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Article: Family cancer syndromes: inherited deficiencies in systems for the maintenance of genomic integrity.

Darbary, Huferesh / Stoler, Daniel L / Anderson, Garth R

Surgical oncology clinics of North America

2008 Volume 18, Issue 1, Page(s) 1–17, vii

Abstract: Familial cancer syndromes have revealed important fundamental features regarding how all cancers arise through destabilization of the genome, such that somatic evolution can select for the disruption of critical cellular coordinating and regulatory ... ...

Abstract	Familial cancer syndromes have revealed important fundamental features regarding how all cancers arise through destabilization of the genome, such that somatic evolution can select for the disruption of critical cellular coordinating and regulatory features. The authors examine those cellular genes and systems whose normal role is to preserve genomic integrity and relate them to the genetic foundations of heritable cancers. By examining how these cellular systems normally function, how family cancer genes are able to affect the process of tumor progression can be learned. In so doing, a clearer picture of how sporadic cancers arise is additionally gained.
MeSH term(s)	Cell Cycle ; DNA Damage ; Genomic Instability/genetics ; Humans ; Neoplastic Syndromes, Hereditary/genetics ; Risk Factors
Language	English
Publishing date	2008-05-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1196919-2
ISSN	1558-5042 ; 1055-3207
ISSN (online)	1558-5042
ISSN	1055-3207
DOI	10.1016/j.soc.2008.08.001
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Article ; Online: Erratum to: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

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
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Article ; Online: Mechanisms and Disease Associations of Haplotype-Dependent Allele-Specific DNA Methylation.

Do, Catherine / Lang, Charles F / Lin, John / Darbary, Huferesh / Krupska, Izabela / Gaba, Aulona / Petukhova, Lynn / Vonsattel, Jean-Paul / Gallagher, Mary P / Goland, Robin S / Clynes, Raphael A / Dwork, Andrew / Kral, John G / Monk, Catherine / Christiano, Angela M / Tycko, Benjamin

American journal of human genetics

2016 Volume 98, Issue 5, Page(s) 934–955

Abstract: Haplotype-dependent allele-specific methylation (hap-ASM) can impact disease susceptibility, but maps of this phenomenon using stringent criteria in disease-relevant tissues remain sparse. Here we apply array-based and Methyl-Seq approaches to multiple ... ...

Abstract	Haplotype-dependent allele-specific methylation (hap-ASM) can impact disease susceptibility, but maps of this phenomenon using stringent criteria in disease-relevant tissues remain sparse. Here we apply array-based and Methyl-Seq approaches to multiple human tissues and cell types, including brain, purified neurons and glia, T lymphocytes, and placenta, and identify 795 hap-ASM differentially methylated regions (DMRs) and 3,082 strong methylation quantitative trait loci (mQTLs), most not previously reported. More than half of these DMRs have cell type-restricted ASM, and among them are 188 hap-ASM DMRs and 933 mQTLs located near GWAS signals for immune and neurological disorders. Targeted bis-seq confirmed hap-ASM in 12/13 loci tested, including CCDC155, CD69, FRMD1, IRF1, KBTBD11, and S100A(∗)-ILF2, associated with immune phenotypes, MYT1L, PTPRN2, CMTM8 and CELF2, associated with neurological disorders, NGFR and HLA-DRB6, associated with both immunological and brain disorders, and ZFP57, a trans-acting regulator of genomic imprinting. Polymorphic CTCF and transcription factor (TF) binding sites were over-represented among hap-ASM DMRs and mQTLs, and analysis of the human data, supplemented by cross-species comparisons to macaques, indicated that CTCF and TF binding likelihood predicts the strength and direction of the allelic methylation asymmetry. These results show that hap-ASM is highly tissue specific; an important trans-acting regulator of genomic imprinting is regulated by this phenomenon; and variation in CTCF and TF binding sites is an underlying mechanism, and maps of hap-ASM and mQTLs reveal regulatory sequences underlying supra- and sub-threshold GWAS peaks in immunological and neurological disorders.
MeSH term(s)	Alleles ; Animals ; Brain/metabolism ; Brain/pathology ; DNA Methylation ; Female ; Genome-Wide Association Study ; Genomic Imprinting ; Haplotypes/genetics ; Humans ; Immune System Diseases/genetics ; Macaca mulatta ; Macaca radiata ; Nervous System Diseases/genetics ; Placenta/metabolism ; Placenta/pathology ; Polymorphism, Single Nucleotide/genetics ; Pregnancy ; Quantitative Trait Loci ; Species Specificity ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; Trans-Activators/genetics
Chemical Substances	Trans-Activators
Language	English
Publishing date	2016-03-24
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2016.03.027
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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
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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
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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
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Article ; Online: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models.

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
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Article: A critical role of tropomyosins in TGF-beta regulation of the actin cytoskeleton and cell motility in epithelial cells.

Bakin, Andrei V / Safina, Alfiya / Rinehart, Cammie / Daroqui, Cecilia / Darbary, Huferesh / Helfman, David M

Molecular biology of the cell

2004 Volume 15, Issue 10, Page(s) 4682–4694

Abstract: We have investigated transforming growth factor beta (TGF-beta)-mediated induction of actin stress fibers in normal and metastatic epithelial cells. We found that stress fiber formation requires de novo protein synthesis, p38Mapk and Smad signaling. We ... ...

Abstract	We have investigated transforming growth factor beta (TGF-beta)-mediated induction of actin stress fibers in normal and metastatic epithelial cells. We found that stress fiber formation requires de novo protein synthesis, p38Mapk and Smad signaling. We show that TGF-beta via Smad and p38Mapk up-regulates expression of actin-binding proteins including high-molecular-weight tropomyosins, alpha-actinin and calponin h2. We demonstrate that, among these proteins, tropomyosins are both necessary and sufficient for TGF-beta induction of stress fibers. Silencing of tropomyosins with short interfering RNAs (siRNAs) blocks stress fiber assembly, whereas ectopic expression of tropomyosins results in stress fibers. Ectopic-expression and siRNA experiments show that Smads mediate induction of tropomyosins and stress fibers. Interestingly, TGF-beta induction of stress fibers was not accompanied by changes in the levels of cofilin phosphorylation. TGF-beta induction of tropomyosins and stress fibers are significantly inhibited by Ras-ERK signaling in metastatic breast cancer cells. Inhibition of the Ras-ERK pathway restores TGF-beta induction of tropomyosins and stress fibers and thereby reduces cell motility. These results suggest that induction of tropomyosins and stress fibers play an essential role in TGF-beta control of cell motility, and the loss of this TGF-beta response is a critical step in the acquisition of metastatic phenotype by tumor cells.
MeSH term(s)	Actinin/genetics ; Actinin/metabolism ; Actins/metabolism ; Animals ; Calcium-Binding Proteins ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Movement/physiology ; DNA-Binding Proteins/metabolism ; Epithelial Cells/cytology ; Epithelial Cells/physiology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression Regulation ; Humans ; MAP Kinase Signaling System/physiology ; Mice ; Microfilament Proteins/genetics ; Microfilament Proteins/metabolism ; Molecular Sequence Data ; Neoplasm Metastasis ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Smad Proteins ; Stress Fibers/drug effects ; Stress Fibers/metabolism ; Trans-Activators/metabolism ; Transforming Growth Factor beta/pharmacology ; Tropomyosin/genetics ; Tropomyosin/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism ; ras Proteins/metabolism ; Calponins
Chemical Substances	Actins ; Calcium-Binding Proteins ; DNA-Binding Proteins ; Microfilament Proteins ; RNA, Small Interfering ; Smad Proteins ; Trans-Activators ; Transforming Growth Factor beta ; Tropomyosin ; Actinin (11003-00-2) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2004-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1098979-1
ISSN	1939-4586 ; 1059-1524
ISSN (online)	1939-4586
ISSN	1059-1524
DOI	10.1091/mbc.e04-04-0353
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Article: Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models

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
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Article: aCGH local copy number aberrations associated with overall copy number genomic instability in colorectal cancer: coordinate involvement of the regions including BCR and ABL.

Bartos, Jeremy D / Gaile, Daniel P / McQuaid, Devin E / Conroy, Jeffrey M / Darbary, Huferesh / Nowak, Norma J / Block, Annemarie / Petrelli, Nicholas J / Mittelman, Arnold / Stoler, Daniel L / Anderson, Garth R

Mutation research

2007 Volume 615, Issue 1-2, Page(s) 1–11

Abstract: In order to identify small regions of the genome whose specific copy number alteration is associated with high genomic instability in the form of overall genome-wide copy number aberrations, we have analyzed array-based comparative genomic hybridization ( ...

Abstract	In order to identify small regions of the genome whose specific copy number alteration is associated with high genomic instability in the form of overall genome-wide copy number aberrations, we have analyzed array-based comparative genomic hybridization (aCGH) data from 33 sporadic colorectal carcinomas. Copy number changes of a small number of specific regions were significantly correlated with elevated overall amplifications and deletions scattered throughout the entire genome. One significant region at 9q34 includes the c-ABL gene. Another region spanning 22q11-q13 includes the breakpoint cluster region (BCR) of the Philadelphia chromosome. Coordinate 22q11-q13 alterations were observed in 9 of 11 tumors with the 9q34 alteration. Additional regions on 1q and 14q were associated with overall genome-wide copy number changes, while copy number aberrations on chromosome 7p, 7q, and 13q21.1-q31.3 were found associated with this instability only in tumors from patients with a smoking history. Our analysis demonstrates there are a small number of regions of the genome where gain or loss is commonly associated with a tumor's overall level of copy number aberrations. Our finding BCR and ABL located within two of the instability-associated regions, and the involvement of these two regions occurring coordinately, suggests a system akin to the BCR-ABL translocation of CML may be involved in genomic instability in about one-third of human colorectal carcinomas.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Chromosomes, Artificial, Bacterial/genetics ; Chromosomes, Human, Pair 14/genetics ; Chromosomes, Human, Pair 22/genetics ; Chromosomes, Human, Pair 7/genetics ; Chromosomes, Human, Pair 9/genetics ; Colorectal Neoplasms/genetics ; Female ; Gene Dosage ; Genes, abl ; Genomic Instability ; Humans ; Male ; Middle Aged ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-bcr/genetics
Chemical Substances	BCR protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins c-bcr (EC 2.7.11.1)
Language	English
Publishing date	2007-02-03
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.2006.09.006
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