troglitazone has been researched along with Pancreatic Neoplasms in 16 studies
Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.
Pancreatic Neoplasms: Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).
| Excerpt | Relevance | Reference |
|---|---|---|
| " We compared the effects of six types of TZDs (troglitazone, RS-1303, RS-1330, RS-1387, RS-1455, and RS-1456) and 9-cis RA, an RXRalpha ligand, on the activation of PPARgamma/RXRalpha and the growth inhibition of six types of adenocarcinoma cell lines (MKN45, HT-29, HCT116, HuCCT1, KMP-2, and BxPC3) established from abdominal malignancies." | 3.72 | Thiazolidinediones inhibit growth of gastrointestinal, biliary, and pancreatic adenocarcinoma cells through activation of the peroxisome proliferator-activated receptor gamma/retinoid X receptor alpha pathway. ( Dono, K; Hayashi, N; Hiraoka, N; Monden, M; Nagano, H; Nakamori, S; Okami, J; Sakon, M; Tsujie, M; Umeshita, K, 2003) |
| "Troglitazone (TGZ) is a peroxisome proliferator-activated receptor gamma agonist that could inhibit the expression of CD73." | 1.62 | CD73 induces gemcitabine resistance in pancreatic ductal adenocarcinoma: A promising target with non-canonical mechanisms. ( Gao, S; Hao, J; Huang, C; Li, X; Liu, J; Liu, W; Ma, Y; Wang, H; Wang, X; Wang, Z; Wu, L; Yang, S; Yu, X; Zhao, T, 2021) |
| "Troglitazone (TGZ) is a peroxisome proliferator-activated receptor gamma (PPARĪ³) agonist that has been investigated as a potential chemopreventive and chemotherapeutic agent." | 1.46 | In vitro and in vivo cytotoxicity of troglitazone in pancreatic cancer. ( Fujita, M; Hasegawa, A; Okamura, N; Yamamori, M, 2017) |
| "Treatment of human pancreatic cancer cells with specific MEK inhibitor, PD98059 or U0126, inhibited ERK1/2 phosphorylation and cell growth." | 1.33 | Involvement of MEK-ERK signaling pathway in the inhibition of cell growth by troglitazone in human pancreatic cancer cells. ( Fukuda, M; Kohgo, Y; Motomura, W; Nagamine, M; Okumura, T; Takahashi, N; Tanno, S, 2005) |
| "PPARgamma ligands inhibit pancreatic cancer cell invasion, suggesting that these agents may represent novel strategies to treat pancreatic cancer." | 1.32 | Selective activation of PPARgamma inhibits pancreatic cancer invasion and decreases expression of tissue plasminogen activator. ( Evers, BM; Farrow, B; Hashimoto, K; Iwamura, T; O'Connor, KL, 2003) |
| "Among three gastric cancer cell lines, MKN28, MKN45, and MKN74, only the most poorly differentiated MKN45 cells survived >36 h." | 1.31 | Remarkable tolerance of tumor cells to nutrient deprivation: possible new biochemical target for cancer therapy. ( Esumi, H; Izuishi, K; Kato, K; Kinoshita, T; Ogura, T, 2000) |
| "Troglitazone showed a potent dose-response effect on the growth inhibition of six pancreatic cancer cell lines, which were suppressed to less than 50% of control at the concentration of 10 microM." | 1.31 | Growth inhibition and differentiation of pancreatic cancer cell lines by PPAR gamma ligand troglitazone. ( Kawa, S; Kiyosawa, K; Nakayama, K; Nikaido, T; Unno, H; Usuda, N, 2002) |
| "In our study, we focused on pancreatic cancers, because the prognosis of advanced pancreatic cancer has not significantly improved due to its resistance to various chemotherapeutic regimens, so that a novel strategy should be required." | 1.31 | Ligands for peroxisome proliferator-activated receptor gamma inhibit growth of pancreatic cancers both in vitro and in vivo. ( Hashimoto, Y; Hosotani, R; Imamura, M; Itami, A; Kato, M; Kawamura, J; Shimada, Y; Watanabe, G, 2001) |
| "Seven human pancreatic cancer cell lines and 7 surgically resected human pancreatic cancer tissues were used as samples." | 1.31 | Activation of peroxisome proliferator-activated receptor gamma inhibits the growth of human pancreatic cancer. ( Chayama, K; Fujimoto, Y; Kawasaki, Y; Kuwada, Y; Sasaki, T; Tsuchida, A, 2001) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 14 (87.50) | 29.6817 |
| 2010's | 1 (6.25) | 24.3611 |
| 2020's | 1 (6.25) | 2.80 |
| Authors | Studies |
|---|---|
| Yu, X | 1 |
| Liu, W | 1 |
| Wang, Z | 1 |
| Wang, H | 1 |
| Liu, J | 1 |
| Huang, C | 1 |
| Zhao, T | 1 |
| Wang, X | 1 |
| Gao, S | 1 |
| Ma, Y | 1 |
| Wu, L | 1 |
| Li, X | 1 |
| Yang, S | 1 |
| Hao, J | 1 |
| Fujita, M | 1 |
| Hasegawa, A | 1 |
| Yamamori, M | 1 |
| Okamura, N | 1 |
| Kumei, S | 1 |
| Motomura, W | 4 |
| Yoshizaki, T | 1 |
| Takakusaki, K | 1 |
| Okumura, T | 4 |
| Tsujie, M | 2 |
| Nakamori, S | 2 |
| Okami, J | 2 |
| Takahashi, Y | 1 |
| Hayashi, N | 2 |
| Nagano, H | 2 |
| Dono, K | 2 |
| Umeshita, K | 2 |
| Sakon, M | 2 |
| Monden, M | 2 |
| Hiraoka, N | 1 |
| Farrow, B | 1 |
| O'Connor, KL | 1 |
| Hashimoto, K | 1 |
| Iwamura, T | 1 |
| Evers, BM | 1 |
| Nagamine, M | 2 |
| Tanno, S | 2 |
| Sawamukai, M | 1 |
| Takahashi, N | 3 |
| Kohgo, Y | 3 |
| Fukuda, M | 1 |
| Yao, CJ | 1 |
| Lai, GM | 1 |
| Chan, CF | 1 |
| Cheng, AL | 1 |
| Yang, YY | 1 |
| Chuang, SE | 1 |
| Obara, T | 1 |
| Izuishi, K | 1 |
| Kato, K | 1 |
| Ogura, T | 1 |
| Kinoshita, T | 1 |
| Esumi, H | 1 |
| Kawa, S | 1 |
| Nikaido, T | 1 |
| Unno, H | 1 |
| Usuda, N | 1 |
| Nakayama, K | 1 |
| Kiyosawa, K | 1 |
| Itami, A | 1 |
| Watanabe, G | 1 |
| Shimada, Y | 1 |
| Hashimoto, Y | 1 |
| Kawamura, J | 1 |
| Kato, M | 1 |
| Hosotani, R | 1 |
| Imamura, M | 1 |
| Kawai, T | 1 |
| Hirose, H | 1 |
| Seto, Y | 1 |
| Fujita, H | 2 |
| Ukeda, K | 1 |
| Saruta, T | 1 |
| Toyota, M | 1 |
| Miyazaki, Y | 1 |
| Kitamura, S | 1 |
| Nagasawa, Y | 1 |
| Kiyohara, T | 1 |
| Shinomura, Y | 1 |
| Matsuzawa, Y | 1 |
| Sasaki, T | 1 |
| Fujimoto, Y | 1 |
| Tsuchida, A | 1 |
| Kawasaki, Y | 1 |
| Kuwada, Y | 1 |
| Chayama, K | 1 |
16 other studies available for troglitazone and Pancreatic Neoplasms
| Article | Year |
|---|---|
CD73 induces gemcitabine resistance in pancreatic ductal adenocarcinoma: A promising target with non-canonical mechanisms.
Topics: 5'-Nucleotidase; Animals; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Deoxycytidine; Down-Regula | 2021 |
In vitro and in vivo cytotoxicity of troglitazone in pancreatic cancer.
Topics: Animals; Antineoplastic Agents; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Cell Cycle; Cell L | 2017 |
Troglitazone increases expression of E-cadherin and claudin 4 in human pancreatic cancer cells.
Topics: Antineoplastic Agents; Butadienes; Cadherins; Cell Line, Tumor; Chromans; Claudin-4; Extracellular S | 2009 |
Growth inhibition of pancreatic cancer cells through activation of peroxisome proliferator-activated receptor gamma/retinoid X receptor alpha pathway.
Topics: Alitretinoin; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; bcl-2-Associated X Protein; | 2003 |
Thiazolidinediones inhibit growth of gastrointestinal, biliary, and pancreatic adenocarcinoma cells through activation of the peroxisome proliferator-activated receptor gamma/retinoid X receptor alpha pathway.
Topics: Adenocarcinoma; Alitretinoin; Antineoplastic Agents; Apoptosis; Biliary Tract Neoplasms; Cell Differ | 2003 |
Selective activation of PPARgamma inhibits pancreatic cancer invasion and decreases expression of tissue plasminogen activator.
Topics: Chromans; Humans; Integrins; Matrix Metalloproteinase Inhibitors; Neoplasm Invasiveness; Pancreatic | 2003 |
Inhibition of cell invasion and morphological change by troglitazone in human pancreatic cancer cells.
Topics: Actins; Antineoplastic Agents; Cell Migration Inhibition; Cell Movement; Chromans; Culture Media, Co | 2004 |
Involvement of MEK-ERK signaling pathway in the inhibition of cell growth by troglitazone in human pancreatic cancer cells.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Cell Survival; Chromans; Dose-Response | 2005 |
Dramatic synergistic anticancer effect of clinically achievable doses of lovastatin and troglitazone.
Topics: Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Cell Survival; Chromans; Cyclin A; | 2006 |
Activation of peroxisome proliferator-activated receptor gamma by troglitazone inhibits cell growth through the increase of p27KiP1 in human. Pancreatic carcinoma cells.
Topics: Adenocarcinoma; Antineoplastic Agents; Blotting, Northern; Cell Cycle Proteins; Cell Division; Chrom | 2000 |
Remarkable tolerance of tumor cells to nutrient deprivation: possible new biochemical target for cancer therapy.
Topics: Antineoplastic Agents; Cell Survival; Chromans; Chromones; Culture Media, Serum-Free; Enzyme Activat | 2000 |
Growth inhibition and differentiation of pancreatic cancer cell lines by PPAR gamma ligand troglitazone.
Topics: Adenocarcinoma; Cell Differentiation; Cell Division; Chromans; Dose-Response Relationship, Drug; Flo | 2002 |
Ligands for peroxisome proliferator-activated receptor gamma inhibit growth of pancreatic cancers both in vitro and in vivo.
Topics: Adipocytes; Animals; Antineoplastic Agents; Cell Cycle; Cell Cycle Proteins; Cell Differentiation; C | 2001 |
Troglitazone ameliorates lipotoxicity in the beta cell line INS-1 expressing PPAR gamma.
Topics: Animals; Base Sequence; Cell Division; Cell Survival; Chromans; DNA Primers; Fatty Acids, Nonesterif | 2002 |
Peroxisome proliferator-activated receptor gamma reduces the growth rate of pancreatic cancer cells through the reduction of cyclin D1.
Topics: Alitretinoin; Animals; Antineoplastic Agents; Blotting, Northern; Blotting, Western; Carcinoma; Cell | 2002 |
Activation of peroxisome proliferator-activated receptor gamma inhibits the growth of human pancreatic cancer.
Topics: Antineoplastic Agents; Cell Division; Chromans; Dose-Response Relationship, Drug; Electrophoretic Mo | 2001 |