Eman Alshehri, Amal M Al-Dogmi, Tahani Mohamed Ibrahim Al-Hazani, Maha Abdulla Alwaili, Fatmah Ahmed Safhi, Lina Mohammed Alneghery, Areej Saud Jalal, Ibtesam Sanad Alanazi, Fatima Abdullah AlQassim, Mashael Alhumaidi Alotaibi, Wedad Saeed Al-Qahtani
{"title":"诊断为膀胱癌的吸烟男性患者中9种癌症相关基因的突变模式和PAF的发展","authors":"Eman Alshehri, Amal M Al-Dogmi, Tahani Mohamed Ibrahim Al-Hazani, Maha Abdulla Alwaili, Fatmah Ahmed Safhi, Lina Mohammed Alneghery, Areej Saud Jalal, Ibtesam Sanad Alanazi, Fatima Abdullah AlQassim, Mashael Alhumaidi Alotaibi, Wedad Saeed Al-Qahtani","doi":"10.3233/TUB-220032","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":23364,"journal":{"name":"Tumor Biology","volume":"45 1","pages":"1-14"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Patterns of mutations in nine cancer-related genes and PAF development among smoking male patients diagnosed with bladder cancer.\",\"authors\":\"Eman Alshehri, Amal M Al-Dogmi, Tahani Mohamed Ibrahim Al-Hazani, Maha Abdulla Alwaili, Fatmah Ahmed Safhi, Lina Mohammed Alneghery, Areej Saud Jalal, Ibtesam Sanad Alanazi, Fatima Abdullah AlQassim, Mashael Alhumaidi Alotaibi, Wedad Saeed Al-Qahtani\",\"doi\":\"10.3233/TUB-220032\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":23364,\"journal\":{\"name\":\"Tumor Biology\",\"volume\":\"45 1\",\"pages\":\"1-14\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Tumor Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3233/TUB-220032\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tumor Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3233/TUB-220032","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
Patterns of mutations in nine cancer-related genes and PAF development among smoking male patients diagnosed with bladder cancer.
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.
期刊介绍:
Tumor Biology is a peer reviewed, international journal providing an open access forum for experimental and clinical cancer research. Tumor Biology covers all aspects of tumor markers, molecular biomarkers, tumor targeting, and mechanisms of tumor development and progression.
Specific topics of interest include, but are not limited to:
Pathway analyses,
Non-coding RNAs,
Circulating tumor cells,
Liquid biopsies,
Exosomes,
Epigenetics,
Cancer stem cells,
Tumor immunology and immunotherapy,
Tumor microenvironment,
Targeted therapies,
Therapy resistance
Cancer genetics,
Cancer risk screening.
Studies in other areas of basic, clinical and translational cancer research are also considered in order to promote connections and discoveries across different disciplines.
The journal publishes original articles, reviews, commentaries and guidelines on tumor marker use. All submissions are subject to rigorous peer review and are selected on the basis of whether the research is sound and deserves publication.
Tumor Biology is the Official Journal of the International Society of Oncology and BioMarkers (ISOBM).