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Age dependence of tumor genetics in unfavorable neuroblastoma: arrayCGH profiles of 34 consecutive cases, using a Swedish 25-year neuroblastoma cohort for validation.

https://arctichealth.org/en/permalink/ahliterature114056
Source
BMC Cancer. 2013;13:231
Publication Type
Article
Date
2013
Author
Cihan Cetinkaya
Tommy Martinsson
Johanna Sandgren
Catarina Träger
Per Kogner
Jan Dumanski
Teresita Díaz de Ståhl
Fredrik Hedborg
Author Affiliation
Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala SE-751 85, Sweden.
Source
BMC Cancer. 2013;13:231
Date
2013
Language
English
Publication Type
Article
Keywords
Adolescent
Age Factors
Base Sequence
Child
Child, Preschool
Chromosome Aberrations
Chromosomes, Human, Pair 11 - genetics
Chromosomes, Human, Pair 12 - genetics
DNA Copy Number Variations
Gene Amplification
Gene Expression Profiling
Humans
Infant
Neuroblastoma - genetics
Nuclear Proteins - genetics
Oligonucleotide Array Sequence Analysis
Oncogene Proteins - genetics
Registries
Sequence Deletion
Sweden
Abstract
Aggressive neuroblastoma remains a significant cause of childhood cancer death despite current intensive multimodal treatment protocols. The purpose of the present work was to characterize the genetic and clinical diversity of such tumors by high resolution arrayCGH profiling.
Based on a 32K BAC whole-genome tiling path array and using 50-250K Affymetrix SNP array platforms for verification, DNA copy number profiles were generated for 34 consecutive high-risk or lethal outcome neuroblastomas. In addition, age and MYCN amplification (MNA) status were retrieved for 112 unfavorable neuroblastomas of the Swedish Childhood Cancer Registry, representing a 25-year neuroblastoma cohort of Sweden, here used for validation of the findings. Statistical tests used were: Fisher's exact test, Bayes moderated t-test, independent samples t-test, and correlation analysis.
MNA or segmental 11q loss (11q-) was found in 28/34 tumors. With two exceptions, these aberrations were mutually exclusive. Children with MNA tumors were diagnosed at significantly younger ages than those with 11q- tumors (mean: 27.4 vs. 69.5 months; p=0.008; n=14/12), and MNA tumors had significantly fewer segmental chromosomal aberrations (mean: 5.5 vs. 12.0; p
Notes
Cites: Nucleic Acids Res. 2002 Feb 15;30(4):e1511842121
Cites: Nat Rev Cancer. 2003 Mar;3(3):203-1612612655
Cites: BMC Genomics. 2004 Sep 20;5:7015380028
Cites: Cancer Genet Cytogenet. 2004 Oct 15;154(2):131-715474148
Cites: Science. 1984 Jun 8;224(4653):1121-46719137
Cites: Hum Genet. 1991 Apr;86(6):562-62026421
Cites: Med Pediatr Oncol. 1992;20(4):292-3001608350
Cites: EMBO J. 1993 Dec 15;12(13):5083-78262051
Cites: Eur J Cancer. 1995;31A(4):520-37576957
Cites: Cancer. 1997 May 15;79(10):2028-359149032
Cites: J Clin Oncol. 2005 Apr 1;23(10):2280-9915800319
Cites: N Engl J Med. 2005 Nov 24;353(21):2243-5316306521
Cites: Bioinformatics. 2006 Apr 15;22(8):1024-616455749
Cites: Genes Chromosomes Cancer. 2007 Dec;46(12):1098-10817823929
Cites: Oncogene. 2007 Nov 22;26(53):7432-4417533364
Cites: Hum Mutat. 2008 Mar;29(3):398-40818058796
Cites: Bioinformatics. 2008 Mar 15;24(6):751-818204059
Cites: BMC Genomics. 2008;9:35318664255
Cites: J Clin Oncol. 2009 Jan 10;27(2):289-9719047291
Cites: Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3368-7316740759
Cites: Cancer Genet Cytogenet. 2007 Jan 15;172(2):127-3817213021
Cites: Genes Chromosomes Cancer. 2007 Oct;46(10):936-4917647283
Cites: J Clin Oncol. 2009 Mar 1;27(7):1026-3319171713
Cites: Hematol Oncol Clin North Am. 2010 Feb;24(1):65-8620113896
Cites: Oncogene. 2010 Feb 11;29(6):865-7519901960
Cites: Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4323-820145112
Cites: Clin Cancer Res. 2010 Jun 1;16(11):2971-820406844
Cites: N Engl J Med. 2010 Jun 10;362(23):2202-1120558371
Cites: J Clin Oncol. 2010 Jul 1;28(19):3122-3020516441
Cites: Cell. 2011 Mar 4;144(5):646-7421376230
Cites: Cancer. 2011 Sep 15;117(18):4286-9321387264
Cites: Nature. 2012 Mar 29;483(7391):589-9322367537
PubMed ID
23656755 View in PubMed
Less detail

Amplification of c-erbB-2, int-2 and c-myc genes in node-negative breast carcinomas. Relationship to prognosis.

https://arctichealth.org/en/permalink/ahliterature24243
Source
Acta Oncol. 1993;32(3):289-94
Publication Type
Article
Date
1993
Author
L. Ottestad
T I Andersen
J M Nesland
M. Skrede
K M Tveit
K. Nustad
A L Børresen
Author Affiliation
Department of Medical Oncology, Norwegian Radium Hospital, Oslo.
Source
Acta Oncol. 1993;32(3):289-94
Date
1993
Language
English
Publication Type
Article
Keywords
Adult
Breast Neoplasms - genetics - mortality - pathology
Carcinoma - genetics - mortality - pathology - secondary
Fibroblast Growth Factor 3
Fibroblast Growth Factors - analysis
Gene Amplification
Gene Expression
Humans
Middle Aged
Neoplasm Recurrence, Local - genetics - mortality
Norway
Prognosis
Proto-Oncogene Proteins - analysis
Proto-Oncogene Proteins c-myc - analysis
Receptor, erbB-2
Receptors, Estrogen
Receptors, Progesterone
Research Support, Non-U.S. Gov't
Survival Analysis
Abstract
Primary tumours from 100 Norwegian node-negative breast carcinoma patients were examined for c-erbB-2, int-2, and c-myc proto-oncogene amplification. c-erbB-2, int-2, and c-myc amplification was found in 12.1% (12 of 99), 8.6% (8 of 93), and 1.1% (1 of 89) of the samples respectively. All the c-erbB-2 amplified tumours were of the ductal type, and all the int-2 amplified tumours were oestrogen receptor positive. No other significant or borderline significant associations between gene amplification and clinical or histopathological parameters were found. Relapse occurred more frequently in patients with c-erbB-2 gene amplification (relapse in 33.3% of the patients with c-erbB-2 amplification compared to 20.7% in the non-amplified group), but the difference was not statistically significant, int-2 amplification was not associated with increased risk of relapse, whereas the prognostic value of the c-myc amplification could not be evaluated.
PubMed ID
8100712 View in PubMed
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Amplification of HER-2(erbB-2/neu) oncogene as the most significant prognostic factor in a group of Russian breast cancer patients.

https://arctichealth.org/en/permalink/ahliterature222515
Source
Neoplasma. 1993;40(1):35-9
Publication Type
Article
Date
1993
Author
E N Imyanitov
O I Chernitsa
O M Serova
I F Nikoforova
G F Pluzhnikova
P G Knyazev
Author Affiliation
N.N. Petrov Research Institute of Oncology, Laboratory of Molecular Genetics of Cancer, St. Petersburg, Russia.
Source
Neoplasma. 1993;40(1):35-9
Date
1993
Language
English
Publication Type
Article
Keywords
Blotting, Northern
Blotting, Southern
Breast Neoplasms - genetics - pathology
Chi-Square Distribution
Chromosomes, Human, Pair 17
DNA - analysis - isolation & purification
Female
Follow-Up Studies
Gene Amplification
Gene Expression Regulation, Neoplastic
Genes, p53
Humans
Menopause
Middle Aged
Oncogene Proteins v-erbB
Oncogene Proteins, Viral - genetics
Oncogenes
Prognosis
RNA - analysis - isolation & purification
Receptor, erbB-2
Receptors, Estrogen - biosynthesis
Receptors, Progesterone - biosynthesis
Retroviridae Proteins, Oncogenic - genetics
Russia
Transcription, Genetic
Abstract
Amplification of HER-2(erbB-2/neu) oncogene was detected in 36 of 142 (25%) breast carcinomas (BC) RNA expression was examined in 42 carcinomas, in 10 of them overexpression was revealed. Amplification was matched by overexpression. No association was found between the increased number of HER-2(erbB-2/neu) copies and tumor size, lymph node involvement, stage of disease, age of onset, and estrogen and progesterone receptor level. HER-2(erbB-2/neu) amplification was shown to be of independent prognostic significance in the group of 32 BC patients with sufficient follow-up (more than 40 months). Six of 7 HER-2(erbB-2/neu) amplification-positive patients and only 2 of 25 HER-2(erbB-2/neu) amplification-negative ones relapsed (p
PubMed ID
7688867 View in PubMed
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Amplification studies of MET and Cdk6 in a rat endometrial tumor model and their correlation to human type I endometrial carcinoma tumors.

https://arctichealth.org/en/permalink/ahliterature85888
Source
Adv Exp Med Biol. 2008;617:511-7
Publication Type
Article
Date
2008
Author
Samuelson Emma
Nordlander Carola
Levan Göran
Behboudi Afrouz
Author Affiliation
Göteborg University Sahlgrenska Academy, Department of Clinical Genetics, Göteborg, Sweden.
Source
Adv Exp Med Biol. 2008;617:511-7
Date
2008
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - genetics - metabolism - secondary
Animals
Carcinoma, Squamous Cell - genetics - metabolism - secondary
Chromosome Aberrations
Chromosomes, Human, Pair 7 - genetics
Cyclin-Dependent Kinase 6 - genetics
Disease Models, Animal
Endometrial Neoplasms - genetics - metabolism - pathology
Female
Gene Amplification
Humans
In Situ Hybridization, Fluorescence
Peritoneal Neoplasms - genetics - metabolism - secondary
Proto-Oncogene Proteins c-met - genetics
Rats
Rats, Inbred BN
Abstract
Cancer is known to be a genetic disease that is both polygenic and heterogeneous, in most cases involving changes in several genes in a stepwise fashion. The spectrum of individual genes involved in the initiation and progression of cancer is greatly influenced by genetic factors unique to each patient. A study of complex diseases such as cancer is complicated by the genetic heterogeneous background and environmental factors in the human population. Endometrial cancer (EC) is ranked fourth among invasive tumors in women. In Sweden, approximately 1300 women (27/100,000 women) are diagnosed annually. To be able to study the genetic alterations in cancer, the use of an animal model is very convenient. Females of the BDII strain are genetically predisposed to EC and 90% of female BDII rats develop EC during their lifetime. Thus, BDII rats have been used to model human EC with respect to the genetics of susceptibility and of tumor development. A set of rat EC tumors was analyzed using conventional cytogenetics and comparative genome hybridization (CGH). Chromosomal aberrations, i.e., gains, were found on rat chromosome 4 (RNO4). Using FISH analysis, we concluded that the Met oncogene and Cdk6 (cyclin-dependent kinase 6) were amplified in this set of EC tumors. The data from this investigation were used to analyze a set of human endometrial tumors for amplification of Cdk6 and Met. Our preliminary data are indicative for a good correlation between our findings in the BDII rat model for EAC and the situation in human EC. These data provide strong support for the use of animal model systems for better understanding and scrutinizing of human complex disease of cancer.
PubMed ID
18497076 View in PubMed
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An Outbreak of Sheep Pox in Zabajkalskij kray of Russia.

https://arctichealth.org/en/permalink/ahliterature270564
Source
Transbound Emerg Dis. 2015 Aug;62(4):453-6
Publication Type
Article
Date
Aug-2015
Author
R A Maksyutov
E V Gavrilova
A P Agafonov
O S Taranov
A G Glotov
V N Miheev
S N Shchelkunov
A N Sergeev
Source
Transbound Emerg Dis. 2015 Aug;62(4):453-6
Date
Aug-2015
Language
English
Publication Type
Article
Keywords
Animals
Capripoxvirus - genetics - isolation & purification
DNA, Viral - genetics
Disease Outbreaks - veterinary
Gene Amplification
Microscopy, Electron - veterinary
Molecular Sequence Data
Phylogeny
Polymerase Chain Reaction - veterinary
Poxviridae Infections - epidemiology - veterinary
Russia - epidemiology
Sheep
Sheep Diseases - epidemiology
Skin - virology
Abstract
In this study, we investigated recent sheep pox outbreaks that occurred in Ononsky and Borzunsky regions of Zabajkalskij kray of Russia. The outbreaks involved in 2756 animals of which 112 were infected and 3 were slaughtered. Samples of injured skin of infected sheep were analysed by electron microscopy and CaPV-specific P32 gene amplification. Following sequence analysis of entire P32 gene showed that both specimens were identical to the sequence of several sheep poxvirus isolates from China and India. The close location of China to the last decade's Russian outbreaks suggest that possible future outbreaks in Russia could occur along the border regions with countries where sheep and goat pox are not controlled.
PubMed ID
24127821 View in PubMed
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Association of Rickettsia helvetica with chronic perimyocarditis in sudden cardiac death.

https://arctichealth.org/en/permalink/ahliterature49967
Source
Lancet. 1999 Oct 2;354(9185):1169-73
Publication Type
Article
Date
Oct-2-1999
Author
K. Nilsson
O. Lindquist
C. Påhlson
Author Affiliation
Department of Medical Sciences, Uppsala University Hospital, Sweden.
Source
Lancet. 1999 Oct 2;354(9185):1169-73
Date
Oct-2-1999
Language
English
Publication Type
Article
Keywords
Adult
Chronic Disease
Death, Sudden, Cardiac - etiology
Gene Amplification
Humans
Male
Microscopy, Electron, Scanning
Myocarditis - microbiology - pathology
Polymerase Chain Reaction
Research Support, Non-U.S. Gov't
Rickettsia - genetics - isolation & purification
Rickettsia Infections - complications
Sweden
Abstract
BACKGROUND: Rickettsia helvetica is the only non-imported rickettsia found in Scandinavia. It was first detected in Ixodes ricinus ticks, but has never been linked to human disease. We studied two young Swedish men who died of sudden cardiac failure during exercise, and who showed signs of perimyocarditis similar to those described in rickettsial disease. METHODS: Samples from the heart and other organs were analysed by PCR and DNA sequencing. May-Gr?nwald-Giemsa, Grocott, and acridine-orange stains were used for histopathological examinations. Staining of R. helvetica grown on shell-vials in vero cells, and the early descriptions of R. rickettsii by H T Ricketts and S B Wohlbach served as controls. Immunohistochemistry was done with Proteus OX-19 rabbit antisera as the primary antibody. The structure of rickettsia-like organisms was investigated by transmission electron microscopy. Serological analyses were carried out by indirect immunofluorescence with R. helvetica as the antigen. FINDINGS: By use of a semi-nested PCR, with primers specific for the 16S rRNA and 17-kDa outer-membrane-protein genes, and sequence analysis of the amplified products, genetic material from R. helvetica was detected in the pericardium and in a lymph node from the pulmonary hilum in case 1, and in a coronary artery and the heart muscle in case 2. A serological response in case 1 revealed an endpoint titre for R. helvetica of 1/320 (1/256 with R. rickettsii as the antigen). Examination of PCR-positive tissue showed chronic interstitial inflammation and the presence of rickettsia-like organisms predominantly located in the endothelium. These organisms reacted with Proteus OX-19 antisera, and their size and form were consistent with rickettsia. Electron microscopy confirmed that the appearance of the organisms was similar to that described for spotted-fever rickettsia. INTERPRETATION: R. helvetica, transmitted by I. ricinus ticks, may be an important pathogen in the aetiology of perimyocarditis, which can result in sudden unexpected cardiac death in young people.
PubMed ID
10513711 View in PubMed
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Aurora-A amplification associated with BRCA2 mutation in breast tumours.

https://arctichealth.org/en/permalink/ahliterature81367
Source
Cancer Lett. 2007 Apr 8;248(1):96-102
Publication Type
Article
Date
Apr-8-2007
Author
Bodvarsdottir Sigridur K
Hilmarsdottir Holmfridur
Birgisdottir Valgerdur
Steinarsdottir Margret
Jonasson Jon G
Eyfjord Jorunn E
Author Affiliation
Icelandic Cancer Society, Skogarhlid 8, 105 Reykjavik, Iceland; University of Iceland, Department of Medicine, Vatnsmyrarvegi 16, 101 Reykjavik, Iceland.
Source
Cancer Lett. 2007 Apr 8;248(1):96-102
Date
Apr-8-2007
Language
English
Publication Type
Article
Keywords
BRCA2 Protein - genetics
Breast Neoplasms - genetics - pathology
Cell Line
DNA Mutational Analysis
Female
Gene Amplification
Heterozygote
Humans
In Situ Hybridization, Fluorescence
Mutation
Odds Ratio
Protein-Serine-Threonine Kinases - genetics
Tumor Suppressor Protein p53 - genetics
Abstract
Potential interaction of Aurora-A amplification and BRCA2 mutation was examined in breast tumours from BRCA2 999del5 mutation carriers (n=20) and non-carriers (n=41). Aurora-A amplification studied by FISH was significantly more common in breast tumours from BRCA2 mutation carriers (p=0.0005). Extensive Aurora-A amplification was also detected on metaphase chromosomes in three breast epithelial cell lines with the same BRCA2 mutation. In addition, significant association was found between Aurora-A amplification and TP53 mutations in non-BRCA2 mutation carrier tumours (p=0.007). These results suggest that breast tumours with mutations in BRCA2 or TP53 could be promising candidates for Aurora-A targeted treatment.
PubMed ID
16860930 View in PubMed
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Automated image analysis of cyclin D1 protein expression in invasive lobular breast carcinoma provides independent prognostic information.

https://arctichealth.org/en/permalink/ahliterature123920
Source
Hum Pathol. 2012 Nov;43(11):2053-61
Publication Type
Article
Date
Nov-2012
Author
Nicholas P Tobin
Katja L Lundgren
Catherine Conway
Lola Anagnostaki
Sean Costello
Göran Landberg
Author Affiliation
Breakthrough Breast Cancer Research Unit, School of Cancer, Enabling Sciences and Technology, University of Manchester, Manchester Academic Health Science Centre, Paterson Institute for Cancer Research, The Christie NHS Foundation Trust, Wilmslow Road, Manchester, M20 4BX, UK.
Source
Hum Pathol. 2012 Nov;43(11):2053-61
Date
Nov-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Algorithms
Breast Neoplasms - diagnosis - metabolism - mortality
Carcinoma, Lobular - diagnosis - metabolism - mortality
Cell Nucleus - metabolism - pathology
Cyclin D1 - metabolism
Disease-Free Survival
Female
Gene Amplification
Humans
Image Processing, Computer-Assisted - methods
Mastectomy
Middle Aged
Neoplasm Invasiveness
Neoplasm Staging
Prognosis
Survival Rate
Sweden - epidemiology
Tumor Markers, Biological - metabolism
Abstract
The emergence of automated image analysis algorithms has aided the enumeration, quantification, and immunohistochemical analyses of tumor cells in both whole section and tissue microarray samples. To date, the focus of such algorithms in the breast cancer setting has been on traditional markers in the common invasive ductal carcinoma subtype. Here, we aimed to optimize and validate an automated analysis of the cell cycle regulator cyclin D1 in a large collection of invasive lobular carcinoma and relate its expression to clinicopathologic data. The image analysis algorithm was trained to optimally match manual scoring of cyclin D1 protein expression in a subset of invasive lobular carcinoma tissue microarray cores. The algorithm was capable of distinguishing cyclin D1-positive cells and illustrated high correlation with traditional manual scoring (?=0.63). It was then applied to our entire cohort of 483 patients, with subsequent statistical comparisons to clinical data. We found no correlation between cyclin D1 expression and tumor size, grade, and lymph node status. However, overexpression of the protein was associated with reduced recurrence-free survival (P=.029), as was positive nodal status (P
PubMed ID
22647349 View in PubMed
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Biological aspects of neuroblastomas identified by mass screening in Quebec.

https://arctichealth.org/en/permalink/ahliterature193977
Source
Med Pediatr Oncol. 2001 Jan;36(1):157-9
Publication Type
Article
Date
Jan-2001
Author
G M Brodeur
A T Look
H. Shimada
V M Hamilton
J M Maris
H W Hann
J M Leclerc
M. Bernstein
L C Brisson
J. Brossard
B. Lemieux
M. Tuchman
W G Woods
Author Affiliation
Division of Oncology, Children's Hospital of Philadelphia, PA 19104-4318, USA. brodeur@email.chop.edu
Source
Med Pediatr Oncol. 2001 Jan;36(1):157-9
Date
Jan-2001
Language
English
Publication Type
Article
Keywords
Age Factors
Catecholamines - urine
Chromosomes, Human, Pair 1 - genetics - ultrastructure
Cohort Studies
Ferritins - analysis - blood
Gene Amplification
Genes, myc
Humans
Infant
Infant, Newborn
Mass Screening
Neonatal Screening
Neuroblastoma - epidemiology - genetics - metabolism - pathology
Physical Examination
Ploidies
Prognosis
Quebec - epidemiology
Tumor Markers, Biological
Abstract
Neuroblastoma has several characteristics that suggest that preclinical diagnosis might improve outcome. Therefore, the Quebec Neuroblastoma Screening Project was undertaken from 1989 to 1994 to examine infants at 3 weeks and 6 months by measuring urinary catecholamine metabolites.
Over the 5-yr period, 45 tumors were detected by screening, 20 were identified clinically prior to the third week, and 64 were identified clinically at a later time. We analyzed available tumors for Shimada histopathology, tumor ploidy, MYCN copy number and serum ferritin.
Of the tumors detected by screening, only 2 of 45 tested had unfavorable histology, 2 of 45 had diploid or tetraploid DNA content, 0 of 43 had MYCN amplification, and 4 of 44 had elevated serum ferritin. All of these patients are alive and well. The 20 patients detected prior to the 3-week screen had similar biological characteristics. In contrast, of the patients detected clinically after 3 weeks of age, 19 of 51 testedhad unfavorable histology, 25 of 66 had diploid or tetraploid tumors, 12 of 56 had MYCN amplification, and 14 of 54 had elevated ferritin.
The difference between the screened and clinically detected cases was highly significant for each biological variable. Preliminary data on other biological variables, such as neurotrophin expression and allelic loss on 1 p in these patients are consistent with the above findings. These data suggest that mass screening for neuroblastoma at or before 6 months of age detects almost exclusively tumors that have favorable biological characteristics, many of which might have regressed spontaneously. Thus, continued mass screening for neuroblastoma at 6 months is unlikely to accomplish its intended goal, and should probably be discontinued.
PubMed ID
11464873 View in PubMed
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66 records – page 1 of 7.