celecoxib has been researched along with Brain Neoplasms in 50 studies
Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
| 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) |
| "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) |
| "The combination of TMZ and celecoxib is safe and potentially effective in the treatment of metastatic melanoma." | 9.12 | Temozolomide in combination with celecoxib in patients with advanced melanoma. A phase II study of the Hellenic Cooperative Oncology Group. ( Fountzilas, G; Frangia, K; Gogas, H; Mantzourani, M; Markopoulos, C; Middleton, M; Panagiotou, P; Papadopoulos, O; Pectasides, D; Polyzos, A; Stavrinidis, I; Tsoutsos, D; Vaiopoulos, G, 2006) |
| "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) |
| "In the current study, the authors report a Phase II trial of irinotecan (CPT-11), a topoisomerase I inhibitor active against malignant glioma (MG), with celecoxib, a selective COX-2 inhibitor, among MG patients with recurrent disease." | 9.11 | Phase II trial of irinotecan plus celecoxib in adults with recurrent malignant glioma. ( Badruddoja, M; Dowell, JM; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Quinn, JA; Reardon, DA; Rich, JN; Vredenburgh, J, 2005) |
| " 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) |
| "Our findings suggest that celecoxib may not be effective on meningioma growth in clinical settings." | 7.79 | Effect of systemic celecoxib on human meningioma after intracranial transplantation into nude mice. ( Friedrich, S; Grote, M; Krauss, JK; Nakamura, M; Schwabe, K, 2013) |
| "This study reports evidence for new targets and synergistic effect of celecoxib/fluvastatin combination in pilocytic astrocytoma." | 7.79 | Evidence for new targets and synergistic effect of metronomic celecoxib/fluvastatin combination in pilocytic astrocytoma. ( André, N; Baeza-Kallee, N; Carré, M; Chappé, C; Colin, C; Fernandez, C; Figarella-Branger, D; Lambert, S; Mercurio, S; Padovani, L; Scavarda, D; Tchoghandjian, A, 2013) |
| "Celecoxib combined with radiation plays a critical role in the suppression of growth of CD133(+) glioblastoma stemlike cells." | 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) |
| "The purpose of this study was to determine whether a combination treatment of temozolomide with celecoxib is effective in the rat orthotopic glioma model." | 7.73 | Combination celecoxib and temozolomide in C6 rat glioma orthotopic model. ( Groves, MD; Kang, SG; Kim, JS; Nam, DH; Park, K, 2006) |
| " To determine whether oral administration of a COX-2-specific inhibitor can inhibit glial tumors, we analyzed the effect of celecoxib on the growth of 9L rat gliosarcoma cells that were orthotopically transplanted into rat brains." | 7.72 | Intracranial inhibition of glioma cell growth by cyclooxygenase-2 inhibitor celecoxib. ( Eoh, W; Hong, SC; Im, YH; Kim, JH; Kim, MH; Lee, S; McDonnell, TJ; Nam, DH; Park, C; Park, K; Shin, HJ, 2004) |
| "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 was never discontinued for toxicity." | 6.73 | Impact of celecoxib on capecitabine tolerability and activity in pretreated metastatic breast cancer: results of a phase II study with biomarker evaluation. ( Carlini, P; Cognetti, F; Fabi, A; Ferretti, G; Gelibter, A; Melucci, E; Metro, G; Milella, M; Mottolese, M; Papaldo, P; Russillo, M; Sperduti, I; Tomao, S, 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 has been utilized with success in the treatment of several types of cancer, including gliomas." | 5.42 | Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine. ( Winfield, LL; Yerokun, T, 2015) |
| "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) |
| "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) |
| "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) |
| "The combination of TMZ and celecoxib is safe and potentially effective in the treatment of metastatic melanoma." | 5.12 | Temozolomide in combination with celecoxib in patients with advanced melanoma. A phase II study of the Hellenic Cooperative Oncology Group. ( Fountzilas, G; Frangia, K; Gogas, H; Mantzourani, M; Markopoulos, C; Middleton, M; Panagiotou, P; Papadopoulos, O; Pectasides, D; Polyzos, A; Stavrinidis, I; Tsoutsos, D; Vaiopoulos, G, 2006) |
| "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) |
| "In the current study, the authors report a Phase II trial of irinotecan (CPT-11), a topoisomerase I inhibitor active against malignant glioma (MG), with celecoxib, a selective COX-2 inhibitor, among MG patients with recurrent disease." | 5.11 | Phase II trial of irinotecan plus celecoxib in adults with recurrent malignant glioma. ( Badruddoja, M; Dowell, JM; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Quinn, JA; Reardon, DA; Rich, JN; Vredenburgh, J, 2005) |
| "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) |
| "Our findings suggest that celecoxib may not be effective on meningioma growth in clinical settings." | 3.79 | Effect of systemic celecoxib on human meningioma after intracranial transplantation into nude mice. ( Friedrich, S; Grote, M; Krauss, JK; Nakamura, M; Schwabe, K, 2013) |
| "This study reports evidence for new targets and synergistic effect of celecoxib/fluvastatin combination in pilocytic astrocytoma." | 3.79 | Evidence for new targets and synergistic effect of metronomic celecoxib/fluvastatin combination in pilocytic astrocytoma. ( André, N; Baeza-Kallee, N; Carré, M; Chappé, C; Colin, C; Fernandez, C; Figarella-Branger, D; Lambert, S; Mercurio, S; Padovani, L; Scavarda, D; Tchoghandjian, A, 2013) |
| "Celecoxib combined with radiation plays a critical role in the suppression of growth of CD133(+) glioblastoma stemlike cells." | 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) |
| "The purpose of this study was to determine whether a combination treatment of temozolomide with celecoxib is effective in the rat orthotopic glioma model." | 3.73 | Combination celecoxib and temozolomide in C6 rat glioma orthotopic model. ( Groves, MD; Kang, SG; Kim, JS; Nam, DH; Park, K, 2006) |
| " To determine whether oral administration of a COX-2-specific inhibitor can inhibit glial tumors, we analyzed the effect of celecoxib on the growth of 9L rat gliosarcoma cells that were orthotopically transplanted into rat brains." | 3.72 | Intracranial inhibition of glioma cell growth by cyclooxygenase-2 inhibitor celecoxib. ( Eoh, W; Hong, SC; Im, YH; Kim, JH; Kim, MH; Lee, S; McDonnell, TJ; Nam, DH; Park, C; Park, K; Shin, HJ, 2004) |
| "Diagnoses included solid tumors (Ewing sarcoma, osteosarcoma, malignant peripheral nerve sheath tumor, rhabdoid tumor, retinoblastoma) and brain tumors (glioblastoma multiforme [GBM], diffuse intrinsic pontine glioma, high-grade glioma [HGG], medulloblastoma, ependymoma, anaplastic astrocytoma, low-grade infiltrative astrocytoma, primitive neuroectodermal tumor, nongerminomatous germ cell tumor]." | 2.94 | A phase I study of sirolimus in combination with metronomic therapy (CHOAnome) in children with recurrent or refractory solid and brain tumors. ( Cash, T; Goldsmith, KC; Katzenstein, HM; Kean, L; MacDonald, TJ; Qayed, M; Suessmuth, Y; Tanos, R; Tighiouart, M; Watkins, B; Wetmore, C, 2020) |
| "Celecoxib was never discontinued for toxicity." | 2.73 | Impact of celecoxib on capecitabine tolerability and activity in pretreated metastatic breast cancer: results of a phase II study with biomarker evaluation. ( Carlini, P; Cognetti, F; Fabi, A; Ferretti, G; Gelibter, A; Melucci, E; Metro, G; Milella, M; Mottolese, M; Papaldo, P; Russillo, M; Sperduti, I; Tomao, S, 2008) |
| "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 was administered at 400 mg/day during the entire course of radiotherapy." | 2.71 | Phase I/II study of selective cyclooxygenase-2 inhibitor celecoxib as a radiation sensitizer in patients with unresectable brain metastases. ( Bonomi, MR; Cabalar, ME; Castro, MA; Cerchietti, LC; Navigante, AH; Roth, BM, 2005) |
| "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) |
| "Celecoxib has been utilized with success in the treatment of several types of cancer, including gliomas." | 1.42 | Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine. ( Winfield, LL; Yerokun, T, 2015) |
| "Breast cancer is among the most common malignancies that metastasize to the brain, with 15% to 20% of patients with metastatic breast cancer eventually developing brain metastases." | 1.40 | COX-2 drives metastatic breast cells from brain lesions into the cerebrospinal fluid and systemic circulation. ( Allen, JE; Dicker, DT; El-Deiry, WS; Glantz, MJ; Patel, AS; Prabhu, VV; Sheehan, JM, 2014) |
| "Celecoxib and anti-Gr1 treatment may be useful for blockade of these processes, thereby preventing brain metastasis in patients with breast cancer." | 1.39 | Premetastatic soil and prevention of breast cancer brain metastasis. ( Fellows-Mayle, W; Ikeura, M; Kohanbash, G; Kosaka, A; Liu, Y; Okada, H; Snyder, LA, 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) |
| "Medulloblastomas are the most common malignant brain tumors in children." | 1.37 | Detection of human cytomegalovirus in medulloblastomas reveals a potential therapeutic target. ( Baryawno, N; Darabi, A; FuskevÅg, OM; Johnsen, JI; Khan, Z; Kogner, P; Nordenskjöld, M; Odeberg, J; Rahbar, A; Segerström, L; Siesjö, P; Söderberg-Nauclér, C; Sveinbjörnsson, B; Taher, C; Wolmer-Solberg, N, 2011) |
| "Celecoxib was incorporated into poly DL-lactide-co-glycolide (PLGA) nanoparticles for antitumor drug delivery." | 1.37 | Preparation of polylactide-co-glycolide nanoparticles incorporating celecoxib and their antitumor activity against brain tumor cells. ( Jeong, YI; Jin, SG; Jung, S; Jung, TY; Kang, SS; Kim, IY; Kim, TH; Moon, KS; Pei, J, 2011) |
| "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) |
| "Chemotherapy for the treatment of brain metastases arising from non-small cell lung cancer (NSCLC) has been limited by poor efficacy and high toxicity." | 1.33 | [A case report of chemotherapy with thalidomide, celecoxib and gemcitabine in the treatment of patients with brain metastases from lung cancer]. ( Hada, M; Horiuchi, T, 2005) |
| "Celecoxib was more potent than rofecoxib in suppressing cell growth." | 1.31 | Overexpression of cyclooxygenase-2 (COX-2) in human primitive neuroectodermal tumors: effect of celecoxib and rofecoxib. ( Gumired, K; Patti, R; Phillips, PC; Reddanna, P; Reddy, CD; Sutton, LN, 2002) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 17 (34.00) | 29.6817 |
| 2010's | 29 (58.00) | 24.3611 |
| 2020's | 4 (8.00) | 2.80 |
| Authors | Studies |
|---|---|
| Qayed, M | 1 |
| Cash, T | 1 |
| Tighiouart, M | 1 |
| MacDonald, TJ | 1 |
| Goldsmith, KC | 1 |
| Tanos, R | 1 |
| Kean, L | 1 |
| Watkins, B | 1 |
| Suessmuth, Y | 1 |
| Wetmore, C | 1 |
| Katzenstein, HM | 1 |
| Tang, B | 1 |
| Guo, ZS | 1 |
| Bartlett, DL | 1 |
| Yan, DZ | 1 |
| Schane, CP | 1 |
| Thomas, DL | 1 |
| Liu, J | 1 |
| McFadden, G | 1 |
| Shisler, JL | 1 |
| Roy, EJ | 1 |
| Uram, Ł | 1 |
| Markowicz, J | 1 |
| Misiorek, M | 1 |
| Filipowicz-Rachwał, A | 1 |
| Wołowiec, S | 1 |
| Wałajtys-Rode, E | 1 |
| Majchrzak-Celińska, A | 1 |
| Misiorek, JO | 1 |
| Kruhlenia, N | 1 |
| Przybyl, L | 1 |
| Kleszcz, R | 1 |
| Rolle, K | 1 |
| Krajka-Kuźniak, V | 1 |
| Skaga, E | 1 |
| Skaga, IØ | 1 |
| Grieg, Z | 1 |
| Sandberg, CJ | 1 |
| Langmoen, IA | 1 |
| Vik-Mo, EO | 1 |
| Liu, Y | 1 |
| Kosaka, A | 1 |
| Ikeura, M | 1 |
| Kohanbash, G | 1 |
| Fellows-Mayle, W | 1 |
| Snyder, LA | 1 |
| Okada, H | 1 |
| Mercurio, S | 1 |
| Padovani, L | 2 |
| Colin, C | 1 |
| Carré, M | 1 |
| Tchoghandjian, A | 1 |
| Scavarda, D | 2 |
| Lambert, S | 1 |
| Baeza-Kallee, N | 1 |
| Fernandez, C | 1 |
| Chappé, C | 1 |
| André, N | 2 |
| Figarella-Branger, D | 1 |
| Zhang, H | 1 |
| Tian, M | 1 |
| Xiu, C | 1 |
| Wang, Y | 1 |
| Tang, G | 1 |
| Hauser, P | 1 |
| Vancsó, I | 1 |
| Pócza, T | 1 |
| Schuler, D | 1 |
| Garami, M | 1 |
| Allen, JE | 1 |
| Patel, AS | 1 |
| Prabhu, VV | 1 |
| Dicker, DT | 1 |
| Sheehan, JM | 1 |
| Glantz, MJ | 1 |
| El-Deiry, WS | 1 |
| Vera, M | 1 |
| Barcia, E | 1 |
| Negro, S | 1 |
| Marcianes, P | 1 |
| García-García, L | 1 |
| Slowing, K | 1 |
| Fernández-Carballido, A | 1 |
| Kast, RE | 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 | 2 |
| Volas-Redd, G | 1 |
| Giglio, P | 2 |
| Conrad, CA | 2 |
| Salacz, ME | 1 |
| Floyd, JD | 1 |
| Loghin, ME | 1 |
| Hsu, SH | 2 |
| Gonzalez, J | 1 |
| Chang, EL | 1 |
| Woo, SY | 1 |
| Mahajan, A | 1 |
| Aldape, KD | 1 |
| Yung, WK | 3 |
| Gilbert, MR | 2 |
| 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 |
| Wickström, M | 1 |
| Dyberg, C | 1 |
| Milosevic, J | 1 |
| Einvik, C | 1 |
| Calero, R | 1 |
| Sveinbjörnsson, B | 2 |
| Sandén, E | 1 |
| Darabi, A | 2 |
| Siesjö, P | 2 |
| Kool, M | 1 |
| Kogner, P | 2 |
| Baryawno, N | 2 |
| Johnsen, JI | 2 |
| Yerokun, T | 1 |
| Winfield, LL | 1 |
| Ju, RJ | 1 |
| Zeng, F | 1 |
| Liu, L | 1 |
| Mu, LM | 1 |
| Xie, HJ | 1 |
| Zhao, Y | 1 |
| Yan, Y | 1 |
| Wu, JS | 1 |
| Hu, YJ | 1 |
| Lu, WL | 1 |
| Sagara, A | 1 |
| Igarashi, K | 1 |
| Otsuka, M | 1 |
| Karasawa, T | 1 |
| Gotoh, N | 1 |
| Narita, M | 2 |
| Kuzumaki, N | 1 |
| Kato, Y | 1 |
| Sato, A | 1 |
| Mizobuchi, Y | 1 |
| Nakajima, K | 1 |
| Shono, K | 1 |
| Fujihara, T | 1 |
| Kageji, T | 1 |
| Kitazato, K | 1 |
| Matsuzaki, K | 1 |
| Mure, H | 1 |
| Kuwayama, K | 1 |
| Sumi, A | 1 |
| Saya, H | 1 |
| Sampetrean, O | 1 |
| Nagahirao, S | 1 |
| Becker, MR | 1 |
| Gaiser, T | 1 |
| Rome, A | 1 |
| Gentet, JC | 1 |
| De Paula, AM | 1 |
| Pasquier, E | 1 |
| Kim, CK | 1 |
| Joe, YA | 1 |
| Lee, SK | 1 |
| Kim, EK | 1 |
| O, E | 1 |
| Kim, HK | 1 |
| Oh, BJ | 1 |
| Hong, SH | 1 |
| Hong, YK | 1 |
| Zhou, R | 1 |
| Zhang, LZ | 1 |
| Wang, RZ | 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 |
| Chlapek, P | 1 |
| Redova, M | 1 |
| Zitterbart, K | 1 |
| Hermanova, M | 1 |
| Sterba, J | 1 |
| Veselska, R | 1 |
| Walbert, T | 1 |
| Bobustuc, GC | 1 |
| Bekele, BN | 1 |
| Qiao, W | 1 |
| Nakano, I | 1 |
| Chiocca, EA | 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 |
| Sareddy, GR | 1 |
| Geeviman, K | 1 |
| Ramulu, C | 1 |
| Babu, PP | 1 |
| Rahbar, A | 1 |
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| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Sirolimus in Combination With Metronomic Therapy in Children With Recurrent and Refractory Solid Tumors: A Phase I Study[NCT01331135] | Phase 1 | 18 participants (Actual) | Interventional | 2011-04-30 | Completed | ||
| 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 | ||
| Oral L-arginine Supplementation in Patients With Non-resectable Brain Metastases Treated With Radiation Therapy With Palliative Intent[NCT02844387] | Phase 1/Phase 2 | 70 participants (Actual) | Interventional | 2004-05-31 | 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 |
10 trials available for celecoxib and Brain Neoplasms
| Article | Year |
|---|---|
A phase I study of sirolimus in combination with metronomic therapy (CHOAnome) in children with recurrent or refractory solid and brain tumors.
Topics: Administration, Metronomic; Adolescent; Antineoplastic Combined Chemotherapy Protocols; Brain Neopla | 2020 |
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 |
Phase II trial of irinotecan plus celecoxib in adults with recurrent malignant glioma.
Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Biological Availability; Brain Neoplasm | 2005 |
Phase I/II study of selective cyclooxygenase-2 inhibitor celecoxib as a radiation sensitizer in patients with unresectable brain metastases.
Topics: Adult; Aged; Brain Neoplasms; Breast Neoplasms; Celecoxib; Combined Modality Therapy; Cyclooxygenase | 2005 |
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 |
Temozolomide in combination with celecoxib in patients with advanced melanoma. A phase II study of the Hellenic Cooperative Oncology Group.
Topics: Antineoplastic Agents, Alkylating; Brain Neoplasms; Celecoxib; Cyclooxygenase 2; Cyclooxygenase Inhi | 2006 |
Phase II study of metronomic chemotherapy for recurrent malignant gliomas in adults.
Topics: Adult; Aged; Angiogenesis Inhibitors; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasm | 2007 |
Impact of celecoxib on capecitabine tolerability and activity in pretreated metastatic breast cancer: results of a phase II study with biomarker evaluation.
Topics: Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Bone Neoplasms; Brain Neoplasms; Br | 2008 |
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 |
40 other studies available for celecoxib and Brain Neoplasms
| Article | Year |
|---|---|
Synergistic Combination of Oncolytic Virotherapy and Immunotherapy for Glioma.
Topics: Animals; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Combined Modality Therapy; Cyclooxygenase 2 I | 2020 |
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 |
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 |
Premetastatic soil and prevention of breast cancer brain metastasis.
Topics: Adenocarcinoma; Animals; Apoptosis; Blotting, Western; Brain Neoplasms; Calgranulin B; CD11b Antigen | 2013 |
Evidence for new targets and synergistic effect of metronomic celecoxib/fluvastatin combination in pilocytic astrocytoma.
Topics: Antineoplastic Combined Chemotherapy Protocols; Astrocytoma; Brain Neoplasms; CD36 Antigens; Celecox | 2013 |
Enhancement of antitumor activity by combination of tumor lysate-pulsed dendritic cells and celecoxib in a rat glioma model.
Topics: Animals; Antineoplastic Agents; Apoptosis; Brain Neoplasms; Cancer Vaccines; Celecoxib; Cell Line, T | 2013 |
[Antiangiogenic treatment of pediatric CNS tumors in Hungary with the Kieran schedule].
Topics: Administration, Oral; Adolescent; Adult; Angiogenesis Inhibitors; Antineoplastic Combined Chemothera | 2013 |
COX-2 drives metastatic breast cells from brain lesions into the cerebrospinal fluid and systemic circulation.
Topics: Animals; Antineoplastic Agents; Brain Neoplasms; Breast Neoplasms; Celecoxib; Cell Line, Tumor; Cycl | 2014 |
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 |
Wnt/β-catenin pathway regulates MGMT gene expression in cancer and inhibition of Wnt signalling prevents chemoresistance.
Topics: Animals; Antineoplastic Agents; Benzeneacetamides; beta Catenin; Brain Neoplasms; Camptothecin; Cele | 2015 |
Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzimidazoles; Brain Neoplasms; Celecoxib; Cell Lin | 2015 |
Destruction of vasculogenic mimicry channels by targeting epirubicin plus celecoxib liposomes in treatment of brain glioma.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Blood-Brain Barrier; Brain Neopl | 2016 |
Intrinsic Resistance to 5-Fluorouracil in a Brain Metastatic Variant of Human Breast Cancer Cell Line, MDA-MB-231BR.
Topics: Aniline Compounds; Brain Neoplasms; Breast Neoplasms; Celecoxib; Cell Line, Tumor; Cell Survival; Cy | 2016 |
Blocking COX-2 induces apoptosis and inhibits cell proliferation via the Akt/survivin- and Akt/ID3 pathway in low-grade-glioma.
Topics: Animals; Apoptosis; Brain; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Cell Proliferation; Cycloox | 2017 |
Impressive regression of visceral and cerebral melanoma metastases under combination treatment including dacarbacine, radiotherapy and celecoxib.
Topics: Adolescent; Antineoplastic Agents, Alkylating; Brain Neoplasms; Celecoxib; Combined Modality Therapy | 2009 |
Metronomic chemotherapy-induced bilateral subdural hematoma in a child with meningeal carcinomatosis.
Topics: Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Celecoxib; Child; Cyclooxygenase 2 | 2009 |
Enhancement of anti-tumor activity by low-dose combination of the recombinant urokinase kringle domain and celecoxib in a glioma model.
Topics: Angiogenesis Inhibitors; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Brain N | 2010 |
Effect of celecoxib on proliferation, apoptosis, and survivin expression in human glioma cell line U251.
Topics: Apoptosis; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Cell Proliferation; Cyclooxygenase Inhibito | 2010 |
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 |
Enhancement of ATRA-induced differentiation of neuroblastoma cells with LOX/COX inhibitors: an expression profiling study.
Topics: Brain Neoplasms; Caffeic Acids; Celecoxib; Cell Differentiation; Cyclooxygenase Inhibitors; Enzyme I | 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 |
Finding drugs against CD133+ glioma subpopulations.
Topics: AC133 Antigen; Antigens, CD; Antineoplastic Agents; Brain Neoplasms; Celecoxib; Combined Modality Th | 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 |
Detection of human cytomegalovirus in medulloblastomas reveals a potential therapeutic target.
Topics: Adult; Animals; Antiviral Agents; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Child; Child, Presch | 2011 |
Preparation of polylactide-co-glycolide nanoparticles incorporating celecoxib and their antitumor activity against brain tumor cells.
Topics: Acetone; Animals; Antineoplastic Agents; Brain Neoplasms; Celecoxib; Cell Line, Tumor; Cell Movement | 2011 |
OSU-03012 interacts with lapatinib to kill brain cancer cells.
Topics: Apoptosis; Apoptosis Regulatory Proteins; Autophagy-Related Protein 5; Beclin-1; Benzoquinones; Brai | 2012 |
Effect of systemic celecoxib on human meningioma after intracranial transplantation into nude mice.
Topics: Aged; Aged, 80 and over; Animals; Brain Neoplasms; Celecoxib; Cell Culture Techniques; Cell Survival | 2013 |
Intracranial inhibition of glioma cell growth by cyclooxygenase-2 inhibitor celecoxib.
Topics: Animals; Antineoplastic Agents; Apoptosis; Brain; Brain Neoplasms; Celecoxib; Cell Division; Cycloox | 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 |
[A case report of chemotherapy with thalidomide, celecoxib and gemcitabine in the treatment of patients with brain metastases from lung cancer].
Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Carcinoma, Non-Small-Cell Lu | 2005 |
R(+)-methanandamide elicits a cyclooxygenase-2-dependent mitochondrial apoptosis signaling pathway in human neuroglioma cells.
Topics: Animals; Apoptosis; Arachidonic Acids; Blotting, Western; Brain Neoplasms; Caspase 3; Caspase 9; Cas | 2006 |
Combination celecoxib and temozolomide in C6 rat glioma orthotopic model.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Celecoxib; Cyclooxygenase | 2006 |
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 |
Overexpression of cyclooxygenase-2 (COX-2) in human primitive neuroectodermal tumors: effect of celecoxib and rofecoxib.
Topics: Antineoplastic Agents; Apoptosis; Blotting, Western; Brain; Brain Neoplasms; Caspase 3; Caspases; Ce | 2002 |