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Article ; Online: Common and distinct patterns of acquired uniparental disomy and homozygous deletions between lung squamous cell carcinomas and lung adenocarcinoma.

Tuna, Musaffe / Mills, Gordon B / Amos, Christopher I

2023 Volume 45, Page(s) 100932

Abstract: Acquired uniparental disomy (aUPD) is a chromosomal alteration that can lead to homozygosity of existing aberrations. We used data from The Cancer Genome Atlas SNP-based arrays to identify distinct and common aUPD profiles in lung adenocarcinoma (LUAD) ... ...

Abstract	Acquired uniparental disomy (aUPD) is a chromosomal alteration that can lead to homozygosity of existing aberrations. We used data from The Cancer Genome Atlas SNP-based arrays to identify distinct and common aUPD profiles in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Moreover, we tested relevance of aUPD for homozygous deletion (HMD), overall survival (OS), and recurrence-free survival (RFS). Overall, we found significantly higher aUPD (q = 5.34E-09) in LUSC than in LUAD. A significant portion of HMD was associated with aUPD in LUSC (24.9%) and LUAD (19.7%). We identified segmental, whole-chromosome arm and whole-chromosome aUPD, in which whole 7p arm aUPD was restricted to LUSC, while whole-chromosome 3 aUPD was observed only in LUAD, and whole-chromosome 21 aUPD was common to both LUSC and LUAD. The most frequent aUPD and HMD were observed at CDKN2A/B region in both LUAD and LUSC. In LUAD, aUPD and HMD at CDKN2A/B region were associated with shorter OS (q < 0.021 and q < 0.005), and RFS (q < 0.005 and q < 0.005), while heterozygous deletion was not associated with OS and RFS. In contrast, no association was found between aUPD at CDKN2A/B region and survival in LUSC. In LUAD, CTLA expression was significantly lower in samples with aUPD at CDKN2A/B regions than in samples without copy number and allele-based changes. Immune infiltration correlated with aUPD or HMD at CDKN2A/B, gain at HLA class I region, and aUPD at whole-chromosome q-arm or whole chromosome in LUAD, but not in LUSC. Both LUSC and LUAD have common and distinct patterns of aUPD regions with differing frequencies of occurrence and associations with outcome.
MeSH term(s)	Humans ; Uniparental Disomy/genetics ; Homozygote ; Sequence Deletion ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/pathology ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Squamous Cell/pathology ; Lung Neoplasms/pathology ; Lung/metabolism
Language	English
Publishing date	2023-10-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2023.100932
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Article ; Online: Whole-chromosome arm acquired uniparental disomy in cancer development is a consequence of isochromosome formation.

Tuna, Musaffe / Amos, Christopher I / Mills, Gordon B

Neoplasia (New York, N.Y.)

2022 Volume 25, Page(s) 9–17

Abstract: Using SNP-based microarray data from The Cancer Genome Atlas (TCGA), we investigated isochromosomes (deletion of one arm and duplication of the other arm) and related acquired uniparental disomy in 12 tumor types. We observed a high frequency of ... ...

Abstract	Using SNP-based microarray data from The Cancer Genome Atlas (TCGA), we investigated isochromosomes (deletion of one arm and duplication of the other arm) and related acquired uniparental disomy in 12 tumor types. We observed a high frequency of isochromosomes (25.98%) across all type of tumors except thyroid cancers. The highest frequency of isochromosomes was found in lung squamous cell carcinoma (54.18%). Moreover, whole-chromosome arm acquired uniparental disomy (aUPD) was common in the deleted arms of isochromosomes. These data are consistent with whole-chromosome arm aUPD likely being a consequence of isochromosomes formation. Our findings implicated aUPD as occurring through error-prone DNA repair of a deleted arm or segment of a chromosome that leads to homozygosity for existing alterations. Isochromosomes were significantly more frequent in TP53 mutated samples than wild types in 6 types of tumors with loss of TP53 function potentially contributing to development of isochromosomes. Isochromosomes are common alterations in cancer, and losing one arm of a chromosome could result in duplication of the lost arm. Duplication of the remaining arm leads promulgation of the effects on any defects in the remaining allele, due to subsequent homozygosity.
MeSH term(s)	Alleles ; Humans ; Isochromosomes/genetics ; Neoplasms/genetics ; Uniparental Disomy/genetics
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2021.12.009
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Article: Acquired Uniparental Disomy Regions Are Associated with Disease Outcome in Patients with Oral Cavity and Oropharynx But Not Larynx Cancers.

Tuna, Musaffe / I Amos, Christopher / B Mills, Gordon

Translational oncology

2020 Volume 13, Issue 5, Page(s) 100763

Abstract: Acquired uniparental disomy (aUPD) regions pinpoint homozygousity and monoallelic expressed genes. We analyzed The Cancer Genome Atlas single-nucleotide polymorphism arrays and expression data from oral cavity, oropharynx, and larynx cancers to identify ... ...

Abstract	Acquired uniparental disomy (aUPD) regions pinpoint homozygousity and monoallelic expressed genes. We analyzed The Cancer Genome Atlas single-nucleotide polymorphism arrays and expression data from oral cavity, oropharynx, and larynx cancers to identify frequency of aUPD in each tumor type and association of aUPD regions and differentially expressed genes in the regions with survival. Cox proportional hazard models were used for survival function; and Student's t test, for differentially expressed genes between groups. The frequency of aUPD was highest in larynx cancers (88.35%) followed by oral cavity (81.11%) and oropharynx cancers (73.85%). In univariate analysis, 11 regions at chromosome 9p were associated with overall survival (OS) in oral cavity cancers. Two regions at chromosome 17p were associated with OS in oropharyngeal cancers, but no aUPD region was associated with survival in patients with larynx cancers. Overexpression of SIGMAR1, C9orf23, and HINT2 was associated with reduced OS in patients with oral cavity cancers, and upregulation of MED27 and YWHAE was associated with shorter OS in patients with oropharynx cancers. In multivariate analysis, four aUPD regions at chromosome 9p and overexpression of HINT2 were associated with shorter OS in oral cavity cancers, and overexpression of MED27 was associated with worse OS in patients with oropharynx cancers. aUPD regions and differentially expressed genes in those regions influence the outcome and may play a role in aggressiveness in oral cavity and oropharynx cancers but not in patients with larynx cancers.
Language	English
Publishing date	2020-04-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2443840-6
ISSN	1936-5233 ; 1936-5233 ; 1944-7124
ISSN (online)	1936-5233
ISSN	1936-5233 ; 1944-7124
DOI	10.1016/j.tranon.2020.100763
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Article ; Online: Next generation sequencing and its applications in HPV-associated cancers.

Tuna, Musaffe / Amos, Christopher I

Oncotarget

2017 Volume 8, Issue 5, Page(s) 8877–8889

Abstract: Approximately 18% of all human cancers have a viral etiology, and human papillomavirus (HPV) has been identified as one of the most prevalent viruses that plays causative role in nearly all cervical cancers and, in addition, in subset of head and neck, ... ...

Abstract	Approximately 18% of all human cancers have a viral etiology, and human papillomavirus (HPV) has been identified as one of the most prevalent viruses that plays causative role in nearly all cervical cancers and, in addition, in subset of head and neck, anal, penile and vulvar cancers. The recent introduction of next generation sequencing (NGS) and other 'omics' approaches have resulted in comprehensive knowledge on the pathogenesis of HPV-driven tumors. Specifically, these approaches have provided detailed information on genomic HPV integration sites, disrupted genes and pathways, and common and distinct genetic and epigenetic alterations in different human HPV-associated cancers. This review focuses on HPV integration sites, its concomitantly disrupted genes and pathways and its functional consequences in both cervical and head and neck cancers. Integration of NGS data with other 'omics' and clinical data is crucial to better understand the pathophysiology of each individual malignancy and, based on this, to select targets and to design effective personalized treatment options.
Language	English
Publishing date	2017-01-31
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.12830
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Article ; Online: Molecular mechanisms and pathobiology of oncogenic fusion transcripts in epithelial tumors.

Tuna, Musaffe / Amos, Christopher I / Mills, Gordon B

Oncotarget

2019 Volume 10, Issue 21, Page(s) 2095–2111

Abstract: Recurrent fusion transcripts, which are one of the characteristic hallmarks of cancer, arise either from chromosomal rearrangements or from transcriptional errors in splicing. DNA rearrangements include intrachromosomal or interchromosomal translocation, ...

Abstract	Recurrent fusion transcripts, which are one of the characteristic hallmarks of cancer, arise either from chromosomal rearrangements or from transcriptional errors in splicing. DNA rearrangements include intrachromosomal or interchromosomal translocation, tandem duplication, deletion, inversion, or result from chromothripsis, which causes complex rearrangements. In addition, fusion proteins can be created through transcriptional read-through. Fusion genes can be transcribed to fusion transcripts and translated to chimeric proteins, with many having demonstrated transforming activities through multiple mechanisms in cells. Fusion proteins represent novel therapeutic targets and diagnostic biomarkers of diagnosis, disease status, or progression. This review focuses on the mechanisms underlying the formation of oncogenic fusion genes and transcripts and their impact on the pathobiology of epithelial tumors.
Language	English
Publishing date	2019-03-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.26777
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Article ; Online: Genome-Wide Analysis of Head and Neck Squamous Cell Carcinomas Reveals HPV, TP53, Smoking and Alcohol-Related Allele-Based Acquired Uniparental Disomy Genomic Alterations.

Tuna, Musaffe / Amos, Christopher I / Mills, Gordon B

Neoplasia (New York, N.Y.)

2019 Volume 21, Issue 2, Page(s) 197–205

Abstract: Smoking and alcohol intake are major risk factors in head and neck squamous cell carcinomas (HNSCCs). Although the link between TP53 mutation and smoking has been well established, very little is known about the link between acquired uniparental disomy ( ... ...

Abstract	Smoking and alcohol intake are major risk factors in head and neck squamous cell carcinomas (HNSCCs). Although the link between TP53 mutation and smoking has been well established, very little is known about the link between acquired uniparental disomy (aUPD) and smoking and/or alcohol consumption or other clinical characteristics. We used TCGA genomic data to investigate whether smoking, alcohol intake, clinical and demographic variables, HPV status and TP53 mutation are associated with aUPD at specific chromosomal regions. In multivariate analysis, we found association between aUPD regions and risk factors and clinical variables of disease. aUPD regions on chromosome 4q, 5q, 9p, 9q, 13q, 17p and CDKN2A occurred significantly more often in patients with TP53-mutated HNSCC than in those with wild-type HNSCC, while aUPD regions on chromosome 9p and at CDKN2A were significantly more frequent in females than in males. Besides, aUPD occurred more frequent in HPV-positive than in HPV-negative samples with all HNSCC and larynx cancers on chromosome 9q 15q and 17p. Moreover, aUPD on CDKN2A region occurred more often in alcohol drinkers than nondrinkers in patients with all HNSCC and oral cavity cancers, while aUPD region on chromosome 5q occurred less in alcohol drinkers than nondrinkers in patients with all HNSCC and oral cavity cancers. Similarly, aUPD region on chromosome 5q occurred less in smokers than nonsmokers in patients with all HNSCC and oral cavity cancers. In conclusion, aUPD regions are not random, and certain regions are associated with risk factors for disease, and with TP53 mutation status.
MeSH term(s)	Alcohol Drinking/adverse effects ; Alleles ; Databases, Genetic ; Genome-Wide Association Study ; Humans ; Mutation ; Neoplasm Grading ; Neoplasm Staging ; Papillomavirus Infections/complications ; Polymorphism, Single Nucleotide ; Smoking/adverse effects ; Squamous Cell Carcinoma of Head and Neck/diagnosis ; Squamous Cell Carcinoma of Head and Neck/etiology ; Tumor Suppressor Protein p53/genetics ; Uniparental Disomy/genetics
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2019-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2018.12.002
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Article ; Online: Genome-Wide Profiling of Acquired Uniparental Disomy Reveals Prognostic Factors in Head and Neck Squamous Cell Carcinoma.

Tuna, Musaffe / Liu, Wenbin / Amos, Christopher I / Mills, Gordon B

Neoplasia (New York, N.Y.)

2019 Volume 21, Issue 11, Page(s) 1102–1109

Abstract: Acquired uniparental disomy (aUPD) leads to homozygosity facilitating identification of monoallelically expressed genes. We analyzed single-nucleotide polymorphism array-based genotyping data of 448 head and neck squamous cell carcinoma (HNSCC) samples ... ...

Abstract	Acquired uniparental disomy (aUPD) leads to homozygosity facilitating identification of monoallelically expressed genes. We analyzed single-nucleotide polymorphism array-based genotyping data of 448 head and neck squamous cell carcinoma (HNSCC) samples from The Cancer Genome Atlas to determine the frequency and distribution of aUPD regions and their association with survival, as well as to gain a better understanding of their influence on the tumor genome. We used expression data from the same dataset to identify differentially expressed genes between groups with and without aUPD. Univariate and multivariable Cox proportional hazards models were performed for survival analysis. We found that 82.14% of HNSCC samples carried aUPD; the most common regions were in chromosome 17p (31.25%), 9p (30.13%), and 9q (27.46%). In univariate analysis, five independent aUPD regions at chromosome 9p, two regions at chromosome 9q, and the CDKN2A region were associated with poor overall survival in all groups, including training and test sets and human papillomavirus (HPV)-negative samples. Forty-three genes in areas of aUPD including PD-L1 and CDKN2A were differentially expressed in samples with aUPD compared to samples without aUPD. In multivariable analysis, aUPD at the CDKN2A region was a significant predictor of overall survival in the whole cohort and in patients with HPV-negative HNSCC. aUPD at specific regions in the genome influences clinical outcomes of HNSCC and may be beneficial for selection of personalized therapy to prolong survival in patients with this disease.
MeSH term(s)	Adult ; Aged ; Databases, Genetic ; Female ; Gene Expression Profiling ; Genome-Wide Association Study ; Genomics/methods ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Polymorphism, Single Nucleotide ; Prognosis ; Squamous Cell Carcinoma of Head and Neck/genetics ; Squamous Cell Carcinoma of Head and Neck/mortality ; Squamous Cell Carcinoma of Head and Neck/pathology ; Uniparental Disomy/genetics
Language	English
Publishing date	2019-11-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1483840-0
ISSN	1476-5586 ; 1522-8002
ISSN (online)	1476-5586
ISSN	1522-8002
DOI	10.1016/j.neo.2019.08.008
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Article ; Online: Insulin-like growth factor I regulates the expression of isoforms of Wilms' tumor 1 gene in breast cancer.

Tuna, Musaffe / Itamochi, Hiroaki

Tumori

2014 Volume 99, Issue 6, Page(s) 715–722

Abstract: Aim and background: The Wilms' tumor 1 gene (WT1) is overexpressed in many cancers, including breast cancer, and its high expression is an adverse prognostic factor. However, the factors that regulate WT1 expression are poorly understood.: Methods and ...

Abstract	Aim and background: The Wilms' tumor 1 gene (WT1) is overexpressed in many cancers, including breast cancer, and its high expression is an adverse prognostic factor. However, the factors that regulate WT1 expression are poorly understood. Methods and study design: Expression of genes at the RNA and protein level was detected by reverse transcriptase-polymerase chain reaction, western blotting, and reverse-phase protein array assays in breast cancer cell lines and tumor samples. Results: In the study, we showed that the treatment of MCF-7 breast cancer cells with insulin-like growth factor I (IGF-I) increases WT1 protein expression by 77%. IGF-I uses Akt to up-regulate WT1 expression. Conversely, inhibition of IGF-I by IGF-binding protein 3 and of IGF-I receptor (IGF-IR) by anti-IGF-IR antibody (α-IR3) uses Akt to decrease WT1 protein levels in MCF-7 cells. We thus newly identified a mechanism by which IGF-I up-regulates WT1, especially the (+exon 5/-KTS) isoform, at the posttranscriptional level in MCF-7 cells and primary breast tumor samples. Conclusions: The results indicate a novel posttranscriptional regulatory factor of WT1 in MCF-7 breast cancer cells.
MeSH term(s)	Blotting, Western ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Wilms Tumor ; Humans ; Insulin-Like Growth Factor I/metabolism ; MCF-7 Cells/metabolism ; Neoplasm Staging ; Predictive Value of Tests ; Prognosis ; RNA Isoforms/metabolism ; RNA Processing, Post-Transcriptional ; RNA, Messenger/metabolism ; RNA, Neoplasm/metabolism ; Receptor, ErbB-2/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Up-Regulation ; WT1 Proteins/genetics
Chemical Substances	RNA Isoforms ; RNA, Messenger ; RNA, Neoplasm ; WT1 Proteins ; WT1 protein, human ; Insulin-Like Growth Factor I (67763-96-6) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2014-03-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	280962-x
ISSN	2038-2529 ; 0300-8916
ISSN (online)	2038-2529
ISSN	0300-8916
DOI	10.1700/1390.15461
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Ud II Zs.43: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Genetic and epigenetic alterations of microRNAs and implications for human cancers and other diseases.

Tuna, Musaffe / Machado, Andreia S / Calin, George A

Genes, chromosomes & cancer

2016 Volume 55, Issue 3, Page(s) 193–214

Abstract: MicroRNAs (miRNAs) are a well-studied group of noncoding RNAs that control gene expression by interacting mainly with messenger RNA. It is known that miRNAs and their biogenesis regulatory machineries have crucial roles in multiple cell processes; thus, ... ...

Abstract	MicroRNAs (miRNAs) are a well-studied group of noncoding RNAs that control gene expression by interacting mainly with messenger RNA. It is known that miRNAs and their biogenesis regulatory machineries have crucial roles in multiple cell processes; thus, alterations in these genes often lead to disease, such as cancer. Disruption of these genes can occur through epigenetic and genetic alterations, resulting in aberrant expression of miRNAs and subsequently of their target genes. This review focuses on the disruption of miRNAs and their key regulatory machineries by genetic alterations, with emphasis on mutations and epigenetic changes in cancer and other diseases.
MeSH term(s)	Epigenesis, Genetic ; Epigenomics ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; Mutation ; Neoplasms/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1018988-9
ISSN	1098-2264 ; 1045-2257
ISSN (online)	1098-2264
ISSN	1045-2257
DOI	10.1002/gcc.22332
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Article: Genomic sequencing in cancer

Tuna, Musaffe / Amos, Christopher I

Cancer letters. 2013 Nov. 1, v. 340, no. 2

2013

Abstract: Genomic sequencing has provided critical insights into the etiology of both simple and complex diseases. The enormous reductions in cost for whole genome sequencing have allowed this technology to gain increasing use. Whole genome analysis has impacted ... ...

Abstract	Genomic sequencing has provided critical insights into the etiology of both simple and complex diseases. The enormous reductions in cost for whole genome sequencing have allowed this technology to gain increasing use. Whole genome analysis has impacted research of complex diseases including cancer by allowing the systematic analysis of entire genomes in a single experiment, thereby facilitating the discovery of somatic and germline mutations, and identification of the insertions, deletions, and structural rearrangements, including translocations and inversions, in novel disease genes. Whole-genome sequencing can be used to provide the most comprehensive characterization of the cancer genome, the complexity of which we are only beginning to understand. Hence in this review, we focus on whole-genome sequencing in cancer.
Keywords	etiology ; genes ; germ cells ; mutation ; sequence analysis
Language	English
Dates of publication	2013-1101
Size	p. 161-170.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2012.11.004
Database	NAL-Catalogue (AGRICOLA)

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