Mutations in codons 12 and 13 of K-ras exon 2 in colorectal tumors of Saudi Arabian patients: frequency, clincopathological associations, and clinical outcomes

Zekri, J; Alshehri, Ahmed; Mahrous, Mervat; S, Al-Rehaily; Darwish, Tarek; Bassi, Sawsan; H, El Taani; A, Al Zahrani; Elsamany, Shereef; Al-Maghrabi, Jaudah; Bb, Sadiq

doi:10.4238/gmr16019369

Cited by 11 publications

(12 citation statements)

References 42 publications

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“…The frequency of KRAS mutations in our study group did not differ when compared with those of most other studies in Europe and the United States (23,24). Previous studies that enrolled a relatively large number of Arabian patients with different stages of the disease, reported KRAS mutation rates of 28-56% in Saudi Arabia (19,(25)(26)(27), 23-32% in Tunisia (22,28,29), 33-44% in Jordan (30,31) and 42% in Egypt (32).…”

Section: Discussionmentioning

confidence: 99%

KRAS mutations in patients with colorectal cancer in Libya

et al. 2021

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Large prospective clinical trials have demonstrated that colorectal cancers (CRCs) with wild-type KRAS respond favorably to anti-epidermal growth factor receptor treatment, thus making mutational analysis obligatory prior to treatment. In our study, frozen CRC tissues from Libyan patients were analyzed for KRAS and HRAS mutations in codons 12/13 by direct sequencing and the correlations with clinical and pathological parameters were investigated. A total of 34 CRC cases, comprising 19 men and 15 women (age range, 24-87 years), were subjected to systematic analysis for RAS mutations. Although HRAS mutations were not detected in any of the patients in the study group, KRAS codon 12/13 mutations were present in 38.2% (13/34) of the patients. The frequent types of codon 12 mutations were glycine to aspartate (G12D, 46.1%); glycine to valine (G12V, 30.8%) and glycine to cysteine (G12C, 15.4%), while the codon 13 mutations were glycine to aspartate (G13D, 7.7%). G→A mutations occurred in 53.8% (7/13) of the patients, while G→T mutations occurred in 46.2% (6/13) of the patients. Mutations occurred at the first base of codon 12 or 13 in 2/13 (15.4%) and at the second base in 11/13 (84.6%) patients. There was no significant association between clinicopathological characteristics and KRAS mutation status, except the site of the tumors harboring KRAS mutations, which was as follows: The frequency was higher among tumors located in the left colon (8/13, 61.5%) compared to other sites (P=0.027). KRAS mutations were correlated with advanced age, with 10/13 being aged >50 years and affected 8/15 female patients (53%) compared with 5/19 male patients (26%). The highest frequency of KRAS mutations was observed in highly differentiated CRCs (8/13).

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Section: Discussionmentioning

confidence: 99%

KRAS mutations in patients with colorectal cancer in Libya

et al. 2021

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“…However, we found no significant association between the overall frequency of K-ras mutations and patients’ characteristics and/or clinicopathological features. In literature, conflicting results were documented regarding the association between K-ras mutations and patients’ characteristics and/or clinicopathological features [ 17 - 21 ]. For example, while some studies showed that females are significantly more likely to have mutant K-ras than males [ 18 , 22 ], other studies showed the opposite (i.e males are significantly more likely to have mutant K-ras than females) [ 17 , 23 ].…”

Section: Discussionmentioning

confidence: 99%

Clinico-Pathological Study of K-ras Mutations in Colorectal Tumors: A Single-Center Retrospective Study of 51 Patients in Madinah, Saudi Arabia

Mulla¹,

Alshareef²,

Syed

et al. 2020

Cureus

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Background Colorectal cancer (CRC) is one of the leading types of cancer worldwide and in Saudi Arabia. At the molecular level, CRC is very complicated and requires establishing comprehensive patient stratification models through identification of patients who will benefit or will not benefit from targeted therapy. We retrospectively investigated and analyzed the frequency of Kirsten-ras (K-ras) mutation and its correlation with patients’ characteristics as weel as its association with clinicopathological features (i.e age, gender, clinical stage, anatomical site, histological subtype, degree of histological differentiation and metastatic site) in patients with CRC. Methods Medical records and paraffin-embedded tumor samples from 51 patients with histologically proven colorectal adenocarcinoma referred to Madinah center in Saudi Arabia were analyzed for the occurrence of rat sarcoma virus (RAS) mutations. Results RAS mutations occurred in 43% of the patients; 91% of these mutations were in K-ras. Seventy-five percent of these K-ras mutations were in codon 12, most commonly p.G12D. Codon 13 mutations occurred in 20% of tumors: all of these were p.G13D (100%). The percentage of K-ras mutations occurrence was higher in young patients (≤50) compared with the older patients (>50) (54.5% and 35%, respectively). Similarly, the percentage of K-ras mutations occurrence was higher in the right-sided tumors compared with the left-sided tumors (57.1% and 32.4%, respectively). Patients’ characteristics and clinicopathological features were not significantly associated with K-ras mutations. Conclusions K-ras mutations are common among Saudi patients diagnosed with CRC in Madinah, especially pG12V and pG12D in codon 12. Further investigation would be required to establish correlation of K-ras mutations in larger cohorts.

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“…The most frequently happens in exon 2 (codons 12 and 13), changing the guanine/adenine that during the formation of protein replaces the amino acid. Exon mutations may occur less often 3 (codons 61) and exon 4 (codons 146) (23).…”

Section: Methodsmentioning

confidence: 99%

“…Since 2009, the American Society of Clinical Oncology has recommended that mAb treatment candidates be screened for K-ras mutations in codons 12 and 13. (23), because mutations in this gene identify patients who do not respond well to therapy with anti-EGFR drugs (24).…”

Section: Introductionmentioning

confidence: 99%

Tumor Diagnosis by Genetic Markers Protein P-53, p16, C-MYC, N-MYC, Protein K-Ras, and Gene Her-2 Neu is this possible? Tumor Diagnosis by Genetic Markers C-MYC, N-MYC, Protein P-53, p16

Al-hassany¹,

Albu-Rghaif²,

Naji³

2021

PJMHS

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Currently, cancer is among the leading causes of death in the world. It is the correct diagnosis that gives the patient a better chance of healing. The detection of genetic markers, macromolecules that are produced directly by the tumor or by the host, has the potential to be one of the diagnostic tests. This paper is a review article, with the objective of addressing tumor markers c-MYC, n-MYC, protein p-53, protein Kras, and the gene HER-2 neu regarding the diagnosis and prognosis of patients with cancer, studies demonstrated that c-MYC is expressed in several malignant tumors because it affects proliferation and cellular metabolism, P-53 in breast and lung tumors is overexpressed, Regarding p16 it has been suggested that cytoplasmic also overexpression as kind of cancer predictor. K-ras is used to determine survival time and free time for neoplasm. It is an effective marker for monoclonal antibody therapy. The marker HER-2 neu and N-MYC are indicative of poor prognosis, conclusions: application of these markers is being increasingly used for expressing specificity and sensitivity in different areas of tumor characterization, in addition to being related to the therapeutic conduct to be followed in tumor treatment. Keywords: genetic marker; p16; Tumor marker; cancer diagnosis;p53

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Mutations in codons 12 and 13 of K-ras exon 2 in colorectal tumors of Saudi Arabian patients: frequency, clincopathological associations, and clinical outcomes

Cited by 11 publications

References 42 publications

KRAS mutations in patients with colorectal cancer in Libya

KRAS mutations in patients with colorectal cancer in Libya

Clinico-Pathological Study of K-ras Mutations in Colorectal Tumors: A Single-Center Retrospective Study of 51 Patients in Madinah, Saudi Arabia

Tumor Diagnosis by Genetic Markers Protein P-53, p16, C-MYC, N-MYC, Protein K-Ras, and Gene Her-2 Neu is this possible? Tumor Diagnosis by Genetic Markers C-MYC, N-MYC, Protein P-53, p16

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