Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients

Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood. To evaluate the relationship between HPV genotypes and genomic alterations in PCa,...

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Published inEuropean journal of medical research Vol. 28; no. 1; pp. 239 - 10
Main Authors Lang, Bin, Cao, Chen, Zhao, Xiaoxiao, Wang, Yi, Cao, Ying, Zhou, Xueying, Zhao, Tong, Wang, Yuyan, Liu, Ting, Liang, Wenjia, Hu, Zheng, Tian, Xun, Zhang, Jingjing, Yan, Yongji
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 17.07.2023
BioMed Central
BMC
Subjects
Age groups
Cancer patients
Capture sequencing
Care and treatment
Development and progression
East Asian People
Genetic aspects
Genomes
Genomics
Genotype
Human papillomavirus
Humans
Infection
Infections
Male
Medical screening
Mutation
Nuclear Proteins - genetics
Papillomavirus infections
Papillomavirus Infections - complications
Papillomavirus Infections - genetics
Prostate cancer
Prostatic Neoplasms - complications
Prostatic Neoplasms - genetics
Prostatic Neoplasms - pathology
Repressor Proteins - genetics
Sexually transmitted diseases
Tumors
Whole-exome sequencing
Xeroderma Pigmentosum Group D Protein - genetics
China
Human papillomavirus
Capture sequencing
Prostate cancer
Whole-exome sequencing
Online AccessGet full text

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Abstract Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood. To evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated. The presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1. The genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.
AbstractList Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood. To evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated. The presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1. The genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.
BackgroundHuman papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood.MethodsTo evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated.ResultsThe presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1.ConclusionsThe genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.
Background Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood. Methods To evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated. Results The presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1. Conclusions The genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy. Keywords: Capture sequencing, Human papillomavirus, Prostate cancer, Whole-exome sequencing
Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood.BACKGROUNDHuman papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood.To evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated.METHODSTo evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated.The presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1.RESULTSThe presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1.The genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.CONCLUSIONSThe genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.
Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood. To evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated. The presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1. The genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.
Abstract Background Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection and relevant genomic changes in PCa is poorly understood. Methods To evaluate the relationship between HPV genotypes and genomic alterations in PCa, HPV capture sequencing of DNA isolated from 59 Han Chinese PCa patients was performed using an Illumina HiSeq2500. Additionally, whole-exome sequencing of DNA from these 59 PCa tissue samples and matched normal tissues was carried out using the BGI DNBSEQ platform. HPV infection status and genotyping were determined, and the genetic disparities between HPV-positive and HPV-negative PCa were evaluated. Results The presence of the high-risk HPV genome was identified in 16.9% of our cohort, and HPV16 was the most frequent genotype detected. The overall mutational burden in HPV-positive and HPV-negative PCa was similar, with an average of 2.68/Mb versus 2.58/Mb, respectively, in the targeted whole-exome region. HPV-negative tumors showed a mutational spectrum concordant with published PCa analyses with enrichment for mutations in SPOP, FOXA1, and MED12. HPV-positive tumors showed more mutations in KMT2C, KMT2D and ERCC2. Copy number alterations per sample were comparable between the two groups. However, the significantly amplified or deleted regions of the two groups only partially overlapped. We identified amplifications in oncogenes, including FCGR2B and CCND1, and deletions of tumor suppressors, such as CCNC and RB1, only in HPV-negative tumors. HPV-positive tumors showed unique deletions of tumor suppressors such as NTRK1 and JAK1. Conclusions The genomic mutational landscape of PCa differs based on HPV infection status. This work adds evidence for the direct involvement of HPV in PCa etiology. Different genomic features render HPV-positive PCa a unique subpopulation that might benefit from virus-targeted therapy.
ArticleNumber 239
Audience Academic
Author Zhao, Tong
Zhao, Xiaoxiao
Wang, Yuyan
Liang, Wenjia
Tian, Xun
Lang, Bin
Yan, Yongji
Wang, Yi
Zhang, Jingjing
Hu, Zheng
Cao, Chen
Zhou, Xueying
Cao, Ying
Liu, Ting
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CitedBy_id crossref_primary_10_1186_s12985_025_02682_1
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Cites_doi 10.1038/ng.2279
10.1016/j.micpath.2022.105503
10.1001/jamanetworkopen.2021.40644
10.7150/jca.25356
10.1002/ijc.30716
10.3322/caac.21660
10.1093/nar/gkq603
10.1038/nbt.2514
10.1002/ctm2.971
10.1093/nar/gkw520
10.1109/IPDPS.2019.00041
10.1371/journal.pone.0176181
10.3892/ol.2017.6367
10.1097/CM9.0000000000002108
10.1186/s13027-022-00427-1
10.1016/j.tips.2021.05.002
10.3390/diagnostics11050908
10.1093/bioinformatics/btp352
10.3390/genes13050840
10.1038/s41568-018-0060-1
10.1186/gb-2011-12-4-r41
10.1186/s13027-020-00305-8
10.1038/s41586-020-2135-x
10.1101/gr.239244.118
10.1016/j.cell.2015.10.025
10.1038/s41379-021-00905-8
10.3390/cancers14194623
10.1111/ajco.13124
10.1016/j.intimp.2020.106913
10.1093/nar/gky719
10.1038/s41586-019-1318-9
10.1038/ng.806
10.1093/carcin/bgz094
10.3390/cancers14133272
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Issue 1
Keywords Human papillomavirus
Capture sequencing
Prostate cancer
Whole-exome sequencing
Language English
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References JS Lawson (1207_CR5) 2020; 15
K Cibulskis (1207_CR17) 2013; 31
VL Porter (1207_CR8) 2022; 14
CH Mermel (1207_CR20) 2011; 12
A Bagherabadi (1207_CR32) 2022; 13
B Yin (1207_CR4) 2017; 14
C de Martel (1207_CR23) 2017; 141
JS Lawson (1207_CR24) 2022; 17
M Moghoofei (1207_CR3) 2019; 15
CE Barbieri (1207_CR26) 2012; 44
1207_CR22
J Zhang (1207_CR25) 2021; 4
K Hjorth-Jensen (1207_CR27) 2018; 46
J Li (1207_CR10) 2020; 580
EJ Adams (1207_CR28) 2019; 571
X Zhai (1207_CR29) 2021; 42
A Mayakonda (1207_CR18) 2018; 28
LA Albacker (1207_CR31) 2017; 12
Cancer Genome Atlas Research (1207_CR9) 2015; 163
H Li (1207_CR15) 2009; 25
Z Sondka (1207_CR21) 2018; 18
F Crocetto (1207_CR35) 2021; 11
Y Liu (1207_CR30) 2018; 9
R Tian (1207_CR11) 2019; 40
K Wang (1207_CR14) 2010; 38
K Mizuno (1207_CR34) 2022; 82
MA DePristo (1207_CR16) 2011; 43
R Shen (1207_CR19) 2016; 44
A Khatami (1207_CR6) 2022; 166
IA González (1207_CR33) 2022; 35
C Xia (1207_CR2) 2022; 135
F Crocetto (1207_CR36) 2022; 14
J Sadri Nahand (1207_CR7) 2020; 88
1207_CR13
H Sung (1207_CR1) 2021; 71
R Tian (1207_CR12) 2022; 12
38926869 - Eur J Med Res. 2024 Jun 26;29(1):348. doi: 10.1186/s40001-024-01935-z
References_xml – volume: 44
  start-page: 685
  issue: 6
  year: 2012
  ident: 1207_CR26
  publication-title: Nat Genet
  doi: 10.1038/ng.2279
– volume: 166
  start-page: 105503
  year: 2022
  ident: 1207_CR6
  publication-title: Microb Pathog
  doi: 10.1016/j.micpath.2022.105503
– volume: 4
  start-page: e2140644
  issue: 12
  year: 2021
  ident: 1207_CR25
  publication-title: JAMA Netw Open
  doi: 10.1001/jamanetworkopen.2021.40644
– volume: 9
  start-page: 2786
  issue: 16
  year: 2018
  ident: 1207_CR30
  publication-title: J Cancer
  doi: 10.7150/jca.25356
– volume: 141
  start-page: 664
  issue: 4
  year: 2017
  ident: 1207_CR23
  publication-title: Int J Cancer
  doi: 10.1002/ijc.30716
– volume: 71
  start-page: 209
  issue: 3
  year: 2021
  ident: 1207_CR1
  publication-title: CA Cancer J Clin
  doi: 10.3322/caac.21660
– volume: 38
  start-page: e164
  issue: 16
  year: 2010
  ident: 1207_CR14
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkq603
– volume: 31
  start-page: 213
  issue: 3
  year: 2013
  ident: 1207_CR17
  publication-title: Nat Biotechnol
  doi: 10.1038/nbt.2514
– volume: 12
  start-page: e971
  issue: 8
  year: 2022
  ident: 1207_CR12
  publication-title: Clin Transl Med
  doi: 10.1002/ctm2.971
– ident: 1207_CR22
– volume: 44
  start-page: e131
  issue: 16
  year: 2016
  ident: 1207_CR19
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkw520
– ident: 1207_CR13
  doi: 10.1109/IPDPS.2019.00041
– volume: 12
  start-page: e0176181
  issue: 11
  year: 2017
  ident: 1207_CR31
  publication-title: PLoS ONE
  doi: 10.1371/journal.pone.0176181
– volume: 14
  start-page: 1855
  issue: 2
  year: 2017
  ident: 1207_CR4
  publication-title: Oncol Lett
  doi: 10.3892/ol.2017.6367
– volume: 135
  start-page: 584
  issue: 5
  year: 2022
  ident: 1207_CR2
  publication-title: Chin Med J (Engl)
  doi: 10.1097/CM9.0000000000002108
– volume: 17
  start-page: 23
  issue: 1
  year: 2022
  ident: 1207_CR24
  publication-title: Infect Agent Cancer
  doi: 10.1186/s13027-022-00427-1
– volume: 42
  start-page: 688
  issue: 8
  year: 2021
  ident: 1207_CR29
  publication-title: Trends Pharmacol Sci
  doi: 10.1016/j.tips.2021.05.002
– volume: 11
  start-page: 908
  issue: 5
  year: 2021
  ident: 1207_CR35
  publication-title: Diagnostics (Basel)
  doi: 10.3390/diagnostics11050908
– volume: 25
  start-page: 2078
  issue: 16
  year: 2009
  ident: 1207_CR15
  publication-title: Bioinformatics (Oxf, Engl)
  doi: 10.1093/bioinformatics/btp352
– volume: 13
  start-page: 840
  issue: 5
  year: 2022
  ident: 1207_CR32
  publication-title: Genes (Basel).
  doi: 10.3390/genes13050840
– volume: 18
  start-page: 696
  issue: 11
  year: 2018
  ident: 1207_CR21
  publication-title: Nat Rev Cancer
  doi: 10.1038/s41568-018-0060-1
– volume: 12
  start-page: R41
  issue: 4
  year: 2011
  ident: 1207_CR20
  publication-title: Genome Biol
  doi: 10.1186/gb-2011-12-4-r41
– volume: 15
  start-page: 41
  year: 2020
  ident: 1207_CR5
  publication-title: Infect Agent Cancer
  doi: 10.1186/s13027-020-00305-8
– volume: 580
  start-page: 93
  issue: 7801
  year: 2020
  ident: 1207_CR10
  publication-title: Nature
  doi: 10.1038/s41586-020-2135-x
– volume: 28
  start-page: 1747
  issue: 11
  year: 2018
  ident: 1207_CR18
  publication-title: Genome Res
  doi: 10.1101/gr.239244.118
– volume: 163
  start-page: 1011
  issue: 4
  year: 2015
  ident: 1207_CR9
  publication-title: Cell
  doi: 10.1016/j.cell.2015.10.025
– volume: 35
  start-page: 4
  issue: 1
  year: 2022
  ident: 1207_CR33
  publication-title: Mod Pathol
  doi: 10.1038/s41379-021-00905-8
– volume: 82
  start-page: S86
  issue: Suppl 1
  year: 2022
  ident: 1207_CR34
  publication-title: Prostate
– volume: 14
  start-page: 4623
  issue: 19
  year: 2022
  ident: 1207_CR8
  publication-title: Cancers (Basel).
  doi: 10.3390/cancers14194623
– volume: 15
  start-page: e59
  issue: 5
  year: 2019
  ident: 1207_CR3
  publication-title: Asia Pac J Clin Oncol
  doi: 10.1111/ajco.13124
– volume: 88
  start-page: 106913
  year: 2020
  ident: 1207_CR7
  publication-title: Int Immunopharmacol
  doi: 10.1016/j.intimp.2020.106913
– volume: 46
  start-page: 9484
  issue: 18
  year: 2018
  ident: 1207_CR27
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gky719
– volume: 571
  start-page: 408
  issue: 7765
  year: 2019
  ident: 1207_CR28
  publication-title: Nature
  doi: 10.1038/s41586-019-1318-9
– volume: 43
  start-page: 491
  issue: 5
  year: 2011
  ident: 1207_CR16
  publication-title: Nat Genet
  doi: 10.1038/ng.806
– volume: 40
  start-page: 1220
  issue: 10
  year: 2019
  ident: 1207_CR11
  publication-title: Carcinogenesis
  doi: 10.1093/carcin/bgz094
– volume: 14
  start-page: 3272
  issue: 13
  year: 2022
  ident: 1207_CR36
  publication-title: Cancers (Basel).
  doi: 10.3390/cancers14133272
– reference: 38926869 - Eur J Med Res. 2024 Jun 26;29(1):348. doi: 10.1186/s40001-024-01935-z
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Snippet Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV infection...
Background Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV...
BackgroundHuman papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association between HPV...
Abstract Background Human papillomavirus (HPV) has been proposed as a potential pathogenetic organism involved in prostate cancer (PCa), but the association...
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SubjectTerms Age groups
Cancer patients
Capture sequencing
Care and treatment
Development and progression
East Asian People
Genetic aspects
Genomes
Genomics
Genotype
Human papillomavirus
Humans
Infection
Infections
Male
Medical screening
Mutation
Nuclear Proteins - genetics
Papillomavirus infections
Papillomavirus Infections - complications
Papillomavirus Infections - genetics
Prostate cancer
Prostatic Neoplasms - complications
Prostatic Neoplasms - genetics
Prostatic Neoplasms - pathology
Repressor Proteins - genetics
Sexually transmitted diseases
Tumors
Whole-exome sequencing
Xeroderma Pigmentosum Group D Protein - genetics
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Title Genomic alterations related to HPV infection status in a cohort of Chinese prostate cancer patients
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