PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “diploidization”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMedDate not supplied

Replication of primate oncornavirus SSV-1 on MRC-5 human diploid cells.

MRC-5 human diploid cells infected with Simian Sarcoma Virus from woolly monkey (SSV-1) were not transformed but an efficient replication of non transforming SiLV was demonstrated. Increase of virus reverse transcriptase activity paralleled cell replication during successive passages. Preliminary results concerning the influence of viral infection on the life span and the karyotype of MRC-5 diploid cells will be reported and several implications of these findings discussed.

Cells, Cultured↗
PubMedDate not supplied

Clinical experience with a human diploid cell rabies vaccine.

Between January 1975 and December 1977 the Center for Disease Control treated 255 persons with the human diploid cell strain rabies vaccine who did not have development of an antibody titer to duck embryo vaccine (DEV) or who were at risk for having a serious reaction to DEV. Two hundred eighteen persons were treated postexposure, and 37 persons were treated preexposure. The antibody response to the vaccine was excellent, and the reaction rates were low. No person treated has had development of rabies. This study corroborates other studies that suggest that the human diploid cell strain rabies vaccines are safe and induce excellent antibody titers to rabies.

Adult↗
PubMed1995

Comparative genomic hybridization of formalin-fixed, paraffin-embedded breast tumors reveals different patterns of chromosomal gains and losses in fibroadenomas and diploid and aneuploid carcinomas.

Comparative genomic hybridization serves as a screening test for regions of copy number changes in tumor genomes. We have applied the technique to map DNA gains and losses in 33 cases of formalin-fixed, paraffin-embedded primary breast tumors (13 fibroadenomas and 10 diploid and 10 aneuploid carcinomas). No genomic imbalances were found in fibroadenomas. Recurrent findings in adenocarcinomas include copy number increases for chromosomes 1q (14 of 20 samples), 8q (10 of 20), 17q (5 of 20), 6p (3 of 20), 13q (3 of 20), and 16p (3 of 20), and copy number decreases for chromosomes 22 (7 of 20), 17p (6 of 20), and 20 (3 of 20). Regional high level copy number increases were observed on chromosome bands 1q32, 8p11, 8q24, 10p, 11q13, 12p, 12q15, 17q11-12, and 17q22-24. The majority of the samples were studied for gene amplification of c-myc, c-erbB2, cycD1, and int-2 by means of Southern blot analysis. The comparison with DNA ploidy measurements revealed a different distribution and a significantly higher number of chromosomal aberrations in aneuploid tumors than in diploid tumors and in fibroadenomas.

Aneuploidy↗
PubMed1995

[Detection of numerical chromosomal aberrations by FISH in "DNA-diploid" head and neck squamous cell carcinomas].

We applied Fluorescence In Situ Hybridization to DNA-diploid head and neck squamous cell carcinomas to detect numerical chromosomal aberrations. Using centromeric repetitive probes of chromosomes 1, 7, 11, 17, X, and Y, we detected numerical aberrations of chromosomes in 4 of the 7 tumors examined, the main line of one tumor showed trisomy 1, while the other 3 tumors had subpopulations that showed trisomy or monosomy of 1 or 2 chromosomes examined. We found polyploidy by cytofluorometry in all 4 tumors with numerical chromosomal aberrations. These results suggest that from DNA-diploid tumors with polyploidy, subpopulation that are aneuploid at the chromosome level may arise before the ploidy of the main line shifts to over DNA-aneuploidy.

Carcinoma, Squamous Cell↗
PubMed1995

[A comparative study on the effect of absorbable components of several drugs on the growth and population doublings of rat diploid fibroblast].

Embryonic skin fibroblast of Sprague-Dawley rats cultivated in vitro was used in this experiment. The cultural medium was added with absorbable components of several drugs. The result reveals that Yan Shou recipe, vitamin E and Huan Jing Jian have conspicuous promotive effect on the growth of diploid fibroblast and also help to increase population doublings. The experiment suggests that all these drugs possess anti-aging effect on the skin diploid fibroblast of rats.

Aging↗
PubMedDate not supplied

A probabilistic approach to the analysis of the frequency of diploid formation in yeast (Saccharomyces cerevisiae) mating.

Conditions of optimizing mating efficiency in the yeast. Saccharomyces cerevisiae were tested and measured as a number of prototrophic diploids. It was found that the process of diploid formation could be controlled by suitably adjusting cell densities in liquid mating medium and alpha: a mating type cell ratio. When the first was about 5 x 10(8) per ml and the second 1:10, respectively, every alpha cell was able to find a partner of opposite mating type. Some mathematical models of the "courtship" in yeast were advanced and the conclusions are discussed in the light of recent data on mating pathway in S. cerevisiae.

Crosses, Genetic↗
PubMed1995

[Genetic structure and origin of the tetraploid toad Bufo danatensis Pisanetz, 1978 (Amphibia, Bufonidae) from Central Asia. Biochemical polymorphism and comparison of the level of heterozygosity of diploid species with tetraploid species].

Comparison of individual variation at 24 biochemical loci in members of the species complex of Palearctic green toads showed that the heterozygosity of the tetraploid species Bufo danatensis (Hobs + 0.45) was significantly higher than that of the diploid species B. viridis, B. sp., and B. raddei (Hobs = 0.009 - 0.103). Such difference can be explained only by a hybrid origin of the tetraploid species. Individual electrophoretic variability of the polyploid toad species is associated with an allelic variation that is manifested in constantly heterozygous spectra as the gene dosage effect. At the population level, this phenomenon found in Pamir toads is caused by irregular meiosis in founders of the population or by directional changes in gene regulation. Genotypic distributions in zones of contact of the diploid and tetraploid taxons demonstrate the possibility of restricted introgressive hybridization.

Animals↗
PubMed1994

Microsatellite instability occurs frequently and in both diploid and aneuploid cell populations of Barrett's-associated esophageal adenocarcinomas.

Alterations of microsatellites consisting of extra or missing copies of these sequences occur at relatively high frequencies in sporadic and hereditary colorectal adenocarcinomas, gastric and pancreatic cancers, and at lower frequencies in endometrial, bladder, ovarian, and other carcinomas. We determined the prevalence of microsatellite instability in esophageal adenocarcinoma, Barrett's esophagus, and squamous cell carcinoma of the esophagus. Assays were performed on 105 patients, including 28 subjects with Barrett's metaplasia, 36 with Barrett's-associated adenocarcinoma, and 42 with primary esophageal squamous cell carcinoma. Flow cytometric nuclear sorting based on DNA content was performed on 25 of the adenocarcinomas prior to DNA extraction. Specimens from 11 of the 106 patients (10%) showed instability at 1 or more chromosomal loci. Instability was seen in 2 of 28 patients (7%) with Barrett's metaplasia alone, in 8 of 36 (22%) with adenocarcinoma, and in 1 of 42 (2%) with squamous cell carcinoma. Among the 25 flow cytometrically sorted adenocarcinomas, instability occurred in 8 (32%); sorted diploid nuclei from these tumors showed instability in 4 of 8 cases (50%). These data indicate that microsatellite instability occurs frequently in Barrett's-associated esophageal adenocarcinoma. They also suggest that in esophageal adenocarcinomas, microsatellite instability can develop as an early event in metaplasia and in diploid tumor cells, before aneuploidy occurs.

Adenocarcinoma↗
PubMed1975

Characterization of the cell kinetics and growth properties of cystic fibrosis diploid fibroblasts in vitro.

The population growth kinetics of human diploid skin fibroblasts derived from cystic fibrosis homozygotes and heterozygotes and from normal subjects were investigated. Our data suggest the following: 1. Population doubling times increase with time in culture, with no significant differences observed among the three genotypes tested, when data were compared at the same subculture times or phases of growth. 2. The fraction of dividing cells in a population decreased with the duration in which the cells were in culture. No significant differences were obtained for cells derived from the three genotypes. 3. Cell cycle times were very similar (18-20 hr) when comparing the normal and cystic fibrosis lines or when comparing cystic fibrosis lines in phases 1 and 2 of growth. 4. No significant variations in population doubling times or growth fractions could be attributed to age or sex of the biopsy donor. 5. Variability in growth fractions and doubling times was minimal through the eighth subculture period but was very great in older cultures (tenth subculture). 6. Changes in growth fractions and doubling times appear to be due to the possibility of "aging" of human diploid fibroblasts in culture rather than to the presence or absence of genes for cystic fibrosis. 7. It is strongly indicated that differences in cell kinetic parameters cannot be used as the basis for differentiation between cells derived from normal or cystic fibrosis genotypes.

Adolescent↗
PubMedDate not supplied

Diploid chromosome number and chromosomal variation in the white rhinoceros (Ceratotherium simum).

Chromosomal studies were conducted on 38 white rhinoceroses representing both the northern and southern subspecies and one subspecies hybrid. Improvements in tissue culture methods and harvesting techniques have made it possible to obtain a highly repeatable diploid number of 82 chromosomes for both subspecies. Comparison of G-banded karyotypes from the two subspecies failed to indicate a difference in banding pattern, but did reveal size polymorphisms involving short arm additions in five individuals. Chromosomal polymorphism, resulting in three individuals with a diploid number of 2n = 81, was noted in northern white rhinoceroses.

Animals↗
PubMed1994

17p allelic losses in diploid cells of patients with Barrett's esophagus who develop aneuploidy.

Inactivation of the p53 gene, located on chromosome 17p, leads to genetic instability and aneuploidy in vitro. Aneuploid cell populations from Barrett's adenocarcinomas have a high prevalence of 17p allelic losses, and there is substantial evidence that the target of these losses is the p53 gene. If 17p allelic losses lead to aneuploidy in Barrett's esophagus, then they should be present in diploid cells from patients who develop aneuploidy. We detected 17p allelic losses in diploid cells from 10 of 11 patients (91%) with Barrett's esophagus who developed aneuploid cell populations. Our data strongly suggest that 17p allelic losses precede the development of aneuploidy during neoplastic progression in Barrett's esophagus in vivo and, therefore, support in vitro evidence for the role of p53 in genetic instability.

Adenocarcinoma↗
PubMed1994

Induction of metastatic ability in a stably diploid benign rat mammary epithelial cell line by transfection with DNA from human malignant breast carcinoma cell lines.

Transfection of the stably diploid rat mammary epithelial cell line, Rama 37, which yields nonmetastasizing, adenomatous tumors in syngeneic rats with HindIII-fragmented DNA from malignant or nonmalignant human breast epithelial cell lines and the drug-resistance plasmid pSV2neo, yields transformants with a frequency of 10(-4) to 10(-5). The resultant cell lines form tumors with varying frequencies when injected s.c. into the mammary fat pads of syngeneic rats. Cells transfected with DNA from the malignant human breast carcinoma cell line, Ca2-83, or DNA from the human pleural effusion-derived cell lines, MCF-7 or ZR-75-1, yield transformants which metastasize to lungs and/or lymph nodes at high frequency, whereas transfection of HindIII-fragmented DNA from nonmetastatic human mammary epithelial cell lines, transfection of the drug-resistance plasmid pSV2neo alone, or nonspecific DNA such as salmon sperm DNA fails to yield transformants expressing the metastatic phenotype. Transfectants which metastasized were reestablished in culture and reinjected into syngeneic rats to confirm their metastatic properties. These transfectants yield rapidly growing tumors with reduced latent periods, which give rise to significant numbers of metastases. The karyotype of selected transfectants after passage in vivo remains stably diploid. Hybridization of a 32P-labeled oligonucleotide probe specific for the human Alu family of sequences to DNA from these transfectants reveals the presence of human-specific DNA sequences integrated into the genome. It is suggested that transfection of specific genomic DNA sequences from the malignant human cell lines can induce the metastatic phenotype in the nonmetastatic Rama 37 cell line in a genetically dominant manner, whereas genomic DNA from the nonmetastatic cells cannot confer metastatic properties to the Rama 37 cell line.

Animals↗
PubMed1994

Nuclear matrix proteins distinguish normal diploid osteoblasts from osteosarcoma cells.

Interrelationships between nuclear architecture and gene expression were examined by comparing the representation of nuclear matrix proteins in ROS 17/2.8 rat and MG-63 human osteosarcoma cells with those in normal diploid osteoblasts. The tumor-derived cells coexpress genes which are expressed in a sequential and mutually exclusive manner during the progressive stages of osteoblast differentiation. In osteosarcoma cells two-dimensional electrophoretic analysis indicates a composite representation of nuclear matrix proteins characteristic of both the proliferative and postproliferative periods of osteoblast phenotype development. In addition, nuclear matrix proteins unique to the tumor cells and the absence of nuclear matrix proteins found only in normal diploid osteoblasts are observed. Tumor-specific nuclear matrix proteins include those expressed in a proliferation-dependent and independent manner. There is a parallel relationship between nuclear matrix proteins and the expression of cell growth and tissue-specific genes during osteoblast differentiation and in osteosarcoma cells where the developmental sequence of gene expression has been abrogated. Nuclear matrix proteins therefore provide markers reflecting defined periods of bone cell differentiation and phenotypic characteristics of an osteosarcoma.

Animals↗
PubMed1993

[Variation of the diploid pattern in tissues used as normal controls of solid tumors: advantages and disadvantages of flow cytometric analysis of paraffin-embedded tissues].

The aim of the present work was to study the factors that influence the variation of diploid patterns in 75 areas of histologically normal gastric tissue, located in surgically resected stomachs due to early gastric cancer. Each sample was used as a diploid reference of its respective tumoral area. Fifty five samples were embedded in formalin and 20 corresponded to fresh tissue. It was found that in the older tissues, the cellular debris increased, the localization channel of the peaks shifted to the left (lower than channel 60) and the peak shape was deformed, with an increase in the variation coefficient (around 6) and an elevation and lengthening of phase S. When fresh tissue was used, the first peak was localized around channel 60-70, with a significant reduction of cellular debris, a lower variation coefficient amplitude (2-5) and a phase S adhered to the basal line. Aiming to observe the influence of paraffin embedding over time, 21 tissue samples originally assayed as fresh tissues, were reanalyzed one year later. The same alterations initially observed in old tissues were again noticed. According to these results, it is necessary to select adequate controls for flow cytometric analysis to obtain an adequate histogram interpretation, and specially to calculate the ADN index.

Adult↗
PubMed1993

[Detection of chromosomal aberration using fluorescence in situ hybridization in DNA diploid colorectal carcinomas].

Numerical aberrations of chromosomes can be detected by fluorescence in situ hybridization (FISH), using chromosome-specific probes. It is possible to observe this in solid tumors from which it is very difficult to obtain metaphase nuclei. The present study employed surgical specimens from 15 cases of colorectal carcinoma, all of which showed DNA diploidy. In the same samples, we analyzed chromosomal numerical aberration by FISH according to the method of Pinkel et al. Biotinylated DNA probes specific to chromosome #7, #11 and #17, were used. The hybridization spots were observed by fluorescent microscopy. As a result, the numerical aberrations of chromosomes detected by FISH were found in DNA diploid cases by FCM. They were trisomy and monosomy. These results indicate that FISH is useful to detect the chromosomal aberrations of DNA diploid cases.

Chromosome Aberrations↗
PubMed1996

Immortalisation of a human diploid fibroblast cell strain: a DT-diaphorase paradox.

Transfection of a normal human diploid fibroblast cell strain, GM38, with a simian virus 40 (SV40) large T antigen containing plasmid, yielded an immortal cell line, G38-8X, which had a similar sensitivity as the parental cell strain to the quinone-containing chemotherapeutic agent mitomycin C (MMC), under both aerobic and hypoxic exposure conditions. The activity level of DT-diaphorase was similar in both the parental GM38 and G38-8X cells. Although DT-diaphorase could be detected by Western blot analysis, using two mouse anti-human monoclonal antibodies, in GM38 cells, it was not detected in the G38-8X cells. G38-8X cells have a slightly increased P450R activity (2-fold), and have elevated P-glycoprotein levels compared with the parental GM38 cell strain. The immortal G38-8X cell line is 2-fold more resistant to ionising radiation than the parental GM38 cell strain (D10 approximately 5 Gy). Although these SV40 large T antigen immortalised human diploid fibroblasts behaved similarly to their parental cell strain in terms of MMC sensitivity and DT-diaphorase activity, careful characterisation revealed that these cells had enhanced P-glycoprotein activity and had a decreased sensitivity to ionising radiation.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Hypoxia-induced tetraploidisation of a diploid human melanoma cell line in vitro.

Many human tumours are hyperdiploid, particularly in advanced stages of growth. The purpose of the present work was to investigate whether exposure to hypoxia followed by reoxygenation might induce hyperploidisation of diploid human tumour cells in vitro. The investigation was performed by using the diploid melanoma cell line BEX-c (median chromosome number, 46; DNA index, 1.10 +/- 0.04) as test line and the hyperdiploid melanoma cell line SAX-c (median chromosome number, 61; DNA index, 1.42 +/- 0.03) as control line. Cell cultures kept in glass dishes in air-tight steel chambers were exposed to hypoxia (O2 concentrations < 10 p.p.m. or < 100 p.p.m.) at 37 degrees C for 24 h. DNA content was measured by flow cytometry. Metaphase spreads banded with trypsin-Versene-Giemsa were examined to determine the number of chromosomes per cell. An electronic particle counter was used to measure cell volume. The expression of p53 and pRb was studied by Western blot analysis. Transient exposure to hypoxia was found to induce a doubling of the number of chromosomes in BEX-c but not in SAX-c. The fraction of the BEX-c metaphase spreads with 92 chromosomes was approximately 10% at 18 h after reoxygenation, decreased to approximately 2% at 7 days after reoxygenation and then increased gradually with time. The whole cell population became tetraploid within 25 weeks. BEX-c and SAX-c behaved differently during the 24 h hypoxia exposure. Cell volume and fraction of cells in G2 + M increased with time in BEX-c but remained essentially unchanged in SAX-c. On the other hand, the expression of p53 and pRb was similar for the two lines; hypoxia induced increased expression of p53 and hypophosphorylation of pRb.

Cell Hypoxia↗