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1.
Curr Mol Med ; 2024 Jan 12.
Artigo em Inglês | MEDLINE | ID: mdl-38243923

RESUMO

Gastrointestinal (GI) cancer is one the most prevalent types of cancer. Despite current chemotherapy's success, patients with GI cancer continue to have a dismal outcome. The onset and progression of cancer are caused by alterations and the abnormal expression of several families of genes, like tumor-suppressor genes, oncogenes, and chemotherapy-resistant genes. The final purpose of tumor therapy is to inhibit cellular development by modifying mutations and editing the irregular expression of genes It has been reported that CDH1, TP53, KRAS, ARID1A, PTEN, and HLA-B are the commonly mutated genes in GI cancer. Gene editing has become one potential approach for cases with advanced or recurrent CRC, who are nonresponsive to conventional treatments and a variety of driver mutations along with progression cause GI progression. CRISPR/Cas9 technique is a reliable tool to edit the genome and understand the functions of mutations driving GI cancer development. CRISPR/Cas9 can be applied to genome therapy for GI cancers, particularly with reference to molecular-targeted medicines and suppressors. Moreover, it can be used as a therapeutic approach by knocking in/out multiple genes. The use of CRISPR/ Cas9 gene editing method for GI cancer therapy has therefore resulted in some improvements. There are several research works on the role of CRISPR/Cas9 in cancer treatment that are summarized in the following separate sections. Here, the use of CRISPR/Cas9-based genome editing in GI and the use of CRISPR/Cas9 is discussed in terms of Targeting Chemotherapy Resistance-related Genes like; KRAS, TP53, PTEN, and ARID1A.

2.
Acta Cardiol ; 78(9): 1033-1044, 2023 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-37694924

RESUMO

OBJECTIVE: To investigate the association between cardiovascular diseases (CVDs) and haematologic factors in a cohort of Iranian adults. METHOD: For a total population of 9,704 aged 35 to 65, a prospective study was designed. Haematologic factors and demographic characteristics (such as gender, age, and smoking status) were completed for all participants. The association between haematologic factors and CVDs was assessed through logistic regression (LR) analysis, decision tree (DT), and bootstrap forest (BF). RESULTS: Almost all of the included factors were significantly associated with CVD (p<.001). Among the included factors, were: age, white blood cell (WBC), and platelet distribution width (PDW) had the strongest correlation with the development of CVD. For unit OR interpretation, WBC has been represented as the most remarkable risk factor for CVD (OR: 1.22 (CI 95% (1.18, 1.27))). Also, age is associated with an increase in the odds of CVD + occurrence (OR: 1.12 (CI 95% (1.11, 1.13))). Moreover, males are times more likely to develop CVD than females (OR: 1.39 (CI 95% (1.22, 1.58))). In DT model, age is the best classifier factor in CVD development, followed by WBC and PDW. Furthermore, based on the BF algorithm, the most crucial factors correlated with CVD are age, WBC, PDW, sex, and smoking status. CONCLUSION: The obtained result from LR, DT, and BF models confirmed that age, WBC, and PDW are the most crucial factors for the development of CVD.

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