Loading…
Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence
BACKGROUND Cervical cancer is a predominantly human papillomavirus (HPV)‐driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C sin...
Saved in:
| Published in: | Cancer 2017-07, Vol.123 (13), p.2459-2466 |
|---|---|
| Main Authors: | , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063 |
| container_end_page | 2466 |
| container_issue | 13 |
| container_start_page | 2459 |
| container_title | Cancer |
| container_volume | 123 |
| creator | Alsbeih, Ghazi A. Al‐Harbi, Najla M. Bin Judia, Sara S. Khoja, Hatim A. Shoukri, Mohamed M. Tulbah, Asma M. |
| description | BACKGROUND
Cervical cancer is a predominantly human papillomavirus (HPV)‐driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C single nucleotide polymorphism (SNP) presumed to affect cancer incidence.
METHODS
Patients treated between 1990 and 2012 were reviewed, and a series of 232 invasive cervical cancer cases were studied and compared with 313 matched controls without cancer. SNP was genotyped by way of direct sequencing. HPV linear array analysis was used to detect and genotype HPV in tumor samples.
RESULTS
The incidence of cervical cancer revealed bimodal peaks at 42.5 years, with a slighter rebound at 60.8 years. Among all cases, 77% were HPV‐positive and 16 HPV genotypes were detected—mostly genotypes 16 (75%) and 18 (9%)—with no difference by age, histology, or geographical region. Although the TP53 G72C genotype was not associated with overall cervical cancer risk, it was significantly associated with HPV positivity (odds ratio, 0.57; 95% confidence interval, 0.36‐0.90; P = .016). Furthermore, the variant C allele was significantly overtransmitted in the population (P |
| doi_str_mv | 10.1002/cncr.30635 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5485004</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1920462317</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063</originalsourceid><addsrcrecordid>eNp9kcuKFDEUhoMoTju68QEk4EaEGnOpVFU2ghTeYFAZRnAX0qmT6QyppEyqauhn8KVN2-OgLlzlhPOd_1x-hJ5SckYJYa9MMOmMk4aLe2hDiWwrQmt2H20IIV0lav7tBD3K-bp8Wyb4Q3TCOi45F2KDflzAsBgYcNIz4Gjxbhl1wJOenPdx1KtLS8YuWDCziwHrMOArCDA7g-MKaU465NHlfEiW8ssvguOW9XiKfj_GNO0KuOrkdJixjzeQsIG0OqM9NjqUuIgbN0AJH6MHVvsMT27fU_T13dvL_kN1_vn9x_7NeWXquhMVCMtbKxttBa-1pk0nBis7zruOSUlBgNluG2nq1m6bBghICYS3kllLhsOZTtHro-60bEcYDISyhVdTcqNOexW1U39ngtupq7gqUdoTUheBF7cCKX5fIM-qXMCA9zpAXLKiXdfwhjAhC_r8H_Q6LimU9RSVjNQN47Qt1MsjZVLMOYG9G4YSdfBYHTxWvzwu8LM_x79Df5taAHoEbpyH_X-kVP-pvziK_gSEhbSL</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1920462317</pqid></control><display><type>article</type><title>Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence</title><source>Wiley-Blackwell Read & Publish Collection</source><source>EZB Electronic Journals Library</source><creator>Alsbeih, Ghazi A. ; Al‐Harbi, Najla M. ; Bin Judia, Sara S. ; Khoja, Hatim A. ; Shoukri, Mohamed M. ; Tulbah, Asma M.</creator><creatorcontrib>Alsbeih, Ghazi A. ; Al‐Harbi, Najla M. ; Bin Judia, Sara S. ; Khoja, Hatim A. ; Shoukri, Mohamed M. ; Tulbah, Asma M.</creatorcontrib><description>BACKGROUND
Cervical cancer is a predominantly human papillomavirus (HPV)‐driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C single nucleotide polymorphism (SNP) presumed to affect cancer incidence.
METHODS
Patients treated between 1990 and 2012 were reviewed, and a series of 232 invasive cervical cancer cases were studied and compared with 313 matched controls without cancer. SNP was genotyped by way of direct sequencing. HPV linear array analysis was used to detect and genotype HPV in tumor samples.
RESULTS
The incidence of cervical cancer revealed bimodal peaks at 42.5 years, with a slighter rebound at 60.8 years. Among all cases, 77% were HPV‐positive and 16 HPV genotypes were detected—mostly genotypes 16 (75%) and 18 (9%)—with no difference by age, histology, or geographical region. Although the TP53 G72C genotype was not associated with overall cervical cancer risk, it was significantly associated with HPV positivity (odds ratio, 0.57; 95% confidence interval, 0.36‐0.90; P = .016). Furthermore, the variant C allele was significantly overtransmitted in the population (P < .0003).
CONCLUSION
Cervical cancer incidence displays bimodal curve peaking at a young age with secondary rebound at older age. The combination of relative low HPV infection and variant TP53 72C allele overtransmission provide a plausible explanation for the low incidence of cervical cancer in our population. Therefore, HPV screening and host SNP genotyping may provide more relevant biomarkers to gauge the risk of developing cervical cancer. Cancer 2017;123:2459–66. © 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Cervical cancer incidence shows bimodal peaks at 43 years and relative rebound at 61 years of age. A reduced rate of human papillomavirus infection and overtransmission of the TP53 72C variant lower cancer incidence.</description><identifier>ISSN: 0008-543X</identifier><identifier>EISSN: 1097-0142</identifier><identifier>DOI: 10.1002/cncr.30635</identifier><identifier>PMID: 28393355</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Adenocarcinoma - epidemiology ; Adenocarcinoma - genetics ; Adenocarcinoma - virology ; Adult ; Age ; Age Distribution ; Aged ; Alleles ; Biomarkers ; Cancer ; cancer predisposition ; Carcinoma, Squamous Cell - epidemiology ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - virology ; Cervical cancer ; Cervix ; Confidence intervals ; Female ; Gene polymorphism ; Genetic Predisposition to Disease ; Genotype ; Genotypes ; Genotyping ; Health risk assessment ; Health risks ; Histology ; HPV genotyping ; Human papillomavirus ; Humans ; Incidence ; Infections ; Invasiveness ; Medical screening ; Middle Aged ; Odds Ratio ; Oncology ; Original ; p53 Protein ; Papillomaviridae ; Papillomavirus Infections - epidemiology ; Papillomavirus Infections - genetics ; Papillomavirus Infections - virology ; Polymorphism ; Polymorphism, Single Nucleotide ; Population genetics ; Saudi Arabia - epidemiology ; Sequences ; Single-nucleotide polymorphism ; TP53 polymorphism ; Tumor Suppressor Protein p53 - genetics ; Uterine Cervical Neoplasms - epidemiology ; Uterine Cervical Neoplasms - genetics ; Uterine Cervical Neoplasms - virology</subject><ispartof>Cancer, 2017-07, Vol.123 (13), p.2459-2466</ispartof><rights>2017 The Authors. published by Wiley Periodicals, Inc. on behalf of</rights><rights>2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society.</rights><rights>2017 American Cancer Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063</citedby><cites>FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063</cites><orcidid>0000-0002-2128-6293</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28393355$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alsbeih, Ghazi A.</creatorcontrib><creatorcontrib>Al‐Harbi, Najla M.</creatorcontrib><creatorcontrib>Bin Judia, Sara S.</creatorcontrib><creatorcontrib>Khoja, Hatim A.</creatorcontrib><creatorcontrib>Shoukri, Mohamed M.</creatorcontrib><creatorcontrib>Tulbah, Asma M.</creatorcontrib><title>Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence</title><title>Cancer</title><addtitle>Cancer</addtitle><description>BACKGROUND
Cervical cancer is a predominantly human papillomavirus (HPV)‐driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C single nucleotide polymorphism (SNP) presumed to affect cancer incidence.
METHODS
Patients treated between 1990 and 2012 were reviewed, and a series of 232 invasive cervical cancer cases were studied and compared with 313 matched controls without cancer. SNP was genotyped by way of direct sequencing. HPV linear array analysis was used to detect and genotype HPV in tumor samples.
RESULTS
The incidence of cervical cancer revealed bimodal peaks at 42.5 years, with a slighter rebound at 60.8 years. Among all cases, 77% were HPV‐positive and 16 HPV genotypes were detected—mostly genotypes 16 (75%) and 18 (9%)—with no difference by age, histology, or geographical region. Although the TP53 G72C genotype was not associated with overall cervical cancer risk, it was significantly associated with HPV positivity (odds ratio, 0.57; 95% confidence interval, 0.36‐0.90; P = .016). Furthermore, the variant C allele was significantly overtransmitted in the population (P < .0003).
CONCLUSION
Cervical cancer incidence displays bimodal curve peaking at a young age with secondary rebound at older age. The combination of relative low HPV infection and variant TP53 72C allele overtransmission provide a plausible explanation for the low incidence of cervical cancer in our population. Therefore, HPV screening and host SNP genotyping may provide more relevant biomarkers to gauge the risk of developing cervical cancer. Cancer 2017;123:2459–66. © 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Cervical cancer incidence shows bimodal peaks at 43 years and relative rebound at 61 years of age. A reduced rate of human papillomavirus infection and overtransmission of the TP53 72C variant lower cancer incidence.</description><subject>Adenocarcinoma - epidemiology</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - virology</subject><subject>Adult</subject><subject>Age</subject><subject>Age Distribution</subject><subject>Aged</subject><subject>Alleles</subject><subject>Biomarkers</subject><subject>Cancer</subject><subject>cancer predisposition</subject><subject>Carcinoma, Squamous Cell - epidemiology</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - virology</subject><subject>Cervical cancer</subject><subject>Cervix</subject><subject>Confidence intervals</subject><subject>Female</subject><subject>Gene polymorphism</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Genotyping</subject><subject>Health risk assessment</subject><subject>Health risks</subject><subject>Histology</subject><subject>HPV genotyping</subject><subject>Human papillomavirus</subject><subject>Humans</subject><subject>Incidence</subject><subject>Infections</subject><subject>Invasiveness</subject><subject>Medical screening</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Oncology</subject><subject>Original</subject><subject>p53 Protein</subject><subject>Papillomaviridae</subject><subject>Papillomavirus Infections - epidemiology</subject><subject>Papillomavirus Infections - genetics</subject><subject>Papillomavirus Infections - virology</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Population genetics</subject><subject>Saudi Arabia - epidemiology</subject><subject>Sequences</subject><subject>Single-nucleotide polymorphism</subject><subject>TP53 polymorphism</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Uterine Cervical Neoplasms - epidemiology</subject><subject>Uterine Cervical Neoplasms - genetics</subject><subject>Uterine Cervical Neoplasms - virology</subject><issn>0008-543X</issn><issn>1097-0142</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNp9kcuKFDEUhoMoTju68QEk4EaEGnOpVFU2ghTeYFAZRnAX0qmT6QyppEyqauhn8KVN2-OgLlzlhPOd_1x-hJ5SckYJYa9MMOmMk4aLe2hDiWwrQmt2H20IIV0lav7tBD3K-bp8Wyb4Q3TCOi45F2KDflzAsBgYcNIz4Gjxbhl1wJOenPdx1KtLS8YuWDCziwHrMOArCDA7g-MKaU465NHlfEiW8ssvguOW9XiKfj_GNO0KuOrkdJixjzeQsIG0OqM9NjqUuIgbN0AJH6MHVvsMT27fU_T13dvL_kN1_vn9x_7NeWXquhMVCMtbKxttBa-1pk0nBis7zruOSUlBgNluG2nq1m6bBghICYS3kllLhsOZTtHro-60bEcYDISyhVdTcqNOexW1U39ngtupq7gqUdoTUheBF7cCKX5fIM-qXMCA9zpAXLKiXdfwhjAhC_r8H_Q6LimU9RSVjNQN47Qt1MsjZVLMOYG9G4YSdfBYHTxWvzwu8LM_x79Df5taAHoEbpyH_X-kVP-pvziK_gSEhbSL</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Alsbeih, Ghazi A.</creator><creator>Al‐Harbi, Najla M.</creator><creator>Bin Judia, Sara S.</creator><creator>Khoja, Hatim A.</creator><creator>Shoukri, Mohamed M.</creator><creator>Tulbah, Asma M.</creator><general>Wiley Subscription Services, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2128-6293</orcidid></search><sort><creationdate>20170701</creationdate><title>Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence</title><author>Alsbeih, Ghazi A. ; Al‐Harbi, Najla M. ; Bin Judia, Sara S. ; Khoja, Hatim A. ; Shoukri, Mohamed M. ; Tulbah, Asma M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenocarcinoma - epidemiology</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - virology</topic><topic>Adult</topic><topic>Age</topic><topic>Age Distribution</topic><topic>Aged</topic><topic>Alleles</topic><topic>Biomarkers</topic><topic>Cancer</topic><topic>cancer predisposition</topic><topic>Carcinoma, Squamous Cell - epidemiology</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - virology</topic><topic>Cervical cancer</topic><topic>Cervix</topic><topic>Confidence intervals</topic><topic>Female</topic><topic>Gene polymorphism</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>Genotyping</topic><topic>Health risk assessment</topic><topic>Health risks</topic><topic>Histology</topic><topic>HPV genotyping</topic><topic>Human papillomavirus</topic><topic>Humans</topic><topic>Incidence</topic><topic>Infections</topic><topic>Invasiveness</topic><topic>Medical screening</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Oncology</topic><topic>Original</topic><topic>p53 Protein</topic><topic>Papillomaviridae</topic><topic>Papillomavirus Infections - epidemiology</topic><topic>Papillomavirus Infections - genetics</topic><topic>Papillomavirus Infections - virology</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Population genetics</topic><topic>Saudi Arabia - epidemiology</topic><topic>Sequences</topic><topic>Single-nucleotide polymorphism</topic><topic>TP53 polymorphism</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Uterine Cervical Neoplasms - epidemiology</topic><topic>Uterine Cervical Neoplasms - genetics</topic><topic>Uterine Cervical Neoplasms - virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alsbeih, Ghazi A.</creatorcontrib><creatorcontrib>Al‐Harbi, Najla M.</creatorcontrib><creatorcontrib>Bin Judia, Sara S.</creatorcontrib><creatorcontrib>Khoja, Hatim A.</creatorcontrib><creatorcontrib>Shoukri, Mohamed M.</creatorcontrib><creatorcontrib>Tulbah, Asma M.</creatorcontrib><collection>Wiley Open Access Journals</collection><collection>Wiley Free Archive</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alsbeih, Ghazi A.</au><au>Al‐Harbi, Najla M.</au><au>Bin Judia, Sara S.</au><au>Khoja, Hatim A.</au><au>Shoukri, Mohamed M.</au><au>Tulbah, Asma M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence</atitle><jtitle>Cancer</jtitle><addtitle>Cancer</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>123</volume><issue>13</issue><spage>2459</spage><epage>2466</epage><pages>2459-2466</pages><issn>0008-543X</issn><eissn>1097-0142</eissn><abstract>BACKGROUND
Cervical cancer is a predominantly human papillomavirus (HPV)‐driven disease worldwide. However, its incidence is unexplainably low in western Asia, including Saudi Arabia. Using this paradigm, we investigated the role of HPV infection rate and host genetic predisposition in TP53 G72C single nucleotide polymorphism (SNP) presumed to affect cancer incidence.
METHODS
Patients treated between 1990 and 2012 were reviewed, and a series of 232 invasive cervical cancer cases were studied and compared with 313 matched controls without cancer. SNP was genotyped by way of direct sequencing. HPV linear array analysis was used to detect and genotype HPV in tumor samples.
RESULTS
The incidence of cervical cancer revealed bimodal peaks at 42.5 years, with a slighter rebound at 60.8 years. Among all cases, 77% were HPV‐positive and 16 HPV genotypes were detected—mostly genotypes 16 (75%) and 18 (9%)—with no difference by age, histology, or geographical region. Although the TP53 G72C genotype was not associated with overall cervical cancer risk, it was significantly associated with HPV positivity (odds ratio, 0.57; 95% confidence interval, 0.36‐0.90; P = .016). Furthermore, the variant C allele was significantly overtransmitted in the population (P < .0003).
CONCLUSION
Cervical cancer incidence displays bimodal curve peaking at a young age with secondary rebound at older age. The combination of relative low HPV infection and variant TP53 72C allele overtransmission provide a plausible explanation for the low incidence of cervical cancer in our population. Therefore, HPV screening and host SNP genotyping may provide more relevant biomarkers to gauge the risk of developing cervical cancer. Cancer 2017;123:2459–66. © 2017 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Cervical cancer incidence shows bimodal peaks at 43 years and relative rebound at 61 years of age. A reduced rate of human papillomavirus infection and overtransmission of the TP53 72C variant lower cancer incidence.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28393355</pmid><doi>10.1002/cncr.30635</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-2128-6293</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-543X |
| ispartof | Cancer, 2017-07, Vol.123 (13), p.2459-2466 |
| issn | 0008-543X 1097-0142 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5485004 |
| source | Wiley-Blackwell Read & Publish Collection; EZB Electronic Journals Library |
| subjects | Adenocarcinoma - epidemiology Adenocarcinoma - genetics Adenocarcinoma - virology Adult Age Age Distribution Aged Alleles Biomarkers Cancer cancer predisposition Carcinoma, Squamous Cell - epidemiology Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - virology Cervical cancer Cervix Confidence intervals Female Gene polymorphism Genetic Predisposition to Disease Genotype Genotypes Genotyping Health risk assessment Health risks Histology HPV genotyping Human papillomavirus Humans Incidence Infections Invasiveness Medical screening Middle Aged Odds Ratio Oncology Original p53 Protein Papillomaviridae Papillomavirus Infections - epidemiology Papillomavirus Infections - genetics Papillomavirus Infections - virology Polymorphism Polymorphism, Single Nucleotide Population genetics Saudi Arabia - epidemiology Sequences Single-nucleotide polymorphism TP53 polymorphism Tumor Suppressor Protein p53 - genetics Uterine Cervical Neoplasms - epidemiology Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - virology |
| title | Reduced rate of human papillomavirus infection and genetic overtransmission of TP53 72C polymorphic variant lower cervical cancer incidence |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T21%3A15%3A17IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Reduced%20rate%20of%20human%20papillomavirus%20infection%20and%20genetic%20overtransmission%20of%20TP53%2072C%20polymorphic%20variant%20lower%20cervical%20cancer%20incidence&rft.jtitle=Cancer&rft.au=Alsbeih,%20Ghazi%20A.&rft.date=2017-07-01&rft.volume=123&rft.issue=13&rft.spage=2459&rft.epage=2466&rft.pages=2459-2466&rft.issn=0008-543X&rft.eissn=1097-0142&rft_id=info:doi/10.1002/cncr.30635&rft_dat=%3Cproquest_pubme%3E1920462317%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4485-e5f37f96af534aa1685df9833882991e5ecbb69c47fb66e0e99e03792ff0d3063%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1920462317&rft_id=info:pmid/28393355&rfr_iscdi=true |