Cell cycle control and cancer.

By P. May. Pathologie et biologie, 2000

1,151 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/4ad60e787dd1dd9cbbf7c384ce600c2872859800

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Citations in the corpus

DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation (2003, background): “Signal-transduction pathways are rapidly activated after exposure to DNA-damaging agents and other cellular stresses, and these pathways affect processes such as gene transcription and cell-cycle progressio”
Awareness and current knowledge of breast cancer (2017, background): “The patients with a family history of breast or ovarian cancer have possibility of developing breast cancer [64].”
The impact of a negligent G2/M checkpoint on genomic instability and cancer induction (2007, background): “Cell cycle checkpoints monitor the structural integrity of chromosomes before progression through crucial cell cycle stage”
Multiple functions of p21 in cell cycle, apoptosis and transcriptional regulation after DNA damage. (2016, background): “In addition, E2F up-regulates ARF hich then elevates p53 levels [93].”
Cell cycle checkpoint signaling through the ATM and ATR kinases. (2001, background): “A central premise of modern cancer cell biology is that cancer development is a hyperevolutionary process fueled by genetic instability (Hartwell and Kastan 1994; Weinert 1997; Lengauer et al. 1998; Cahill et al. 1999).”
Involvement of Brca1 in S-Phase and G2-Phase Checkpoints after Ionizing Irradiation (2001, background): “The cellular responses to DNA damage induced by ionizing radiation (IR) include activation of cell cycle checkpoints that delay progression of cells through the cell cycle (6, 7).”
Ultrashort electrical pulses open a new gateway into biological cells (2004, methodology): “Here, different methods were used to examine ultrashort pulse effects on DNA, including the comet assay, which allows the measurement of DNA fragmentation for single cells [35]; cell lysis and DNA extraction [36]; and cytogenic analysis (studying the damage to individual chromosomes) and changes in ”
PRMT6 increases cytoplasmic localization of p21CDKN1A in cancer cells through arginine methylation and makes more resistant to cytotoxic agents (2015, background): “Cells possess several cell-cycle checkpoints to induce cell cycle arrest or to induce apoptosis when the genomic integrity is threatened, preventing the transmission of dangerous genetic mutations into subsequent cell generations [3].”
Chromosome aberrations in solid tumors (2003, background): “This variability may be due to differences in the mechanisms by which tumors are initiated, the manner in which genome stability is compromise”
Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, unknown): “Based on karyotypic and mutational analyses, it is clear that tumors, especially solid tumors, pass through stages of extreme genomic instability that result in the accumulation of point mutations, deletions, complex chromosomal rearrangements , and extensive aneuploidy (Hartwell and Kastan, 1994).”