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The cancer therapeutic potential of Chk1 inhibitors: how mechanistic studies impact on clinical trial design.
Thompson R, Eastman A. Thompson R, et al. Among authors: eastman a. Br J Clin Pharmacol. 2013 Sep;76(3):358-69. doi: 10.1111/bcp.12139. Br J Clin Pharmacol. 2013. PMID: 23593991 Free PMC article. Review.
Chk1 was initially recognized as a regulator of the G2/M checkpoint, but has since been demonstrated to have additional roles in replication fork stability, replication origin firing and homologous recombination. ...
Chk1 was initially recognized as a regulator of the G2/M checkpoint, but has since been demonstrated to have additional roles in repl …
Activation of programmed cell death by anticancer agents: cisplatin as a model system.
Eastman A. Eastman A. Cancer Cells. 1990 Aug-Sep;2(8-9):275-80. Cancer Cells. 1990. PMID: 2223389 Review.
The anticancer drug cisplatin exerts its action as a consequence of interaction with DNA. Cell cycle progression facilitates sensitivity to the drug, but inhibition of DNA synthesis is not necessarily the critical step. ...Certain features of cisplatin-induced cell death, …
The anticancer drug cisplatin exerts its action as a consequence of interaction with DNA. Cell cycle progression facilitates sensitiv …
Activation of programmed cell death (apoptosis) by cisplatin, other anticancer drugs, toxins and hyperthermia.
Barry MA, Behnke CA, Eastman A. Barry MA, et al. Among authors: eastman a. Biochem Pharmacol. 1990 Nov 15;40(10):2353-62. doi: 10.1016/0006-2952(90)90733-2. Biochem Pharmacol. 1990. PMID: 2244936
The results suggest that, irrespective of the primary site of action of a drug, cell death by most pharmacologic agents is mediated by activation of the signal transduction pathway for apoptosis. The results also suggest two signal pathways for apoptosis, one directly asso …
The results suggest that, irrespective of the primary site of action of a drug, cell death by most pharmacologic agents is mediated b …
Survival factors, intracellular signal transduction, and the activation of endonucleases in apoptosis.
Eastman A. Eastman A. Semin Cancer Biol. 1995 Feb;6(1):45-52. doi: 10.1006/scbi.1995.0006. Semin Cancer Biol. 1995. PMID: 7548841 Review.
It is suggested that a Ras/Raf/MAP kinase-dependent pathway is critical for cell survival. Apoptosis results from loss of these survival factors or deregulation of survival pathways. ...
It is suggested that a Ras/Raf/MAP kinase-dependent pathway is critical for cell survival. Apoptosis results from loss of these survi …
The role of cell cycle progression in cisplatin-induced apoptosis in Chinese hamster ovary cells.
Demarcq C, Bunch RT, Creswell D, Eastman A. Demarcq C, et al. Among authors: eastman a. Cell Growth Differ. 1994 Sep;5(9):983-93. Cell Growth Differ. 1994. PMID: 7819136
The current experiments establish a detailed sequence of events that occur in Chinese hamster ovary CHO/UV41 cells following incubation with cisplatin. ...These cells subsequently lost contact with the extracellular matrix, and only then digested their DNA in a mann …
The current experiments establish a detailed sequence of events that occur in Chinese hamster ovary CHO/UV41 cells following incubati …
Apoptosis: a product of programmed and unprogrammed cell death.
Eastman A. Eastman A. Toxicol Appl Pharmacol. 1993 Jul;121(1):160-4. doi: 10.1006/taap.1993.1141. Toxicol Appl Pharmacol. 1993. PMID: 8337697 Review.
Apoptosis is a form of cell death defined by morphological and biochemical characteristics. Although originally described in 1972, it is only very recently that significant interest in the subject has occurred, possibly as a result of the identification of genes tha …
Apoptosis is a form of cell death defined by morphological and biochemical characteristics. Although originally described in 1972, it …
Phorbol ester augments butyrate-induced apoptosis of colon cancer cells.
McBain JA, Eastman A, Simmons DL, Pettit GR, Mueller GC. McBain JA, et al. Among authors: eastman a. Int J Cancer. 1996 Sep 4;67(5):715-23. doi: 10.1002/(SICI)1097-0215(19960904)67:5<715::AID-IJC21>3.0.CO;2-2. Int J Cancer. 1996. PMID: 8782664
In each of these lines, butyrate inhibited cell replication in a reversible manner, similar to that seen in VACO 5. However, the combination of butyrate and TPA led to high levels of cell death in only a subset of these lines. ...Our findings indicate that the PKC s …
In each of these lines, butyrate inhibited cell replication in a reversible manner, similar to that seen in VACO 5. However, the comb …
7-Hydroxystaurosporine (UCN-01) causes redistribution of proliferating cell nuclear antigen and abrogates cisplatin-induced S-phase arrest in Chinese hamster ovary cells.
Bunch RT, Eastman A. Bunch RT, et al. Among authors: eastman a. Cell Growth Differ. 1997 Jul;8(7):779-88. Cell Growth Differ. 1997. PMID: 9218872
A variety of agents, such as caffeine, have been shown to abrogate the DNA damage-dependent G2 checkpoint and enhance cytotoxicity. ...PCNA acts as a sliding clamp for DNA polymerase delta. Sequestering of PCNA by p21waf1/cip1 is required for p53-dependent G1 arrest
A variety of agents, such as caffeine, have been shown to abrogate the DNA damage-dependent G2 checkpoint and enhance cytotoxicity. .
Enhancement of cisplatin-induced cytotoxicity by 7-hydroxystaurosporine (UCN-01), a new G2-checkpoint inhibitor.
Bunch RT, Eastman A. Bunch RT, et al. Among authors: eastman a. Clin Cancer Res. 1996 May;2(5):791-7. Clin Cancer Res. 1996. PMID: 9816232
A variety of agents such as caffeine have been shown to abrogate the DNA damage-dependent G2 checkpoint and enhance cytotoxicity. ...Furthermore, the same concentrations of UCN-01 that resulted in abrogation of the cisplatin-induced G2 arrest also enhanced cisplatin-induce
A variety of agents such as caffeine have been shown to abrogate the DNA damage-dependent G2 checkpoint and enhance cytotoxicity. ...
Comparison of the efficacy of 7-hydroxystaurosporine (UCN-01) and other staurosporine analogs to abrogate cisplatin-induced cell cycle arrest in human breast cancer cell lines.
Lee SI, Brown MK, Eastman A. Lee SI, et al. Among authors: eastman a. Biochem Pharmacol. 1999 Dec 1;58(11):1713-21. doi: 10.1016/s0006-2952(99)00258-0. Biochem Pharmacol. 1999. PMID: 10571245
Hence, K252a did not enhance cisplatin-induced cytotoxicity because it failed to push the cells through a lethal mitosis. None of the other analogs influenced cell cycle progression at the concentrations tested. ...
Hence, K252a did not enhance cisplatin-induced cytotoxicity because it failed to push the cells through a lethal mitosis. None of the …
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