Imperial College London
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DrAdamFrampton

Faculty of Medicine, Department of Surgery & Cancer

Honorary Clinical Lecturer
 
 
 
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Contact

 

+44 (0)20 7594 2125a.frampton

 
 
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Location

 

4005Institute of Reproductive and Developmental BiologyHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Mantini:2021:10.3390/cancers13010066,
author = {Mantini, G and Meijer, LL and Glogovitis, I and In't, Veld SGJG and Paleckyte, R and Capula, M and Le, Large TYS and Morelli, L and Pham, TV and Piersma, SR and Frampton, AE and Jimenez, CR and Kazemier, G and Koppers-Lalic, D and Wurdinger, T and Giovannetti, E},
doi = {10.3390/cancers13010066},
journal = {Cancers},
title = {Omics analysis of educated platelets in cancer and benign disease of the pancreas},
url = {http://dx.doi.org/10.3390/cancers13010066},
volume = {13},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Pancreatic ductal adenocarcinoma (PDAC) is traditionally associated with thrombocytosis/hypercoagulation and novel insights on platelet-PDAC “dangerous liaisons” are warranted. Here we performed an integrative omics study investigating the biological processes of mRNAs and expressed miRNAs, as well as proteins in PDAC blood platelets, using benign disease as a reference for inflammatory noise. Gene ontology mining revealed enrichment of RNA splicing, mRNA processing and translation initiation in miRNAs and proteins but depletion in RNA transcripts. Remarkably, correlation analyses revealed a negative regulation on SPARC transcription by isomiRs involved in cancer signaling, suggesting a specific ”education” in PDAC platelets. Platelets of benign patients were enriched for non-templated additions of G nucleotides (#ntaG) miRNAs, while PDAC presented length variation on 3′ (lv3p) as the most frequent modification on miRNAs. Additionally, we provided an actionable repertoire of PDAC and benign platelet-ome to be exploited for future studies. In conclusion, our data show that platelets change their biological repertoire in patients with PDAC, through dysregulation of miRNAs and splicing factors, supporting the presence of de novo protein machinery that can “educate” the platelet. These novel findings could be further exploited for innovative liquid biopsies platforms as well as possible therapeutic targets.
AU  - Mantini,G
AU  - Meijer,LL
AU  - Glogovitis,I
AU  - In't,Veld SGJG
AU  - Paleckyte,R
AU  - Capula,M
AU  - Le,Large TYS
AU  - Morelli,L
AU  - Pham,TV
AU  - Piersma,SR
AU  - Frampton,AE
AU  - Jimenez,CR
AU  - Kazemier,G
AU  - Koppers-Lalic,D
AU  - Wurdinger,T
AU  - Giovannetti,E
DO  - 10.3390/cancers13010066
PY  - 2021///
SN  - 2072-6694
TI  - Omics analysis of educated platelets in cancer and benign disease of the pancreas
T2  - Cancers
UR  - http://dx.doi.org/10.3390/cancers13010066
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000605898500001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://www.mdpi.com/2072-6694/13/1/66
UR  - http://hdl.handle.net/10044/1/96030
VL  - 13
ER  -
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