celecoxib has been researched along with Cell Transformation, Neoplastic in 23 studies
Cell Transformation, Neoplastic: Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Celecoxib selectively affects genes and pathways involved in inflammation and malignant transformation in tumor but not normal tissues, this may assist in the development of safer and more effective chemopreventive agents." | 7.77 | Gene expression following exposure to celecoxib in humans: pathways of inflammation and carcinogenesis are activated in tumors but not normal tissues. ( Arber, N; Domany, E; Kazanov, D; Kraus, S; Naumov, I; Sagiv, E; Shapira, S; Sheffer, M, 2011) |
| "The expression of the putative markers LGR-5 (leucine-rich-repeat-containing G-protein-coupled receptor 5), MSI-1 (Musashi-1) and DCAMKL-1 (doublecortin and calcium/calmodulin-dependent protein kinase-like-1) was studied in normal colon mucosa (NM), in the precancerous lesions Mucin Depleted Foci (MDF) and in macroscopic tumours (adenomas) of 1,2-dimethylhydrazine-treated rats." | 3.79 | Expression of LGR-5, MSI-1 and DCAMKL-1, putative stem cell markers, in the early phases of 1,2-dimethylhydrazine-induced rat colon carcinogenesis: correlation with nuclear β-catenin. ( Caderni, G; Dolara, P; Femia, AP; Salvadori, M, 2013) |
| "Celecoxib selectively affects genes and pathways involved in inflammation and malignant transformation in tumor but not normal tissues, this may assist in the development of safer and more effective chemopreventive agents." | 3.77 | Gene expression following exposure to celecoxib in humans: pathways of inflammation and carcinogenesis are activated in tumors but not normal tissues. ( Arber, N; Domany, E; Kazanov, D; Kraus, S; Naumov, I; Sagiv, E; Shapira, S; Sheffer, M, 2011) |
| "The low survival rate of patients with pancreatic cancer points towards an increased need for novel therapeutic and chemopreventive strategies and also early detection of this disease." | 2.46 | Chemoprevention strategies for pancreatic cancer. ( Brand, RE; Singh, SV; Stan, SD, 2010) |
| " We demonstrate that a reduction of cyclooxygenase 2 gene dosage rescued the ovarian aging phenotype of the Wv mice, whereas homozygous deletion was accompanied by a compensatory increase in ovarian cyclooxygenase 1 expression and prostaglandin E(2) synthesis." | 1.34 | A reduction of cyclooxygenase 2 gene dosage counters the ovarian morphological aging and tumor phenotype in Wv mice. ( Cai, KQ; Hamilton, TC; Klein-Szanto, A; Smedberg, JL; Smith, ER; Xu, XX; Yang, WL, 2007) |
| "Celecoxib is a newly developed cyclo-oxygenase (COX)-2 inhibitor with significantly less toxicity." | 1.31 | Antiangiogenic and chemopreventive activities of celecoxib in oral carcinoma cell. ( Fuentes, CF; Shapshay, SM; Wang, Z, 2002) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (4.35) | 18.2507 |
| 2000's | 8 (34.78) | 29.6817 |
| 2010's | 14 (60.87) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Jain, S | 1 |
| Ghanghas, P | 1 |
| Rana, C | 1 |
| Sanyal, SN | 1 |
| Zheng, Y | 1 |
| Comaills, V | 1 |
| Burr, R | 1 |
| Boulay, G | 1 |
| Miyamoto, DT | 1 |
| Wittner, BS | 1 |
| Emmons, E | 1 |
| Sil, S | 1 |
| Koulopoulos, MW | 1 |
| Broderick, KT | 1 |
| Tai, E | 1 |
| Rengarajan, S | 1 |
| Kulkarni, AS | 1 |
| Shioda, T | 1 |
| Wu, CL | 1 |
| Ramaswamy, S | 1 |
| Ting, DT | 1 |
| Toner, M | 1 |
| Rivera, MN | 1 |
| Maheswaran, S | 1 |
| Haber, DA | 1 |
| Xu, K | 1 |
| Wang, L | 1 |
| Shu, HK | 1 |
| Park, GB | 1 |
| Hur, DY | 1 |
| Kim, D | 1 |
| Xu, HB | 1 |
| Shen, FM | 1 |
| Lv, QZ | 1 |
| Evageliou, NF | 1 |
| Haber, M | 1 |
| Vu, A | 1 |
| Laetsch, TW | 1 |
| Murray, J | 1 |
| Gamble, LD | 1 |
| Cheng, NC | 1 |
| Liu, K | 1 |
| Reese, M | 1 |
| Corrigan, KA | 1 |
| Ziegler, DS | 1 |
| Webber, H | 1 |
| Hayes, CS | 1 |
| Pawel, B | 1 |
| Marshall, GM | 1 |
| Zhao, H | 1 |
| Gilmour, SK | 1 |
| Norris, MD | 1 |
| Hogarty, MD | 1 |
| Colby, JK | 1 |
| Klein, RD | 1 |
| McArthur, MJ | 1 |
| Conti, CJ | 1 |
| Kiguchi, K | 1 |
| Kawamoto, T | 1 |
| Riggs, PK | 1 |
| Pavone, AI | 1 |
| Sawicki, J | 1 |
| Fischer, SM | 1 |
| Brown, PH | 1 |
| Subbaramaiah, K | 1 |
| Salmon, AP | 1 |
| Baker, R | 1 |
| Newman, RA | 1 |
| Yang, P | 1 |
| Zhou, XK | 1 |
| Bissonnette, RP | 1 |
| Dannenberg, AJ | 1 |
| Howe, LR | 1 |
| Stan, SD | 1 |
| Singh, SV | 1 |
| Brand, RE | 1 |
| Carothers, AM | 1 |
| Davids, JS | 1 |
| Damas, BC | 1 |
| Bertagnolli, MM | 1 |
| Ferrario, A | 1 |
| Gomer, CJ | 1 |
| Oshima, H | 1 |
| Hioki, K | 1 |
| Popivanova, BK | 1 |
| Oguma, K | 1 |
| Van Rooijen, N | 1 |
| Ishikawa, TO | 1 |
| Oshima, M | 1 |
| Elmets, CA | 1 |
| Viner, JL | 1 |
| Pentland, AP | 1 |
| Cantrell, W | 1 |
| Lin, HY | 1 |
| Bailey, H | 1 |
| Kang, S | 1 |
| Linden, KG | 1 |
| Heffernan, M | 1 |
| Duvic, M | 1 |
| Richmond, E | 1 |
| Elewski, BE | 1 |
| Umar, A | 1 |
| Bell, W | 1 |
| Gordon, GB | 1 |
| Sagiv, E | 1 |
| Sheffer, M | 1 |
| Kazanov, D | 1 |
| Shapira, S | 1 |
| Naumov, I | 1 |
| Kraus, S | 1 |
| Domany, E | 1 |
| Arber, N | 1 |
| Konger, RL | 1 |
| Xu, Z | 1 |
| Sahu, RP | 1 |
| Rashid, BM | 1 |
| Mehta, SR | 1 |
| Mohamed, DR | 1 |
| DaSilva-Arnold, SC | 1 |
| Bradish, JR | 1 |
| Warren, SJ | 1 |
| Kim, YL | 1 |
| Femia, AP | 1 |
| Dolara, P | 1 |
| Salvadori, M | 1 |
| Caderni, G | 1 |
| Wang, Z | 1 |
| Fuentes, CF | 1 |
| Shapshay, SM | 1 |
| Zielinski, SL | 1 |
| Li, N | 1 |
| Sood, S | 1 |
| Wang, S | 1 |
| Fang, M | 1 |
| Wang, P | 1 |
| Sun, Z | 1 |
| Yang, CS | 1 |
| Chen, X | 1 |
| Mernitz, H | 1 |
| Smith, DE | 1 |
| Zhu, AX | 1 |
| Wang, XD | 1 |
| Yang, WL | 1 |
| Cai, KQ | 1 |
| Smedberg, JL | 1 |
| Smith, ER | 1 |
| Klein-Szanto, A | 1 |
| Hamilton, TC | 1 |
| Xu, XX | 1 |
| Ziegler, J | 1 |
| Kawamori, T | 1 |
| Wakabayashi, K | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase II/III Randomized, Double-Blind, Placebo-Controlled Clinical Trial Of Celecoxib In Subjects With Actinic Keratoses[NCT00027976] | Phase 2/Phase 3 | 0 participants (Actual) | Interventional | 2001-12-31 | Withdrawn | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
1 review available for celecoxib and Cell Transformation, Neoplastic
| Article | Year |
|---|---|
Chemoprevention strategies for pancreatic cancer.
Topics: Alkyl and Aryl Transferases; Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Pr | 2010 |
1 trial available for celecoxib and Cell Transformation, Neoplastic
| Article | Year |
|---|---|
Chemoprevention of nonmelanoma skin cancer with celecoxib: a randomized, double-blind, placebo-controlled trial.
Topics: Adult; Aged; Aged, 80 and over; Anticarcinogenic Agents; Carcinoma, Basal Cell; Carcinoma, Squamous | 2010 |
21 other studies available for celecoxib and Cell Transformation, Neoplastic
| Article | Year |
|---|---|
Role of GSK-3β in Regulation of Canonical Wnt/β-catenin Signaling and PI3-K/Akt Oncogenic Pathway in Colon Cancer.
Topics: 1,2-Dimethylhydrazine; Animals; Anticarcinogenic Agents; Apoptosis; Celecoxib; Cell Transformation, | 2017 |
COX-2 mediates tumor-stromal prolactin signaling to initiate tumorigenesis.
Topics: Animals; Carcinogenesis; Celecoxib; Cell Transformation, Neoplastic; Cyclooxygenase 2; Cyclooxygenas | 2019 |
COX-2 overexpression increases malignant potential of human glioma cells through Id1.
Topics: Animals; Celecoxib; Cell Line, Tumor; Cell Transformation, Neoplastic; Cyclooxygenase 2; Cyclooxygen | 2014 |
Combining CAL-101 with Celecoxib Enhances Apoptosis of EBV-transformed B-Cells Through MAPK-induced ER Stress.
Topics: Apoptosis; B-Lymphocytes; Celecoxib; Cell Line; Cell Proliferation; Cell Transformation, Neoplastic; | 2015 |
Celecoxib enhanced the cytotoxic effect of cisplatin in chemo-resistant gastric cancer xenograft mouse models through a cyclooxygenase-2-dependent manner.
Topics: Animals; Antineoplastic Agents; Apoptosis; ATP Binding Cassette Transporter, Subfamily B; Celecoxib; | 2016 |
Polyamine Antagonist Therapies Inhibit Neuroblastoma Initiation and Progression.
Topics: Animals; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Celecoxib; Cell Line | 2016 |
Progressive metaplastic and dysplastic changes in mouse pancreas induced by cyclooxygenase-2 overexpression.
Topics: Animals; Biomarkers, Tumor; Carcinoma, Pancreatic Ductal; Celecoxib; Cell Transformation, Neoplastic | 2008 |
Combination chemoprevention of HER2/neu-induced breast cancer using a cyclooxygenase-2 inhibitor and a retinoid X receptor-selective retinoid.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Bexarotene; Carcinoma; Celecoxib; Cell Tran | 2008 |
Persistent cyclooxygenase-2 inhibition downregulates NF-{kappa}B, resulting in chronic intestinal inflammation in the min/+ mouse model of colon tumorigenesis.
Topics: Animals; Antigens, CD34; Celecoxib; Cell Transformation, Neoplastic; Colitis; Colonic Neoplasms; Cyc | 2010 |
Targeting the tumor microenvironment using photodynamic therapy combined with inhibitors of cyclooxygenase-2 or vascular endothelial growth factor.
Topics: Animals; Celecoxib; Cell Line, Tumor; Cell Transformation, Neoplastic; Combined Modality Therapy; Cy | 2010 |
Prostaglandin E₂ signaling and bacterial infection recruit tumor-promoting macrophages to mouse gastric tumors.
Topics: Animals; Antibodies, Neutralizing; Benzamides; Celecoxib; Cell Line; Cell Transformation, Neoplastic | 2011 |
Gene expression following exposure to celecoxib in humans: pathways of inflammation and carcinogenesis are activated in tumors but not normal tissues.
Topics: Adenocarcinoma; Celecoxib; Cell Cycle; Cell Transformation, Neoplastic; Colonic Polyps; Colorectal N | 2011 |
Spatiotemporal assessments of dermal hyperemia enable accurate prediction of experimental cutaneous carcinogenesis as well as chemopreventive activity.
Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Anti-Inflammatory Agents; Carcinogens; Celecoxib; Cell Tr | 2013 |
Expression of LGR-5, MSI-1 and DCAMKL-1, putative stem cell markers, in the early phases of 1,2-dimethylhydrazine-induced rat colon carcinogenesis: correlation with nuclear β-catenin.
Topics: 1,2-Dimethylhydrazine; Adenoma; Animals; beta Catenin; Biomarkers, Tumor; Celecoxib; Cell Nucleus; C | 2013 |
Antiangiogenic and chemopreventive activities of celecoxib in oral carcinoma cell.
Topics: Administration, Oral; Angiogenesis Inhibitors; Animals; Carcinoma, Squamous Cell; Celecoxib; Cell Di | 2002 |
Despite positive studies, popularity of chemoprevention drugs increasing slowly.
Topics: Adenomatous Polyposis Coli; Androgen Antagonists; Anti-Inflammatory Agents, Non-Steroidal; Anticarci | 2004 |
Overexpression of 5-lipoxygenase and cyclooxygenase 2 in hamster and human oral cancer and chemopreventive effects of zileuton and celecoxib.
Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Arachidonate 5-Lipoxygenase; Arachidonic Acid; Carcinogen | 2005 |
9-cis-Retinoic acid inhibition of lung carcinogenesis in the A/J mouse model is accompanied by increased expression of RAR-beta but no change in cyclooxygenase-2.
Topics: Alitretinoin; Animals; Antineoplastic Agents; Carcinogens; Celecoxib; Cell Transformation, Neoplasti | 2006 |
A reduction of cyclooxygenase 2 gene dosage counters the ovarian morphological aging and tumor phenotype in Wv mice.
Topics: Adenoma; Aging; Animals; Blotting, Western; Celecoxib; Cell Transformation, Neoplastic; Cyclooxygena | 2007 |
Cancer and arthritis share underlying processes.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Anticarcinogenic Agents; Arthritis; Celecoxib; Cell Transfo | 1998 |
COX-2 and prostanoid receptors: good targets for chemoprevention.
Topics: Animals; Breast Neoplasms; Celecoxib; Cell Transformation, Neoplastic; Chemoprevention; Colonic Neop | 2002 |