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Article: Th2 Cytokines and Atopic Dermatitis.

Brandt, Eric B / Sivaprasad, Umasundari

Journal of clinical & cellular immunology

2010 Volume 2, Issue 3

Abstract: Atopic dermatitis (AD), a chronic relapsing inflammatory skin disease, is increasing in prevalence around the world. Intensive research is ongoing to understand the mechanisms involved in the development of AD and offer new treatment options for patients ...

Abstract	Atopic dermatitis (AD), a chronic relapsing inflammatory skin disease, is increasing in prevalence around the world. Intensive research is ongoing to understand the mechanisms involved in the development of AD and offer new treatment options for patients suffering from AD. In this review, we highlight the importance of allergic Th2 responses in the development of the disease and summarize relevant literature, including genetic studies, studies of human skin and mechanistic studies on keratinocytes and mouse models of AD. We discuss the importance of the skin barrier and review recent findings on the pro-Th2 cytokines TSLP, IL-25, and IL-33, notably their ability to polarize dendritic cells and promote Th2 responses. After a brief update on the contribution of different T-cell subsets to AD, we focus on Th2 cells and the respective contributions of each of the Th2 cytokines (IL-4, IL-13, IL-5, IL-31, and IL-10) to AD. We conclude with a brief discussion of the current gaps in our knowledge and technical limitations.
Language	English
Publishing date	2010-09-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2684688-3
ISSN	2155-9899
ISSN	2155-9899
DOI	10.4172/2155-9899.1000110
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Article ; Online: Multiple Transcriptome Data Analysis Reveals Biologically Relevant Atopic Dermatitis Signature Genes and Pathways.

Ghosh, Debajyoti / Ding, Lili / Sivaprasad, Umasundari / Geh, Esmond / Biagini Myers, Jocelyn / Bernstein, Jonathan A / Khurana Hershey, Gurjit K / Mersha, Tesfaye B

PloS one

2015 Volume 10, Issue 12, Page(s) e0144316

Abstract: Several studies have identified genes that are differentially expressed in atopic dermatitis (AD) compared to normal skin. However, there is also considerable variation in the list of differentially expressed genes (DEGs) reported by different groups and ...

Abstract	Several studies have identified genes that are differentially expressed in atopic dermatitis (AD) compared to normal skin. However, there is also considerable variation in the list of differentially expressed genes (DEGs) reported by different groups and the exact cause of AD is still not fully understood. Using a rank-based approach, we analyzed gene expression data from five different microarray studies, comprising a total of 127 samples and more than 250,000 transcripts. A total of 89 AD gene expression signatures '89ADGES', including FLG gene, were identified to show dysregulation consistently across these studies. Using a Support Vector Machine, we showed that the '89ADGES' discriminates AD from normal skin with 98% predictive accuracy. Functional annotation of these genes implicated their roles in immune responses (e.g., betadefensin, microseminoprotein), keratinocyte differentiation/epidermal development (e.g., FLG, CORIN, AQP, LOR, KRT16), inflammation (e.g., IL37, IL27RA, CCL18) and lipid metabolism (e.g., AKR1B10, FAD7, FAR2). Subsequently, we validated a subset of signature genes using quantitative PCR in a mouse model. Using a bioinformatic approach, we identified keratinocyte pathway over-represented (P = <0.0006) among the 89 signature genes. Keratinocytes are known to play a major role in barrier function due to their location in the epidermis. Our result suggests that besides immune- mediated pathway, skin barrier pathways such as the keratinocyte differentiation pathway play a key role in AD pathogenesis. A better understanding of the role of keratinocytes in AD will be important for developing novel "barrier therapy" for this disease.
MeSH term(s)	Animals ; Case-Control Studies ; Cell Differentiation/genetics ; Cluster Analysis ; Computational Biology/methods ; Databases, Genetic ; Dermatitis, Atopic/genetics ; Dermatitis, Atopic/metabolism ; Discriminant Analysis ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Regulatory Networks ; Humans ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Mice ; Molecular Sequence Annotation ; Reproducibility of Results ; Signal Transduction ; Support Vector Machine ; Transcriptome
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0144316
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Article ; Online: APC/C--the master controller of origin licensing?

Sivaprasad, Umasundari / Machida, Yuichi J / Dutta, Anindya

Cell division

2007 Volume 2, Page(s) 8

Abstract: DNA replication must be tightly controlled to prevent initiation of a second round of replication until mitosis is complete. So far, components of the pre-replicative complex (Cdt1, Cdc6 and geminin) were considered key players in this regulation. In a ... ...

Abstract	DNA replication must be tightly controlled to prevent initiation of a second round of replication until mitosis is complete. So far, components of the pre-replicative complex (Cdt1, Cdc6 and geminin) were considered key players in this regulation. In a new study, Machida and Dutta have shown that depletion of Emi1 caused cells to replicate their DNA more than once per cell cycle 1. This effect was dependent on the ability of Emi1 to inhibit the APC/C. In addition to its role in regulating entry into mitosis, oscillation of APC/C activity regulates pre-RC formation: high APC/C activity in late M/G1 allows pre-RC formation and low APC/C activity in S/G2 prevents pre-RC formation for a second time thereby preventing rereplication. Each redundant pathway to prevent rereplication is dependent on regulating one of the pre-RC components, and all of the pathways are co-regulated by Emi1 through the APC/C. In this commentary we discuss how this new role of Emi1 adds to our understanding of the regulation of replication initiation. We also review the literature to analyze whether APC/C has a role in regulating endoreduplication (a normal state of polyploidy in some differentiated cells). Similarly a role of premature APC/C activation in genomic instability of tumors is discussed.
Language	English
Publishing date	2007-02-23
Publishing country	England
Document type	Journal Article
ISSN	1747-1028
ISSN (online)	1747-1028
DOI	10.1186/1747-1028-2-8
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Article ; Online: APC/C – the master controller of origin licensing?

Dutta Anindya / Machida Yuichi J / Sivaprasad Umasundari

Cell Division, Vol 2, Iss 1, p

2007 Volume 8

Abstract: Abstract DNA replication must be tightly controlled to prevent initiation of a second round of replication until mitosis is complete. So far, components of the pre-replicative complex (Cdt1, Cdc6 and geminin) were considered key players in this ... ...

Abstract	Abstract DNA replication must be tightly controlled to prevent initiation of a second round of replication until mitosis is complete. So far, components of the pre-replicative complex (Cdt1, Cdc6 and geminin) were considered key players in this regulation. In a new study, Machida and Dutta have shown that depletion of Emi1 caused cells to replicate their DNA more than once per cell cycle 1 . This effect was dependent on the ability of Emi1 to inhibit the APC/C. In addition to its role in regulating entry into mitosis, oscillation of APC/C activity regulates pre-RC formation: high APC/C activity in late M/G1 allows pre-RC formation and low APC/C activity in S/G2 prevents pre-RC formation for a second time thereby preventing rereplication. Each redundant pathway to prevent rereplication is dependent on regulating one of the pre-RC components, and all of the pathways are co-regulated by Emi1 through the APC/C. In this commentary we discuss how this new role of Emi1 adds to our understanding of the regulation of replication initiation. We also review the literature to analyze whether APC/C has a role in regulating endoreduplication (a normal state of polyploidy in some differentiated cells). Similarly a role of premature APC/C activation in genomic instability of tumors is discussed.
Keywords	Cytology ; QH573-671 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Cytology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	570 ; 572
Language	English
Publishing date	2007-02-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Differential efficacy of 3-hydroxy-3-methylglutaryl CoA reductase inhibitors on the cell cycle of prostate cancer cells.

Sivaprasad, Umasundari / Abbas, Tarek / Dutta, Anindya

Molecular cancer therapeutics

2006 Volume 5, Issue 9, Page(s) 2310–2316

Abstract: Members of the statin family of 3-hydroxy-3-methylglutaryl CoA reductase inhibitors are being investigated for the therapy and prevention of cancers because of their growth-inhibitory effects on epithelial cells. Some epidemiologic studies show that ... ...

Abstract	Members of the statin family of 3-hydroxy-3-methylglutaryl CoA reductase inhibitors are being investigated for the therapy and prevention of cancers because of their growth-inhibitory effects on epithelial cells. Some epidemiologic studies show that patients taking statins show a lower incidence of cancer compared with those taking other cholesterol-lowering medication. In contrast, other studies show that statin use does not correlate with cancer risk. To address this discrepancy, we investigated the efficacy of different statins on the PC-3 prostate cancer cell line and the androgen-dependent LNCaP prostate cancer cell line. Clinically used statins, lovastatin, fluvastatin, and simvastatin inhibit proliferation of the two prostate cancer cells by inducing a G1 arrest. Lovastatin induced the arrest at 0.5 micromol/L, a concentration easily reached in the serum after oral administration. Pravastatin, however, was less effective at inhibiting 3-hydroxy-3-methylglutaryl CoA reductase in PC-3 cells and had to be present at 200 times higher concentrations to effect a cell cycle arrest. Another potential source of variability is the different levels of the cyclin-dependent kinase (cdk) inhibitor p27 noted in prostate cancers particularly because statins have been suggested to act through the induction of cdk inhibitors. All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Therefore, p27 status is unlikely to confound the epidemiologic data on the efficacy of statins in prostate cancer. To make definitive conclusions about the efficacy of statins on cancer prevention, however, the epidemiologic studies should take into account the type of statin used and the serum concentrations achieved and ensure that the tested statin inhibits the specific type of cancer in vitro at those concentrations.
MeSH term(s)	Cell Cycle/drug effects ; Cell Line, Tumor ; Cyclin E/metabolism ; Cyclin-Dependent Kinase 2/antagonists & inhibitors ; Cyclin-Dependent Kinase 2/metabolism ; Fatty Acids, Monounsaturated/pharmacology ; Fluvastatin ; G1 Phase/drug effects ; Humans ; Hydroxymethylglutaryl CoA Reductases/metabolism ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Indoles/pharmacology ; Lovastatin/pharmacology ; Male ; Phosphorylation/drug effects ; Pravastatin/pharmacology ; Proliferating Cell Nuclear Antigen/metabolism ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/enzymology ; Prostatic Neoplasms/pathology ; Protein-Serine-Threonine Kinases/metabolism ; Simvastatin/pharmacology ; p21-Activated Kinases
Chemical Substances	Cyclin E ; Fatty Acids, Monounsaturated ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Indoles ; Proliferating Cell Nuclear Antigen ; p27 antigen ; Fluvastatin (4L066368AS) ; Lovastatin (9LHU78OQFD) ; Simvastatin (AGG2FN16EV) ; Hydroxymethylglutaryl CoA Reductases (EC 1.1.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; p21-Activated Kinases (EC 2.7.11.1) ; Cyclin-Dependent Kinase 2 (EC 2.7.11.22) ; Pravastatin (KXO2KT9N0G)
Language	English
Publishing date	2006-09-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-06-0175
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Article ; Online: Rhinovirus infection results in stronger and more persistent genomic dysregulation: Evidence for altered innate immune response in asthmatics at baseline, early in infection, and during convalescence.

Heymann, Peter W / Nguyen, Huyen-Tran / Steinke, John W / Turner, Ronald B / Woodfolk, Judith A / Platts-Mills, Thomas A E / Martin, Lisa / He, Hua / Biagini Myers, Jocelyn / Lindsey, Mark / Sivaprasad, Umasundari / Medvedovic, Mario / Mahi, Naim / Carper, Holliday / Murphy, Deborah D / Patrie, James / Khurana Hershey, Gurjit K

PloS one

2017 Volume 12, Issue 5, Page(s) e0178096

Abstract: Background: Rhinovirus (HRV) is associated with the large majority of virus-induced asthma exacerbations in children and young adults, but the mechanisms remain poorly defined.: Methods: Asthmatics and non-asthmatic controls were inoculated with HRV- ... ...

Abstract	Background: Rhinovirus (HRV) is associated with the large majority of virus-induced asthma exacerbations in children and young adults, but the mechanisms remain poorly defined. Methods: Asthmatics and non-asthmatic controls were inoculated with HRV-A16, and nasal epithelial samples were obtained 7 days before, 36 hours after, and 7 days after viral inoculation. RNA was extracted and subjected to RNA-seq analysis. Results: At baseline, 57 genes were differentially expressed between asthmatics and controls, and the asthmatics had decreased expression of viral replication inhibitors and increased expression of genes involved in inflammation. At 36 hours (before the emergence of peak symptoms), 1329 genes were significantly altered from baseline in the asthmatics compared to 62 genes in the controls. At this time point, asthmatics lacked an increase in IL-10 signaling observed in the controls. At 7 days following HRV inoculation, 222 genes were significantly dysregulated in the asthmatics, whereas only 4 genes were dysregulated among controls. At this time point, the controls but not asthmatics demonstrated upregulation of SPINK5. Conclusions: As judged by the magnitude and persistence of dysregulated genes, asthmatics have a substantially different host response to HRV-A16 infection compared with non-asthmatic controls. Gene expression differences illuminate biologically plausible mechanisms that contribute to a better understanding of the pathogenesis of HRV-induced asthma exacerbations.
MeSH term(s)	Adult ; Asthma/immunology ; Case-Control Studies ; Female ; Humans ; Immunity, Innate ; Male ; Picornaviridae Infections/immunology ; Rhinovirus/pathogenicity ; Young Adult
Language	English
Publishing date	2017-05-26
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0178096
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Article: Genomic architecture of asthma differs by sex

Mersha, Tesfaye B / Lisa J. Martin / Jocelyn M. Biagini Myers / Melinda Butsch Kovacic / Hua He / Mark Lindsey / Umasundari Sivaprasad / Weiguo Chen / Gurjit K. Khurana Hershey

Genomics. 2015 July, v. 106

2015

Abstract: Asthma comprised of highly heterogeneous subphenotypes resulting from complex interplay between genetic and environmental stimuli. While much focus has been placed on extrinsic environmental stimuli, intrinsic environment such as sex can interact with ... ...

Abstract	Asthma comprised of highly heterogeneous subphenotypes resulting from complex interplay between genetic and environmental stimuli. While much focus has been placed on extrinsic environmental stimuli, intrinsic environment such as sex can interact with genes to influence asthma risk. However, few studies have examined sex-specific genetic effects. The overall objective of this study was to evaluate if sex-based differences exist in genomic associations with asthma. We tested 411 asthmatics and 297 controls for presence of interactions and sex-stratified effects in 51 genes using both SNP and gene expression data. Logistic regression was used to test for association. Over half (55%) of the genetic variants identified in sex-specific analyses were not identified in the sex-combined analysis. Further, sex-stratified genetic analyses identified associations with significantly higher median effect sizes than sex-combined analysis for girls (p-value=6.5E-15) and for boys (p-value=1.0E-7). When gene expression data were analyzed to identify genes that were differentially expressed in asthma versus non-asthma, nearly one third (31%) of the probes identified in the sex-specific analyses were not identified in the sex-combined analysis. Both genetic and gene expression data suggest that the biologic underpinnings for asthma may differ by sex. Failure to recognize sex interactions in asthma greatly decreases the ability to detect significant genomic variation and may result in significant misrepresentation of genes and pathways important in asthma in different environments.
Keywords	asthma ; boys ; gene expression ; gene expression regulation ; genes ; genetic techniques and protocols ; genetic variation ; girls ; regression analysis ; risk ; single nucleotide polymorphism
Language	English
Dates of publication	2015-07
Size	p. 15-22.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	356334-0
ISSN	1089-8646 ; 0888-7543
ISSN (online)	1089-8646
ISSN	0888-7543
DOI	10.1016/j.ygeno.2015.03.003
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 2367: Show issues

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Article ; Online: Genomic architecture of asthma differs by sex.

Mersha, Tesfaye B / Martin, Lisa J / Biagini Myers, Jocelyn M / Kovacic, Melinda Butsch / He, Hua / Lindsey, Mark / Sivaprasad, Umasundari / Chen, Weiguo / Khurana Hershey, Gurjit K

Genomics

2015 Volume 106, Issue 1, Page(s) 15–22

Abstract	Asthma comprised of highly heterogeneous subphenotypes resulting from complex interplay between genetic and environmental stimuli. While much focus has been placed on extrinsic environmental stimuli, intrinsic environment such as sex can interact with genes to influence asthma risk. However, few studies have examined sex-specific genetic effects. The overall objective of this study was to evaluate if sex-based differences exist in genomic associations with asthma. We tested 411 asthmatics and 297 controls for presence of interactions and sex-stratified effects in 51 genes using both SNP and gene expression data. Logistic regression was used to test for association. Over half (55%) of the genetic variants identified in sex-specific analyses were not identified in the sex-combined analysis. Further, sex-stratified genetic analyses identified associations with significantly higher median effect sizes than sex-combined analysis for girls (p-value=6.5E-15) and for boys (p-value=1.0E-7). When gene expression data were analyzed to identify genes that were differentially expressed in asthma versus non-asthma, nearly one third (31%) of the probes identified in the sex-specific analyses were not identified in the sex-combined analysis. Both genetic and gene expression data suggest that the biologic underpinnings for asthma may differ by sex. Failure to recognize sex interactions in asthma greatly decreases the ability to detect significant genomic variation and may result in significant misrepresentation of genes and pathways important in asthma in different environments.
MeSH term(s)	Asthma/genetics ; Child ; Female ; Gene Expression ; Genome, Human ; Humans ; Male ; Polymorphism, Single Nucleotide ; Sex Factors
Language	English
Publishing date	2015-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	356334-0
ISSN	1089-8646 ; 0888-7543
ISSN (online)	1089-8646
ISSN	0888-7543
DOI	10.1016/j.ygeno.2015.03.003
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Article: Mechanism for ordered receptor binding by human prolactin.

Sivaprasad, Umasundari / Canfield, Jeffrey M / Brooks, Charles L

Biochemistry

2004 Volume 43, Issue 43, Page(s) 13755–13765

Abstract: Prolactin, a lactogenic hormone, binds to two prolactin receptors sequentially, the first receptor binding at site 1 of the hormone followed by the second receptor binding at site 2. We have investigated the mechanism by which human prolactin (hPRL) ... ...

Abstract	Prolactin, a lactogenic hormone, binds to two prolactin receptors sequentially, the first receptor binding at site 1 of the hormone followed by the second receptor binding at site 2. We have investigated the mechanism by which human prolactin (hPRL) binds the extracellular domain of the human prolactin receptor (hPRLbp) using surface plasmon resonance (SPR) technology. We have covalently coupled hPRL to the SPR chip surface via coupling chemistries that reside in and block either site 1 or site 2. Equilibrium binding experiments using saturating hPRLbp concentrations show that site 2 receptor binding is dependent on site 1 receptor occupancy. In contrast, site 1 binding is independent of site 2 occupancy. Thus, sites 1 and 2 are functionally coupled, site 1 binding inducing the functional organization of site 2. Site 2 of hPRL does not have a measurable binding affinity prior to hPRLbp binding at site 1. After site 1 receptor binding, site 2 affinity is increased to values approaching that of site 1. Corruption of either site 1 or site 2 by mutagenesis is consistent with a functional coupling of sites 1 and 2. Fluorescence resonance energy transfer (FRET) experiments indicate that receptor binding at site 1 induces a conformation change in the hormone. These data support an "induced-fit" model for prolactin receptor binding where binding of the first receptor to hPRL induces a conformation change in the hormone creating the second receptor-binding site.
MeSH term(s)	Binding, Competitive/genetics ; Cysteine/genetics ; Dextrans/chemistry ; Fluorescence Resonance Energy Transfer/methods ; Glycine/genetics ; Glycine/metabolism ; Humans ; Kinetics ; Methionine/genetics ; Methionine/metabolism ; Models, Chemical ; Mutagenesis, Site-Directed ; Prolactin/chemistry ; Prolactin/genetics ; Prolactin/isolation & purification ; Prolactin/metabolism ; Protein Binding/genetics ; Protein Conformation ; Receptors, Prolactin/antagonists & inhibitors ; Receptors, Prolactin/chemistry ; Receptors, Prolactin/isolation & purification ; Receptors, Prolactin/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; Spectrophotometry, Ultraviolet ; Surface Plasmon Resonance/methods
Chemical Substances	Dextrans ; Receptors, Prolactin ; Recombinant Proteins ; Prolactin (9002-62-4) ; Methionine (AE28F7PNPL) ; Cysteine (K848JZ4886) ; Glycine (TE7660XO1C)
Language	English
Publishing date	2004-11-02
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1108-3
ISSN	1520-4995 ; 0006-2960
ISSN (online)	1520-4995
ISSN	0006-2960
DOI	10.1021/bi049333p
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Article ; Online: Oral human papillomavirus is common in individuals with Fanconi anemia.

Sauter, Sharon L / Wells, Susanne I / Zhang, Xue / Hoskins, Elizabeth E / Davies, Stella M / Myers, Kasiani C / Mueller, Robin / Panicker, Gitika / Unger, Elizabeth R / Sivaprasad, Umasundari / Brown, Darron R / Mehta, Parinda A / Butsch Kovacic, Melinda

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

2015 Volume 24, Issue 5, Page(s) 864–872

Abstract: Background: Fanconi anemia is a rare genetic disorder resulting in a loss of function of the Fanconi anemia-related DNA repair pathway. Individuals with Fanconi anemia are predisposed to some cancers, including oropharyngeal and gynecologic cancers, ... ...

Abstract	Background: Fanconi anemia is a rare genetic disorder resulting in a loss of function of the Fanconi anemia-related DNA repair pathway. Individuals with Fanconi anemia are predisposed to some cancers, including oropharyngeal and gynecologic cancers, with known associations with human papillomavirus (HPV) in the general population. As individuals with Fanconi anemia respond poorly to chemotherapy and radiation, prevention of cancer is critical. Methods: To determine whether individuals with Fanconi anemia are particularly susceptible to oral HPV infection, we analyzed survey-based risk factor data and tested DNA isolated from oral rinses from 126 individuals with Fanconi anemia and 162 unaffected first-degree family members for 37 HPV types. Results: Fourteen individuals (11.1%) with Fanconi anemia tested positive, significantly more (P = 0.003) than family members (2.5%). While HPV prevalence was even higher for sexually active individuals with Fanconi anemia (17.7% vs. 2.4% in family; P = 0.003), HPV positivity also tended to be higher in the sexually inactive (8.7% in Fanconi anemia vs. 2.9% in siblings). Indeed, having Fanconi anemia increased HPV positivity 4.9-fold (95% CI, 1.6-15.4) considering age and sexual experience, but did not differ by other potential risk factors. Conclusion: Our studies suggest that oral HPV is more common in individuals with Fanconi anemia. It will be essential to continue to explore associations between risk factors and immune dysfunction on HPV incidence and persistence over time. Impact: HPV vaccination should be emphasized in those with Fanconi anemia as a first step to prevent oropharyngeal cancers, although additional studies are needed to determine whether the level of protection it offers in this population is adequate.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Fanconi Anemia/virology ; Female ; Head and Neck Neoplasms/virology ; Humans ; Incidence ; Infant ; Male ; Middle Aged ; Mouth Diseases/virology ; Mouth Mucosa/virology ; Papillomaviridae/isolation & purification ; Papillomavirus Infections/virology ; Young Adult
Language	English
Publishing date	2015-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1153420-5
ISSN	1538-7755 ; 1055-9965
ISSN (online)	1538-7755
ISSN	1055-9965
DOI	10.1158/1055-9965.EPI-15-0097-T
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