Evidence map›Paper›PMID 36060016›Full record

ArticleCancer diagnosis & prognosis

Jehison Alirio Herrera-Pulido, Orlando Ricaurte Guerrero, Jinneth Acosta Forero, Pablo Moreno-Acosta, Alfredo Romero-Rojas, Carolina Sanabria, Gustavo Hernández, Martha Lucía Serrano

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Article in Cancer diagnosis & prognosis. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jehison Alirio Herrera-PulidoCancer Biology Research Group, National Cancer Institute, Bogotá, Colombia.
Orlando Ricaurte GuerreroDepartment of Pathology, Faculty of Medicine, Universidad Nacional de Colombia, Bogotá, Colombia.
Jinneth Acosta ForeroDepartment of Pathology, Faculty of Medicine, Universidad Nacional de Colombia, Bogotá, Colombia.
Pablo Moreno-AcostaCancer Biology Research Group, National Cancer Institute, Bogotá, Colombia.
Alfredo Romero-RojasOncological Pathology Group, National Cancer Institute, Bogotá, Colombia.
Carolina SanabriaCancer Biology Research Group, National Cancer Institute, Bogotá, Colombia.
Gustavo HernándezPublic Health and Cancer Epidemiology Group, National Cancer Institute, Bogotá, Colombia.
Martha Lucía SerranoCancer Biology Research Group, National Cancer Institute, Bogotá, Colombia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimAlthough some mutations of KRAS proto-oncogene, GTPase (KRAS) have been associated with the prognosis and therapeutic management of colorectal cancer (CRC), the epigenetic mechanisms (DNA methylation and microRNA expression) that regulate wild-type KRAS expression in patients with CRC are poorly known. The aim of this study was to establish whether there is a relationship between the expression of the wild-type KRAS gene, the methylation status of its distal promoter, and miR-143 and miR-18a-3p levels in samples of sporadic CRC. PATIENTS AND

methodsA total of 51 cases of sporadic CRC with wild-type KRAS were analyzed. The expression levels of KRAS mRNA, miR-18a-3p, miR-143, and KRAS protein, as well as methylation in the distal promoter of the KRAS gene were evaluated.

resultsIn the analyzed cases, KRAS mRNA expression was detected in 51.1%; wild-type KRAS protein was found in the membrane in 31.4% and in the cytoplasm in 98% of cases. An inverse relationship of marginal significance was observed between miR-18a-3p and KRAS protein expression in the cytoplasm (odds ratio=0.14, 95% confidence interval=0.012-1.092; p=0.08). The methylation status of the distal promoter of KRAS at four CpG islands was analyzed in 30 cases (58.8%): partial methylation of the four CpG islands evaluated was observed in two cases (6.7%). In these cases, KRAS protein expression was not evidenced at the membrane level; miR-18a-3p expression was not detected either but high expression of miR-143 was observed.

conclusionNo association was found between the expression levels of KRAS mRNA, miR-18a-3p, miR-143 and methylation status. Methylation status was detected with low frequency, thus being the first report of methylation in wild-type KRAS.

Indexed as

colorectal cancerDNA methylationKRASmiR-143miR-18a-3p

Identifiers

PMID36060016
PMCPMC9425578

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