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Differential effects of selective COX-2 inhibitors on cell cycle regulation and proliferation of glioblastoma cell lines.
Kardosh A, Blumenthal M, Wang WJ, Chen TC, Schönthal AH. Kardosh A, et al. Cancer Biol Ther. 2004 Jan;3(1):55-62. doi: 10.4161/cbt.3.1.571. Epub 2004 Jan 22. Cancer Biol Ther. 2004. PMID: 14726653
As patients with brain tumors, such as glioblastoma, exhibit a very poor prognosis, we began to explore whether COX inhibitors could be useful for the treatment of this type of tumor. ...In an effort to determine the underlying molecular processes that might mediate celeco …
As patients with brain tumors, such as glioblastoma, exhibit a very poor prognosis, we began to explore whether COX inhibitors could …
Antiangiogenic activities of 2,5-dimethyl-celecoxib on the tumor vasculature.
Virrey JJ, Liu Z, Cho HY, Kardosh A, Golden EB, Louie SG, Gaffney KJ, Petasis NA, Schönthal AH, Chen TC, Hofman FM. Virrey JJ, et al. Among authors: kardosh a. Mol Cancer Ther. 2010 Mar;9(3):631-41. doi: 10.1158/1535-7163.MCT-09-0652. Epub 2010 Mar 2. Mol Cancer Ther. 2010. PMID: 20197398 Free article.
Green tea polyphenols block the anticancer effects of bortezomib and other boronic acid-based proteasome inhibitors.
Golden EB, Lam PY, Kardosh A, Gaffney KJ, Cadenas E, Louie SG, Petasis NA, Chen TC, Schönthal AH. Golden EB, et al. Among authors: kardosh a. Blood. 2009 Jun 4;113(23):5927-37. doi: 10.1182/blood-2008-07-171389. Epub 2009 Feb 3. Blood. 2009. PMID: 19190249
COX-2 inhibition is neither necessary nor sufficient for celecoxib to suppress tumor cell proliferation and focus formation in vitro.
Chuang HC, Kardosh A, Gaffney KJ, Petasis NA, Schönthal AH. Chuang HC, et al. Among authors: kardosh a. Mol Cancer. 2008 May 16;7:38. doi: 10.1186/1476-4598-7-38. Mol Cancer. 2008. PMID: 18485224 Free PMC article.
Rather, the drug's ability to trigger ERS, a known effector of cell death, might provide an alternative explanation for its acute cytotoxicity. In addition, the newly discovered ability of this drug to restore contact inhibition and block focus formation during chronic dru …
Rather, the drug's ability to trigger ERS, a known effector of cell death, might provide an alternative explanation for its acute cyt …
Aggravated endoplasmic reticulum stress as a basis for enhanced glioblastoma cell killing by bortezomib in combination with celecoxib or its non-coxib analogue, 2,5-dimethyl-celecoxib.
Kardosh A, Golden EB, Pyrko P, Uddin J, Hofman FM, Chen TC, Louie SG, Petasis NA, Schönthal AH. Kardosh A, et al. Cancer Res. 2008 Feb 1;68(3):843-51. doi: 10.1158/0008-5472.CAN-07-5555. Cancer Res. 2008. PMID: 18245486
The selective cyclooxygenase-2 (COX-2) inhibitor celecoxib (Celebrex) causes ER stress through a different mechanism (i.e., by causing leakage of calcium from the ER into the cytosol). ...We propose that this novel drug combination should receive further evaluation as a
The selective cyclooxygenase-2 (COX-2) inhibitor celecoxib (Celebrex) causes ER stress through a different mechanism (i.e., by causin …
HIV-1 protease inhibitors nelfinavir and atazanavir induce malignant glioma death by triggering endoplasmic reticulum stress.
Pyrko P, Kardosh A, Wang W, Xiong W, Schönthal AH, Chen TC. Pyrko P, et al. Among authors: kardosh a. Cancer Res. 2007 Nov 15;67(22):10920-8. doi: 10.1158/0008-5472.CAN-07-0796. Cancer Res. 2007. PMID: 18006837
Induction of ESR seems to play a central role in PI-induced cell death because small interfering RNA-mediated knockdown of the protective ER chaperone GRP78 sensitizes cells; whereas knockdown of proapoptotic caspase-4 protects cells from PI-induced cell death. ...Thus, ou …
Induction of ESR seems to play a central role in PI-induced cell death because small interfering RNA-mediated knockdown of the protec …
Celecoxib transiently inhibits cellular protein synthesis.
Pyrko P, Kardosh A, Schönthal AH. Pyrko P, et al. Among authors: kardosh a. Biochem Pharmacol. 2008 Jan 15;75(2):395-404. doi: 10.1016/j.bcp.2007.08.029. Epub 2007 Sep 1. Biochem Pharmacol. 2008. PMID: 17920040
Here, we report a COX-2-independent effect of celecoxib that might have profound consequences for the interpretation of previous results obtained at elevated concentrations of this drug in vitro. ...This appears to be a consequence of endoplasmic reticulum (ER) stre …
Here, we report a COX-2-independent effect of celecoxib that might have profound consequences for the interpretation of previous resu …
Reduced survivin expression and tumor cell survival during chronic hypoxia and further cytotoxic enhancement by the cyclooxygenase-2 inhibitor celecoxib.
Kardosh A, Soriano N, Pyrko P, Liu YT, Jabbour M, Hofman FM, Schönthal AH. Kardosh A, et al. J Biomed Sci. 2007 Sep;14(5):647-62. doi: 10.1007/s11373-007-9173-3. Epub 2007 Apr 18. J Biomed Sci. 2007. PMID: 17440835
Hypoxia is a characteristic feature of advanced solid tumors and may worsen prognosis. The development of tumor-targeted and hypoxia-inducible gene therapy vectors holds promise to selectively deliver and express suicidal or cytotoxic genes in hypoxic regions of tumors. .. …
Hypoxia is a characteristic feature of advanced solid tumors and may worsen prognosis. The development of tumor-targeted and hypoxia- …
Calcium-activated endoplasmic reticulum stress as a major component of tumor cell death induced by 2,5-dimethyl-celecoxib, a non-coxib analogue of celecoxib.
Pyrko P, Kardosh A, Liu YT, Soriano N, Xiong W, Chow RH, Uddin J, Petasis NA, Mircheff AK, Farley RA, Louie SG, Chen TC, Schönthal AH. Pyrko P, et al. Among authors: kardosh a. Mol Cancer Ther. 2007 Apr;6(4):1262-75. doi: 10.1158/1535-7163.MCT-06-0629. Mol Cancer Ther. 2007. PMID: 17431104
A drawback of extensive coxib use for antitumor purposes is the risk of life-threatening side effects that are thought to be a class effect and probably due to the resulting imbalance of eicosanoid levels. 2,5-Dimethyl-celecoxib (DMC) is a close structural an
A drawback of extensive coxib use for antitumor purposes is the risk of life-threatening side effects that are thought to be a
Glioma-associated endothelial cells show evidence of replicative senescence.
Charalambous C, Virrey J, Kardosh A, Jabbour MN, Qazi-Abdullah L, Pen L, Zidovetzki R, Schönthal AH, Chen TC, Hofman FM. Charalambous C, et al. Among authors: kardosh a. Exp Cell Res. 2007 Apr 1;313(6):1192-202. doi: 10.1016/j.yexcr.2006.12.027. Epub 2007 Jan 12. Exp Cell Res. 2007. PMID: 17291495
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