Evidence map›Paper›PMID 31881025›Full record

ArticlePloS one2019

KRAS and NRAS mutational gene profile of metastatic colorectal cancer patients in Jordan.

Muhammad Awidi, Nidaa Ababneh, Maha Shomaf, Feras Al Fararjeh, Laila Owaidi, Mohammad AlKhatib, Buthaina Al Tarawneh, Abdalla Awidi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% of its field
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Therapeutic and diagnostic applications of exosomes in colorectal cancer.Medical oncology (Northwood, London, England) · 2024
    Review
  4. Clinical Medicine Insights. Oncology · 2024
    Review
  5. Article
  6. Cancer control : journal of the Moffitt Cancer Center
    Article
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

8 authors at 2 institutions in 2 countries.

Muhammad AwidiBeth Israel Lahey Health-Lahey Hospital and Medical Center, Burlington, Massachusetts, United States of America.ORCID 0000-0002-4205-8417
Nidaa AbabnehCell Therapy Center, The University of Jordan, Amman, Jordan.
Maha ShomafDepartment of Pathology and Microbiology and Forensic Medicine, The University of Jordan, Amman, Jordan.
Feras Al FararjehDepartment of Medicine, The University of Jordan, School of Medicine, Amman, Jordan.
Laila OwaidiHemostasis and Thrombosis Laboratory, School of Medicine, The University of Jordan, Amman, Jordan.
Mohammad AlKhatibHemostasis and Thrombosis Laboratory, School of Medicine, The University of Jordan, Amman, Jordan.
Buthaina Al TarawnehHemostasis and Thrombosis Laboratory, School of Medicine, The University of Jordan, Amman, Jordan.
Abdalla AwidiCell Therapy Center, The University of Jordan, Amman, Jordan.
University of Jordan · JOLahey Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA constitutively active RAS protein in the absence of stimulation of the epidermal growth factor receptor (EGFR) is the result of mutations in KRAS and NRAS genes. Mutations in the KRAS exon 2 and outside exon 2 have been found to predict the resistance to anti-EGFR monoclonal therapy. A substantial proportion of metastatic colorectal cancer cases (mCRC) exhibit RAS mutations outside KRAS exon 2, particularly in KRAS exon 3 and 4 and NRAS exons 2 and 3. No data about RAS mutations outside KRAS exon 2 are available for Jordanian patients with mCRC. We aim to study the molecular spectrum, frequency, and distribution pattern of KRAS and NRAS mutations in Jordanian patients with mCRC.

methodsA cohort of 190 Jordanian metastatic colorectal cancer patients were enrolled in the trial. We detected mutations in exon 2 of the KRAS and NRAS gene as well as mutations outside of exon 2 using the StripAssay technique. The KRAS StripAssay covered 29 mutations and 22 NRAS mutations.

resultsMutations were observed in 92 (48.42%) cases, and KRAS exon 2 mutations accounted for 76 cases (83.69%). KRAS G12D was the most common mutation, occurring in 18 cases, followed by KRAS G12A in 16 cases, and G12T in 13 cases. Mutations outside of KRAS exon 2 represented 16.3% of the mutated cases. Among those, 6 cases (6.48%) carried mutations in NRAS exon 2 and 3, and 10 cases (10.87%) in KRAS exon 3 and 4.

conclusionThe frequency of NRAS and KRAS mutations outside of exon 2 appears to be higher in Jordanian patients in comparison with patients from western countries. KRAS mutations outside of exon 2 should be tested routinely to identify patients who should not be treated with anti-EGFR antibodies.

Indexed as

AdultAgedAged, 80 and overColorectal NeoplasmsDNA Mutational AnalysisExonsFemaleGTP PhosphohydrolasesHumansJordanMaleMembrane ProteinsMiddle AgedNeoplasm MetastasisProto-Oncogene Proteins p21(ras)Young AdultGTP PhosphohydrolasesKRAS protein, humanMembrane ProteinsNRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID31881025
PMCPMC6934288
OpenAlexW2997573493

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.