Corrigendum to “Design and synthesis of novel isatin-based derivatives targeting cell cycle checkpoint pathways as potential anticancer agents” [Bioorg. Chem. 105 (2020) 104366]

Unrestrained proliferation is a common feature of malignant neoplasms. Targeting the cell cycle is a therapeutic strategy to prevent unlimited cell division. Recently developed rationales for these selective inhibitors can be subdivided into two categories with antithetical functionality. One applies a “brake” to the cell cycle to halt cell proliferation, such as with inhibitors of cell cycle kinases. The other “accelerates” the cell cycle to initiate replication/mitotic catastrophe, such as with inhibitors of cell cycle checkpoint kinases. The fate of cell cycle progression or arrest is tightly regulated by the presence of tolerable or excessive DNA damage, respectively. This suggests that there is compatibility between inhibitors of DNA repair kinases, such as PARP inhibitors, and inhibitors of cell cycle checkpoint kinases. In the present review, we explore alterations to the cell cycle that are concomitant with altered DNA damage repair machinery in unfavorable neuroblastomas, with respect to their unique genomic and molecular features. We highlight the vulnerabilities of these alterations that are attributable to the features of each. Based on the assessment, we offer possible therapeutic approaches for personalized medicine, which are seemingly antithetical, but both are promising strategies for targeting the altered cell cycle in unfavorable neuroblastomas.

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A DNA-Damage-Induced Cell Cycle Checkpoint in Arabidopsis

Genetics ◽

10.1093/genetics/164.1.323 ◽

2003 ◽

Vol 164 (1) ◽

pp. 323-334

Author(s):

S B Preuss ◽

A B Britt

Keyword(s):

Cell Cycle ◽

Gamma Radiation ◽

Cell Cycle Progression ◽

Cell Cycle Checkpoint ◽

Phase Cell ◽

Cycle Arrest ◽

Cycle Checkpoint ◽

Radiation Induced ◽

High Doses ◽

Regulation Of Cell Cycle

Abstract Although it is well established that plant seeds treated with high doses of gamma radiation arrest development as seedlings, the cause of this arrest is unknown. The uvh1 mutant of Arabidopsis is defective in a homolog of the human repair endonuclease XPF, and uvh1 mutants are sensitive to both the toxic effects of UV and the cytostatic effects of gamma radiation. Here we find that gamma irradiation of uvh1 plants specifically triggers a G2-phase cell cycle arrest. Mutants, termed suppressor of gamma (sog), that suppress this radiation-induced arrest and proceed through the cell cycle unimpeded were recovered in the uvh1 background; the resulting irradiated plants are genetically unstable. The sog mutations fall into two complementation groups. They are second-site suppressors of the uvh1 mutant's sensitivity to gamma radiation but do not affect the susceptibility of the plant to UV radiation. In addition to rendering the plants resistant to the growth inhibitory effects of gamma radiation, the sog1 mutation affects the proper development of the pollen tetrad, suggesting that SOG1 might also play a role in the regulation of cell cycle progression during meiosis.

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Attenuation of G 2 -Phase Cell Cycle Checkpoint Control Is Associated with Increased Frequencies of Unrejoined Chromosome Breaks in Human Tumor Cells

Radiation Research ◽

10.2307/3579585 ◽

1996 ◽

Vol 146 (2) ◽

pp. 139 ◽

Cited By ~ 7

Author(s):

Jeffrey L. Schwartz ◽

Janet Cowan ◽

David J. Grdina ◽

Ralph R. Weichselbaum

Keyword(s):

Cell Cycle ◽

Tumor Cells ◽

Human Tumor ◽

Cell Cycle Checkpoint ◽

Phase Cell ◽

Checkpoint Control ◽

Human Tumor Cells ◽

Chromosome Breaks ◽

Cycle Checkpoint

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