celecoxib has been researched along with Astrocytoma, Grade IV in 30 studies
| Excerpt | Relevance | Reference |
|---|---|---|
| "Chemoradiation, followed by adjuvant temozolomide, is the standard treatment for newly diagnosed glioblastoma." | 9.20 | Randomized phase II adjuvant factorial study of dose-dense temozolomide alone and in combination with isotretinoin, celecoxib, and/or thalidomide for glioblastoma. ( Aldape, KD; Chang, EL; Colman, H; Conrad, CA; De Groot, JF; Fisch, MJ; Floyd, JD; Giglio, P; Gilbert, MR; Gonzalez, J; Groves, MD; Hess, KR; Hsu, SH; Lagrone, LW; Levin, VA; Loghin, ME; Mahajan, A; Penas-Prado, M; Puduvalli, VK; Salacz, ME; Volas-Redd, G; Woo, SY; Yung, WK, 2015) |
| "External beam radiation therapy (XRT) with concomitant temozolomide and 6 cycles of adjuvant temozolomide (5/28-day schedule) improves survival in patients with newly diagnosed glioblastoma compared with XRT alone." | 9.14 | A phase I factorial design study of dose-dense temozolomide alone and in combination with thalidomide, isotretinoin, and/or celecoxib as postchemoradiation adjuvant therapy for newly diagnosed glioblastoma. ( Chang, E; Colman, H; Conrad, C; de Groot, J; Giglio, P; Gilbert, MR; Gonzalez, J; Groves, MD; Hess, K; Hunter, K; Levin, V; Mahajan, A; Puduvalli, V; Woo, S; Yung, WK, 2010) |
| "We conducted a phase II study of the combination of temozolomide and angiogenesis inhibitors for treating adult patients with newly diagnosed glioblastoma." | 9.13 | Phase II study of temozolomide, thalidomide, and celecoxib for newly diagnosed glioblastoma in adults. ( Batchelor, TT; Black, PM; Ciampa, A; Doherty, L; Drappatz, J; Folkman, J; Gigas, DC; Henson, JW; Kesari, S; Kieran, M; Laforme, A; Ligon, KL; Longtine, JA; Muzikansky, A; Ramakrishna, N; Schiff, D; Weaver, S; Wen, PY, 2008) |
| "In a phase II clinical trial, we sought to determine if combining celecoxib with 13-cis-retinoic acid (13-cRA, Accutane) was efficacious in the treatment of recurrent (progressive) glioblastoma multiforme (GBM)." | 9.12 | Combination chemotherapy with 13-cis-retinoic acid and celecoxib in the treatment of glioblastoma multiforme. ( Giglio, P; Groves, MD; Hess, K; Jochec, J; Levin, VA; Puduvalli, VK; Yung, WK, 2006) |
| " Celecoxib (CXB), a selective COX-2 inhibitor, is able to control inflammation and pain, to improve the efficacy of radiotherapy, and to inhibit at high doses the growth of cancer cells." | 7.80 | New celecoxib multiparticulate systems to improve glioblastoma treatment. ( Barcia, E; Fernández-Carballido, A; García-García, L; Marcianes, P; Negro, S; Slowing, K; Vera, M, 2014) |
| "Cells positive for CD133 were isolated from glioblastoma specimens and characterized by flow cytometry, then treated with celecoxib and/or ionizing radiation (IR)." | 7.77 | Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects. Laboratory investigation. ( Chen, YW; Chiou, SH; Huang, PI; Hueng, DY; Kao, CL; Ma, HI; Sytwu, HK; Tai, LK, 2011) |
| "Toward improved glioblastoma multiforme treatment, we determined whether celecoxib, a selective cyclooxygenase (COX)-2 inhibitor, could enhance glioblastoma radiosensitivity by inducing tumor necrosis and inhibiting tumor angiogenesis." | 7.74 | Enhancement of glioblastoma radioresponse by a selective COX-2 inhibitor celecoxib: inhibition of tumor angiogenesis with extensive tumor necrosis. ( Cheah, ES; Kang, KB; Moore, XL; Wang, TT; Wong, MC; Woon, CT; Zhu, C, 2007) |
| "Celecoxib (400) mg was administered orally twice a day until tumor progression or dose-limiting toxicity." | 6.73 | Effect of phenytoin on celecoxib pharmacokinetics in patients with glioblastoma. ( Batchelor, T; Desideri, S; Grossman, SA; Hammour, T; Lesser, G; Olson, J; Peereboom, D; Supko, JG; Ye, X, 2008) |
| "Celecoxib and 2,5-DMC were the most cytotoxic." | 5.62 | COXIBs and 2,5-dimethylcelecoxib counteract the hyperactivated Wnt/β-catenin pathway and COX-2/PGE2/EP4 signaling in glioblastoma cells. ( Kleszcz, R; Krajka-Kuźniak, V; Kruhlenia, N; Majchrzak-Celińska, A; Misiorek, JO; Przybyl, L; Rolle, K, 2021) |
| "Celecoxib treatment significantly down-regulated TNF-α induced NF-κB nuclear translocation, NF-κB DNA binding activity, and NF-κB-dependent reporter gene expression in U373 and T98G cells in a dose-dependent manner." | 5.38 | The nonsteroidal anti-inflammatory drug celecoxib suppresses the growth and induces apoptosis of human glioblastoma cells via the NF-κB pathway. ( Babu, PP; Geeviman, K; Ramulu, C; Sareddy, GR, 2012) |
| "Glioblastoma multiforme is the most common and most malignant primary brain tumour." | 5.36 | Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib. ( Freyschlag, CF; Nölte, I; Pechlivanis, I; Schmieder, K; Seiz, M; Tuettenberg, J; Vajkoczy, P, 2010) |
| " We propose that this novel drug combination should receive further evaluation as a potentially effective anticancer therapy." | 5.35 | 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. ( Chen, TC; Golden, EB; Hofman, FM; Kardosh, A; Louie, SG; Petasis, NA; Pyrko, P; Schönthal, AH; Uddin, J, 2008) |
| "Chemoradiation, followed by adjuvant temozolomide, is the standard treatment for newly diagnosed glioblastoma." | 5.20 | Randomized phase II adjuvant factorial study of dose-dense temozolomide alone and in combination with isotretinoin, celecoxib, and/or thalidomide for glioblastoma. ( Aldape, KD; Chang, EL; Colman, H; Conrad, CA; De Groot, JF; Fisch, MJ; Floyd, JD; Giglio, P; Gilbert, MR; Gonzalez, J; Groves, MD; Hess, KR; Hsu, SH; Lagrone, LW; Levin, VA; Loghin, ME; Mahajan, A; Penas-Prado, M; Puduvalli, VK; Salacz, ME; Volas-Redd, G; Woo, SY; Yung, WK, 2015) |
| "External beam radiation therapy (XRT) with concomitant temozolomide and 6 cycles of adjuvant temozolomide (5/28-day schedule) improves survival in patients with newly diagnosed glioblastoma compared with XRT alone." | 5.14 | A phase I factorial design study of dose-dense temozolomide alone and in combination with thalidomide, isotretinoin, and/or celecoxib as postchemoradiation adjuvant therapy for newly diagnosed glioblastoma. ( Chang, E; Colman, H; Conrad, C; de Groot, J; Giglio, P; Gilbert, MR; Gonzalez, J; Groves, MD; Hess, K; Hunter, K; Levin, V; Mahajan, A; Puduvalli, V; Woo, S; Yung, WK, 2010) |
| "We conducted a phase II study of the combination of temozolomide and angiogenesis inhibitors for treating adult patients with newly diagnosed glioblastoma." | 5.13 | Phase II study of temozolomide, thalidomide, and celecoxib for newly diagnosed glioblastoma in adults. ( Batchelor, TT; Black, PM; Ciampa, A; Doherty, L; Drappatz, J; Folkman, J; Gigas, DC; Henson, JW; Kesari, S; Kieran, M; Laforme, A; Ligon, KL; Longtine, JA; Muzikansky, A; Ramakrishna, N; Schiff, D; Weaver, S; Wen, PY, 2008) |
| "In a phase II clinical trial, we sought to determine if combining celecoxib with 13-cis-retinoic acid (13-cRA, Accutane) was efficacious in the treatment of recurrent (progressive) glioblastoma multiforme (GBM)." | 5.12 | Combination chemotherapy with 13-cis-retinoic acid and celecoxib in the treatment of glioblastoma multiforme. ( Giglio, P; Groves, MD; Hess, K; Jochec, J; Levin, VA; Puduvalli, VK; Yung, WK, 2006) |
| "Constructed from a theoretical framework, the coordinated undermining of survival paths in glioblastoma (GBM) is a combination of nine drugs approved for non-oncological indications (CUSP9; aprepitant, auranofin, captopril, celecoxib, disulfiram, itraconazole, minocycline, quetiapine, and sertraline) combined with temozolomide (TMZ)." | 3.91 | The efficacy of a coordinated pharmacological blockade in glioblastoma stem cells with nine repurposed drugs using the CUSP9 strategy. ( Grieg, Z; Langmoen, IA; Sandberg, CJ; Skaga, E; Skaga, IØ; Vik-Mo, EO, 2019) |
| " Celecoxib (CXB), a selective COX-2 inhibitor, is able to control inflammation and pain, to improve the efficacy of radiotherapy, and to inhibit at high doses the growth of cancer cells." | 3.80 | New celecoxib multiparticulate systems to improve glioblastoma treatment. ( Barcia, E; Fernández-Carballido, A; García-García, L; Marcianes, P; Negro, S; Slowing, K; Vera, M, 2014) |
| "Cells positive for CD133 were isolated from glioblastoma specimens and characterized by flow cytometry, then treated with celecoxib and/or ionizing radiation (IR)." | 3.77 | Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects. Laboratory investigation. ( Chen, YW; Chiou, SH; Huang, PI; Hueng, DY; Kao, CL; Ma, HI; Sytwu, HK; Tai, LK, 2011) |
| "Toward improved glioblastoma multiforme treatment, we determined whether celecoxib, a selective cyclooxygenase (COX)-2 inhibitor, could enhance glioblastoma radiosensitivity by inducing tumor necrosis and inhibiting tumor angiogenesis." | 3.74 | Enhancement of glioblastoma radioresponse by a selective COX-2 inhibitor celecoxib: inhibition of tumor angiogenesis with extensive tumor necrosis. ( Cheah, ES; Kang, KB; Moore, XL; Wang, TT; Wong, MC; Woon, CT; Zhu, C, 2007) |
| " Here, we report administration of celecoxib rather than dexamethasone to prevent brain edema in a patient with a cerebellar glioblastoma multiforme WHO grade IV (GBM) upon the patient's request, as well as determining cerebrospinal fluid (CSF) and serum concentrations." | 3.73 | Avoiding glucocorticoid administration in a neurooncological case. ( Bernays, RL; Gutteck-Amsler, U; Hofer, S; Meier, UR; Meier-Abt, PJ; Peghini, PE; Rentsch, K; Rutz, HP, 2005) |
| "Celecoxib (400) mg was administered orally twice a day until tumor progression or dose-limiting toxicity." | 2.73 | Effect of phenytoin on celecoxib pharmacokinetics in patients with glioblastoma. ( Batchelor, T; Desideri, S; Grossman, SA; Hammour, T; Lesser, G; Olson, J; Peereboom, D; Supko, JG; Ye, X, 2008) |
| "Celecoxib and 2,5-DMC were the most cytotoxic." | 1.62 | COXIBs and 2,5-dimethylcelecoxib counteract the hyperactivated Wnt/β-catenin pathway and COX-2/PGE2/EP4 signaling in glioblastoma cells. ( Kleszcz, R; Krajka-Kuźniak, V; Kruhlenia, N; Majchrzak-Celińska, A; Misiorek, JO; Przybyl, L; Rolle, K, 2021) |
| "Treatment with celecoxib alone promoted the membrane translocation of phosphatase and tensin homolog (PTEN), indicating PTEN activation, and consequently led to protein kinase B (AKT) dephosphorylation (inactivation)." | 1.46 | Synergistic antitumor effects of the combined treatment with an HDAC6 inhibitor and a COX-2 inhibitor through activation of PTEN. ( Gan, YH; Zhang, G, 2017) |
| "For the treatment of glioblastoma multiforme, an "anticancer drug cocktail" delivered by biodegradable poly-lactide-co-glycolide (PLGA)-microspheres is proposed." | 1.39 | A "drug cocktail" delivered by microspheres for the local treatment of rat glioblastoma. ( Allhenn, D; Béduneau, A; Lamprecht, A; Neumann, D; Pellequer, Y, 2013) |
| "Celecoxib treatment significantly down-regulated TNF-α induced NF-κB nuclear translocation, NF-κB DNA binding activity, and NF-κB-dependent reporter gene expression in U373 and T98G cells in a dose-dependent manner." | 1.38 | The nonsteroidal anti-inflammatory drug celecoxib suppresses the growth and induces apoptosis of human glioblastoma cells via the NF-κB pathway. ( Babu, PP; Geeviman, K; Ramulu, C; Sareddy, GR, 2012) |
| "Glioblastoma multiforme is the most common and most malignant primary brain tumour." | 1.36 | Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib. ( Freyschlag, CF; Nölte, I; Pechlivanis, I; Schmieder, K; Seiz, M; Tuettenberg, J; Vajkoczy, P, 2010) |
| "Celecoxib is a cyclooxygenase 2-selective nonsteroidal anti-inflammatory drug (NSAID) that exhibited therapeutic activity in cancer." | 1.35 | TRAIL-mediated apoptosis in malignant glioma cells is augmented by celecoxib through proteasomal degradation of survivin. ( Becker, MR; Ehemann, V; Gaiser, T; Habel, A; Rami, A; Reuss, DE; Siegelin, MD, 2008) |
| " We propose that this novel drug combination should receive further evaluation as a potentially effective anticancer therapy." | 1.35 | 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. ( Chen, TC; Golden, EB; Hofman, FM; Kardosh, A; Louie, SG; Petasis, NA; Pyrko, P; Schönthal, AH; Uddin, J, 2008) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 9 (30.00) | 29.6817 |
| 2010's | 17 (56.67) | 24.3611 |
| 2020's | 4 (13.33) | 2.80 |
| Authors | Studies |
|---|---|
| Yin, D | 1 |
| Jin, G | 1 |
| He, H | 1 |
| Zhou, W | 1 |
| Fan, Z | 1 |
| Gong, C | 1 |
| Zhao, J | 1 |
| Xiong, H | 1 |
| Uram, Ł | 2 |
| Misiorek, M | 2 |
| Pichla, M | 1 |
| Filipowicz-Rachwał, A | 2 |
| Markowicz, J | 2 |
| Wołowiec, S | 2 |
| Wałajtys-Rode, E | 2 |
| Kast, RE | 2 |
| Majchrzak-Celińska, A | 1 |
| Misiorek, JO | 1 |
| Kruhlenia, N | 1 |
| Przybyl, L | 1 |
| Kleszcz, R | 1 |
| Rolle, K | 1 |
| Krajka-Kuźniak, V | 1 |
| Zhang, G | 1 |
| Gan, YH | 1 |
| Skaga, E | 1 |
| Skaga, IØ | 1 |
| Grieg, Z | 1 |
| Sandberg, CJ | 1 |
| Langmoen, IA | 1 |
| Vik-Mo, EO | 1 |
| Allhenn, D | 1 |
| Neumann, D | 1 |
| Béduneau, A | 1 |
| Pellequer, Y | 1 |
| Lamprecht, A | 1 |
| Suzuki, K | 1 |
| Gerelchuluun, A | 1 |
| Hong, Z | 1 |
| Sun, L | 1 |
| Zenkoh, J | 1 |
| Moritake, T | 1 |
| Tsuboi, K | 1 |
| Sareddy, GR | 2 |
| Kesanakurti, D | 1 |
| Kirti, PB | 1 |
| Babu, PP | 2 |
| Vera, M | 1 |
| Barcia, E | 1 |
| Negro, S | 1 |
| Marcianes, P | 1 |
| García-García, L | 1 |
| Slowing, K | 1 |
| Fernández-Carballido, A | 1 |
| Karpel-Massler, G | 1 |
| Halatsch, ME | 1 |
| Penas-Prado, M | 1 |
| Hess, KR | 1 |
| Fisch, MJ | 1 |
| Lagrone, LW | 1 |
| Groves, MD | 4 |
| Levin, VA | 3 |
| De Groot, JF | 1 |
| Puduvalli, VK | 3 |
| Colman, H | 3 |
| Volas-Redd, G | 1 |
| Giglio, P | 3 |
| Conrad, CA | 2 |
| Salacz, ME | 1 |
| Floyd, JD | 1 |
| Loghin, ME | 1 |
| Hsu, SH | 2 |
| Gonzalez, J | 2 |
| Chang, EL | 1 |
| Woo, SY | 1 |
| Mahajan, A | 2 |
| Aldape, KD | 1 |
| Yung, WK | 4 |
| Gilbert, MR | 3 |
| Wong, ET | 1 |
| Lok, E | 1 |
| Swanson, KD | 1 |
| Welzel, G | 1 |
| Gehweiler, J | 1 |
| Brehmer, S | 1 |
| Appelt, JU | 1 |
| von Deimling, A | 1 |
| Seiz-Rosenhagen, M | 1 |
| Schmiedek, P | 1 |
| Wenz, F | 1 |
| Giordano, FA | 1 |
| Gaiser, T | 1 |
| Becker, MR | 1 |
| Habel, A | 1 |
| Reuss, DE | 1 |
| Ehemann, V | 1 |
| Rami, A | 1 |
| Siegelin, MD | 1 |
| Seiz, M | 1 |
| Nölte, I | 1 |
| Pechlivanis, I | 1 |
| Freyschlag, CF | 1 |
| Schmieder, K | 1 |
| Vajkoczy, P | 2 |
| Tuettenberg, J | 2 |
| Stockhammer, F | 1 |
| Misch, M | 1 |
| Koch, A | 1 |
| Czabanka, M | 1 |
| Plotkin, M | 1 |
| Blechschmidt, C | 1 |
| Walbert, T | 1 |
| Bobustuc, GC | 1 |
| Bekele, BN | 1 |
| Qiao, W | 1 |
| Hunter, K | 1 |
| Hess, K | 2 |
| Chang, E | 1 |
| Puduvalli, V | 1 |
| Conrad, C | 1 |
| Levin, V | 1 |
| Woo, S | 1 |
| de Groot, J | 1 |
| Ma, HI | 1 |
| Chiou, SH | 1 |
| Hueng, DY | 1 |
| Tai, LK | 1 |
| Huang, PI | 1 |
| Kao, CL | 1 |
| Chen, YW | 1 |
| Sytwu, HK | 1 |
| Geeviman, K | 1 |
| Ramulu, C | 1 |
| Kardosh, A | 2 |
| Blumenthal, M | 1 |
| Wang, WJ | 1 |
| Chen, TC | 2 |
| Schönthal, AH | 2 |
| Kang, KB | 2 |
| Wang, TT | 2 |
| Woon, CT | 2 |
| Cheah, ST | 1 |
| Lim, YK | 1 |
| Moore, XL | 2 |
| Wong, MC | 2 |
| Rutz, HP | 1 |
| Hofer, S | 1 |
| Peghini, PE | 1 |
| Gutteck-Amsler, U | 1 |
| Rentsch, K | 1 |
| Meier-Abt, PJ | 1 |
| Meier, UR | 1 |
| Bernays, RL | 1 |
| Jochec, J | 1 |
| Cheah, ES | 1 |
| Zhu, C | 1 |
| Golden, EB | 1 |
| Pyrko, P | 1 |
| Uddin, J | 1 |
| Hofman, FM | 1 |
| Louie, SG | 1 |
| Petasis, NA | 1 |
| Grossman, SA | 1 |
| Olson, J | 1 |
| Batchelor, T | 1 |
| Peereboom, D | 1 |
| Lesser, G | 1 |
| Desideri, S | 1 |
| Ye, X | 1 |
| Hammour, T | 1 |
| Supko, JG | 1 |
| Kesari, S | 1 |
| Schiff, D | 1 |
| Henson, JW | 1 |
| Muzikansky, A | 1 |
| Gigas, DC | 1 |
| Doherty, L | 1 |
| Batchelor, TT | 1 |
| Longtine, JA | 1 |
| Ligon, KL | 1 |
| Weaver, S | 1 |
| Laforme, A | 1 |
| Ramakrishna, N | 1 |
| Black, PM | 1 |
| Drappatz, J | 1 |
| Ciampa, A | 1 |
| Folkman, J | 1 |
| Kieran, M | 1 |
| Wen, PY | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Randomized, Factorial-Design, Phase II Trial of Temozolomide Alone and in Combination With Possible Permutations of Thalidomide, Isotretinoin and/or Celecoxib as Post-Radiation Adjuvant Therapy of Glioblastoma Multiforme[NCT00112502] | Phase 2 | 178 participants (Actual) | Interventional | 2005-09-30 | Completed | ||
| A Pharmacokinetic Study of the Interaction Between Celecoxib and Anticonvulsant Drugs in Patients With Newly Diagnosed Glioblastoma Multiforme Undergoing Radiation Therapy[NCT00068770] | Phase 2 | 35 participants (Actual) | Interventional | 2003-10-31 | Terminated (stopped due to EORTC trail showed TMZ & RT conferred significant survivial in this population) | ||
| Phase II Study Of Temozolomide, Thalidomide And Celecoxib In Patients With Newly Diagnosed Glioblastoma Multiforme In The Post-Radiation Setting[NCT00047294] | Phase 2 | 0 participants | Interventional | 2001-04-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Celecoxib versus not Celecoxib analysis: We compared the median OS outcome of participants in arms III, V, VI and VIII, versus participants in arms I, II, IV and VII. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Celecoxib: Arm III, Arm V, Arm VI and Arm VIII | 20.2 |
| No Celecoxib: Arm I, Arm II, Arm IV and Arm VII | 17.1 |
Doublet (2 agents) versus Triplet (3 agents) therapy analysis: We compared the median OS outcome of participants in arms II, III, IV, versus participants in arms V, VI and VII. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Doublet (2 Agents): Arm II, Arm III and Arm IV | 17.0 |
| Triplet (3 Agents): Arm V, Arm VI and Arm VII | 20.1 |
Isotretinoin versus not Isotretinoin analysis: We compared the median OS outcome of participants in arms IV, V, VII and VIII, versus participants in arms I, II, III and VI. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Isotretinoin: Arm IV, Arm V, Arm VII and ARM VIII | 17.1 |
| No Isotretinoin: Arm I, Arm II, Arm III and ARM VI | 19.9 |
Thalidomide versus not Thalidomide analysis: We compared the median OS outcome of participants in arms II, VI, VII and VIII, versus participants in arms I, III, IV and V. Median OS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Thalidomide: Arm II, Arm VI, Arm VII and Arm VIII | 18.3 |
| No Thalidomide: Arm I, Arm III, Arm IV and Arm V | 17.4 |
Celecoxib versus not Celecoxib analysis: We compared the median PFS outcome of participants in arms III, V, VI and VIII, versus participants in arms I, II, IV and VII. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Celecoxib: Arm III, Arm V, Arm VI and Arm VIII | 8.3 |
| No Celecoxib: Arm I, Arm II, Arm IV and Arm VII | 7.4 |
Doublet (2 agents) versus Triplet (3 agents) therapy analysis: We compared the median PFS outcome of participants in arms II, III, IV, versus participants in arms V, VI and VII. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Doublet (2 Agents): Arm II, Arm III and Arm IV | 8.3 |
| Triplet (3 Agents): Arm V, Arm VI and Arm VII | 8.2 |
Isotretinoin versus not Isotretinoin analysis: We compared the median PFS outcome of participants in arms IV, V, VII and VIII, versus participants in arms I, II, III and VI. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Isotretinoin: Arm IV, Arm V, Arm VII and Arm VIII | 6.6 |
| No Isotretinoin: Arm I, Arm II, Arm III and Arm VI | 9.1 |
Thalidomide versus not Thalidomide analysis: Comparison of median PFS outcome of participants in arms II, VI, VII and VIII, versus participants in arms I, III, IV and V. Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up, up to one year (12 study cycles).
| Intervention | months (Median) |
|---|---|
| Thalidomide: Arm II, Arm VI, Arm VII and Arm VIII | 7.6 |
| No Thalidomide: Arm I, Arm III, Arm IV and Arm V | 8.7 |
Median PFS was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 2 cycles (1 cycle = 28 days) from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Arm I: TMZ | 10.5 |
| Arm II: TMZ + Thalidomide | 7.7 |
| Arm III: TMZ + Celecoxib | 13.4 |
| Arm IV: TMZ + Isotretinoin | 6.5 |
| Arm V: TMZ + Isotretinoin + Celecoxib | 11.6 |
| Arm VI: TMZ + Thalidomide + Celecoxib | 7.9 |
| Arm VII: TMZ + Thalidomide + Isotretinoin | 6.2 |
| Arm VIII: TMZ + Thalidomide + Isotretinoin + Celecoxib | 5.8 |
Overall Survival (OS) was estimated using the Kaplan-Meier method from time of randomization to time of progression, death, or last follow-up. Progression defined as 25% increase in the sum of products of all measurable lesions over smallest sum observed (over baseline if no decrease) using the same techniques as baseline, OR clear worsening of any evaluable disease, OR appearance of any new lesion/site, OR failure to return for evaluation due to death or deteriorating condition (unless clearly unrelated to this cancer). (NCT00112502)
Timeframe: Every 3 months from randomization until progression of disease, death or last follow-up.
| Intervention | months (Median) |
|---|---|
| Arm I: TMZ | 21.2 |
| Arm II: TMZ + Thalidomide | 17.4 |
| Arm III: TMZ + Celecoxib | 18.1 |
| Arm IV: TMZ + Isotretinoin | 11.7 |
| Arm V: TMZ + Isotretinoin + Celecoxib | 23.1 |
| Arm VI: TMZ + Thalidomide + Celecoxib | 20.2 |
| Arm VII: TMZ + Thalidomide + Isotretinoin | 17.9 |
| Arm VIII: TMZ + Thalidomide + Isotretinoin + Celecoxib | 18.5 |
subjects will take one dose of celecoxib and will then have 6 hours of blood draws, day 2 subject will take 2 doses of celecoxib 8 hours apart with 2 additional blood samples, one hour apart. Subject, will continue to take 2 doses of celecoxib for 6 weeks, with a sample (PK) drawn every week prior to the first dose of the week. Comparison of Cmax of Celecoxib is reported (NCT00068770)
Timeframe: First dose of celecoxib through completion of radiation, 6 weeks.
| Intervention | (ng/ml) (Geometric Mean) |
|---|---|
| nonp450 | 1752 |
| p450 | 1813 |
duration of survival when celecoxib is administered concurrently with radiation in pts with newly diagnosed glioblastoma multiforme (NCT00068770)
Timeframe: date pt started treatment to date pt last known alive
| Intervention | months (Mean) |
|---|---|
| p450 ( +EIASD) | 11.5 |
| nonp450 (-EIASD) | 16 |
1 review available for celecoxib and Astrocytoma, Grade IV
| Article | Year |
|---|---|
Adding high-dose celecoxib to increase effectiveness of standard glioblastoma chemoirradiation.
Topics: Celecoxib; Cyclooxygenase 2; Glioblastoma; Humans; Temozolomide | 2021 |
5 trials available for celecoxib and Astrocytoma, Grade IV
| Article | Year |
|---|---|
Randomized phase II adjuvant factorial study of dose-dense temozolomide alone and in combination with isotretinoin, celecoxib, and/or thalidomide for glioblastoma.
Topics: Adolescent; Adult; Aged; Aged, 80 and over; Antineoplastic Agents, Alkylating; Brain Neoplasms; Cele | 2015 |
A phase I factorial design study of dose-dense temozolomide alone and in combination with thalidomide, isotretinoin, and/or celecoxib as postchemoradiation adjuvant therapy for newly diagnosed glioblastoma.
Topics: Adolescent; Adult; Aged; Antineoplastic Agents; Celecoxib; Chemotherapy, Adjuvant; Combined Modality | 2010 |
Combination chemotherapy with 13-cis-retinoic acid and celecoxib in the treatment of glioblastoma multiforme.
Topics: Adult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Celecoxib; Di | 2006 |
Effect of phenytoin on celecoxib pharmacokinetics in patients with glioblastoma.
Topics: Aged; Aged, 80 and over; Anticonvulsants; Antineoplastic Agents; Area Under Curve; Brain Neoplasms; | 2008 |
Phase II study of temozolomide, thalidomide, and celecoxib for newly diagnosed glioblastoma in adults.
Topics: Adult; Aged; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasm | 2008 |
24 other studies available for celecoxib and Astrocytoma, Grade IV
| Article | Year |
|---|---|
Celecoxib reverses the glioblastoma chemo-resistance to temozolomide through mitochondrial metabolism.
Topics: Celecoxib; Cell Line, Tumor; Cell Survival; Drug Resistance, Neoplasm; Drug Therapy, Combination; Gl | 2021 |
The Effect of Biotinylated PAMAM G3 Dendrimers Conjugated with COX-2 Inhibitor (celecoxib) and PPARγ Agonist (Fmoc-L-Leucine) on Human Normal Fibroblasts, Immortalized Keratinocytes and Glioma Cells in Vitro.
Topics: Antineoplastic Agents; Apoptosis; Biotinylation; Celecoxib; Cell Line, Tumor; Cell Movement; Cell Pr | 2019 |
Celecoxib substituted biotinylated poly(amidoamine) G3 dendrimer as potential treatment for temozolomide resistant glioma therapy and anti-nematode agent.
Topics: Antineoplastic Agents, Alkylating; Apoptosis; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Dendrime | 2020 |
COXIBs and 2,5-dimethylcelecoxib counteract the hyperactivated Wnt/β-catenin pathway and COX-2/PGE2/EP4 signaling in glioblastoma cells.
Topics: Aged; Antineoplastic Agents, Alkylating; Apoptosis; beta Catenin; Brain Neoplasms; Celecoxib; Cell C | 2021 |
Synergistic antitumor effects of the combined treatment with an HDAC6 inhibitor and a COX-2 inhibitor through activation of PTEN.
Topics: Anilides; Animals; Celecoxib; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Cy | 2017 |
The efficacy of a coordinated pharmacological blockade in glioblastoma stem cells with nine repurposed drugs using the CUSP9 strategy.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aprepitant; Auranofin; Brain Neoplasms; Cap | 2019 |
A "drug cocktail" delivered by microspheres for the local treatment of rat glioblastoma.
Topics: Acridines; Animals; Antineoplastic Agents, Phytogenic; Celecoxib; Cyclooxygenase 2 Inhibitors; Drug | 2013 |
Celecoxib enhances radiosensitivity of hypoxic glioblastoma cells through endoplasmic reticulum stress.
Topics: Animals; Celecoxib; Cell Hypoxia; Cell Line, Tumor; Cell Survival; Endoplasmic Reticulum Stress; Gam | 2013 |
Nonsteroidal anti-inflammatory drugs diclofenac and celecoxib attenuates Wnt/β-catenin/Tcf signaling pathway in human glioblastoma cells.
Topics: Anti-Inflammatory Agents, Non-Steroidal; beta Catenin; Celecoxib; Cell Line, Tumor; Cell Movement; C | 2013 |
New celecoxib multiparticulate systems to improve glioblastoma treatment.
Topics: Animals; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Cell Proliferation; Cyclooxygenase 2 Inhibito | 2014 |
CUSP9* treatment protocol for recurrent glioblastoma: aprepitant, artesunate, auranofin, captopril, celecoxib, disulfiram, itraconazole, ritonavir, sertraline augmenting continuous low dose temozolomide.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Aprepitant; Artemisinins; Artesunate; Auran | 2014 |
Clinical benefit in recurrent glioblastoma from adjuvant NovoTTF-100A and TCCC after temozolomide and bevacizumab failure: a preliminary observation.
Topics: Adult; Aged; Angiogenesis Inhibitors; Antimetabolites, Antineoplastic; Antineoplastic Agents, Alkyla | 2015 |
Metronomic chemotherapy with daily low-dose temozolomide and celecoxib in elderly patients with newly diagnosed glioblastoma multiforme: a retrospective analysis.
Topics: Aged; Aged, 80 and over; Antineoplastic Agents; Brain Neoplasms; Celecoxib; Chemoradiotherapy; Comor | 2015 |
TRAIL-mediated apoptosis in malignant glioma cells is augmented by celecoxib through proteasomal degradation of survivin.
Topics: Apoptosis; Celecoxib; Cell Line, Tumor; Cyclooxygenase Inhibitors; Dose-Response Relationship, Drug; | 2008 |
Far-distant metastases along the CSF pathway of glioblastoma multiforme during continuous low-dose chemotherapy with temozolomide and celecoxib.
Topics: Adult; Antineoplastic Agents; Antineoplastic Agents, Alkylating; Brain Neoplasms; Celecoxib; Central | 2010 |
Continuous low-dose temozolomide and celecoxib in recurrent glioblastoma.
Topics: Adult; Aged; Antineoplastic Agents, Alkylating; Antineoplastic Combined Chemotherapy Protocols; Brai | 2010 |
Combination of 6-thioguanine, capecitabine, and celecoxib with temozolomide or lomustine for recurrent high-grade glioma.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Capecitabine; Celecoxi | 2011 |
Celecoxib and radioresistant glioblastoma-derived CD133+ cells: improvement in radiotherapeutic effects. Laboratory investigation.
Topics: AC133 Antigen; Aged; Animals; Antigens, CD; Antineoplastic Agents; Apoptosis; Blotting, Western; Bra | 2011 |
The nonsteroidal anti-inflammatory drug celecoxib suppresses the growth and induces apoptosis of human glioblastoma cells via the NF-κB pathway.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Blotting, Western; Brain Neoplasms; Celecoxib; C | 2012 |
Differential effects of selective COX-2 inhibitors on cell cycle regulation and proliferation of glioblastoma cell lines.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Celecoxib; Cell Cycle; Cell Division; Cell Line, Tumor; Cyc | 2004 |
Celecoxib enhances brain tumour cell radiosensitivity leading to massive tumour necrosis.
Topics: Angiopoietin-1; Angiopoietin-2; Animals; Brain Neoplasms; Celecoxib; Cell Survival; Cyclooxygenase I | 2004 |
Avoiding glucocorticoid administration in a neurooncological case.
Topics: Antineoplastic Agents, Alkylating; Blood-Brain Barrier; Celecoxib; Cerebellum; Cyclooxygenase Inhibi | 2005 |
Enhancement of glioblastoma radioresponse by a selective COX-2 inhibitor celecoxib: inhibition of tumor angiogenesis with extensive tumor necrosis.
Topics: Angiopoietin-1; Angiopoietin-2; Animals; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Combined Moda | 2007 |
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.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Boronic Acids; Bortezomib; Celecoxib; Cell | 2008 |