scholarly journals Cell cycle dynamics of NG2 cells in the postnatal and ageing brain

2009 ◽  
Vol 5 (3-4) ◽  
pp. 57-67 ◽  
Author(s):  
Konstantina Psachoulia ◽  
Francoise Jamen ◽  
Kaylene M. Young ◽  
William D. Richardson
Keyword(s):  
Cell Cycle ◽  
Corpus Callosum ◽  
Biological Significance ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Active Population ◽  
Dorsal Telencephalon ◽  
Ng2 Cells ◽  
Cell Cycle Dynamics ◽  
Ageing Brain

Oligodendrocyte precursors (OLPs or ‘NG2 cells’) are abundant in the adult mouse brain, where they continue to proliferate and generate new myelinating oligodendrocytes. By cumulative BrdU labelling, we estimated the cell cycle timeTCand the proportion of NG2 cells that is actively cycling (the growth fraction) at ~ postnatal day 6 (P6), P60, P240 and P540. In the corpus callosum,TCincreased from <2 days at P6 to ~9 days at P60 to ~70 days at P240 and P540. In the cortex,TCincreased from ~2 days to >150 days over the same period. The growth fraction remained relatively invariant at ~50% in both cortex and corpus callosum – that is, similar numbers of mitotically active and inactive NG2 cells co-exist at all ages. Our data imply that a stable population of quiescent NG2 cells appears before the end of the first postnatal week and persists throughout life. The mitotically active population acts as a source of new oligodendrocytes during adulthood, while the biological significance of the quiescent population remains to be determined. We found that the mitotic status of adult NG2 cells is unrelated to their developmental site of origin in the ventral or dorsal telencephalon. We also report that new oligodendrocytes continue to be formed at a slow rate from NG2 cells even after P240 (8 months of age).

scholarly journals A method to estimate cell cycle time and growth fraction using bromodeoxyuridine-flow cytometry data from a single sample

BMC Cancer ◽  
2005 ◽  
Vol 5 (1) ◽  
Author(s):  
Rimantas Eidukevicius ◽  
Dainius Characiejus ◽  
Ramunas Janavicius ◽  
Nijole Kazlauskaite ◽  
Vita Pasukoniene ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cycle Time ◽  
Single Sample ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Flow Cytometry Data

The biological significance of variation in satellite DNA and heterochromatin in newts of the genus Triturus : an evolutionary perspective

1986 ◽  
Vol 312 (1154) ◽  
pp. 243-259 ◽  
Keyword(s):  
Cell Cycle ◽  
Satellite Dna ◽  
Biological Significance ◽  
Evolutionary Significance ◽  
Sequence Structure ◽  
Cell Cycle Time ◽  
Satellite Dnas ◽  
Evolutionary Changes ◽  
Available Information ◽  
Simple Sequence

The functional and evolutionary significance of highly repetitive, simple sequence (satellite) DNA is analysed by examining available information on the patterns of variation of heterochromatin and cloned satellites among newts (family Salamandridae), and particularly species of the European genus Triturus . This information is used to develop a model linking evolutionary changes in satellite DNAs and chromosome structure. In this model, satellites accumulate initially in large tandem blocks around centromeres of some or all of the chromosomes, mainly by repeated chromosomal exchanges in these regions. Centromeric blocks later become broken up and dispersed by small, random chromosome rearrangements in these regions. They are dispersed first to pericentric locations and then gradually more distally into the chromosome arms and telomeres. Dispersal of a particular satellite is accompanied by changes in sequence structure (for example, base substitutions, deletions, etc.) and a corresponding decrease in its detectability at either the molecular or cytological level. On the basis of this model, observed satellites in newt species may be classified as ‘old ’, ‘young’, or of ‘intermediate’ phylogenetic age. The functions and effects of satellite DNA and heterochromatin at the cellular and organismal levels are also discussed. It is suggested that satellite DNA may have an impact on cell proliferation through the effect of late-replicating satellite-rich heterochromatin on the duration of S-phase of the cell cycle. It is argued that even small alterations in cell cycle time due to changes in heterochromatin am ount may have magnified effects on organismal growth that may be of adaptive significance.

Review of basic concepts of cell kinetics as applied to brain tumors

1975 ◽  
Vol 42 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Takao Hoshino ◽  
Charles B. Wilson
Keyword(s):  
Cell Cycle ◽  
Brain Tumors ◽  
Cycle Time ◽  
Doubling Time ◽  
Cell Kinetics ◽  
Cell Loss ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Tumor Doubling Time ◽  
Basic Concepts

✓ The authors review and discuss the basic concepts of cell kinetics as applied to brain tumors. Uncontrolled growth of a neoplasm represents an expanding tumor cell population. Four growth parameters characterize the behavior of a neoplastic population: cell cycle time, growth fraction, tumor doubling time, and cell loss. The concept of provisionally nondividing cells explains the disparity between cell cycle time and tumor doubling time. Human gliomas, like many non-neural solid tumors, contain variable proportions of actively proliferating and nonproliferating tumor cells; this ratio is expressed by the growth fraction. The major kinetic difference between glioblastomas and differentiated astrocytomas resides in their respective growth fractions, in all likelihood an inherent biological characteristic of each tumor. Glioblastoma proliferates at a rapid rate, and only a high rate of cell loss prevents this tumor from doubling its volume in less than 1 week. The selection of drugs and design of drug schedules for treatment of glioblastomas should be made with the knowledge that 60% to 70% of the cells in this tumor are resting (nonproliferating). If experience with other solid tumors is any guide, judicious selection and combined use of drugs according to kinetically sound schedules will produce more effective chemotherapy of brain tumors.

scholarly journals Erratum to: a method to estimate cell cycle time and growth fraction using bromodeoxyuridine-flow cytometry data from a single sample

BMC Cancer ◽  
2006 ◽  
Vol 6 (1) ◽  
Author(s):  
Rimantas Eidukevicius ◽  
Dainius Characiejus ◽  
Ramunas Janavicius ◽  
Nijole Kazlauskaite ◽  
Vita Pasukoniene ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cycle Time ◽  
Single Sample ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Flow Cytometry Data

scholarly journals Cell cycle kinetics in malignant lymphoma studied with in vivo iododeoxyuridine administration, nuclear Ki-67 staining, and flow cytometry

Blood ◽  
1992 ◽  
Vol 80 (9) ◽  
pp. 2336-2343 ◽  
Author(s):  
PP Brons ◽  
JM Raemaekers ◽  
MJ Bogman ◽  
PE van Erp ◽  
JB Boezeman ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Lymphoma ◽  
Production Rate ◽  
S Phase ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Ki 67 ◽  
Cell Production ◽  
Reactive Hyperplasia

Abstract Cell cycle kinetics of malignant lymphoma were investigated using in vivo labeling with iododeoxyuridine (IdUrd) and subsequent flow cytometry (FCM) of IdUrd/DNA and Ki-67/DNA. This approach provides an extensive cell kinetic profile from only one single tumor biopsy, including data upon the percentage of S-phase cells, the IdUrd labeling index (LI), Ki-67-derived growth fraction, duration of the S-phase, duration of the G1-phase, potential doubling time, cell production rate, and total cell cycle time. Tissue samples from 33 patients were studied: non-Hodgkin's lymphoma (NHL; n = 22), Hodgkin's disease (HD; n = 7), and reactive hyperplasia (n = 4). In NHL, the percentage of S- phase cells, LI, growth fraction, duration of the S-phase, and cell production rate were significantly correlated with the histologic malignancy grade according to the Working Formulation (P < or = .02). Data found in HD were not essentially different from those in low-grade NHL and reactive hyperplasia. Remarkably, the duration of the S-phase, the duration of the G1-phase, and the total cell cycle time appeared to be rather independent of histologic malignancy grade within the NHL category. A significant correlation was observed between the IdUrd LI and the percentage of S-phase cells, the growth fraction, the potential doubling time, and the cell production rate (P < .001), but not with the duration of the separate cell cycle phases (P > .05). Our data show (1) that it is feasible to obtain detailed information on the in vivo growth characteristics of malignant lymphoma; and (2) that the transition time through the different cell cycle phases widely varies, even within distinct histologic subgroups.

Estimation of growth fraction with bromodeoxyuridine in human central nervous system tumors

1986 ◽  
Vol 65 (5) ◽  
pp. 659-663 ◽  
Author(s):  
Yoshihiko Yoshii ◽  
Yutaka Maki ◽  
Koji Tsuboi ◽  
Yuji Tomono ◽  
Kunio Nakagawa ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cycle Time ◽  
Doubling Time ◽  
Malignant Gliomas ◽  
Cell Loss ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Tumor Doubling Time ◽  
Content Type ◽  
Fine Print

✓ Twenty-five patients with tumors of the central nervous system received bromodeoxyuridine (BUdR), 200 mg/sq m, by intravenous infusion every 8 hours for 3 days before surgery. Excised tumor specimens were fixed in chilled 70% ethanol, embedded in paraffin, and cut into 6-µm sections. Each section was reacted with monoclonal antibodies against BUdR and stained with immunoperoxidase to identify nuclei that had incorporated BUdR. The growth fraction of each tumor was estimated by calculating the ratio of BUdR-positive nuclei to the total number of tumor cells in three to six microscopic fields in viable areas of the tumor. In seven cases, the tumor doubling time was measured from the serial computerized tomography scans and an attempt was made to estimate the cell cycle time. The growth fractions ranged from 9.1% to 46.5% in malignant gliomas, 2.0% to 6.7% in low-grade gliomas, 11.2% to 43.2% in metastatic brain tumors, 0.8% to 1.9% in pituitary adenomas, 3.9% to 4.6% in acoustic neurinomas, and 6.2% to 8.2% in meningiomas and cerebellar hemangioblastomas. The estimated cell cycle time was 5 to 12 days in most malignant gliomas and brain metastases; however, the actual cell cycle time should be substantially shorter because cell loss was not considered in the calculation. Although the growth fraction appeared to correlate with the biological malignancy of each tumor, the tumor doubling time did not reflect growth potential. It is possible that unpredictable cell loss plays an important role in tumor growth at certain sizes. Therefore, the cell cycle times calculated in this study are considerably overestimated and should be interpreted with caution.

Chemotherapeutic implications of growth fraction and cell cycle time in glioblastomas

1975 ◽  
Vol 43 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Takao Hoshino ◽  
Charles B. Wilson ◽  
Mark L. Rosenblum ◽  
Marvin Barker
Keyword(s):  
Cell Cycle ◽  
Tumor Cell ◽  
Cycle Time ◽  
Malignant Gliomas ◽  
Chemotherapeutic Agents ◽  
Tumor Growth Rate ◽  
Growth Fraction ◽  
Cycle Phase ◽  
Combination Drug ◽  
Cell Cycle Time

✓Four patients received 3H-thymidine 4 to 7 days and vinblastine 4 to 6 hours prior to operation for recurrent malignant gliomas (three glioblastomas and one anaplastic astrocytoma). Tumor biopsies obtained at operation were fixed for routine histological studies and radioautography. The tumors' growth fractions averaged 0.28 with a range of 0.14 to 0.39. The tumor cell cycle time calculated in three patients had a mean duration of 57 hours with a standard deviation of 6 hours. The authors concluded that: 1) single short-term courses of cell-cycle specific chemotherapeutic agents alone will probably fail to achieve either significant reduction in tumor mass or dramatic clinical improvement; 2) cell-cycle phase-specific drugs should be administered to maintain effective blood levels over 2 to 3 days for maximal tumor cell kill. Tumor growth rate appears to correlate with the fraction of proliferating cells rather than the length of the tumor cell cycle. The scientific basis for combination drug and multimodality therapy is discussed.

scholarly journals Cell cycle kinetics in malignant lymphoma studied with in vivo iododeoxyuridine administration, nuclear Ki-67 staining, and flow cytometry

Blood ◽  
1992 ◽  
Vol 80 (9) ◽  
pp. 2336-2343 ◽  
Author(s):  
PP Brons ◽  
JM Raemaekers ◽  
MJ Bogman ◽  
PE van Erp ◽  
JB Boezeman ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Lymphoma ◽  
Production Rate ◽  
S Phase ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Ki 67 ◽  
Cell Production ◽  
Reactive Hyperplasia

Cell cycle kinetics of malignant lymphoma were investigated using in vivo labeling with iododeoxyuridine (IdUrd) and subsequent flow cytometry (FCM) of IdUrd/DNA and Ki-67/DNA. This approach provides an extensive cell kinetic profile from only one single tumor biopsy, including data upon the percentage of S-phase cells, the IdUrd labeling index (LI), Ki-67-derived growth fraction, duration of the S-phase, duration of the G1-phase, potential doubling time, cell production rate, and total cell cycle time. Tissue samples from 33 patients were studied: non-Hodgkin's lymphoma (NHL; n = 22), Hodgkin's disease (HD; n = 7), and reactive hyperplasia (n = 4). In NHL, the percentage of S- phase cells, LI, growth fraction, duration of the S-phase, and cell production rate were significantly correlated with the histologic malignancy grade according to the Working Formulation (P < or = .02). Data found in HD were not essentially different from those in low-grade NHL and reactive hyperplasia. Remarkably, the duration of the S-phase, the duration of the G1-phase, and the total cell cycle time appeared to be rather independent of histologic malignancy grade within the NHL category. A significant correlation was observed between the IdUrd LI and the percentage of S-phase cells, the growth fraction, the potential doubling time, and the cell production rate (P < .001), but not with the duration of the separate cell cycle phases (P > .05). Our data show (1) that it is feasible to obtain detailed information on the in vivo growth characteristics of malignant lymphoma; and (2) that the transition time through the different cell cycle phases widely varies, even within distinct histologic subgroups.

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