Evidence map›Paper›PMID 28150169›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2017

KRAS genetic variant as a prognostic factor for recurrence in resectable non-small cell lung cancer.

I Sullivan, J Salazar, C Arqueros, M Andrés, A Sebio, M Majem, J Szafranska, E Martínez, D Páez, A López-Pousa and 2 more

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Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Review
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  11. Prognostic value ofCancer management and research · 2018
    Article
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4 · The record

Corrections and comments

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

12 authors.

I SullivanMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
J SalazarGenetics Department, Hospital de la Santa Creu i Sant Pau, Sant Antoni Maria Claret 167, 08025, Barcelona, Spain. jsalazar@santpau.cat.
C ArquerosMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
M AndrésMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
A SebioMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
M MajemMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
J SzafranskaPathology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
E MartínezThoracic Surgery Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
D PáezMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
A López-PousaMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
M BaigetGenetics Department, Hospital de la Santa Creu i Sant Pau, Sant Antoni Maria Claret 167, 08025, Barcelona, Spain.
A BarnadasMedical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeSeveral angiogenic prognostic markers are under investigation because of their potential clinical utility, aiming to improve patient outcomes. We hypothesized that genetic variant in the VEGF pathway could be used as prognostic markers of survival in non-small cell lung cancer (NSCLC) patients undergoing pulmonary resection.

methodsWe evaluated the relationship between genetic variants in the VEGF pathway and relapse-free survival (RFS, main endpoint) and overall survival (OS, secondary endpoint) among 131 patients with stage I-III NSCLC treated with surgical resection from 2009 to 2013. Clinical, pathological and surgical data were prospectively collected. Twenty-five variants in sixteen relevant genes were selected and genotyped in tumor samples by real time PCR. The Kaplan-Meier method with the log-rank test and Cox's regression models were used for RFS and OS analyses.

resultsWith a median follow-up of 36 (min = 2.8; max = 67.4) months, there were 31 (24%) relapses and 31 (24%) deaths. Overall, median RFS was not reached and median OS was 65 [95% confidence interval (CI) 56-75] months. The KRAS rs1137282 and PIK3C2A rs4356203 variants were significantly associated with RFS. For KRAS rs1137282, the 3-year RFS was 76% [95% CI 64-84%] in patients harboring an A/A genotype compared to 53% [95% CI 37-69%] in patients harboring an A/G or G/G genotype (p = 0.02). For PIK3C2A rs4356203, patients with an A/A or an A/G genotype had a 3-year RFS of 72% [95% CI 58-76%], whereas in patients with a G/G genotype was 49% [95% CI 28-70%] (p = 0.02). These associations remained statistically significant after adjusting for all the relevant clinical parameters in the multivariable analysis.

conclusionGenetic variants in VEGF pathway may be associated with recurrence in stage I-III NSCLC. Specifically, the KRAS rs1137282 could be considered as a prognostic factor for recurrence in resectable NSCLC patients. Although PIK3C2A rs4356203 was associated with RFS, further analyses are necessary to confirm these data.

Indexed as

Polymorphism, GeneticAdenocarcinomaAdultAgedAged, 80 and overCarcinoma, Large CellCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellFemaleFollow-Up StudiesHumansLung NeoplasmsLymphatic MetastasisMaleMiddle AgedNeoplasm InvasivenessKRAS protein, humanPhosphatidylinositol 3-KinasesPIK3C2A protein, humanProto-Oncogene Proteins p21(ras)Genetic variantsKRASPrognostic markerResectable non-small cell lung cancerVEGF pathway

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.