Evidence map›Paper›PMID 24763823›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

Implication of K-ras and p53 in colorectal cancer carcinogenesis in Tunisian population cohort.

Chaar Ines, Ounissi Donia, Boughriba Rahma, Azza Ben Ammar, Amara Sameh, Taher Khalfallah, Ben Hmida Abdelmajid, Mzabi Sabeh, Bouraoui Saadia

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Clinical Medicine Insights. Oncology · 2024
    Review
  4. Article
  5. Article
  6. Review
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  14. Article
  15. CpG methylation of ubiquitin carboxyl-terminal hydrolase 1 (UCHL1) and P53 mutation pattern in sporadic colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Cancer diagnosis & prognosis
    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

9 authors at 3 institutions in 1 country.

Chaar InesLaboratory of Colorectal Cancer Research UR03ES04, Science University Tunis, 2047 Sidi Daoud, Tunis, Tunisia, ines_chaar@hotmail.com.
Ounissi Donia
Boughriba Rahma
Azza Ben Ammar
Amara Sameh
Taher Khalfallah
Ben Hmida Abdelmajid
Mzabi Sabeh
Bouraoui Saadia
Hôpital Mongi Slim · TNTunis El Manar University · TNTunis University · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

According to the multistep route of genetic alterations in the colorectal adenoma-carcinoma sequence, the complex K-ras/p53 mutation is one of the first alterations to occur and represent an important genetic event in colorectal cancer (CRC). An evaluation of the mutation spectra in K-ras and p53 gene was effected in 167 Tunisian patients with sporadic CRC to determine whether our populations have similar pattern of genetic alteration as in Maghrebin's population. Mutation patterns of codon 12-13 of K-ras and exon 5-8 of p53 were analyzed by immunohistochemistry and PCR-SSCP and confirmed by sequencing. Mutations in the K-ras gene were detected in 31.13 % and affect the women more than the men (p = 0.008). Immunostaining showed that expression of p21 ras was correlated with the advanced age (p = 0.004), whereas loss of signal was associated with mucinous histotype (p = 0.003). Kaplan-Meier survival curve found that patients with the K-ras mutation had a shorter survival compared with patients without mutation (p = 0.005). Alteration in p53 was seen in 17.4 % of patients and affects three hot spot codons such as 175, 245, and 248. Overexpression of p53 was seen in 34.1 % and correlated with tumor node metastasis (TNM) advanced stage (p = 0.037) and mucinous histotype (p = 0.001). A high concordance between p53 expression and alteration (p<0.005) was shown. Concomitant mutations in K-ras and p53 gene were detected in only 4 % of tumors. K-ras and p53 undergo separate pathways in colorectal tumorogenesis. Interestingly, mutations in the K-ras gene might be considered a valuable prognostic factor correlated to poor outcome. p53 gene alterations were rather low in our set, and methylation pattern of p53 is required to elucidate the molecular basis of this protein in CRC.

Indexed as

AgedCarcinogenesisColorectal NeoplasmsFemaleHumansKaplan-Meier EstimateLymphatic MetastasisMaleMiddle AgedMutationPrognosisProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTumor Suppressor Protein p53TunisiaKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24763823
OpenAlexW1966018333

What OpenQuestion holds

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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.