About: PRSS contributes to cetuximab resistance in colorectal cancer

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About: PRSS contributes to cetuximab resistance in colorectal cancer Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	PRSS contributes to cetuximab resistance in colorectal cancer
Creator	Wang, Yan Zhang, Yun Fu, Ling Wang, Youliang Chen, Hongxing Du, Peng Gao, Lihua Hu, Xianwen Jia, Ru Qiu, Weiyi Shao, Yong Shen, Wenlong Sun, Zhiwei Tan, Zhaoli Wu, Xiaojie Xi, Yongyi Xu, Jianming Yin, Huihui Zhao, Chuanhua Zhao, Zhihu
topic	covid:a4490fc5ca8fea133b9a5beb9258df89cf4945b6#this
Source	Medline; PMC
abstract	Cetuximab improves the survival of patients with metastatic colorectal cancer. The main limitation is primary and secondary resistance, the underlying mechanism of which requires extensive investigation. We proved that PRSS expression levels are significantly negatively associated with the sensitivity of cancer cells to cetuximab. Detailed mechanistic analysis indicated that PRSS can cleave cetuximab, leading to resistance. Cetuximab or bevacizumab combined with SPINK1, a PRSS inhibitor, inhibited cell growth more efficiently than cetuximab or bevacizumab alone in xenograft models. PRSS levels in the serum of 156 patients with mCRC were analyzed, and poor efficacy of cetuximab therapy was observed in patients with aberrant PRSS expression. PRSS expression in monoclonal antibody (mAb)–treated patients with cancer from The Cancer Genome Atlas database was also evaluated to determine whether patients with higher PRSS expression have significantly reduced progression-free survival. Our work provides a strong scientific rationale for targeting PRSS in combination with cetuximab therapy.
has issue date	2020-01-01(xsd:dateTime)
bibo:doi	10.1126/sciadv.aax5576
bibo:pmid	31911942
has license	cc-by-nc
sha1sum (hex)	a4490fc5ca8fea133b9a5beb9258df89cf4945b6
schema:url	https://doi.org/10.1126/sciadv.aax5576
resource representing a document's title	PRSS contributes to cetuximab resistance in colorectal cancer
has PubMed Central identifier	PMC6938705
has PubMed identifier	31911942
schema:publication	Sci Adv
resource representing a document's body	covid:a4490fc5ca8fea133b9a5beb9258df89cf4945b6#body_text
is http://vocab.deri.ie/void#inDataset of	https://covidontheweb.inria.fr:4443/about/id/http/ns.inria.fr/covid19/a4490fc5ca8fea133b9a5beb9258df89cf4945b6
is schema:about of	named entity 'MCRC' named entity 'COMBINED' named entity 'STRONG' named entity 'RATIONALE' named entity 'HIGHER' named entity 'TARGETING' named entity '156' named entity 'DETAILED' named entity 'DETERMINE' named entity 'ASSOCIATED WITH' named entity 'TREATED' named entity 'THE CANCER GENOME ATLAS' named entity 'POOR' named entity 'LEVELS' named entity 'MONOCLONAL ANTIBODY' named entity 'EXTENSIVE' named entity 'OUR' named entity 'mechanistic' named entity 'bevacizumab' named entity 'levels' named entity 'sensitivity' named entity 'primary' named entity 'determine' named entity 'CETUXIMAB' named entity 'PRSS' named entity 'REDUCED' named entity 'INHIBITED' named entity 'THERAPY' named entity 'RESISTANCE' named entity 'CELL GROWTH' named entity 'LEADING' named entity 'PROVIDES' named entity 'COLORECTAL CANCER' named entity 'RESISTANCE' named entity 'EFFICACY' named entity 'WORK' named entity 'CANCER CELLS' named entity 'UNDERLYING' named entity 'SPINK1' named entity 'BEVACIZUMAB' named entity 'ANALYSIS' named entity 'MAIN' named entity 'OBSERVED' named entity 'ANALYZED' named entity 'SERUM' named entity 'SURVIVAL' named entity 'EVALUATED' named entity 'PATIENTS' named entity 'PRSS' named entity 'INDICATED' named entity 'METASTATIC COLORECTAL CANCER' named entity 'SECONDARY' named entity 'DATABASE' named entity 'ABERRANT' named entity 'LIMITATION' named entity 'MECHANISM' named entity 'INVESTIGATION' named entity 'IMPROVES' named entity 'CANCER' named entity 'EXPRESSION'

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