Dysregulation of KRAS signaling in pancreatic cancer is not associated with KRAS mutations and outcome

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F75010330%3A_____%2F17%3A00011832" target="_blank" >RIV/75010330:_____/17:00011832 - isvavai.cz</a>

Alternative codes found

RIV/65269705:_____/17:00067254 RIV/00216224:14110/17:00097981 RIV/00216208:11140/17:10362957 RIV/00023001:_____/17:00076262 RIV/61989592:15110/17:73583806

Result on the web

<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661609/" target="_blank" >https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661609/</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3892/ol.2017.6946" target="_blank" >10.3892/ol.2017.6946</a>

Result language

angličtina

Original language name

Dysregulation of KRAS signaling in pancreatic cancer is not associated with KRAS mutations and outcome

Original language description

Pancreatic ductal adenocarcinoma (PDAC) is a tumor with a poor prognosis, and no targeted therapy is currently available. The aim of the present study was to investigate the prognostic significance of the expression of V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS), downstream signaling pathway genes and the association with clinical characteristics in PDAC patients undergoing radical surgery. Tumors and adjacent non-neoplastic pancreatic tissues were examined in 45 patients with histologically verified PDAC. The transcript profile of 52 KRAS downstream signaling pathway genes was assessed using quantitative-polymerase chain reaction. KRAS mutation was detected in 80% of cases. The genes of four signaling pathways downstream of KRAS, including the phosphoinositide 3-kinase/3-phosphoinositide-dependent protein kinase 1/V-akt murine thymoma viral oncogene homolog 1, RAL guanine nucleotide exchange factor, Ras and Rab interactor 1/ABL proto-oncogene-1, non-receptor tyrosine kinase, and RAF proto-oncogene serine/threonine-protein kinase/mitogen-activated protein kinase pathways, exhibited differential expression in PDAC compared with that in the adjacent normal tissues. However, no significant differences in expression were evident between patients with KRAS-mutated and wild-type tumors. The expression of KRAS downstream signaling pathways genes did not correlate with angioinvasion, perineural invasion, grade or presence of lymph node metastasis. Additionally, the presence of KRAS mutations was not associated with overall survival. Among the KRAS downstream effective signaling pathways molecules investigated, only v-raf-1 murine leukemia viral oncogene homolog 1 expression was predictive of prognosis. Overall, KRAS mutation is present in the majority of cases of PDAC, but is not associated with changes in the expression of KRAS downstream signaling pathways and the clinical outcome. This may partly explain the failure of KRAS-targeted therapies in PDAC.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30101 - Human genetics

Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Oncology Letters

ISSN

1792-1074

e-ISSN

1792-1082

Volume of the periodical

14

Issue of the periodical within the volume

5

Country of publishing house

GR - GREECE

Number of pages

9

Pages from-to

5980-5988

UT code for WoS article

000415083000127

EID of the result in the Scopus database

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