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Evidence for suppression of cellular growth in vitro and selection against the indigenous mouse X chromosome in A9 cell hybrids after microcell-mediated transfer of an X from other mammalian species.

https://arctichealth.org/en/permalink/ahliterature198826
Source
Cytogenet Cell Genet. 2000;88(1-2):110-3
Publication Type
Article
Date
2000
Author
M Q Islam
K. Islam
Author Affiliation
Laboratory of Cancer Genetics, Division of Cell Biology, Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping University, Sweden. quais@mcb.liu.se
Source
Cytogenet Cell Genet. 2000;88(1-2):110-3
Date
2000
Language
English
Publication Type
Article
Keywords
Animals
Cell Division - genetics
Cell Fusion
Cell Size - genetics
Cell Transformation, Neoplastic - genetics - pathology
Chromosome Banding
Clone Cells - cytology - metabolism - pathology - transplantation
Cricetinae
Gene Dosage
Gene Transfer Techniques
Genes, Tumor Suppressor - genetics
Genetic Markers - genetics
Humans
Hybrid Cells - cytology - metabolism - pathology - transplantation
Karyotyping
Mesocricetus
Mice
Mice, Nude
Neoplasm Transplantation
Neoplasms, Experimental - genetics - pathology
Phenotype
X Chromosome - genetics
Abstract
Introduction of a human or Syrian hamster X chromosome (derived from BHK-191-5C cell hybrids) into tumorigenic mouse A9 cells via microcell fusion induced changes in cellular morphology and a retardation of cellular growth. The suppression of growth of the hybrids could be abolished, however, by daily changes of medium containing 20% serum. G-banding analysis showed the absence of a single, cytogenetically identifiable, indigenous X chromosome (marker Z) in two of four hybrid clones after an X chromosome was transferred from either hamster or human cells. All hybrids were tumorigenic when tested in nude mice. Together, these data suggest that the loss of the mouse X chromosome took place probably because of growth inhibitory effects imposed on hybrid cells due to the increase in X chromosome dosage. In addition, our results show a lack of association between the phenotype of cellular growth suppression in vitro and the phenotype of suppression of tumorigenicity in vivo.
PubMed ID
10773682 View in PubMed
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Family history of breast and ovarian cancers and BRCA1 and BRCA2 mutations in a population-based series of early-onset breast cancer.

https://arctichealth.org/en/permalink/ahliterature19615
Source
J Natl Cancer Inst. 2001 Aug 15;93(16):1215-23
Publication Type
Article
Date
Aug-15-2001
Author
N. Loman
O. Johannsson
U. Kristoffersson
H. Olsson
A. Borg
Author Affiliation
Department of Oncology, Lund University Hospital, Sweden. Niklas.Loman@onk.lu.se
Source
J Natl Cancer Inst. 2001 Aug 15;93(16):1215-23
Date
Aug-15-2001
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Breast Neoplasms - epidemiology - genetics
Female
Genes, BRCA1 - genetics
Genes, Tumor Suppressor - genetics
Genetic Screening
Germ-Line Mutation
Heterozygote
Humans
Ovarian Neoplasms - epidemiology - genetics
Population Surveillance
Prevalence
Research Support, Non-U.S. Gov't
Sweden - epidemiology
Abstract
BACKGROUND: BRCA1 and BRCA2 are the two major susceptibility genes involved in hereditary breast cancer. This study was undertaken to provide reliable population-based estimates of genetic influence and to characterize the nature and prevalence of BRCA1 and BRCA2 germline mutations in early-onset breast cancer. METHODS: In a series comprising all women diagnosed with breast cancer under the age of 41 years in southern Sweden during 1990 through 1995 (n = 262), family history of cancer was evaluated in 95% (n = 250) of the case subjects and germline mutations in BRCA1 and BRCA2 were analyzed in 89% (n = 234). All statistical tests were two-sided. RESULTS: A total of 97 case subjects had at least one first- or second-degree relative with breast or ovarian cancer; 34 (14%; 95% confidence interval [CI] = 9.6% to 18%) cases had at least two first- or second-degree relatives, 22 (8.8%; 95%CI = 5.3% to 12%) had one first-degree relative, and 41 (16%; 95% CI = 12% to 21%) had one second-degree relative with either cancer. If two females affected with breast or ovarian cancer who were related through an unaffected male were also defined as first-degree relatives, then a higher number of case subjects, 120 (48%; 95% CI = 42% to 54%), had at least one first-degree or second-degree relative with breast or ovarian cancer. Sixteen (6.8%; 95% CI = 4.0% to 11%) BRCA1 mutation carriers and five (2.1%; 95% CI = 0.70% to 4.9%) BRCA2 mutation carriers were identified. Among case subjects with one first- or more than one first- or second-degree relative with breast or ovarian cancer, BRCA mutations were more frequent (P
Notes
Comment In: J Natl Cancer Inst. 2001 Aug 15;93(16):1188-911504754
PubMed ID
11504767 View in PubMed
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Genetic alterations of the tumour suppressor gene regions 3p, 11p, 13q, 17p, and 17q in human breast carcinomas.

https://arctichealth.org/en/permalink/ahliterature24506
Source
Genes Chromosomes Cancer. 1992 Mar;4(2):113-21
Publication Type
Article
Date
Mar-1992
Author
T I Andersen
A. Gaustad
L. Ottestad
G W Farrants
J M Nesland
K M Tveit
A L Børresen
Author Affiliation
Department of Genetics, Norwegian Radium Hospital, Montebello, Oslo.
Source
Genes Chromosomes Cancer. 1992 Mar;4(2):113-21
Date
Mar-1992
Language
English
Publication Type
Article
Keywords
Adult
Aged
Aged, 80 and over
Alleles
Breast Neoplasms - genetics - pathology
Chromosome Deletion
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 13
Chromosomes, Human, Pair 17
Chromosomes, Human, Pair 3
Female
Gene Amplification
Genes, Tumor Suppressor - genetics
Heterozygote
Humans
Male
Middle Aged
Neoplasm Metastasis - genetics
Norway
Proto-Oncogene Proteins - genetics
Receptor, erbB-2
Research Support, Non-U.S. Gov't
Survival Rate
Abstract
Fifty-nine primary breast carcinomas and 11 metastases were examined to identify genetic alterations in the tumour suppressor gene regions 3p, 11p, 13q, 17p, and 17q. Loss of heterozygosity (LOH) was frequently observed on chromosome arms 17p (p144D6 lost in 75%, pYNZ22.1 in 55%, and TP53 in 48% of the primary tumours), 13q (RBI lost in 40% of the primary tumours), and 17q (pRMU3 lost in 35%, pTHH59 in 29%, and NM23HI in 26% of the primary tumours). Loss of all the markers except p144D6 was observed even more frequently in the metastases. Pairwise comparisons for concordance of allele losses on 17p indicated that there might be two genes on 17p implicated in breast cancer development; the TP53 gene and a gene located close to the p144D6 and pYNZ22.1 markers. LOH of the RBI gene was associated with LOH of pYNZ22.1 and p144D6, but not with LOH of TP53. LOH of RBI and TP53 was associated with occurrence of ductal carcinomas, RBI and p144D6 losses with tumour size, and p144D6 losses with positive node status as well. LOH of TP53 and the three 17q markers NM23HI, pTHH59, and pRMU3 was most frequently observed in tumours from postmenopausal women. p144D6 losses occurred most frequently in progesterone receptor-negative tumours, whereas pTHH59 losses occurred most frequently in oestrogen receptor-negative tumours. LOH of the investigated loci was not associated with ERBB2 protooncogene amplification, with positive family history of breast cancer, or with survival.
PubMed ID
1373310 View in PubMed
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Genetic studies of human primary hepatocellular carcinoma.

https://arctichealth.org/en/permalink/ahliterature4129
Source
Prog Clin Biol Res. 1992;376:155-72
Publication Type
Article
Date
1992
Author
K H Buetow
Author Affiliation
Division of Population Science, Fox Chase Cancer Center, Philadelphia, PA 19111.
Source
Prog Clin Biol Res. 1992;376:155-72
Date
1992
Language
English
Geographic Location
U.S.
Publication Type
Article
Keywords
Alaska - epidemiology
Alleles
Carcinoma, Hepatocellular - epidemiology - genetics
Chromosomes, Human, Pair 4
Genes, Tumor Suppressor - genetics
Humans
Liver Neoplasms - epidemiology - genetics
PubMed ID
1326768 View in PubMed
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Germline mutations of the PTEN gene in Cowden disease, an inherited breast and thyroid cancer syndrome.

https://arctichealth.org/en/permalink/ahliterature208635
Source
Nat Genet. 1997 May;16(1):64-7
Publication Type
Article
Date
May-1997
Author
D. Liaw
D J Marsh
J. Li
P L Dahia
S I Wang
Z. Zheng
S. Bose
K M Call
H C Tsou
M. Peacocke
C. Eng
R. Parsons
Author Affiliation
Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
Source
Nat Genet. 1997 May;16(1):64-7
Date
May-1997
Language
English
Publication Type
Article
Keywords
Breast Neoplasms - diagnosis - genetics
DNA Mutational Analysis
Female
Genes, Tumor Suppressor - genetics
Germ-Line Mutation
Hamartoma Syndrome, Multiple - genetics
Humans
Male
PTEN Phosphohydrolase
Pedigree
Phosphoric Monoester Hydrolases
Polymorphism, Genetic
Protein Tyrosine Phosphatases - genetics
Tumor Suppressor Proteins
Abstract
Cowden disease (CD) is an autosomal dominant cancer predisposition syndrome associated with an elevated risk for tumours of the breast, thyroid and skin. Lhermitte-Duclos disease (LDD) cosegregates with a subset of CD families and is associated with macrocephaly, ataxia and dysplastic cerebellar gangliocytomatosis. The common feature of these diseases is a predisposition to hamartomas, benign tumours containing differentiated but disorganized cells indigenous to the tissue of origin. Linkage analysis has determined that a single locus within chromosome 10q23 is likely to be responsible for both of these diseases. A candidate tumour suppressor gene (PTEN) within this region is mutated in sporadic brain, breast and prostate cancer. Another group has independently isolated the same gene, termed MMAC1, and also found somatic mutations throughout the gene in advanced sporadic cancers. Mutational analysis of PTEN in CD kindreds has identified germline mutations in four of five families. We found nonsense and missense mutations that are predicted to disrupt the protein tyrosine/dual-specificity phosphatase domain of this gene. Thus, PTEN appears to behave as a tumour suppressor gene in the germline. Our data also imply that PTEN may play a role in organizing the relationship of different cell types within an organ during development.
PubMed ID
9140396 View in PubMed
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Hepatocellular carcinoma in patients from northern Sweden with acute intermittent porphyria: morphology and mutations.

https://arctichealth.org/en/permalink/ahliterature22637
Source
Cancer Epidemiol Biomarkers Prev. 1996 May;5(5):393-7
Publication Type
Article
Date
May-1996
Author
L. Bjersing
C. Andersson
F. Lithner
Author Affiliation
Department of Pathology, University Hospital, Umea, Sweden.
Source
Cancer Epidemiol Biomarkers Prev. 1996 May;5(5):393-7
Date
May-1996
Language
English
Publication Type
Article
Keywords
Adenine
Aged
Aged, 80 and over
Alleles
Base Sequence
Carcinoma, Hepatocellular - genetics - pathology
Cell Division - genetics
Codon - genetics
DNA Damage
DNA, Viral - genetics
Female
Fixatives
Formaldehyde
Genes, Tumor Suppressor - genetics
Genes, p53 - genetics
Genes, ras - genetics
Guanine
Heme - biosynthesis - genetics
Hepatitis B virus - genetics
Humans
Hydroxymethylbilane Synthase - genetics
Liver Cirrhosis - genetics - pathology
Liver Neoplasms - genetics - pathology
Male
Middle Aged
Mutation - genetics
Porphyria, Acute Intermittent - genetics - pathology
Research Support, Non-U.S. Gov't
Sweden
Tissue Fixation
Abstract
More than a decade ago an association between acute intermittent porphyria (AIP) and hepatocellular carcinoma (HCC) was reported, but still the cause of the increased prevalence is unknown. Paraffin sections of formalin-fixed HCC from 17 AIP patients were reexamined and also screened for relevant mutations using several methods. The tumor diagnosis was verified, and in several cases precirrhosis and cirrhosis were also found. The clinically founded AIP diagnosis was verified at the gene level in most cases, demonstrating the Norrland type of mutation, i.e., G(593)-to-A substitution in codon 198 of the porphobilinogen deaminase (PBGD) gene. The second allele was neither mutated nor missing, contradicting the possibility that the PBGD gene might function as a tumor suppressor gene. Subsequent sequencing showed that cases not cleaved by the restriction enzyme NheI lacked the specific Norrland mutation. In recent years, selective mutations at codons 249 and 166 of the p53 gene have been described in HCC associated with aflatoxin and hepatitis B virus. In our area, with low exposure to those agents, no mutations in codon 249 were found, and mutation in codon 166 was excluded in all tumors except one; no traces of hepatitis B DNA were observed. Nor did we find mutations in H-ras 12 or 61. Intrinsic aberrations in AIP, including reduced heme synthesis and endogenous oxidative damage to DNA, may incite carcinogenic mutations elsewhere in the genome of liver cells. The increased cell proliferation coupled to precirrhosis and cirrhosis perhaps represents promotion in the initiation-promotion sequence of hepatocarcinogenesis.
PubMed ID
9162306 View in PubMed
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High frequency of chromosome 9p allelic loss and CDKN2 tumor suppressor gene alterations in squamous cell carcinoma of the bladder.

https://arctichealth.org/en/permalink/ahliterature23079
Source
J Natl Cancer Inst. 1995 Sep 20;87(18):1383-93
Publication Type
Article
Date
Sep-20-1995
Author
M. Gonzalez-Zulueta
A. Shibata
P F Ohneseit
C H Spruck
C. Busch
M. Shamaa
M. El-Baz
P W Nichols
M L Gonzalgo
M ] Elbaz M [corrected to El-Baz
Author Affiliation
Urologic Research Laboratory, University of Southern California, Los Angeles, USA.
Source
J Natl Cancer Inst. 1995 Sep 20;87(18):1383-93
Date
Sep-20-1995
Language
English
Publication Type
Article
Keywords
Alleles
Base Sequence
Bladder Neoplasms - genetics
Carcinoma, Squamous Cell - genetics
Carcinoma, Transitional Cell - genetics
Chromosome Deletion
Chromosomes, Human, Pair 17 - genetics
Chromosomes, Human, Pair 9 - genetics
Egypt
Genes, Tumor Suppressor - genetics
Genes, p53 - genetics
Homozygote
Humans
Immunohistochemistry
Molecular Sequence Data
Point Mutation
Polymerase Chain Reaction - methods
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Sweden
Tumor Suppressor Protein p53 - analysis
Abstract
BACKGROUND: In the Western Hemisphere, 90% of bladder cancers are transitional cell carcinomas, while only 7% are classified as squamous cell carcinomas. In contrast, in Egypt and regions of the Middle East and Africa, where infection by the trematode Schistosoma haematobium is endemic, squamous cell carcinoma is the most common bladder cancer as well as the most common cancer in men. PURPOSE: We planned experiments to understand the genetic defects underlying the development of squamous cell carcinoma and to determine if the morphologically and clinically distinct squamous cell carcinoma and transitional cell carcinoma of the bladder evolve following different genetic alterations. METHODS: Squamous cell carcinoma specimens from high-risk (Egypt, n = 19) and low-risk (Sweden, n = 12) populations were examined for genetic defects known to be involved in transitional cell carcinoma tumorigenesis. Homozygous deletions of the CDKN2 tumor suppressor gene were detected by comparative multiplex polymerase chain reaction. Mutations in the CDKN2 and p53 (also known as TP53) genes were analyzed by single-strand conformation polymorphism and DNA sequencing. Immunohistochemical staining of p53 protein was also performed. Allelic losses in chromosome arms 9p, 9q, and 17p were determined by microsatellite analysis. RESULTS: Homozygous deletions and sequence mutations in the CDKN2 gene were found in 67% (eight of 12) of squamous cell carcinoma specimens, a frequency three times higher than that reported for uncultured transitional cell carcinomas (P = .009). Hemizygous and homozygous deletions in 9p, where CDKN2 resides, were found in 92% (11 of 12) of uncultured squamous cell carcinomas, while only about 39% (35 of 90) of transitional cell carcinomas showed these losses (P = .001). Deletions in 9p with no change in 9q were found in 92% (10 of 11) of squamous cell carcinomas compared with only 10% (11 of 110) of transitional cell carcinomas (P
Notes
Erratum In: J Natl Cancer Inst 1995 Dec 6;87(23):1807
PubMed ID
7658499 View in PubMed
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Lack of tumor suppression but induced loss of copies of indigenous chromosome 10 in vitro following microcell-mediated transfer of a deleted human der(9)t(X;9) chromosome to Syrian hamster BHK-191-5C cells.

https://arctichealth.org/en/permalink/ahliterature199715
Source
Cytogenet Cell Genet. 1999;87(1-2):11-8
Publication Type
Article
Date
1999
Author
M Q Islam
K. Islam
Author Affiliation
Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping University, Linköping, Sweden. quais@mcb.liu.se
Source
Cytogenet Cell Genet. 1999;87(1-2):11-8
Date
1999
Language
English
Publication Type
Article
Keywords
Animals
Cell Division
Cell Fusion
Cell Line
Cell Size
Cell Transformation, Neoplastic - genetics - pathology
Chromosome Deletion
Chromosomes, Human, Pair 9 - genetics
Contact Inhibition
Cricetinae
DNA Replication - genetics
Fibroblasts - metabolism - pathology
Gene Amplification - genetics
Gene Dosage
Gene Transfer Techniques
Genes, Tumor Suppressor - genetics
Humans
Hybrid Cells - metabolism - pathology
Karyotyping
Mesocricetus
Phenotype
Polyploidy
Suppression, Genetic - genetics
X Chromosome - genetics
Abstract
We have previously shown that microcell-mediated transfer of a der(9)t(X;9) chromosome, containing an almost complete human chromosome (HSA) 9 derived from the human fibroblast strain GM0705, into the Syrian hamster (Mesocricetus auratus) cell line BHK-191-5C suppressed the anchorage independence and tumorigenicity of the hybrids. Transfer of a normal HSA X did not have any effect on these phenotypes. Although the recipient cell line contained a 1:1 ratio of near-diploid and near-tetraploid cells, all hybrids retaining the der(9) chromosome were near-tetraploid, in contrast to hybrids retaining a normal X chromosome. In the present study, we have generated microcell hybrids by transferring another der(9)t(X;9) chromosome derived from the human fibroblast strain GM01429. This derivative chromosome contained a deletion on the short arm of HSA 9 and was also missing the distal part of the long arm of HSA 9 due to the involvement in a reciprocal (constitutive) translocation of this chromosome with HSA X. Cytogenetic analysis showed that all hybrid clones were near-tetraploid, confirming our previous finding. We also observed that the introduction of the deleted der(9) chromosome forced the hybrids to lose Syrian hamster chromosome 10. A soft agar test and nude mice assay indicated that none of the hybrids was suppressed for either anchorage independent growth or tumor formation. These data suggest that there is an antagonistic relationship between growth-promoting genes and antiproliferative genes. The observed dosage effects of both growth-promoting and growth-suppressing genes indicate that cellular growth may be a quantitative trait.
PubMed ID
10640804 View in PubMed
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Linkage to BRCA2 region in hereditary male breast cancer.

https://arctichealth.org/en/permalink/ahliterature23121
Source
Lancet. 1995 Aug 26;346(8974):544-5
Publication Type
Article
Date
Aug-26-1995
Author
S. Thorlacius
L. Tryggvadottir
G H Olafsdottir
J G Jonasson
H M Ogmundsdottir
H. Tulinius
J E Eyfjord
Author Affiliation
Molecular and Cell Biology Research Laboratory, Reykjavik, Iceland.
Source
Lancet. 1995 Aug 26;346(8974):544-5
Date
Aug-26-1995
Language
English
Publication Type
Article
Keywords
Aged
Alleles
Breast Neoplasms - genetics
Breast Neoplasms, Male - genetics
Chromosome Mapping
Chromosomes, Human, Pair 13
DNA, Neoplasm - genetics
Female
Genes, Tumor Suppressor - genetics
Genes, p53 - genetics
Haplotypes
Heterozygote
Humans
Linkage (Genetics) - genetics
Lod Score
Male
Middle Aged
Pedigree
Research Support, Non-U.S. Gov't
Abstract
Breast cancer is rare in men, and family history of the disease is a risk factor. The recently discovered BRCA2 gene on chromosome 13q is thought to account for some families with increased risk of breast cancer, including male breast cancer. We describe a family with multiple cases of male breast cancer but, interestingly, no increase in female breast cancer. Linkage to the BRCA2 region is demonstrated and all the affected men share the same haplotype for the BCRA2 markers and loss of the other alleles in their tumours.
PubMed ID
7658781 View in PubMed
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15 records – page 1 of 2.