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Article ; Online: The 8q24 gene desert: an oasis of non-coding transcriptional activity.

Huppi, Konrad / Pitt, Jason J / Wahlberg, Brady M / Caplen, Natasha J

2012 Volume 3, Page(s) 69

Abstract: Understanding the functional effects of the wide-range of aberrant genetic characteristics associated with the human chromosome 8q24 region in cancer remains daunting due to the complexity of the locus. The most logical target for study remains the MYC ... ...

Abstract	Understanding the functional effects of the wide-range of aberrant genetic characteristics associated with the human chromosome 8q24 region in cancer remains daunting due to the complexity of the locus. The most logical target for study remains the MYC proto-oncogene, a prominent resident of 8q24 that was first identified more than a quarter of a century ago. However, many of the amplifications, translocation breakpoints, and viral integration sites associated with 8q24 are often found throughout regions surrounding large expanses of the MYC locus that include other transcripts. In addition, chr.8q24 is host to a number of single nucleotide polymorphisms associated with cancer risk. Yet, the lack of a direct correlation between cancer risk alleles and MYC expression has also raised the possibility that MYC is not always the target of these genetic associations. The 8q24 region has been described as a "gene desert" because of the paucity of functionally annotated genes located within this region. Here we review the evidence for the role of other loci within the 8q24 region, most of which are non-coding transcripts, either in concert with MYC or independent of MYC, as possible candidate gene targets in malignancy.
Language	English
Publishing date	2012-04-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021 ; 1664-8021
ISSN (online)	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2012.00069
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Article ; Online: Genomic instability and mouse microRNAs.

Huppi, Konrad / Pitt, Jason / Wahlberg, Brady / Caplen, Natasha J

Toxicology mechanisms and methods

2011 Volume 21, Issue 4, Page(s) 325–333

Abstract: Tumor progression is the continual selection of variant subpopulations of malignant cells that have acquired increasing levels of genetic instability (Nowell Science 1976, 194, 23-28). This instability is manifested as chromosomal aneuploidy or ... ...

Abstract	Tumor progression is the continual selection of variant subpopulations of malignant cells that have acquired increasing levels of genetic instability (Nowell Science 1976, 194, 23-28). This instability is manifested as chromosomal aneuploidy or translocations, viral integration or somatic mutations that typically affect the expression of a gene (oncogene) that is especially damaging to the proper function of a cell. With the recent discovery of non-coding RNAs such as microRNAs (miRNAs), the concept that a target of genetic instability must be a protein-encoding gene is no longer tenable. Over the years, we have conducted several studies comparing the location of miRNA genes to positions of genetic instability, principally retroviral integration sites and chromosomal translocations in the mouse as a means of identifying miRNAs of importance in carcinogenesis. In this current study, we have used the most recent annotation of the mouse miRome (miRBase, release 16.0), and several datasets reporting the sites of integration of different retroviral vectors in a variety of mouse strains and mouse models of cancer, including for the first time a model that shows a propensity to form solid tumors, as a means to further identify or define, candidate oncogenic miRNAs. Several miRNA genes and miRNA gene clusters stand out as interesting new candidate oncogenes due to their close proximity to common retroviral integration sites including miR-29a/b/c and miR106a~363. We also discussed some recently identified miRNAs including miR-1965, miR-1900, miR-1945, miR-1931, miR-1894, and miR-1936 that are close to common retroviral integration sites and are therefore likely to have some role in cell homeostasis.
MeSH term(s)	Animals ; Gene Expression Profiling ; Genomic Instability ; Mice ; MicroRNAs/genetics ; Mutagenesis ; Neoplasms, Experimental/genetics ; Retroviridae/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2011-04-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2081252-8
ISSN	1537-6524 ; 1537-6516 ; 1051-7235
ISSN (online)	1537-6524
ISSN	1537-6516 ; 1051-7235
DOI	10.3109/15376516.2011.562759
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Article: Molecular profiling of prostate cancer.

Huppi, Konrad / Chandramouli, G V R

Current urology reports

2003 Volume 5, Issue 1, Page(s) 45–51

Abstract: The ability to distinguish between aggressive and nonaggressive tumors has not changed despite vast improvements in the detection of prostate cancer (PCA). To improve predictive accuracy, additional PCA-specific biomarkers must be identified and it is ... ...

Abstract	The ability to distinguish between aggressive and nonaggressive tumors has not changed despite vast improvements in the detection of prostate cancer (PCA). To improve predictive accuracy, additional PCA-specific biomarkers must be identified and it is the emerging microarray technology and gene expression profiling that appear to be capable of achieving this goal. Through comparisons of a number of published microarray studies of PCA, several potential biomarkers appear on the horizon, including the serine protease Hepsin, a-methylacyl CoA racemase, and the human homologue of the Drosophila protein Enhancer of Zeste. Although these markers will move toward validation by eventual protein expression studies, another aspect of microarray expression, global signature expression patterns through multidimensional scaling, appears to be promising in distinguishing between aggressive and nonaggressive forms of PCA or in distinguishing PCA from benign prostatic hyperplasia or normal prostate tissue.
MeSH term(s)	Gene Expression Profiling ; Humans ; Male ; Oligonucleotide Array Sequence Analysis ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism
Language	English
Publishing date	2003-09-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057354-6
ISSN	1534-6285 ; 1527-2737
ISSN (online)	1534-6285
ISSN	1527-2737
DOI	10.1007/s11934-004-0011-0
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Article ; Online: Insertional hypermutation in mineral oil-induced plasmacytomas.

Knittel, Gero / Metzner, Mirjam / Beck-Engeser, Gabriele / Kan, Ada / Ahrends, Tomasz / Eilat, Dan / Huppi, Konrad / Wabl, Matthias

European journal of immunology

2014 Volume 44, Issue 9, Page(s) 2785–2801

Abstract: Unless stimulated by a chronic inflammatory agent, such as mineral oil, plasma cell tumors are rare in young BALB/c mice. This raises the questions: What do inflammatory tissues provide to promote mutagenesis? And what is the nature of mutagenesis? We ... ...

Abstract	Unless stimulated by a chronic inflammatory agent, such as mineral oil, plasma cell tumors are rare in young BALB/c mice. This raises the questions: What do inflammatory tissues provide to promote mutagenesis? And what is the nature of mutagenesis? We determined that mineral oil-induced plasmacytomas produce large amounts of endogenous retroelements--ecotropic and polytropic murine leukemia virus and intracisternal A particles. Therefore, plasmacytoma formation might occur, in part, by de novo insertion of these retroelements, induced or helped by the inflammation. We recovered up to ten de novo insertions in a single plasmacytoma, mostly in genes with common retroviral integration sites. Additional integrations accompany tumor evolution from a solid tumor through several generations in cell culture. The high frequency of de novo integrations into cancer genes suggests that endogenous retroelements are coresponsible for plasmacytoma formation and progression in BALB/c mice.
MeSH term(s)	Animals ; Cell Line ; Emollients/adverse effects ; Emollients/pharmacology ; Mice ; Mice, Inbred BALB C ; Mineral Oil/adverse effects ; Mineral Oil/pharmacology ; Mutagenesis, Insertional/drug effects ; Mutagenesis, Insertional/immunology ; Neoplasms, Experimental/chemically induced ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/immunology ; Neoplasms, Experimental/pathology ; Plasmacytoma/chemically induced ; Plasmacytoma/genetics ; Plasmacytoma/immunology ; Plasmacytoma/pathology ; Retroelements
Chemical Substances	Emollients ; Retroelements ; Mineral Oil (8020-83-5)
Language	English
Publishing date	2014-06-27
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201344322
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: p53-Dependent induction of PVT1 and miR-1204.

Barsotti, Anthony M / Beckerman, Rachel / Laptenko, Oleg / Huppi, Konrad / Caplen, Natasha J / Prives, Carol

The Journal of biological chemistry

2011 Volume 287, Issue 4, Page(s) 2509–2519

Abstract: p53 is a tumor suppressor protein that acts as a transcription factor to regulate (either positively or negatively) a plethora of downstream target genes. Although its ability to induce protein coding genes is well documented, recent studies have ... ...

Abstract	p53 is a tumor suppressor protein that acts as a transcription factor to regulate (either positively or negatively) a plethora of downstream target genes. Although its ability to induce protein coding genes is well documented, recent studies have implicated p53 in the regulation of non-coding RNAs, including both microRNAs (e.g. miR-34a) and long non-coding RNAs (e.g. lincRNA-p21). We have identified the non-protein coding locus PVT1 as a p53-inducible target gene. PVT1, a very large (>300 kb) locus located downstream of c-myc on chromosome 8q24, produces a wide variety of spliced non-coding RNAs as well as a cluster of six annotated microRNAs: miR-1204, miR-1205, miR-1206, miR-1207-5p, miR-1207-3p, and miR-1208. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA), and luciferase assays reveal that p53 binds and activates a canonical response element within the vicinity of miR-1204. Consistently, we demonstrate the p53-dependent induction of endogenous PVT1 transcripts and consequent up-regulation of mature miR-1204. Finally, we have shown that ectopic expression of miR-1204 leads to increased p53 levels and causes cell death in a partially p53-dependent manner.
MeSH term(s)	Cell Death/physiology ; Cell Line, Tumor ; Chromosomes, Human, Pair 8/genetics ; Chromosomes, Human, Pair 8/metabolism ; Genetic Loci/physiology ; Humans ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; Proteins/genetics ; Proteins/metabolism ; RNA Processing, Post-Transcriptional/physiology ; RNA, Long Noncoding ; Response Elements/physiology ; Transcription, Genetic/physiology ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	MIRN1206 microRNA, human ; MicroRNAs ; PVT1 long-non-coding RNA, human ; Proteins ; RNA, Long Noncoding ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2011-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M111.322875
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Article ; Online: Identification of the receptor tyrosine kinase AXL in breast cancer as a target for the human miR-34a microRNA.

Mackiewicz, Mark / Huppi, Konrad / Pitt, Jason J / Dorsey, Tiffany H / Ambs, Stefan / Caplen, Natasha J

Breast cancer research and treatment

2011 Volume 130, Issue 2, Page(s) 663–679

Abstract: The identification of molecular features that contribute to the progression of breast cancer can provide valuable insight into the pathogenesis of this disease. Deregulated microRNA expression represents one type of molecular event that has been ... ...

Abstract	The identification of molecular features that contribute to the progression of breast cancer can provide valuable insight into the pathogenesis of this disease. Deregulated microRNA expression represents one type of molecular event that has been associated with many different human cancers. In order to identify a miRNA/mRNA regulatory interaction that is biologically relevant to the triple-negative breast cancer genotype/phenotype, we initially conducted a miRNA profiling experiment to detect differentially expressed miRNAs in cell line models representing triple-negative (MDA-MB-231), ER(+) (MCF7), and HER-2 overexpressed (SK-BR-3) histotypes. We identified human miR-34a expression as being >3-fold down (from its median expression value across all cell lines) in MDA-MB-231 cells, and identified AXL as a putative mRNA target using multiple miRNA/target prediction algorithms. The miR-34a/AXL interaction was functionally characterized through ectopic overexpression experiments with a miR-34a mimic in two independent triple-negative breast cancer cell lines. In reporter assays, miR-34a binds to its putative target site within the AXL 3'UTR to inhibit luciferase expression. We also observed degradation of AXL mRNA and decreased AXL protein levels, as well as cell signaling effects on AKT phosphorylation and phenotypic effects on cell migration. Finally, we present an inverse correlative trend in miR-34a and AXL expression for both cell line and patient tumor samples.
MeSH term(s)	3' Untranslated Regions ; Apoptosis ; Base Sequence ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Down-Regulation ; Female ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Humans ; Luciferases, Renilla/biosynthesis ; Luciferases, Renilla/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Phosphorylation ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-met/metabolism ; RNA Interference ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Signal Transduction
Chemical Substances	3' Untranslated Regions ; MIRN34 microRNA, human ; MicroRNAs ; Proto-Oncogene Proteins ; Luciferases, Renilla (EC 1.13.12.5) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; axl receptor tyrosine kinase (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2011-08-04
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604563-7
ISSN	1573-7217 ; 0167-6806
ISSN (online)	1573-7217
ISSN	0167-6806
DOI	10.1007/s10549-011-1690-0
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Article: Defining and assaying RNAi in mammalian cells.

Huppi, Konrad / Martin, Scott E / Caplen, Natasha J

Molecular cell

2005 Volume 17, Issue 1, Page(s) 1–10

Abstract: The investigation of protein function through the inhibition of activity has been critical to our understanding of many normal and abnormal biological processes. Until recently, functional inhibition in biological systems has been induced using a variety ...

Abstract	The investigation of protein function through the inhibition of activity has been critical to our understanding of many normal and abnormal biological processes. Until recently, functional inhibition in biological systems has been induced using a variety of approaches including small molecule antagonists, antibodies, aptamers, ribozymes, antisense oligonucleotides or transcripts, morpholinos, dominant-negative mutants, and knockout transgenic animals. Although all of these approaches have made substantial advances in our understanding of the function of many proteins, a lack of specificity or restricted applicability has limited their utility. Recently, exploitation of the naturally occurring posttranscriptional gene silencing mechanism triggered by double-stranded RNA (dsRNA), termed RNA interference (RNAi), has gained much favor as an alternative means for analyzing gene function. Aspects of the basic biology of RNAi, its application as a functional genomics tool, and its potential as a therapeutic approach have been extensively reviewed (Hannon and Rossi, 2004; Meister and Tuschl, 2004); however, there has been only limited discussion as to how to design and validate an individual RNAi effector molecule and how to interpret RNAi data overall, particularly with reference to experimentation in mammalian cells. This perspective will aim to consider some of the issues encountered when conducting and interpreting RNAi experiments in mammalian cells.
MeSH term(s)	Animals ; Cells/metabolism ; Genetic Techniques ; Mammals ; Phenotype ; Proteins/genetics ; Proteins/metabolism ; RNA Interference ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; RNA-Induced Silencing Complex/genetics ; RNA-Induced Silencing Complex/metabolism ; Terminology as Topic
Chemical Substances	Proteins ; RNA, Small Interfering ; RNA-Induced Silencing Complex
Language	English
Publishing date	2005-01-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2004.12.017
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Article: Impact of prematurity and intrauterine growth retardation on neonatal hemorrhagic and ischemic brain damage.

Amato, M / Konrad, D / Hüppi, P / Donati, F

European neurology

1993 Volume 33, Issue 4, Page(s) 299–303

Abstract: Low birth weight and intrauterine growth retardation are well-recognized risk factors for increased mortality, morbidity and poor neurologic outcome. Risk assessment is different considering true preterm (appropriate-for-gestational-age, AGA) or growth- ... ...

Abstract	Low birth weight and intrauterine growth retardation are well-recognized risk factors for increased mortality, morbidity and poor neurologic outcome. Risk assessment is different considering true preterm (appropriate-for-gestational-age, AGA) or growth-retarded (small-for-gestational-age, SGA) infants. Therefore, we carried out a study on the incidence of hemorrhagic (peri-intraventricular hemorrhage, PIVH) and ischemic (periventricular leukomalacia) brain lesions in two groups of AGA and SGA very-low-birth-weight (VLBW) infants. In the study period (1987-1990), 111 VLBW babies (< 1,500 g body weight) were serially studied at days 1, 3 and 7 and weekly until discharge by cerebral ultrasonography (ATL, MK 4, 7.5 MHz). 57 were VLBW-AGA babies (mean gestational age 28 weeks, mean body weight 1,106 g). 54 were VLBW-SGA babies (mean gestational age 31 weeks, mean body weight 990 g). PIVH was graded according to the system of Papile et al. Periventricular leukomalacia was defined as an echodensity (> 3 mm) adjacent to the lateral border of the ventricular body. We noted a higher incidence of PIVH in the AGA group (36.8%) than in SGA babies (18.5%; p < 0.01, Fisher test). The AGA subgroup < 1,000 g body weight had 72.2% PIVH compared to AGA babies > 1,000 g (20.5%; p < 0.01). The same relationship was observed in SGA babies (34.8% in < 1,000 g and 6.4% in > 1,000 g babies). Ischemic brain lesions (periventricular leukomalacia) were equally distributed between AGA and SGA babies (10.5 vs. 3.7%, p > 0.5) independently of body weight category.(ABSTRACT TRUNCATED AT 250 WORDS)
MeSH term(s)	Brain Damage, Chronic/diagnosis ; Cerebral Hemorrhage/diagnosis ; Cerebral Ventricles/pathology ; Cohort Studies ; Echoencephalography ; Female ; Fetal Growth Retardation/diagnosis ; Humans ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature, Diseases/diagnosis ; Infant, Small for Gestational Age ; Leukomalacia, Periventricular/diagnosis ; Male ; Neurologic Examination ; Prognosis ; Risk Factors
Language	English
Publishing date	1993
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	209426-5
ISSN	1421-9913 ; 0014-3022
ISSN (online)	1421-9913
ISSN	0014-3022
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Article: Pillars article: generation of antibody diversity in the immune response of BALB/c mice to influenza virus hemagglutinin. Proc. Natl. Acad. Sci. USA, 81: 3180-3184, May 1984.

McKean, David / Huppi, Konrad / Bell, Michael / Staudt, Louis / Gerhard, Walter / Weigert, Martin

Journal of immunology (Baltimore, Md. : 1950)

2008 Volume 180, Issue 9, Page(s) 5765–5769

MeSH term(s)	Amino Acid Sequence/genetics ; Animals ; Antibodies, Monoclonal/genetics ; Antibodies, Monoclonal/immunology ; Antibodies, Viral/genetics ; Antibodies, Viral/immunology ; Complementarity Determining Regions/genetics ; Complementarity Determining Regions/immunology ; Gene Rearrangement, B-Lymphocyte, Light Chain/immunology ; Hemagglutinins, Viral/immunology ; Hybridomas/cytology ; Hybridomas/immunology ; Immunoglobulin Variable Region/genetics ; Immunoglobulin Variable Region/immunology ; Immunoglobulin kappa-Chains/genetics ; Immunoglobulin kappa-Chains/immunology ; Influenza A Virus, H1N1 Subtype/immunology ; Mice ; Mice, Inbred BALB C ; Quantitative Trait Loci/immunology ; Somatic Hypermutation, Immunoglobulin
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Viral ; Complementarity Determining Regions ; Hemagglutinins, Viral ; Immunoglobulin Variable Region ; Immunoglobulin kappa-Chains
Language	English
Publishing date	2008-05-01
Publishing country	United States
Document type	Classical Article ; Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
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Article ; Online: Pvt1-encoded microRNAs in oncogenesis.

Beck-Engeser, Gabriele B / Lum, Amy M / Huppi, Konrad / Caplen, Natasha J / Wang, Bruce B / Wabl, Matthias

Retrovirology

2008 Volume 5, Page(s) 4

Abstract: Background: The functional significance of the Pvt1 locus in the oncogenesis of Burkitt's lymphoma and plasmacytomas has remained a puzzle. In these tumors, Pvt1 is the site of reciprocal translocations to immunoglobulin loci. Although the locus encodes ...

Abstract	Background: The functional significance of the Pvt1 locus in the oncogenesis of Burkitt's lymphoma and plasmacytomas has remained a puzzle. In these tumors, Pvt1 is the site of reciprocal translocations to immunoglobulin loci. Although the locus encodes a number of alternative transcripts, no protein or regulatory RNA products were found. The recent identification of non-coding microRNAs encoded within the PVT1 region has suggested a regulatory role for this locus. Results: The mouse Pvt1 locus encodes several microRNAs. In mouse T cell lymphomas induced by retroviral insertions into the locus, the Pvt1 transcripts, and at least one of their microRNA products, mmu-miR-1204 are overexpressed. Whereas up to seven co-mutations can be found in a single tumor, in over 2,000 tumors none had insertions into both the Myc and Pvt1 loci. Conclusion: Judging from the large number of integrations into the Pvt1 locus - more than in the nearby Myc locus - Pvt1 and the microRNAs encoded by it are as important as Myc in T lymphomagenesis, and, presumably, in T cell activation. An analysis of the co-mutations in the lymphomas likely place Pvt1 and Myc into the same pathway.
MeSH term(s)	Animals ; Gene Expression ; Genes, myc ; Lymphoma, T-Cell/genetics ; Lymphoma, T-Cell/virology ; Male ; Mice ; Mice, Inbred BALB C ; MicroRNAs/genetics ; Mutation ; Retroviridae/genetics ; Reverse Transcriptase Polymerase Chain Reaction/methods ; Spleen/virology ; Thymus Gland/virology ; Virus Integration/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2008-01-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ISSN	1742-4690
ISSN (online)	1742-4690
DOI	10.1186/1742-4690-5-4
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