter Georgeson10,13, Matthew K H Hong3, Natalie Kurganovs3,14,15, Sebastian Lunke8,16,17, Michael J Clarkson3, Marek Cmero3,5, Michael Kerger4, Ryan Stuchbery4, Ken Chow3, Izhak Haviv18, Andrew Ryan19, Anthony J Costello3,4, Niall M Corcoran3,20,21, Christopher M Hovens3,4.   

Abstract

BACKGROUND: Recent publications have shown patients with defects in the DNA mismatch repair (MMR) pathway driven by either MSH2 or MSH6 loss experience a significant increase in the incidence of prostate cancer. Moreover, this increased incidence of prostate cancer is accompanied by rapid disease progression and poor clinical outcomes. METHODS AND
RESULTS: We show that androgen-receptor activation, a key driver of prostate carcinogenesis, can disrupt the MSH2 gene in prostate cancer. We screened tumours from two cohorts (recurrent/non-recurrent) of prostate cancer patients to confirm the loss of MSH2 protein expression and identified decreased MSH2 expression in recurrent cases. Stratifying the independent TCGA prostate cancer cohort for MSH2/6 expression revealed that patients with lower levels of MSH2/6 had significant worse outcomes, in contrast, endometrial and colorectal cancer patients with lower MSH2/6 levels. MMRd endometrial and colorectal tumours showed the expected increase in mutational burden, microsatellite instability and enhanced immune cell mobilisation but this was not evident in prostate tumours.
CONCLUSIONS: We have shown that loss or reduced levels of MSH2/MSH6 protein in prostate cancer is associated with poor outcome. However, our data indicate that this is not associated with a statistically significant increase in mutational burden, microsatellite instability or immune cell mobilisation in a cohort of primary prostate cancers.
© 2021. The Author(s), under exclusive licence to Springer Nature Limited.

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Year:  2021        PMID: 34108644     DOI: 10.1038/s41391-021-00379-4

Source DB:  PubMed          Journal:  Prostate Cancer Prostatic Dis        ISSN: 1365-7852            Impact factor:   5.554


  52 in total

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Journal:  Cell       Date:  2013-04-25       Impact factor: 41.582

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Journal:  J Clin Oncol       Date:  2013-03-25       Impact factor: 44.544

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7.  Cancer statistics, 2016.

Authors:  Rebecca L Siegel; Kimberly D Miller; Ahmedin Jemal
Journal:  CA Cancer J Clin       Date:  2016-01-07       Impact factor: 508.702

8.  Chromoplexy: a new category of complex rearrangements in the cancer genome.

Authors:  Michael M Shen
Journal:  Cancer Cell       Date:  2013-05-13       Impact factor: 31.743

9.  Androgen-induced TOP2B-mediated double-strand breaks and prostate cancer gene rearrangements.

Authors:  Michael C Haffner; Martin J Aryee; Antoun Toubaji; David M Esopi; Roula Albadine; Bora Gurel; William B Isaacs; G Steven Bova; Wennuan Liu; Jianfeng Xu; Alan K Meeker; George Netto; Angelo M De Marzo; William G Nelson; Srinivasan Yegnasubramanian
Journal:  Nat Genet       Date:  2010-07-04       Impact factor: 38.330

10.  Nuclear receptor-induced chromosomal proximity and DNA breaks underlie specific translocations in cancer.

Authors:  Chunru Lin; Liuqing Yang; Bogdan Tanasa; Kasey Hutt; Bong-gun Ju; Kenny Ohgi; Jie Zhang; David W Rose; Xiang-Dong Fu; Christopher K Glass; Michael G Rosenfeld
Journal:  Cell       Date:  2009-12-11       Impact factor: 41.582

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