Kras Mutations and Egfr Expression as Prognostic and Predictive Factors in Cancer Patients

被引:1
作者
Hussein, Alaa Ramthan [1 ]
Dawood, Wedad Salih [1 ]
机构
[1] Univ Diyala, Coll Sci, Biol Dept, Dhi Qar Publ Educ, Baqubah, Iraq
关键词
Cancer patients; Baghdad; K-ras; polymorphism; genotype; PCR; COLORECTAL-CANCER; GASTRIC-CANCER; ADENOCARCINOMA; EPIDEMIOLOGY;
D O I
10.47750/jptcp.2023.30.03.041
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cell proliferation is largely believed to be under the control of the epidermal growth factor receptor (EGFR), a member of the tyrosine kinase family of proteins. The existence of point mutations in the K-ras proto-oncogene, a member of the RAS gene family, is an essential determinant in cancer development. These alterations, which are involved in the control of signal transmission across the plasma membrane, play a significant role in cancer development. Mutations in the K-ras gene are frequently discovered in pancreatic, lung, colon, and stomach cancer patients. K-ras mutations are most commonly seen in codons 12 and 13, with codon 61 being the least prevalent. This study examined the prognostic and predictive effect of EGFR expression and K-ras mutations in gastric cancer patients. The study group consisted of patients with stomach cancer who were followed up at Baghdad Teaching Hospital between March 2018 and April 2022. They were all diagnosed using paraffin blocks and slides. The Department of Pathology records at Baghdad Medical College in Iraq were searched for information on these patients' demographic and pathological characteristics and their survival rates. The immunohistochemistry method was utilised to examine the epidermal growth factor receptor (EGFR) expression in 62 patients' stomach tissues. The stomach tissues were paraffin -fixed, and sections were cut from them. Mutagenic PCR and RFLP methods were used to investigate the occurrence of K-ras oncogene codon 12-and 13-point mutations. DNA was isolated from paraffin tissue samples acquired from EGFR-positive people. In 62 gastric cancer patients, the genotype frequencies of the K-ras gene codon 12 were determined to be 93.62 %, 6.38 %, and 0%, respectively. The genotype frequencies of the gene codon 13 were found to be 73.08 %, 26.02 %, and 0%, respectively. From previous studies it was clear that patients with wild-type K-ras polymorphism alleles responded favourably to Cetuximab and had their growth reduced. Individuals with these genotypes are also prevalent in our patient population. We have reason to believe that polymorphism research will be advantageous, notably in the treatment of personalised cancer care.
引用
收藏
页码:E393 / E403
页数:11
相关论文
共 22 条
[1]   Gastric cancer: epidemiology, pathology and treatment [J].
Alberts, SR ;
Cervantes, A ;
van de Velde, CJH .
ANNALS OF ONCOLOGY, 2003, 14 :31-36
[2]  
Bissada Eric, 2013, Int J Otolaryngol, V2013, P848021, DOI 10.1155/2013/848021
[3]   K-ras oncogene mutations in sporadic colorectal cancer in The Netherlands Cohort Study [J].
Brink, M ;
de Goeij, AFPM ;
Weijenberg, MP ;
Roemen, GMJM ;
Lentjes, MHFM ;
Pachen, MMM ;
Smits, KM ;
de Bruïne, AP ;
Goldbohm, RA ;
van den Brandt, PA .
CARCINOGENESIS, 2003, 24 (04) :703-710
[4]  
Bugra D, 2004, GASTRIC TUMORS S
[5]   FREQUENCY AND SPECTRUM OF MUTATIONS AT CODON-12 AND CONDON-13 OF THE C-K-RAS GENE IN HUMAN TUMORS [J].
CAPELLA, G ;
CRONAUERMITRA, S ;
PEINADO, MA ;
PERUCHO, M .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1991, 93 :125-131
[6]   Detection of N-, H-, and KRAS codons 12, 13, and 61 mutations with universal RAS primer multiplex PCR and N-, H-, and KRAS-specific primer extension [J].
Chang, Ya-Sian ;
Yeh, Kun-Tu ;
Hsu, Nicholas C. ;
Lin, Shu-Hui ;
Chang, Tien-Jye ;
Chang, Jan-Gowth .
CLINICAL BIOCHEMISTRY, 2010, 43 (03) :296-301
[7]  
Cox Adrienne D, 2010, Small GTPases, V1, P2
[8]  
Demir G, 2008, TOG GASTROINTESTINAL
[9]   Estimating the global cancer incidence and mortality in 2018: GLOBOCAN sources and methods [J].
Ferlay, J. ;
Colombet, M. ;
Soerjomataram, I. ;
Mathers, C. ;
Parkin, D. M. ;
Pineros, M. ;
Znaor, A. ;
Bray, F. .
INTERNATIONAL JOURNAL OF CANCER, 2019, 144 (08) :1941-1953
[10]  
Ferlay J, 2015, INT J CANCER, V136, pE359, DOI [10.14343/jcscr.2016.4e1003, 10.1002/ijc.29210]