Evidence map›Paper›PMID 26749281›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Investigation of FIH-1 and SOCS3 expression in KRAS mutant and wild-type patients with colorectal cancer.

Ladan Vakil, Reza Najafipour, Nasser Rakhshani, Farhad Zamani, Arman Morakabati, Amir Javadi

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Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. [Role of cytokine signal suppressor 3 in the regulatory mechanism of colon cancer invasion and proliferation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019
    Article
  7. 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

6 authors at 5 institutions in 1 country.

Ladan VakilDepartment of Molecular Medicine, School of Medicine, Qazvin University of Medical Sciences, Qazvin, IR, Iran.
Reza NajafipourDepartment of Molecular Medicine, School of Medicine, Qazvin University of Medical Sciences, Qazvin, IR, Iran. rnajafipour@gmail.com.
Nasser RakhshaniGI and Liver Disease Research Center, Firoozgar Hospital, Iran University of Medical Sciences, Tehran, Iran. n_rakhshani@yahoo.com.
Farhad ZamaniGI and Liver Disease Research Center, Firoozgar Hospital, Iran University of Medical Sciences, Tehran, Iran.
Arman MorakabatiMolecular Pathology Department of Mehr General Hospital, Tehran, Iran.
Amir JavadiDepartments of Medical Informatics, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran.
Firoozgar General Hospital · IRDay General Hospital · IRIran University of Medical Sciences · IRQazvin University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is a multistep process based on the accumulation of somatic mutations in genes such as APC and KRAS. Data on the presence of mutations in KRAS gene in CRC and its relationship with clinicopathological parameters and expression of genes involved in tumor progression are scarce. We unbiasedly examined the KRAS status in samples from 99 patients and its correlation with clinicopathological parameters such as age, sex, tumor location, lymph node metastasis, tumor stage, tumor grade, and vascular invasion. Consistent with reports of other researchers, 38.4 % of our samples harbored KRAS mutation in their genomes with preferential mutation in codon 12 (89.4 %). Nevertheless, unlike previous reports, we were not able to correlate KRAS status with clinicopathological parameters (P > 0.05) except for vascular invasion. Patients with KRAS mutation have more vascular invasion compared with patient having wild-type KRAS. Next, we investigated the expression of two tumor suppressor genes, factor-inhibiting hypoxia-inducible factor 1 (FIH-1) and suppressor of cytokine signaling (SOCS3), in both KRAS mutant and wild-type groups and looked for any correlation between their expression and clinicopathological parameters. Although the expression of both genes was not regular, none of the clinicopathological parameters were associated with the expressions of FIH-1 and SOCS3 at mRNA level (P > 0.05). However, decline in FIH-1 expression at protein level in KRAS mutant group was correlated with stage IV and grade 2 of tumor (P ≤ 0.05). Our results demonstrated that there is no or low correlation between KRAS status, FIH-1, and SOCS3 expression with epidemiologic and clinicpathological characteristics in CRC.

Indexed as

AdultAgedAged, 80 and overCodonColorectal NeoplasmsFemaleHumansLymphatic MetastasisMaleMiddle AgedMixed Function OxygenasesMutationNeoplasm StagingProto-Oncogene Proteins p21(ras)Repressor ProteinsSuppressor of Cytokine Signaling 3 ProteinCodonHIF1AN protein, humanKRAS protein, humanMixed Function OxygenasesProto-Oncogene Proteins p21(ras)Repressor ProteinsSOCS3 protein, humanSuppressor of Cytokine Signaling 3 ProteinColorectal cancerFIH-1 and SOCS3KRAS mutation

Identifiers

PMID26749281
OpenAlexW2224314569

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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.