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  1. Article ; Online: Human papillomavirus and tobacco use in tongue base cancers.

    Stoler, Daniel L / Smaldino, Philip J / Darbary, Huferesh K / Sullivan, Maureen A / Popat, Saurin R / Hicks, Wesley L / Merzianu, Mihai / Gaile, Daniel P / Anderson, Garth R / Loree, Thom R

    Ear, nose, & throat journal

    2013  Volume 92, Issue 8, Page(s) 372–380

    Abstract: Human papillomavirus 16 (HPV-16) infection and tobacco use are associated with human oropharyngeal cancers. We conducted a study of the role of HPV and tobacco use in base of the tongue (BOT) cancers. DNA from 34 such cancers was subjected to HPV-16 and ... ...

    Abstract Human papillomavirus 16 (HPV-16) infection and tobacco use are associated with human oropharyngeal cancers. We conducted a study of the role of HPV and tobacco use in base of the tongue (BOT) cancers. DNA from 34 such cancers was subjected to HPV-16 and HPV-18-specific polymerase chain reaction analysis. Demographic and clinicopathologic data were obtained from each patient's medical record. HPV-16 was detected in 68% of tumors. Tobacco use was the only factor found to be significantly associated with HPV status. Tumors from 100% of patients who had never used tobacco tested positive for HPV, compared with only 56% of those who had ever used tobacco (Fisher exact test, p = 0.024). All tumors were associated with either tobacco use or HPV infection. These findings are consistent with the hypothesis that either tobacco use or HPV infection is necessary to the etiology of BOT tumors, and they suggest that tongue base carcinoma may be prevented by combining HPV vaccination with tobacco avoidance.
    MeSH term(s) Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell/etiology ; Carcinoma, Squamous Cell/virology ; DNA, Viral/analysis ; Female ; Human papillomavirus 16/genetics ; Human papillomavirus 16/isolation & purification ; Human papillomavirus 18/genetics ; Human papillomavirus 18/isolation & purification ; Humans ; Incidence ; Male ; Middle Aged ; Papillomavirus Infections/complications ; Papillomavirus Infections/epidemiology ; Smoking/adverse effects ; Smoking/epidemiology ; Tongue Neoplasms/etiology ; Tongue Neoplasms/virology
    Chemical Substances DNA, Viral
    Language English
    Publishing date 2013-08-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 750153-5
    ISSN 1942-7522 ; 0145-5613
    ISSN (online) 1942-7522
    ISSN 0145-5613
    DOI 10.1177/014556131309200812
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 107: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Uniparentalism in sporadic colorectal cancer is independent of imprint status, and coordinate for chromosomes 14 and 18.

    Darbary, Huferesh K / Dutt, Smitha S / Sait, Sheila J / Nowak, Norma J / Heinaman, Roy E / Stoler, Daniel L / Anderson, Garth R

    Cancer genetics and cytogenetics

    2009  Volume 189, Issue 2, Page(s) 77–86

    Abstract: Our previous allelotyping studies of 59 sporadic colorectal cancers revealed that loss of heterozygosity is most frequent for regions of chromosomes 14 and 18. Yet subsequent BAC microarray comparative genomic hybridization studies of the same tumor DNAs ...

    Abstract Our previous allelotyping studies of 59 sporadic colorectal cancers revealed that loss of heterozygosity is most frequent for regions of chromosomes 14 and 18. Yet subsequent BAC microarray comparative genomic hybridization studies of the same tumor DNAs showed no corresponding pattern of copy number alteration for chromosome 14. To clarify this apparent discrepancy, we utilized hybridization to SNP microarrays; this revealed frequent uniparentalism for chromosome 14 and for chromosome 18. Based on the BAC array results combined with fluorescent in situ hybridization data, it was evident that uniparental disomy was occurring in many colorectal cancers as well as in additional chromosomes, and often coordinately involved chromosomes 14 and 18. Further studies examined the possibility that uniparentalism was directed towards the selection for imprinted genes, but no association with imprinting was observed.
    MeSH term(s) Carcinoma/genetics ; Chromosomes, Human, Pair 14 ; Chromosomes, Human, Pair 18 ; Colorectal Neoplasms/genetics ; Comparative Genomic Hybridization ; DNA Methylation ; Genomic Imprinting/physiology ; Genomic Instability/physiology ; Humans ; Karyotyping/methods ; Loss of Heterozygosity ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Uniparental Disomy/genetics
    Language English
    Publishing date 2009-02-12
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 800806-1
    ISSN 1873-4456 ; 0165-4608
    ISSN (online) 1873-4456
    ISSN 0165-4608
    DOI 10.1016/j.cancergencyto.2008.10.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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    Jg. 1995 - 2021: Lesesall (1.OG)
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  3. Article: Colorectal cancers in patients with the (9A/6A) polymorphism of TGFBR1 exhibit lesser inter-(simple sequence repeat) PCR genomic instability and present clinically at greater age.

    Dutt, Smitha S / Chen, Neng / Darbary, Huferesh K / Swede, Helen / Petrelli, Nicholas J / Stoler, Daniel L / Anderson, Garth R

    Mutation research

    2008  Volume 645, Issue 1-2, Page(s) 27–32

    Abstract: TGFbeta is involved in the response to DNA damage and signaling the cell cycle checkpoint response, in large part achieved by modulating the activity of the ATM kinase. We have investigated if the presence of a common polymorphism in the TGFbeta receptor ...

    Abstract TGFbeta is involved in the response to DNA damage and signaling the cell cycle checkpoint response, in large part achieved by modulating the activity of the ATM kinase. We have investigated if the presence of a common polymorphism in the TGFbeta receptor TGFBR1 might impact genomic instability in human colorectal cancer. In order to obtain statistically significant numbers of patients with the lesser polymorphism, 177 colorectal cancer patients were genotyped for either the major form of the TGFBR1 receptor gene, homozygous for an internal segment of 9 alanines (9A/9A), or the lesser form, heterozygous for the polymorphism containing 6 alanines (9A/6A). Intrachromosomal genomic instability in the tumors was then quantified by the robust inter-(simple sequence repeat) PCR method. Tumors from all 26 patients heterozygous with the (9A/6A) polymorphism in TGFBR1 exhibited significantly lower genomic instability than from a randomly selected set [the first identified] of 37 patients with the (9A/9A) polymorphism (p=0.0002, Mann-Whitney). The median age of onset for the (9A/6A) patients was 70 years, compared with a median age of onset of 63 years for the patients carrying the (9A/9A) form (p=0.031, Mann-Whitney). These results are consistent with the model wherein genomic instability facilitates tumor progression, with lesser instability associated with later disease presentation. Clinically, our findings may be developed into improved screening guidelines with respect to the age at which colonoscopy is initiated in carriers of the TGFBR1*6A allele.
    MeSH term(s) Adult ; Age of Onset ; Aged ; Aged, 80 and over ; Alleles ; Base Sequence ; Colorectal Neoplasms/genetics ; DNA Damage ; DNA Primers/genetics ; DNA, Neoplasm/genetics ; Female ; Genomic Instability ; Heterozygote ; Homozygote ; Humans ; Male ; Middle Aged ; Minisatellite Repeats ; Polymorphism, Genetic ; Protein-Serine-Threonine Kinases/genetics ; Receptor, Transforming Growth Factor-beta Type I ; Receptors, Transforming Growth Factor beta/genetics ; Signal Transduction/genetics
    Chemical Substances DNA Primers ; DNA, Neoplasm ; Receptors, Transforming Growth Factor beta ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Receptor, Transforming Growth Factor-beta Type I (EC 2.7.11.30) ; TGFBR1 protein, human (EC 2.7.11.30)
    Language English
    Publishing date 2008-08-20
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 206607-5
    ISSN 1873-135X ; 0027-5107 ; 1383-5718 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
    ISSN (online) 1873-135X
    ISSN 0027-5107 ; 1383-5718 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
    DOI 10.1016/j.mrfmmm.2008.08.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models

    Mendioroz, Maite / Do, Catherine / Jiang, Xiaoling / Liu, Chunhong / Darbary, Huferesh K / Lang, Charles F / Lin, John / Thomas, Anna / Abu-Amero, Sayeda / Stanier, Philip / Temkin, Alexis / Yale, Alexander / Liu, Meng-Min / Li, Yang / Salas, Martha / Kerkel, Kristi / Capone, George / Silverman, Wayne / Yu, Y. Eugene /
    Moore, Gudrun / Wegiel, Jerzy / Tycko, Benjamin

    Genome biology. 2015 Dec., v. 16, no. 1

    2015  

    Abstract: BACKGROUND: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood. RESULTS: Here, we profile CpG methylation in DS and control cerebral and ... ...

    Abstract BACKGROUND: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood. RESULTS: Here, we profile CpG methylation in DS and control cerebral and cerebellar cortex of adults and cerebrum of fetuses. We purify neuronal and non-neuronal nuclei and T lymphocytes and find biologically relevant genes with DS-specific methylation (DS-DM) in each of these cell types. Some genes show brain-specific DS-DM, while others show stronger DS-DM in T cells. Both 5-methyl-cytosine and 5-hydroxy-methyl-cytosine contribute to the DS-DM. Thirty percent of genes with DS-DM in adult brain cells also show DS-DM in fetal brains, indicating early onset of these epigenetic changes, and we find early maturation of methylation patterns in DS brain and lymphocytes. Some, but not all, of the DS-DM genes show differential expression. DS-DM preferentially affected CpGs in or near specific transcription factor binding sites (TFBSs), implicating a mechanism involving altered TFBS occupancy. Methyl-seq of brain DNA from mouse models with sub-chromosomal duplications mimicking DS reveals partial but significant overlaps with human DS-DM and shows that multiple chromosome 21 genes contribute to the downstream epigenetic effects. CONCLUSIONS: These data point to novel biological mechanisms in DS and have general implications for trans effects of chromosomal duplications and aneuploidies on epigenetic patterning.
    Keywords DNA ; DNA methylation ; Down syndrome ; T-lymphocytes ; adults ; animal models ; binding sites ; cerebral cortex ; chromosomes ; early development ; epigenetics ; fetus ; gene expression regulation ; genes ; humans ; immune response ; neurons ; transcription factors ; trisomics
    Language English
    Dates of publication 2015-12
    Size p. 263.
    Publishing place BioMed Central
    Document type Article
    ZDB-ID 2040529-7
    ISSN 1474-760X ; 1465-6906
    ISSN (online) 1474-760X
    ISSN 1465-6906
    DOI 10.1186/s13059-015-0827-6
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Erratum to: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

    Mendioroz, Maite / Do, Catherine / Jiang, Xiaoling / Liu, Chunhong / Darbary, Huferesh K / Lang, Charles F / Lin, John / Thomas, Anna / Abu-Amero, Sayeda / Stanier, Philip / Temkin, Alexis / Yale, Alexander / Liu, Meng-Min / Li, Yang / Salas, Martha / Kerkel, Kristi / Capone, George / Silverman, Wayne / Yu, Y Eugene /
    Moore, Gudrun / Wegiel, Jerzy / Tycko, Benjamin

    Genome biology

    2016  Volume 17, Issue 1, Page(s) 123

    Language English
    Publishing date 2016-06-09
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2040529-7
    ISSN 1474-760X ; 1465-6914 ; 1465-6906
    ISSN (online) 1474-760X ; 1465-6914
    ISSN 1465-6906
    DOI 10.1186/s13059-016-0949-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

    Mendioroz, Maite / Do, Catherine / Jiang, Xiaoling / Liu, Chunhong / Darbary, Huferesh K / Lang, Charles F / Lin, John / Thomas, Anna / Abu-Amero, Sayeda / Stanier, Philip / Temkin, Alexis / Yale, Alexander / Liu, Meng-Min / Li, Yang / Salas, Martha / Kerkel, Kristi / Capone, George / Silverman, Wayne / Yu, Y Eugene /
    Moore, Gudrun / Wegiel, Jerzy / Tycko, Benjamin

    Genome biology

    2015  Volume 16, Page(s) 263

    Abstract: Background: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood.: Results: Here, we profile CpG methylation in DS and control cerebral and ... ...

    Abstract Background: Trisomy 21 causes Down syndrome (DS), but the mechanisms by which the extra chromosome leads to deficient intellectual and immune function are not well understood.
    Results: Here, we profile CpG methylation in DS and control cerebral and cerebellar cortex of adults and cerebrum of fetuses. We purify neuronal and non-neuronal nuclei and T lymphocytes and find biologically relevant genes with DS-specific methylation (DS-DM) in each of these cell types. Some genes show brain-specific DS-DM, while others show stronger DS-DM in T cells. Both 5-methyl-cytosine and 5-hydroxy-methyl-cytosine contribute to the DS-DM. Thirty percent of genes with DS-DM in adult brain cells also show DS-DM in fetal brains, indicating early onset of these epigenetic changes, and we find early maturation of methylation patterns in DS brain and lymphocytes. Some, but not all, of the DS-DM genes show differential expression. DS-DM preferentially affected CpGs in or near specific transcription factor binding sites (TFBSs), implicating a mechanism involving altered TFBS occupancy. Methyl-seq of brain DNA from mouse models with sub-chromosomal duplications mimicking DS reveals partial but significant overlaps with human DS-DM and shows that multiple chromosome 21 genes contribute to the downstream epigenetic effects.
    Conclusions: These data point to novel biological mechanisms in DS and have general implications for trans effects of chromosomal duplications and aneuploidies on epigenetic patterning.
    MeSH term(s) Adult ; Aneuploidy ; Animals ; Brain/growth & development ; Brain/metabolism ; Brain/pathology ; Chromosomes, Human, Pair 21/genetics ; CpG Islands/genetics ; DNA Methylation/genetics ; Disease Models, Animal ; Down Syndrome/genetics ; Down Syndrome/pathology ; Epigenesis, Genetic ; Fetus ; Humans ; Mice ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology
    Language English
    Publishing date 2015-11-25
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2040529-7
    ISSN 1474-760X ; 1474-760X
    ISSN (online) 1474-760X
    ISSN 1474-760X
    DOI 10.1186/s13059-015-0827-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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