Studies on the Sensitivity of Anticancer Agents of Normal Human Cells in Culture

1975 ◽  
pp. 511-519
Author(s):  
L. Morasca ◽  
G. Balconi ◽  
E. Erba ◽  
E. Cvitkovic
Keyword(s):  
Anticancer Agents ◽  
Human Cells ◽  
Cells In Culture ◽  
Normal Human ◽  
Normal Human Cells

Chemotherapy in malignant disease

1970 ◽  
Vol 8 (4) ◽  
pp. 13-16
Keyword(s):  
Cancer Cells ◽  
Cancer Chemotherapy ◽  
Anticancer Agents ◽  
Antimicrobial Chemotherapy ◽  
Malignant Disease ◽  
Human Cells ◽  
Normal Cells ◽  
Different Types ◽  
Normal Human ◽  
Normal Human Cells

Cancer chemotherapy, unlike antimicrobial chemotherapy, is not based on absolute metabolic differences between cancer cells and normal human cells. Anticancer agents inhibit the growth of cells, whether normal or malignant, though different types of cell vary in their susceptibility to these agents, and in their capacity for recovery. The usefulness of these drugs is thus limited by their effects on normal cells.

scholarly journals Knockdown of αII spectrin in normal human cells by siRNA leads to chromosomal instability and decreased DNA interstrand cross-link repair

2009 ◽  
Vol 381 (2) ◽  
pp. 288-293 ◽  
Author(s):  
Laura W. McMahon ◽  
Pan Zhang ◽  
Deepa M. Sridharan ◽  
Joel A. Lefferts ◽  
Muriel W. Lambert
Keyword(s):  
Chromosomal Instability ◽  
Human Cells ◽  
Cross Link ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals DNA amplification is rare in normal human cells.

1990 ◽  
Vol 87 (5) ◽  
pp. 1791-1795 ◽  
Author(s):  
J. A. Wright ◽  
H. S. Smith ◽  
F. M. Watt ◽  
M. C. Hancock ◽  
D. L. Hudson ◽  
...  
Keyword(s):  
Dna Amplification ◽  
Human Cells ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals Reduction of X-ray-induced DNA damage in normal human cells treated with the PrC-210 radioprotector

Biology Open ◽  
2018 ◽  
Vol 7 (10) ◽  
pp. bio035113 ◽  
Author(s):  
Michael Brand ◽  
Matthias Sommer ◽  
Frank Jermusek ◽  
William E. Fahl ◽  
Michael Uder
Keyword(s):  
Dna Damage ◽  
Human Cells ◽  
X Ray ◽  
Normal Human ◽  
Normal Human Cells

scholarly journals Qualitative and quantitative difference in mutation induction between carbon- and neon-ion beams in normal human cells.

2003 ◽  
Vol 17 (4) ◽  
pp. 302-306 ◽  
Author(s):  
Masao Suzuki ◽  
Chizuru Tsuruoka ◽  
Tatsuaki Kanai ◽  
Takeshi Kato ◽  
Fumio Yatagai ◽  
...  
Keyword(s):  
Quantitative Difference ◽  
Ion Beams ◽  
Human Cells ◽  
Mutation Induction ◽  
Qualitative And Quantitative ◽  
Normal Human ◽  
Normal Human Cells ◽  
Neon Ion

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).

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