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

Autor:	Alshehri E; Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia., Al-Dogmi AM; Department of Biology, College of Science, Jouf University, Sakakah, Saudi Arabia., Al-Hazani TMI; Department of Biology, College of Sciences and Humanities, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia., Alwaili MA; Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia., Safhi FA; Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia., Alneghery LM; Department of Biology, College of Science, Al-Imam Mohammad Ibn Saud Islamic University, Riyadh, Saudi Arabia., Jalal AS; Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia., Alanazi IS; Department of Biology, Faculty of Sciences, University of Hafr Al-Batin, Hafar al-Batin, Saudi Arabia., AlQassim FA; Regional Laboratory and Blood Bank, Dammam, Saudi Arabia., Alhumaidi Alotaibi M; Department of Biology, College of Science, Jouf University, Sakakah, Saudi Arabia., Al-Qahtani WS; Department of Forensic Sciences, College of Criminal Justice, Naif Arab University for Security Sciences, Riyadh, Saudi Arabia.
Jazyk:	angličtina
Zdroj:	Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine [Tumour Biol] 2023; Vol. 45 (1), pp. 1-14.
DOI:	10.3233/TUB-220032
Abstrakt:	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.
Databáze:	MEDLINE
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