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PubMed2000

Elevated expression of hepatic proliferative markers during early hepatocarcinogenesis in hepatitis-B virus transgenic mice lacking mdr1a-encoded P-glycoprotein.

Recent studies have shown that expression levels of the multidrug resistance gene MDR1, which encodes the drug transporter P-glycoprotein, correlate with prognostic outcomes of certain tumor types. These findings suggest that expression of MDR1 may affect tumor behaviors. To address this issue further, we investigated the expression of mdr1a, a human MDR1 homolog, on the development of hepatocellular carcinoma in a transgenic mouse model carrying the liver-targeted expression of human hepatitis-B virus (HBV) surface antigen. The pathogenetic program was compared in HBV mice carrying either mdr1a(+/+) or mdr1a(-/-). We found that the expressions of proliferative activity markers, Ki67 nuclear antigen, and proliferating cell nuclear antigen were elevated in mdr1a(-/-) mice younger than 10 wk in comparison with those in the same age group of wild-type animals. Replication in the hepatic population as determined by bromodeoxyuridine incorporation tended to support observation that mdr1a(-/-) mice exhibited elevated labeling indices in this age group. Moreover, histologic staining and flow-cytometric analysis showed that the mdr1a(-/-) animals exhibited a higher cell population with polyploidy than did the mdr1a(+/+) counterparts of the same age. However, no significant differences in the expression of the liver-injury markers serum alanine transaminase and aspartate transaminase were observed. Although our results showed that absence of mdr1a expression is correlated with modest enhanced proliferative characteristics in the livers at stage before the development of hepatocellular carcinoma, the overall life spans between these two strains of mice were not significantly different. The implication of these findings to the role of P-glycoprotein in tumor development and cancer chemotherapy is discussed.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2001

Oncoprotein 18 levels and phosphorylation mediate megakaryocyte polyploidization in human erythroleukemia cells.

Megakaryocytes undergo an unusual cell cycle during differentiation that results in polyploidy through largely unknown mechanism(s). It has been shown that serine phosphorylation of oncoprotein 18 (Op18) is required for cell cycle progression specifically at the G2/M transition. Moreover, mutant forms of Op18 that are defective in one or more of the four serine residues induce G2/M arrest and subsequent polyploidization. Op18 phosphorylation is rapidly induced with phorbol myristate acetate (PMA) treatment in a wide range of human cells. In this study, we investigated the role of Op18 in PMA induced polyploidization during megakaryocyte differentiation of the human erythroleukemia cell line. Crucial to the molecular analysis of megakaryocyte differentiation, is the ability to fractionate cell populations with different ploidy levels. We have utilized cell elutriation as a fractionation strategy to analyze Op18 expression in synchronized cell subpopulations in different phases of the cell cycle or with progressive megakaryocyte polyploidization. In the absence of PMA, increased phosphorylation of Op18 was observed in HEL cells during cell cycle progression, as for other proliferating cells. However, in contrast to Jurkat leukemia cells chosen as control, HEL cells exhibited a lack of Op18 phosphorylation in response to PMA, which was accompanied by polyploidization and differentiation along the megakaryocytic lineage. To further determine the role of Op18 in polyploidization, HEL cells were transfected with different Op18 expression constructs. Differences in cell survival and polyploidization were observed between high and low Op18 expressors. An increased Op18 level reduced cell survival during the early stage of PMA induced megakaryocyte differentiation, but enhanced polyploidization efficiency. Our findings suggest that maintenance of a high level of unphosphorylated Op18 is required for efficient polyploidization during the differentiation program of megakaryocytes.

Cell Cycle↗
PubMed1998

Gene silencing in plants: relevance for genome evolution and the acquisition of genomic methylation patterns.

Transgenes often become silenced in plants because of repressive influences exerted by flanking plant DNA and/or because of interactions among multiple copies of closely linked transgenes. Repeated transgenes on different chromosomes can also interact in a way that leads to silencing and methylation, suggesting a previously unrecognized ability of unlinked homologous sequences to cross-talk in complex genomes. Non-Mendelian inheritance is a frequent consequence of these interactions because the silenced genes do not fully reactivate or lose methylation after segregating in progeny. Several examples of gene silencing in plants appear to reflect the action of genome defence system that methylates and inactivates foreign or invasive sequences such as transgenes and transposable elements. Because certain types of transposable elements are embedded in regulatory regions of plant genes and have become greatly amplified in plant genomes, they could contribute substantially to normal gene expression and to the generation of genomic methylation patterns. Polyploidy, which has been a major force in plant and vertebrate evolution, might encourage proliferation of transposable elements because genes in polyploids are duplicated and hence less susceptible to the consequences of insertional mutagenesis. Accordingly, the appearance of genome-wide methylation has often coincided with episodes of polyploidization.

DNA Methylation↗
PubMed2026

Untangling the Arisaema enigma: Investigating the complex evolutionary history and species relationships in North American Arisaema.

PREMISE: The evolutionary history of morphologically variable plant groups is often obscured by cryptic diversity, morphological convergence, and limited genetic data. Arisaema, a diverse genus within Araceae, exemplifies these challenges. Although some taxonomic treatments recognize only two species of North American Arisaema (A. dracontium and A. triphyllum), other studies have identified morphologically distinct groups within both taxa. Here, we reconstructed evolutionary relationships in North American Arisaema, assessed genetic structure and admixture, and tested the monophyly of proposed species. METHODS: We used 2b-RAD sequencing to generate genome-wide SNP data for 146 samples from 31 populations across the eastern United States. Phylogenetic relationships were inferred using maximum-likelihood and Bayesian approaches. Population structure and admixture were assessed using the program structure and principal component analysis (PCA). RESULTS: Both the Arisaema triphyllum and A. dracontium complexes formed well-supported monophyletic groups. Within the A. dracontium complex, we recovered three monophyletic lineages: A. dracontium, A. calciphilum, and A. macrospathum. In the A. triphyllum complex, A. quinatum, A. stewardsonii, and A. allegheniense consistently formed distinct groups. Relationships between A. pusillum and A. acuminatum, and among A. triphyllum s.s., A. purpurascens, and A. striatum were less clearly resolved, likely due to recent or incomplete divergence, gene flow, or polyploidy. CONCLUSIONS: The results support the monophyly of multiple newly proposed taxa within North American Arisaema, but additional sampling across the species' ranges is needed to fully resolve species boundaries. Our study provides the first evolutionary framework for this group, providing a foundation for future ecological, taxonomic, and conservation research in the genus.

Araceae↗
PubMed1987

The Montana Fetal Genetic Pathology Program and a review of prenatal death in humans.

Western medicine is being sensitized to the enormous extent of prenatal death in humans at a time when such deaths, occurring after the first missed period, involve to an ever increasing degree wanted pregnancies conceived by women with rising mean maternal age, decreasing mean fertility, and ever greater desire and intention to assure a good pregnancy outcome. Available data suggest that about two-thirds of human ova, embryos, and fetuses fail to reach birth or the end of the first year of life, with infant mortality of 1.06%, stillbirth rate of 8/1,000, abortion rate of about 15%, and death rate around the time of implantation estimated at 34%. Based on limited data on sperm, ova aspirated from Graafian follicles in infertile women, direct observation of a few implanting ova, the low rate of human fecundity, and the high failure rate of in vitro fertilization, it seems reasonable to suppose that about 30% of human ova perish at the time of fertilization and before implantation. Most of this prenatal death is attributable to chromosome abnormalities (aneuploidy and polyploidy), estimated to be present at the beginning of development in about half of all human ova or embryos. Parent's anguish about prenatal death and their desire to understand its causes and to prevent recurrence is putting the medical profession under severe pressure to provide diagnostic and counseling services and make available prenatal diagnosis and preventive approaches; this comes at a low point in the ability of Western medicine to respond adequately, especially in the fields of embryology and developmental genetics, clinical teratology, anatomical pathology, and genetic pathology. Unless drastic ameliorative measures are taken, the situation is likely to get much worse, since health insurance pays for only a minute fraction of costs involved and the number of pediatric pathologists devoting major effort to this work in North America has dwindled to a small number without great hope for replacement from younger ranks, primarily as a result of the lack of incentive by the tertiary centers to make fetal genetic pathology ("morphology") an attractive field to work in. Here we report an effort by a secondary care center to provide such a service--presently more on demand than as systematic effort to reach all at need--in a huge, underpopulated state with birthrate of less than 13,000 and lacking any specially trained pathologist with a strong interest in the field.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed2004

Implementation of DNA cytometric measurements in fine-needle aspiration biopsy diagnostics of breast disease.

BACKGROUND: For this study, the diagnostic protocol included fine-needle aspiration biopsy (FNAB) and DNA cytometric measurements. The objective of the study was to improve the diagnostic sensitivity of FNAB. METHODS: Sixty-eight FNAB samples were stained using the Feulgen stain, and DNA histograms were produced by selecting the nuclei of cell groups and free cells separately. RESULTS: Among 28 samples that were classified as definitely benign (n = 17 samples) or atypical but benign (n = 11 samples), DNA cytometry generally showed diploid/peridiploid peaks. Three of those samples were associated later with carcinoma. In those samples DNA cytometry did not improve sensitivity. Among moderately atypical samples (n = 17 samples), 8 samples were diagnosed later as carcinoma. DNA cytometry helped the diagnostic procedure in 62.5% of those samples. Among 21 samples that were classified as highly suspicious (n = 10 samples) or definitely malignant (n = 11 samples), DNA cytometry generally showed atypical DNA histograms (20 of 21 histograms), and DNA cytometry supported the diagnosis of carcinoma in 95.2%. Histograms that were based on free cells frequently were more abnormal compared with histograms that were based on cell groups. Histologically verified benign lesions also could show abnormalities in DNA histograms. Accepting wider gates than are used normally for primarily Feulgen stained samples on these restained samples resulted in improved specificity, efficiency, and predictive values. CONCLUSIONS: DNA cytometry has a potential to support the differential diagnosis of breast lesions, and sampling of free cells increases sensitivity. Benign breast lesions (fibrocystic disease, fibroadenoma) included DNA-cytometrically abnormal cell clones and showed tendencies toward polyploidy, which should be included in the diagnostic criteria.

Biopsy, Needle↗
PubMed1987

Flow cytometric analysis of isolated rat liver nuclei during growth.

The development of hepatocyte polyploidy in rats aged up to 4 months was analyzed by flow cytometry using both scatter and fluorescent parameters to distinguish DNA diploid and DNA tetraploid populations and to discriminate between parenchymal and non-parenchymal compartments. The precise origin of each class of nuclei was assessed in whole liver homogenate using purified hepatocytes, obtained by liver perfusion followed by separation on Percoll gradient, and identifying the peaks corresponding to parenchymal nuclei. The results indicate that preparative procedures involving homogenization of the rat liver tissue caused loss of the DNA octaploid population. Data on the relative proportion of the different DNA ploidy elements during rat liver development, which are in good agreement with those observed by cell analysis by means of microspectrophotometry, indicate the usefulness of flow cytometry as a choice method for the analysis of ploidy distribution.

Animals↗
PubMed1990

DNA ploidy and cytophotometric analysis of cervical intraepithelial neoplasia grade III and invasive squamous cell carcinoma.

Cervical intraepithelial neoplasia grade III (CIN III) and squamous cell carcinoma (INV) were examined using DNA ploidy and cytophotometric analysis. Based on hysterectomy, exconisation, and biopsy material from 69 patients in two age categories, analysis was performed in nuclei isolated from selected areas of paraffin-embedded tissue. High percentages of DNA-diploidy in INV lesions were found mainly in the group of patients age 45 years or younger. CIN III lesions in women age 46 or older demonstrated high percentages of DNA-aneuploidy. DNA-polyploidy was most frequent in CIN III lesions in the younger age category. The results of cytophotometric analysis indicated that the overall mean values of 16 nuclear photometric features discriminated significantly between the whole groups of CIN III (n = 37) and INV (n = 32). On an individual patient level, however, the mean feature values showed a large overlap. Based on the results of a stepwise linear discriminant analysis of patient mean values, a combination of geometrical and run-length texture features was used to discriminate between CIN III and INV lesions. The correct classification rate was highest in the category of patients in the older age category. The results of this study indicate age related differences in CIN III and invasive squamous cell carcinoma, and they may be of help in assessing cytophotometric features in the study of progressive and non-progressive CIN lesions.

Adult↗
PubMed2007

Chromatin supraorganization and extensibility in mouse hepatocytes with development and aging.

BACKGROUND: Chromatin supraorganization and extensibility, which lead to the formation of extended chromatin fibers (ECF), are affected by starvation and refeeding in adult mouse hepatocytes. It is expected that they could also change with mouse development and aging. METHODS: Methods used involved topochemistry, image analysis, microspectrophotometry, gravity action, and polarization microscopy. RESULTS: Increased nuclear areas and Feulgen-DNA amounts with advancing hepatocyte polyploidy were found with development and aging. A slightly less packed chromatin with more heterogeneously distributed condensation levels was detected in young and old mice. Con-A responsiveness was almost absent in young mice but very deep in aged mice. ECFs formed from nuclei of adult and aged mice but not from nuclei of young mice. The frequency of ECF formation with the long lysis protocol increased with aging. CONCLUSIONS: In young mice, a less packed chromatin state may be associated with more intense gene activity, thus increasing the DNA-nuclear matrix interactions, and inhibiting ECF formation. Reduced DNA-nuclear matrix interactions besides defects in heterochromatin formation may induce higher ECF formation and chromatin unpackaging in old mice. We suggest that differences in Con-A staining relate to different gene activity with advancing development and aging.

Aging↗
PubMed1985

Studies in comparative chemical mutagenesis.

This paper presents a review of various collaborative studies in comparative mutagenesis. The following studies are briefly described: (1) the chemical mutagenesis programme of the European Community, (2) Drosophila studies with various alkylating agents of different s (Swain-Scott) factors, (3) the evaluation by the International Commission for Protection against Environmental Mutagens and Carcinogens (ICPEMC) Committee 1, (4) the Environmental Protection Agency's Gene-Tox Programme, (5) the first and second United Kingdom Environmental Mutagen Society (UKEMS) collaborative studies, and (6) the International Programme on Chemical Safety (IPCS) collaborative study on in vitro tests. The need for chemical dosimetry is emphasized. One of the main conclusions is that, of the mammalian point mutation assays, the L5178Y (TFTR, trifluorothymidine resistant) system showed greatest detection capability in the second UKEMS study. The consensus conclusion of the IPCS in vitro study was that chromosomal aberrations are considered to be the optimal assay for complementing the Salmonella assay and offer the additional advantage that aneuploidy, polyploidy, and sister chromatid exchanges can also be easily assessed.

Alkylating Agents↗
PubMed1988

Cytotoxic and genotoxic effects of extract of particulate emission from a gasoline-powered engine.

Extract of particulate matter (EPM) from gasoline engine exhaust has been investigated for cytotoxic and genotoxic effects in the concentration range 0.16-10 micrograms/ml by means of short-term bioassays using mammalian cell culture systems. Cytotoxicity is demonstrated by a strong dose-dependent reduction of cloning efficiency after treatment of V79 cells with EPM. Employing the dye exclusion test with erythrosin B, no considerable loss of cell viability was observed. Using the same cell system, EPM revealed a highly increased number of aberrant mitoses, whereby the occurrence of C mitoses and metaphases with chromosome clusters was especially pronounced. This effect led to mitotic arrest as shown by a highly increased mitotic index at 5 and 10 micrograms/ml EPM. The results indicate disturbances of the mitotic spindle in a way similar to the known spindle poison colcemid. As a consequence of spindle disturbances, EPM produced numerical chromosome alterations such as aneuploidy and polyploidy. Cytogenetic analyses using human lymphocyte cultures treated with EPM revealed a slight increase of chromosomal aberrations at 10 micrograms/ml and a dose-dependent induction of sister chromatid exchanges in the range 2.5-10 micrograms/ml. At least, EPM showed a dose-dependent increase in the cell transformation assay using SV 40-infected Syrian hamster kidney cultures. The great variety of cytotoxic and genotoxic effects found with EPM suggests a potential health hazard to human populations exposed to gasoline engine exhaust. The possible contribution to cytotoxic and genotoxic activity by organolead compounds derived from antiknock additives is discussed.

Animals↗
PubMed1992

Recurring chromosome abnormalities in Hodgkin's disease.

Cytogenetic analysis was performed on lymph nodes or other tumor masses from 33 patients with Hodgkin's disease. Metaphase cells were obtained in 25 of the 33 cases. Analyzable abnormal clones were found in nine cases. Characteristic abnormalities included polyploidy and complex structural rearrangements nonrandomly involving certain chromosomal regions. Chromosomes most commonly gained were 2, 9, 11, 19, and 20, and those most often lost were 10, 13, 15, 16, 21, and Y. Translocation breakpoints clustered in bands 1p11-1p13, 1p36, 4q35, 14q11, and 15p11. In five patients, breakpoints were in bands to which T-cell receptor genes have been mapped. No specific, recurring translocation was identified. There was, however, recurring loss of chromosomal material from 1q, 4q, 6q, and 17p. Loss or deletions of chromosomes 4 and 6 were found in five and six patients, respectively. Deletions overlapped; the smallest overlapping segments included bands 4q25-4q27 and 6q21-6q23. The data suggest that loss of specific chromosomal regions may be important in the pathogenesis of Hodgkin's disease. With respect to tumor specificity, deletions of 4q are of particular interest because these have not been previously reported to occur nonrandomly in other human malignancies.

Adolescent↗
PubMed1995

Cytogenetic studies of breast carcinomas: different karyotypic profiles detected by direct harvesting and short-term culture.

Chromosome analysis was performed on samples from 85 consecutive patients with breast cancer by one or more of three different methods: direct harvest, culture after mechanical disaggregation, and culture after collagenase digestion. Metaphases suitable for karyotyping were obtained in 70% of the cases; direct harvest yielded metaphases in 29% and cultures without and with digestion in 40% and 59%, respectively. Chromosomal abnormalities were detected in 37 cases. Cells judged to be phenotypically abnormal in culture were twice as likely to reveal chromosomal aberrations as normal-looking cells. Eight cases showed multiclonal abnormalities. Significant differences were detected in the karyotypic profile depending on the method used. With direct harvest, the yield of complex chromosomal changes was 87%, compared to 44% after culture of digested tissue (P < 0.01), and also polyploidy was more common in direct-harvested samples. Detailed karyotypic analysis was possible in 29 primary tumors. The chromosomes most frequently involved were 1, 3, 7, 11, 16, and 17. Recurrent structural abnormalities were der(1;16)(q10;p10), i(1)(q10), del(6)(q21), and del(1)(p22). Breakpoints clustered to the centromere regions of chromosomes 1, 3, 11, 15, and 16 and to the short arms of chromosomes 7, 17, and 19. Seven of twenty-nine fully analyzed cases had a family history of breast cancer, and changes of chromosomes 1, 3, and 15 seemed to be more common in these cases. There was an association between karyotype and survival: The 3 year survival was 63% in patients with complex karyotypic changes and 92% in those without complex changes.

Breast Neoplasms↗
PubMedDate not supplied

Prognostic significance of DNA-analysis by flow cytometry in non-Hodgkin's lymphoma.

DNA analysis by flow cytometry was performed on lymph node cells obtained from 65 untreated patients with non-Hodgkin's lymphoma. According to the Kiel classification 41 cases were of low grade malignancy and 24 cases belonged to the high grade malignancy group. 47 out of 61 evaluable cases were diploid/near-diploid, 12 were aneuploid and 2 cases showed polyploidy. No difference in survival was found between diploid/near-diploid and aneuploid cases. The percentage of S-phase cells was found to be a valuable prognostic parameter. Using a cut point at 4 per cent S-phase cells between low and high S-phase lymphomas a highly significant difference in survival was demonstrated (p = 0.0004). The actuarial survival up to 3 years was about 77 per cent for lymphomas with less than 4 per cent S-phase cells to be compared with 20 per cent for patients with high S-phase (greater than or equal to 4 per cent) lymphomas. Subdivision according to the percentage of S-phase cells seemed to be a better prognostic predictor than morphologic subclassification.

DNA, Neoplasm↗
PubMed2004

Allelic loss on chromosomes 2q21 and 19p 13.2 in oxyphilic thyroid tumors.

Hürthle thyroid tumors are characterized by frequent numerical chromosomal aberrations, including aneuploidy or polyploidy, losses and gains of some chromosomal regions and DNA fragmentation. In recent years, great attention has been paid to the combined analysis of morphologic and genetic features of oxyphilic tumors and to the elucidation of their pathogenesis. We analyzed for loss of heterozygosity (LOH) of the candidate regions for TCO (thyroid tumor with cell oxyphilia) and NMTC1 (nonmedullary thyroid carcinoma 1), 2 loci already mapped on chromosomes 19p13.2 and 2q21, respectively. Matched normal and tumor DNA samples from 70 patients with sporadic oxyphilic thyroid tumors and 20 with sporadic follicular tumors were subjected to microsatellite analysis using 10 markers on 19p13.2 and 6 markers on 2q21. This approach led us to the observation of a more significant LOH in oxyphilic than in follicular tumors. Allelic loss in tumor samples was evenly distributed in both 19p13.2 and 2q21 regions, in accordance with the established linkage of TCO and NMTC1 for inherited tumors. In order to investigate the possible contribution of both susceptibility loci in oxyphilic tumors, the family that led to the original mapping of TCO locus was reanalyzed for the markers in the 2q21 region. This led to the exclusion of linkage with the NMTC1 locus and to the refutation of the digenic inheritance hypothesis at least in this family.

Adenocarcinoma↗
PubMed2006

Bystander effects are induced by CENU treatment and associated with altered protein secretory activity of treated tumor cells: a relay for chemotherapy?

In a previous study, it was reported that secondary untreated melanoma tumors implanted several weeks after and at distance from primary chloroethylnitrosourea (CENU)-treated tumors underwent differentiation and growth inhibition. To see whether the primary treated tumor released soluble factors that mediated the secondary tumor response, serum transfer experiments were performed in vivo. Administration of serum from CENU-treated tumor-bearing donors arrested tumor proliferation, decreased vessel formation and induced tumor metabolite alterations encompassing glutathione decrease and polyunsaturated fatty acid and phosphoethanolamine increase. These changes mimicked secondary tumor phenotype. To reproduce the model in vitro, cell culture supernatant transfer experiments were performed. CENU-treated cell cultures showed polyploidy and reactive oxygen species (ROS) production. Cell cultures challenged by a conditioned medium of CENU-treated cells underwent growth inhibition, cytoskeleton disorders, cytokinesis retardation, metabolite alterations, glutathione decrease and phosphoethanolamine increase, without ROS elicitation. Proteomics of CENU-treated cell conditioned media revealed altered protein secretion activity by CENU-treated cells. Among de novo secreted proteins, the most expressed were phosphatidylethanolamine-binding protein (PEBP), cardiovascular heat shock protein (cHsp), Rho-associated coiled-coil forming kinase 2 (ROCK) and actin fragments. These proteins testified of cytoskeleton disorders, growth inhibition and metabolite alterations. This article demonstrates the release by CENU-treated tumors of growth inhibitory differentiation-inducing soluble factors. These factors mediate remote bystander effects and attest persistent biological activity of residual tumors after chemotherapy.

Actins↗
PubMed1985

Endocrine sensitivity of the receptor-positive T61 human breast carcinoma serially grown in nude mice.

A study was made on the effect of ovariectomy, 17 beta-oestradiol, and tamoxifen on the oestrogen and progesterone receptor-positive T61 human breast carcinoma grown in nude mice. The effect of the treatment was evaluated by the specific growth delay calculated on the basis of Gompertz growth curves, and by the changes in the cell cycle distribution monitored by flow cytometric DNA analysis. The results demonstrated that both oestradiol and tamoxifen induced a temporary growth delay, whereas ovariectomy of the host had no effect on the growth of the tumour. The oestradiol-induced tumour growth delay was accompanied by a decrease in the G1 fraction, an accumulation of cells in the S-phase, and polyploidy, whereas neither treatment with tamoxifen nor ovariectomy influenced cell cycle distribution. The results indicate that oestradiol and tamoxifen have different mechanisms of action. In addition, they were interpreted as indicating different mechanisms regulating ovarian-dependent tumour growth, on the one hand, and oestrogen and tamoxifen-induced tumour growth inhibition, on the other. The results support the view that the presence of receptors may be of importance but is not a sufficiently clear marker to allow prediction of the endocrine sensitivity of individual breast tumours.

Animals↗
PubMed1982

Altered cell cycle progression and aberrant mitosis in adenovirus-infected rodent cells.

Actively growing mouse or rat embryo cells suffered structural chromosome damage, mitotic anomalies, and polyploidy after infection by human adenovirus type 5. Chromosome damage required expression of one or more early viral genes and showed regular periodicity in its frequency. The growth cycle time of some of the infected cells was reduced by about 5 hours due to a decrease in G1, and the interval between successive waves of chromosome damage corresponded to this reduced cycle time. After infection there was a decrease in cells with G1 DNA content and an increase in cells with G2 diploid, aneuploid, and polyploid DNA contents. We suggest these effects are due to the expression in semipermissive cells fo early viral gene(s), whose function in productive infection in vivo is to alter cell cycle controls in order to maximize the number of cells able to replicate viral DNA and the time such cells spend in DNA replication.

Adenoviridae Infections↗