celecoxib has been researched along with Hyperplasia in 11 studies
Hyperplasia: An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Celecoxib treatment led to decreased PGE2 and corticosterone levels, reduced proliferation and increased apoptosis of adrenocortical cells, and decreased steroidogenic gene expression." | 5.43 | Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia. ( Berthon, A; Faucz, FR; Liu, S; Martinez, A; Sahut-Barnola, I; Saloustros, E; Salpea, P; Starost, MF; Stratakis, CA; Szarek, E, 2016) |
| "Celecoxib treatment significantly decreased MCP-1 expression (P < 0." | 5.33 | Celecoxib, a selective cyclooxygenase-2 inhibitor, decreases monocyte chemoattractant protein-1 expression and neointimal hyperplasia in the rabbit atherosclerotic balloon injury model. ( Forudi, F; Keller, BT; Koki, AT; Lincoff, AM; Penn, MS; Smith, ME; Tarakji, K; Topol, EJ; Wang, K; Zhang, M; Zhou, X; Zhou, Z, 2005) |
| "Celecoxib is a potential inhibitor of neointimal formation by blocking injury-induced Akt activation." | 5.32 | Celecoxib, a cyclooxygenase-2 inhibitor, reduces neointimal hyperplasia through inhibition of Akt signaling. ( Jeon, SI; Kim, HS; Kim, SH; Lee, MM; Oh, BH; Park, KW; Park, YB; Walsh, K; Yang, HM; You, HJ; Youn, SW, 2004) |
| "Celecoxib was generally well tolerated." | 2.73 | Pilot randomized phase II study of celecoxib in oral premalignant lesions. ( Atwell, A; Boyle, JO; Dannenberg, AJ; Du, B; El-Naggar, AK; Feng, L; Helman, JI; Lee, JJ; Lippman, SM; Nathan, CO; Ondrey, FG; Papadimitrakopoulou, VA; Peterson, DE; William, WN; Yueh, B, 2008) |
| "Prostatic inflammation is the driving force in benign prostatic hyperplasia (BPH)." | 1.91 | Cyclooxygenase-2 activates EGFR-ERK1/2 pathway via PGE2-mediated ADAM-17 signaling in testosterone-induced benign prostatic hyperplasia. ( Abdel-Fattah, MM; Abo-El Fetoh, ME; Afify, H; Mohamed, WR; Ramadan, LAA, 2023) |
| "Celecoxib treatment led to decreased PGE2 and corticosterone levels, reduced proliferation and increased apoptosis of adrenocortical cells, and decreased steroidogenic gene expression." | 1.43 | Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia. ( Berthon, A; Faucz, FR; Liu, S; Martinez, A; Sahut-Barnola, I; Saloustros, E; Salpea, P; Starost, MF; Stratakis, CA; Szarek, E, 2016) |
| "In patients with ESRD who underwent parathyroidectomy, clusters of cells within the parathyroid glands had increased COX2 expression." | 1.37 | Cyclooxygenase 2 promotes parathyroid hyperplasia in ESRD. ( Chen, J; Gu, Y; Hao, CM; Li, H; Lu, Y; Qiu, J; Wang, S; Wang, X; Yang, J; Zhang, L; Zhang, Q, 2011) |
| "Celecoxib treatment significantly decreased MCP-1 expression (P < 0." | 1.33 | Celecoxib, a selective cyclooxygenase-2 inhibitor, decreases monocyte chemoattractant protein-1 expression and neointimal hyperplasia in the rabbit atherosclerotic balloon injury model. ( Forudi, F; Keller, BT; Koki, AT; Lincoff, AM; Penn, MS; Smith, ME; Tarakji, K; Topol, EJ; Wang, K; Zhang, M; Zhou, X; Zhou, Z, 2005) |
| "Esophageal and tongue cancers have both been associated with dietary zinc deficiency (ZD), and cyclooxygenase (COX-2) is often overexpressed in these cancers." | 1.33 | Dietary zinc modulation of COX-2 expression and lingual and esophageal carcinogenesis in rats. ( Farber, JL; Fong, LY; Jiang, Y; Zhang, L, 2005) |
| "Celecoxib is a potential inhibitor of neointimal formation by blocking injury-induced Akt activation." | 1.32 | Celecoxib, a cyclooxygenase-2 inhibitor, reduces neointimal hyperplasia through inhibition of Akt signaling. ( Jeon, SI; Kim, HS; Kim, SH; Lee, MM; Oh, BH; Park, KW; Park, YB; Walsh, K; Yang, HM; You, HJ; Youn, SW, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 5 (45.45) | 29.6817 |
| 2010's | 5 (45.45) | 24.3611 |
| 2020's | 1 (9.09) | 2.80 |
| Authors | Studies |
|---|---|
| Abo-El Fetoh, ME | 1 |
| Abdel-Fattah, MM | 1 |
| Mohamed, WR | 1 |
| Ramadan, LAA | 1 |
| Afify, H | 1 |
| Xu, X | 1 |
| Lan, W | 1 |
| Jin, X | 1 |
| Wang, B | 1 |
| Yan, H | 1 |
| Chen, X | 1 |
| Lai, X | 1 |
| Zhang, L | 3 |
| Zhang, X | 1 |
| Li, Z | 1 |
| Liu, S | 1 |
| Saloustros, E | 1 |
| Berthon, A | 1 |
| Starost, MF | 1 |
| Sahut-Barnola, I | 1 |
| Salpea, P | 1 |
| Szarek, E | 1 |
| Faucz, FR | 1 |
| Martinez, A | 1 |
| Stratakis, CA | 1 |
| Kusunoki, N | 1 |
| Yamazaki, R | 1 |
| Kawai, S | 1 |
| Zhang, Q | 1 |
| Qiu, J | 1 |
| Li, H | 1 |
| Lu, Y | 1 |
| Wang, X | 1 |
| Yang, J | 1 |
| Wang, S | 1 |
| Gu, Y | 1 |
| Hao, CM | 1 |
| Chen, J | 1 |
| Hebert, VY | 1 |
| Jones, BC | 1 |
| Mifflin, RC | 1 |
| Dugas, TR | 1 |
| Kang, HJ | 1 |
| Oh, IY | 1 |
| Chung, JW | 1 |
| Yang, HM | 2 |
| Suh, JW | 1 |
| Park, KW | 2 |
| Kwon, TK | 1 |
| Lee, HY | 1 |
| Cho, YS | 1 |
| Youn, TJ | 1 |
| Koo, BK | 1 |
| Kang, WY | 1 |
| Kim, W | 1 |
| Rha, SW | 1 |
| Bae, JH | 1 |
| Chae, IH | 1 |
| Choi, DJ | 1 |
| Kim, HS | 2 |
| You, HJ | 1 |
| Jeon, SI | 1 |
| Youn, SW | 1 |
| Kim, SH | 1 |
| Oh, BH | 1 |
| Lee, MM | 1 |
| Park, YB | 1 |
| Walsh, K | 1 |
| Wang, K | 1 |
| Tarakji, K | 1 |
| Zhou, Z | 1 |
| Zhang, M | 1 |
| Forudi, F | 1 |
| Zhou, X | 1 |
| Koki, AT | 1 |
| Smith, ME | 1 |
| Keller, BT | 1 |
| Topol, EJ | 1 |
| Lincoff, AM | 1 |
| Penn, MS | 1 |
| Fong, LY | 1 |
| Jiang, Y | 1 |
| Farber, JL | 1 |
| Papadimitrakopoulou, VA | 1 |
| William, WN | 1 |
| Dannenberg, AJ | 1 |
| Lippman, SM | 1 |
| Lee, JJ | 1 |
| Ondrey, FG | 1 |
| Peterson, DE | 1 |
| Feng, L | 1 |
| Atwell, A | 1 |
| El-Naggar, AK | 1 |
| Nathan, CO | 1 |
| Helman, JI | 1 |
| Du, B | 1 |
| Yueh, B | 1 |
| Boyle, JO | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| [NCT00500279] | Phase 4 | 900 participants (Anticipated) | Interventional | 2006-11-30 | Recruiting | ||
| Phase II Double-Blind, Placebo Controlled, Randomized Study Of Celecoxib, A Selective COX-2 Inhibitor, In Oral Premalignant Lesions[NCT00014404] | Phase 2 | 0 participants | Interventional | 2000-10-31 | Completed | ||
| Clinical Evaluation of Bioadhesive Gels for Oral Cancer Chemoprevention[NCT01192204] | Phase 1/Phase 2 | 41 participants (Actual) | Interventional | 2010-10-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
The remaining oral dysplasia lesion will be inspected at each follow up appointment (every 10-14 days). Biopsies will be immediately conducted on patients with any indication of malignant transformation including indurated, rolled borders, nonhealing ulcers, etc. Accordingly, these patients will withdraw from the trial. Participants will also be monitored for any changes consistent with contact mucositis e.g. soreness and erythema at application site. Clinical photographs were taken for the patients records. Pre treatment and post treatment photographs, with a ruler in place, were used for accurate pre and post treatment size measurement. NOTE: if treatment is beneficial, lesional size will decrease which will be reflected as a negative number. (NCT01192204)
Timeframe: pretreatment and posttreatment (3 months treatment duration)
| Intervention | mm^2 (Mean) |
|---|---|
| 10% FBR Gel | -26.12 |
| Placebo Gel | 18.12 |
Laboratory experiments will be conducted to assess the effects of gel treatment on pre and post loss of heterozygosity (LOH) events at loci associated with tumor suppressor genes. (NCT01192204)
Timeframe: Before and after the 3 month treatment duration
| Intervention | LOH events (Mean) |
|---|---|
| 10% FBR Gel | 0.9 |
| Placebo Gel | 0.4 |
A hemisection of lesional tissue will be conducted before the 3 month treatment to establish a diagnosis and provide a pretreatment baseline for the experimental parameters. Anl excisional biopsy of the treatment site including any remaining residual lesional tissue (excision of oral dysplastic lesions is consistent with current standards of care) will be obtained after 3 months of treatment to provide a posttreatment diagnosis. The 0 to 8 histologic scale was:0=normal with or without hyperkeratosis BEST OUTCOME, 1=atypia, 2=mild dysplasia, 3=mild-moderate dysplasia, 4=moderate dysplasia,5=moderate-severe dysplasia,6=severe dysplasia, 7=carcinoma in situ, 8=invasive oral squamous cell carcinoma (WORST OUTCOME). (NCT01192204)
Timeframe: Before and after the 3 month treatment.
| Intervention | unit on histologic grade scale (Mean) | |
|---|---|---|
| Pretreatment | Posttreatment | |
| 10% FBR Gel | 2.36 | 1.9 |
| Placebo Gel | 2.83 | 2.58 |
1 review available for celecoxib and Hyperplasia
| Article | Year |
|---|---|
Pro-apoptotic effect of nonsteroidal anti-inflammatory drugs on synovial fibroblasts.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Apoptosis; Caspase Inhibitors; Celecoxib; Cell Proliferatio | 2008 |
2 trials available for celecoxib and Hyperplasia
| Article | Year |
|---|---|
Effects of celecoxib on restenosis after coronary intervention and evolution of atherosclerosis (Mini-COREA) trial: celecoxib, a double-edged sword for patients with angina.
Topics: Angina Pectoris; Angioplasty, Balloon, Coronary; Atherosclerosis; Blood Pressure; Celecoxib; Coronar | 2012 |
Pilot randomized phase II study of celecoxib in oral premalignant lesions.
Topics: Adult; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Celecoxib; Cyclooxygenase 2 | 2008 |
Pilot randomized phase II study of celecoxib in oral premalignant lesions.
Topics: Adult; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Celecoxib; Cyclooxygenase 2 | 2008 |
Pilot randomized phase II study of celecoxib in oral premalignant lesions.
Topics: Adult; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Celecoxib; Cyclooxygenase 2 | 2008 |
Pilot randomized phase II study of celecoxib in oral premalignant lesions.
Topics: Adult; Aged; Aged, 80 and over; Anti-Inflammatory Agents, Non-Steroidal; Celecoxib; Cyclooxygenase 2 | 2008 |
8 other studies available for celecoxib and Hyperplasia
| Article | Year |
|---|---|
Cyclooxygenase-2 activates EGFR-ERK1/2 pathway via PGE2-mediated ADAM-17 signaling in testosterone-induced benign prostatic hyperplasia.
Topics: ADAM17 Protein; Animals; Celecoxib; Cyclooxygenase 2; Dinoprostone; ErbB Receptors; Hyperplasia; Inf | 2023 |
Regulated expression of PTPRJ by COX-2/PGE2 axis in endothelial cells.
Topics: Animals; Celecoxib; Cells, Cultured; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Disease Models, | 2014 |
Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia.
Topics: Adrenal Cortex; Animals; Celecoxib; Cushing Syndrome; Disease Models, Animal; Down-Regulation; Femal | 2016 |
Cyclooxygenase 2 promotes parathyroid hyperplasia in ESRD.
Topics: Adult; Animals; Celecoxib; Cell Proliferation; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Diseas | 2011 |
Role of COX-2 in the bioactivation of methylenedianiline and in its proliferative effects in vascular smooth muscle cells.
Topics: Aniline Compounds; Animals; Biotransformation; Carcinogens; Celecoxib; Cell Proliferation; Cells, Cu | 2011 |
Celecoxib, a cyclooxygenase-2 inhibitor, reduces neointimal hyperplasia through inhibition of Akt signaling.
Topics: Animals; Apoptosis; Arterial Occlusive Diseases; Celecoxib; Cell Proliferation; Cell Survival; Cyclo | 2004 |
Celecoxib, a selective cyclooxygenase-2 inhibitor, decreases monocyte chemoattractant protein-1 expression and neointimal hyperplasia in the rabbit atherosclerotic balloon injury model.
Topics: Angioplasty, Balloon; Animals; Arteriosclerosis; Celecoxib; Chemokine CCL2; Cyclooxygenase 1; Cycloo | 2005 |
Dietary zinc modulation of COX-2 expression and lingual and esophageal carcinogenesis in rats.
Topics: 4-Nitroquinoline-1-oxide; Animals; Apoptosis; Blotting, Western; Carcinogens; Carcinoma, Squamous Ce | 2005 |