The socioeconomic and cultural impact of tobacco and smoking in Saudi Arabia: a review

Alzahrani, Waleed; Harthi, Mohammed; Aljabri, Abdullatif; Alshaikh, Amani; Almubaddil, Mohammed; Darwish, Naif A.

doi:10.24911/ijmdc.51-1575925960

Cited by 1 publication

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“…at 22.1%, with Saudis using cigarettes each day. Statistically, 43.7% of smokers are males, with the female population of smokers representing 16.5% [33]. An average cigarette contains approximately 7,000 chemicals, and more than 70 are scientifically categorised as carcinogenic.…”

Section: Discussionmentioning

confidence: 99%

“…Other research demonstrated that PAF triggers pro-inflammatory cells, including macrophages and neutrophils through selected inflammatory channels; this was claimed to contribute to diverse biological processes, such as epithelial apoptosis, growth of vascular permeability, and smooth muscle contractions [33,36,39,40]. In connection with reproductive function, anti-apoptosis, and DNA repair, it was suggested as a potential cause of cancer progression [36].…”

Section: Discussionmentioning

confidence: 99%

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Patterns of mutations in nine cancer-related genes and PAF development among smoking male patients diagnosed with bladder cancer

Alshehri

Al-Dogmi

Al-Hazani

et al. 2023

TUB

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BACKGROUND: Smoking is one of the most popular risk factors provoking bladder cancer (BC). This research intended to estimate cigarette smoking effect involving PAF signs between smoking patients with BC and non-smoking patients with same diagnosis to define relations with pathological characteristics and their prognosis on zero-relapse and disease-associated recovery. METHODS: Two groups of smokers (n = 54) and non-smokers (n = 62) were selected. Both cohorts of patients had BC. They were evaluated utilizing NGS on 9 cancer-related genes and confirmed through the Sanger DNA sequencing and histopathological tests based on H&E staining. The factor of smoking and impact of PAF development by ELISA assay and PAF-R manifestation in terms of immunochemical evaluation on BC areas comparing to a control group (n = 30) was examined involving healthy contributors, including the use of well-designed statistical trials. RESULTS: The multivariate evaluation showed considerable rise in mutation patterns related to smoking among BC patients (group 3), increase in PAF development (***P<0.001) and vivid signs of PAF-R contrasted to non-smokers with BC (group 2) and control group (group 1). All the identified biological changes (gains/losses) were recorded at the same locations in both groups. Patients from group 3 held 3-4 various mutations, while patients from group 2 held 1-3 various mutations. Mutations were not identified in 30 respondents from control group. The most repeated mutations were identified in 3 of 9 examined genes, namely TP53, PIK3CA and PTEN, with highest rates of increase in Group 3. Moreover, histopathological tests revealed barely identifiable and abnormal traits in BC tissues, i.e. were without essential histopathological changes between groups 2 and 3. CONCLUSION: Smoking of cigarettes provokes PAF development due to urothelial inflammation and rise of mutations in 9 cancer-related genes. These are indicative factors of inducing BC.

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Section: Discussionmentioning

confidence: 99%