scholarly journals Reinitiation of DNA synthesis in senescent human fibroblasts upon fusion with cells of unlimited growth potential.

1975 ◽  
Vol 64 (3) ◽  
pp. 551-556 ◽  
Author(s):  
T H Norwood ◽  
W R Pendergrass ◽  
G M Martin
Keyword(s):  
Dna Synthesis ◽  
Sendai Virus ◽  
Human Fibroblasts ◽  
Growth Potential ◽  
Labeling Index ◽  
Thymidine Labeling Index ◽  
Unlimited Growth

Postreplicative, "senescent" human fibroblasts were fused to HeLa or to SV-40 transformed human fibroblasts with Sendai virus. DNA synthesis was reinitiated in senescent nuclei in a high proportion of the heterodikaryons. The [3H]thymidine labeling index of senescent fibroblast nuclei in heteropolykaryons was a function of the ratio of HeLa to senescent nuclei.

Increased tritiated thymidine-labeling index of bone marrow myeloblasts following BCG administration in man

1978 ◽  
Vol 4 (3) ◽  
pp. 197-199
Author(s):  
M. Rozencweig ◽  
P. Stryckmans ◽  
J.P. Fichefet ◽  
Mireille Socquet
Keyword(s):  
Bone Marrow ◽  
Tritiated Thymidine ◽  
Labeling Index ◽  
Thymidine Labeling Index

scholarly journals Induction of pancreatic acinar cell proliferation by thyroid hormone

2005 ◽  
Vol 185 (3) ◽  
pp. 393-399 ◽  
Author(s):  
G M Ledda-Columbano ◽  
A Perra ◽  
M Pibiri ◽  
F Molotzu ◽  
A Columbano
Keyword(s):  
Cell Proliferation ◽  
Thyroid Hormone ◽  
Dna Synthesis ◽  
Acinar Cell ◽  
Acinar Cells ◽  
Pancreatic Acinar Cell ◽  
Labeling Index ◽  
Metabolic Effects ◽  
Brdu Incorporation ◽  
Pancreatic Cell

Thyroid hormone is known to elicit diverse cellular and metabolic effects in various organs, including mitogenesis in the rat liver. In the present study, experiments were carried out to determine whether thyroid hormone is able to stimulate cell proliferation in another quiescent organ such as the pancreas. 3,5,3′-l-tri-iodothyronine (T3) added to the diet at a concentration of 4 mg/kg caused a striking increase in nuclear bromodeoxyuridine (BrdU) incorporation of rat acinar cells 7 days after treatment (the labeling index was 46.7% in T3-treated rats vs 7.1% in controls). BrdU incorporation was limited to the acinar cells, with duct cells and islet cells being essentially negative. The increase in DNA synthesis was accompanied by the presence of several mitotic figures. Histological examination of the pancreas did not exhibit any sign of T3-induced toxicity. Determination of the apoptotic index, measurement of the serum levels of α-amylase and lipase, and glycemia determination did not show any increase over control values, suggesting that the enhanced proliferation of acinar cells was a direct effect induced by T3 and not a regenerative response consequent to acinar or β-cell injury. Additional experiments showed that DNA synthesis was induced as early as 2 days after T3 treatment (the labeling index was 9.4 vs 1.9% in controls) and was associated with increased protein levels of cyclin D1, cyclin A and proliferating cell nuclear antigen, with no substantial differences in the expression of the cyclin-dependent kinase inhibitor p27. The mitogenic effect of T3 on the pancreas was not limited to the rat, since extensive acinar cell proliferation was also observed in the pancreas of mice treated with T3 for 1 week (the labeling index was 28% in T3-treated mice vs 1.8% in controls). Treatment with three other ligands of nuclear receptors, ciprofibrate, all-trans retinoic acid and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, induced little or no pancreatic cell proliferation. These results demonstrated that T3 is a powerful inducer of cell proliferation in the pancreas and suggested that pancreatic acinar cell proliferation by selected agents may have potential for therapeutic use.

scholarly journals Antitumor activity of L-asparaginase from Erwinia Carotovora from against different leukemic and solid tumours cell lines

2013 ◽  
Vol 59 (5) ◽  
pp. 498-513 ◽  
Author(s):  
O.Yu. Abakumova ◽  
O.V. Podobed ◽  
P.A. Karalkin ◽  
L.I. Kondakova ◽  
N.N. Sokolov
Keyword(s):  
Dna Synthesis ◽  
Tumor Cells ◽  
Solid Tumor ◽  
Human Fibroblasts ◽  
Erwinia Carotovora ◽  
Cell Number ◽  
Jurkat Cells ◽  
Leukemic Cells ◽  
Cycle Phase ◽  
Tumor Cell Death

We have studied dose- and time-dependent antitumor and cytotoxic effects of Erwinia carotovora L-asparaginase (ECAR LANS) and Escherichia coli L-asparaginase (MEDAC) on human leukemic cells and human and animal solid tumor cells. We determined the sensitivity of tumor cells to L-asparaginases, as well the effect L-asparaginases on cell growth rate, protein and DNA synthesis per se and with addition of different cytostatics. The data obtained demonstrated that ECAR LANS L-asparaginase suppressed growth of all tested solid tumor cells. Evaluation of leukemic cell number after treatment with L-asparaginases for 24, 48 and 72 h demonstrated that asparagine deficiency did not kill cells but stopped normal cell division and had no effect on protein and DNA synthesis. Cytofluorometric study of solid and leukemic cells demonstrated that the treatment with L-asparaginase for 72 h did not change cell cycle phase distribution and did not increase the number of apoptotic cells. The HL-60 cell line was only exemption. At the same time, cells treatment with L-asparaginase and doxorubicin combination leaded to increase of apoptotypical cell number to 60% for MCF7 cells, to 40% for Jurkat cells and to 99% for HL-60 cells. We have excluded apoptosis as main reason for tumor cell death after asparaginase treatment because multi resistant Jurkat/A4 cells have been asparaginase sensitive. We have not found ECAR LANS L-asparaginase effect on normal human fibroblasts growth ability and we had come to conclusion that enzyme cytotoxcisity related only with asparagine deficiency.

scholarly journals Adenovirus E1B 55-Kilodalton Protein Is Required for both Regulation of mRNA Export and Efficient Entry into the Late Phase of Infection in Normal Human Fibroblasts

2006 ◽  
Vol 80 (2) ◽  
pp. 964-974 ◽  
Author(s):  
Ramon Gonzalez ◽  
Wenying Huang ◽  
Renee Finnen ◽  
Courtney Bragg ◽  
S. J. Flint
Keyword(s):  
Dna Synthesis ◽  
Hela Cells ◽  
Human Fibroblasts ◽  
Late Phase ◽  
Mrna Export ◽  
Human Cells ◽  
Insertion Mutation ◽  
Viral Dna ◽  
Normal Human ◽  
Normal Human Cells

ABSTRACT The human adenovirus type 5 (Ad5) E1B 55-kDa protein is required for selective nuclear export of viral late mRNAs from the nucleus and concomitant inhibition of export of cellular mRNAs in HeLa cells and some other human cell lines, but its contributions(s) to replication in normal human cells is not well understood. We have therefore examined the phenotypes exhibited by viruses carrying mutations in the E1B 55-kDa protein coding sequence in normal human fibroblast (HFFs). Ad5 replicated significantly more slowly in HFFs than it does in tumor cells, a difference that is the result of delayed entry into the late phase of infection. The A143 mutation, which specifically impaired export of viral late mRNAs from the nucleus in infected HeLa cells (R. A. Gonzalez and S. J. Flint, J. Virol. 76:4507-4519, 2002), induced a more severe defect in viral mRNA export in HFFs. This observation indicates that the E1B 55-kDa protein regulates mRNA export during the late phase of infection of normal human cells. Other mutants exhibited phenotypes not observed in HeLa cells. In HFFs infected by the null mutant Hr6, synthesis of viral late mRNAs and proteins was severely impaired. Such defects in late gene expression were the result of inefficient progression into the late phase of infection, for viral DNA synthesis was 10-fold less efficient in Hr6-infected HFFs than in cells infected by Ad5. Similar, but less severe, defects in viral DNA synthesis were induced by the insertion mutation H224, which has been reported to inhibit binding of the E1B 55-kDa protein to p53 (C. C. Kao, P. R. Yew, and A. J. Berk, Virology 179:806-814, 1990).

scholarly journals An overexpressed gene transcript in senescent and quiescent human fibroblasts encoding a novel protein in the epidermal growth factor-like repeat family stimulates DNA synthesis.

1995 ◽  
Vol 15 (1) ◽  
pp. 120-128 ◽  
Author(s):  
B Lecka-Czernik ◽  
C K Lumpkin ◽  
S Goldstein
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Dna Synthesis ◽  
Cellular Proliferation ◽  
Werner Syndrome ◽  
Human Fibroblasts ◽  
Extracellular Proteins ◽  
Gene Transcript ◽  
Epidermal Growth ◽  
Novel Protein

We carried out subtractive enrichment of a cDNA library derived from mRNA of senescent human diploid fibroblasts (HDF) established from a subject with Werner syndrome of premature aging. By differential screening, we isolated an overexpressed cDNA sequence (S1-5) that codes for a novel protein containing epidermal growth factor (EGF)-like domains which match the EGF-like consensus sequences within several known extracellular proteins that play a role in cell growth, development, and cell signalling. S1-5 mRNA is overexpressed in Werner syndrome and senescent normal HDF, is induced by growth arrest of young normal cells, but is significantly decreased by high serum, conditions which promote cellular proliferation. Paradoxically, microinjection into young HDF of two different lengths of S1-5 mRNA, containing different putative AUG translational start sites, consistently stimulated rather than inhibited DNA synthesis by an apparent autocrine/paracrine mechanism. Thus, the S1-5 gene product may represent a negative and/or positive factor whose ultimate activity is modulated by the cell environment as occurs with other members of EGF-like family.

Thymidine Labeling Index Analysis in Early Breast Cancer Patients Randomized to Receive Perioperative Chemotherapy

Oncology ◽  
2000 ◽  
Vol 60 (1) ◽  
pp. 88-93 ◽  
Author(s):  
Paolo Pronzato ◽  
Paola Queirolo ◽  
Stefania Vecchio ◽  
Rita Lionetto ◽  
Lucia Del Mastro ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Early Breast Cancer ◽  
Labeling Index ◽  
Perioperative Chemotherapy ◽  
Breast Cancer Patients ◽  
Index Analysis ◽  
Thymidine Labeling Index ◽  
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