Expression of Angiogenesis-related Genes in a Group of Iranian Cases of Breast Cancer

Abstract

Aims: This study aims to design an angiogenesis gene expression profile; to study angiogenesis gene expression profile in breast cancer; and to map angiogenesis gene expression profile in individual participants. Background: In molecular etiology of each disease, there are some important molecules involved in the related pathways. From the viewpoint of precision medicine, molecular etiology of a disease is different person by person because of genetic variations of the genes involved in these pathways. This point of view intends researchers of drug development to design novel drugs for targeted therapy based on the exact etiology. In the case of angiogenesis, there is a drug profile parallel to the molecular profile. Bevacizumab, sunitinib and aflibercept are examples of anti-angiogenic drugs. Objectives: A hallmark of solid tumors is sustained angiogenesis. Vascular endothelial growth factors (VEGF), VEGF receptors (VEGFR) and placental growth factor (PlGF) are involved in angiogenesis. We aimed to study the gene expression profile of angiogenesis including VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGFR-1, VEGFR-2, VEGFR-3 and PlGF in an Iranian group of patients undergoing breast surgery due to breast cancer and breast fibroadenoma. Methods: Tumor tissue samples of a group of patients with invasive ductal carcinoma (IDC) and a group of patients with fibroadenoma (Fib) were used. Gene expression was studied by real-time quantitative polymerase chain reaction (q-PCR) and fold changes (FC) with their 95% confidence intervals (CI) were reported based on calibration with normal breast tissue. Results: All the genes showed significant up-regulation in IDC group. The extensive up-regulation was for VEGFR-2 (FC=52.68; 95% CI=17.96-154.47; P<0.001). In Fib group, PlGF showed a significant upregulation (FC=10.41; 95% CI=5.35-20.26; P=0.002). Comparison of IDC group with Fib group showed significant up-regulation of VEGFR-1, VEGFR-2 and VEGFR-3 in IDC group (P<0.05). Conclusion: Malignancy of breast tumors is associated with overexpression of all the genes of this profile. However, only VEGFRs showed up-regulation in comparison to benign tumors. Individualized targeted therapy, according to this profile, should be studied in the future.

A Meta-Analysis for Association of XRCC3 rs861539, MTHFR rs1801133, IL-6 rs1800795, IL-12B rs3212227, TNF-α rs1800629, and TLR9 rs352140 Polymorphisms with Susceptibility to Cervical Carcinoma

“…However, the specific molecular mechanisms and potential single gene require further studies. Familial based studies and evaluation of inherited genetic variations revealed that host genetic factors have a role in cervical cancer pathogenesis (Yang et al, 2020;Ahmadi et al, 2021). Recently, a comprehensive review study showed that CDK1, CCNB1, ITGB1, FN1, MMP9 and STAT1 played different roles in the progression of cervical cancer through different signaling pathways (Sayad, Ahmadi, Nekouian, et al, 2020;Yi et al, 2020).…”

VEGF-B, VEGF-A, FLT-1, KDR, ERBB2, EGFR, GRB2, RAC1, CDH1 and HYAL-1 Genes Expression Analysis in Canine Mammary Gland Tumors and the Association with Tumor ClinicoPathological Parameters and Dog Breed Assessment

“…While multiple studies were done in the research of importance of VEGF family members, the knowledge about VEGF-B is scarce. VEGF-B (together with VEGF-A , FLT1 and KDR ) was found to be upregulated in invasive ductal carcinoma BC group compared to patients with fibroadenoma, while another study did not find a significant difference in VEGF-B mRNA levels between normal and neoplastic breast [ 52 , 53 ]. To our knowledge, there are no studies that evaluated VEGF-B gene expression in CMTs.…”

Lack of Association between TP73 G4C14-A4T14 Polymorphism and Cervical Cancer Risk in Overall and Asian Women: A Meta-Analysis

“…There were reported a few familial clustering of cervical cancer cases indicating that high-penetrance germline variants are rare in this cancer and heritable risk of cervical cancer may be accounted for by low- and intermediate-penetrant genetic factors [ 21 , 22 ]. However, some evidence from epidemiological studies have been shown that a genetic background could predispose to cervical cancer, and that some of the genes likely to be involved are IRF3, TLR2, EXO1, CYBA, XRCC1 and FANCA, OAS3, SULF1, IFNG, DUT, DMC1, GTF2H4, EVER1/2, ERAP1, LMP7, TAP2, TP53, TERT and IL-17 [ 23 , 24 ]. Several studies showed that TP73 expression is up-regulated in cervical cancer tissues in comparison in normal cervical squamous epithelium, and negatively associated with clinical progression in cervical cancer patients [ 25 , 19 ].…”