P1678ASSOCIATION OF EPIDERMAL GROWTH FACTOR(EGF) AND EGF RECEPTOR POLYMORPHISMS WITH END STAGE RENAL DISEASE AND ACUTE RENAL ALLOGRAFT REJECTION IN KOREAN POPULATION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sunwoo Kang ◽  
Byeong Woo KIm

Abstract Background and Aims Epidermal growth factor (EGF) has been found to be associated with development and repair mechanisms of several renal diseases. In this study, we hypothesized that single nucleotide polymorphisms (SNPs) of the EGF or its receptor genes might have association with end stage renal disease (ESRD) or acute renal allograft rejection (AR) in Korean patients. Method 347 recipients of the first renal transplants for ESRD including 63 AR patients among them and 289 healthy adults were included in the study. Five EGF gene SNPs (rs11568835, rs11568943, rs2237051, rs11569017, rs3756261) and four EGFR gene SNPs (rs1140475, rs2293347, rs1050171, rs6965469) were analyzed. The genotypes of these SNPs were analyzed using AxiomTM genome-wide human assay. For statistical analysis we used SNPStats and Haploview version 4.2. Multiple logistic regression models (codominant, dominant, recessive and Log-additive) were produced to obtain odds ratio (OR), 95% confidence interval (CI), and p value. Results One SNP (rs11569017) in EGF gene showed significant association with ESRD but not with AR. Another SNP (rs11568835) in EGF gene showed significant association with susceptibility to AR but not with ESRD. One SNP (rs1050171) in EGFR gene showed significant association with susceptibility to AR but not with ESRD. Conclusion We suggest that genetic polymorphisms of EGF and EGFR gene may be associated with the risk of development of ESRD and AR in the Korean population.

1994 ◽  
Vol 46 (4) ◽  
pp. 1207-1215 ◽  
Author(s):  
Alicia N. Stein-Oakley ◽  
Alex Tzanidis ◽  
Peter J. Fuller ◽  
Paula Jablonski ◽  
Napier M. Thomson

2005 ◽  
Vol 23 (11) ◽  
pp. 2445-2459 ◽  
Author(s):  
José Baselga ◽  
Carlos L. Arteaga

The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase of the ErbB receptor family that is abnormally activated in many epithelial tumors. The aberrant activation of the EGFR leads to enhanced proliferation and other tumor-promoting activities, which provide a strong rationale to target this receptor family. There are two classes of anti-EGFR agents: monoclonal antibodies (MAbs) directed at the extracellular domain of the receptor and small molecule, adenosine triphosphate–competitive inhibitors of the receptor's tyrosine kinase. Anti-EGFR MAbs have shown antitumor activity in advanced colorectal carcinoma, squamous cell carcinomas of the head and neck, non–small-cell lung cancer (NSCLC) and renal cell carcinomas. The tyrosine kinase inhibitors (TKIs) have a partially different activity profile. They are active against NSCLC, and a specific EGFR inhibitor has shown improvement in survival. Recently, mutations and amplifications of the EGFR gene have been identified in NSCLC and predict for enhanced sensitivity to anti-EGFR TKIs. In addition to specific anti-EGFR TKIs, there are broader acting inhibitors such as dual EGFR HER-2 inhibitors and combined anti-pan-ErbB and antivascular endothelial growth factor receptor inhibitors. Current research efforts are directed at selecting the optimal dose and schedule and identifying predictive factors of response and resistance beyond EGFR gene mutations and/or amplifications. Finally, there is a need for improved strategies to integrate anti-EGFR agents with conventional therapies and to explore combinations with other molecular targeted approaches including other antireceptor therapies, receptor-downstream signaling transduction inhibitors, and targeted approaches interfering with other essential drivers of cancer, such as angiogenesis.


2000 ◽  
Vol 36 (5) ◽  
pp. 945-952 ◽  
Author(s):  
Lorenzo S. Malatino ◽  
Francesca Mallamaci ◽  
Francesco A. Benedetto ◽  
Ignazio Bellanuova ◽  
Alessandro Cataliotti ◽  
...  

Lung Cancer ◽  
2010 ◽  
Vol 68 (3) ◽  
pp. 498-500 ◽  
Author(s):  
Teruhisa Takuwa ◽  
Fumihiro Tanaka ◽  
Kazue Yoneda ◽  
Ikuko Torii ◽  
Masaki Hashimoto ◽  
...  

1998 ◽  
Vol 53 (3) ◽  
pp. 639-644 ◽  
Author(s):  
Manikkam Suthanthiran ◽  
Ashwani Khanna ◽  
David Cukran ◽  
Rohini Adhikarla ◽  
Vijay K. Sharma ◽  
...  

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