2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one has been researched along with Pancreatic Neoplasms in 35 studies
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one: specific inhibitor of phosphatidylinositol 3-kinase; structure in first source
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 |
|---|---|---|
| "These data demonstrate that hypoxia can induce resistance of pancreatic cancer cells to gemcitabine mainly through the PI3K/Akt/NF-kappa B pathways and partially through the MAPK(Erk) signaling pathway." | 7.72 | Hypoxia increases resistance of human pancreatic cancer cells to apoptosis induced by gemcitabine. ( Fidler, IJ; Yokoi, K, 2004) |
| "Curcumin is a potential anticancer agent for pancreatic cancer." | 5.51 | Curcumin attenuates hyperglycemia-driven EGF-induced invasive and migratory abilities of pancreatic cancer via suppression of the ERK and AKT pathways. ( Cao, L; Han, L; Li, W; Ma, Q; Wang, Z; Wu, Z; Xiao, X, 2019) |
| "These data demonstrate that hypoxia can induce resistance of pancreatic cancer cells to gemcitabine mainly through the PI3K/Akt/NF-kappa B pathways and partially through the MAPK(Erk) signaling pathway." | 3.72 | Hypoxia increases resistance of human pancreatic cancer cells to apoptosis induced by gemcitabine. ( Fidler, IJ; Yokoi, K, 2004) |
| "Human pancreatic adenocarcinoma cell lines PK1 and PK8 are resistant to the clinically relevant chemotherapy agent gemcitabine." | 3.70 | Inhibition of phosphatidylinositide 3-kinase enhances gemcitabine-induced apoptosis in human pancreatic cancer cells. ( Chow, S; Hedley, DW; Tsao, MS, 2000) |
| "Leptin is an adipokine that is significantly increased in obese patients and that functions in various biological processes of cancer, such as tumor growth and metastasis." | 1.56 | Leptin receptor mediates the proliferation and glucose metabolism of pancreatic cancer cells via AKT pathway activation. ( Chen, J; Sheng, H; Tan, M; Tian, X; Xu, W; Xu, Y; Zhang, J, 2020) |
| "Curcumin is a potential anticancer agent for pancreatic cancer." | 1.51 | Curcumin attenuates hyperglycemia-driven EGF-induced invasive and migratory abilities of pancreatic cancer via suppression of the ERK and AKT pathways. ( Cao, L; Han, L; Li, W; Ma, Q; Wang, Z; Wu, Z; Xiao, X, 2019) |
| " LY294002 and gemcitabine hydrochloride combined with IR better inhibited cell migration, VM formation and MMP-2 mRNA expression of Panc-1 cells in vitro, and we also proved that the novel therapeutic regimen better inhibited tumor growth, tumor metastasis and VM formation of orthotopic Panc-1 xenografts by suppressing the PI3K/MMPs/Ln-5γ2 signaling pathway in vivo." | 1.43 | The effect of PI3K inhibitor LY294002 and gemcitabine hydrochloride combined with ionizing radiation on the formation of vasculogenic mimicry of Panc-1 cells in vitro and in vivo. ( Bai, R; Ding, T; Lan, X; Liu, S; Yin, L; Yu, Y; Zhang, L; Zhao, J, 2016) |
| "Pancreatic cancer has a poor prognosis." | 1.43 | Regulation of cell apoptosis and proliferation in pancreatic cancer through PI3K/Akt pathway via Polo-like kinase 1. ( Cai, Z; Lai, Y; Li, Q; Mao, Y; Xi, L; Yu, C; Zhang, X, 2016) |
| "Two human pancreatic cancer cell lines were used to evaluate the in vitro effects of the GLP-1R agonist liraglutide on cell growth, migration and invasion." | 1.40 | Activation of glucagon-like peptide-1 receptor inhibits tumourigenicity and metastasis of human pancreatic cancer cells via PI3K/Akt pathway. ( Hong, T; Ke, J; Liu, Y; Tao, M; Wang, L; Wei, R; Xiu, D; Yang, J; Zhao, H, 2014) |
| "Human pancreatic cancer cell lines were used." | 1.38 | Transforming growth factor β and Ras/MEK/ERK signaling regulate the expression level of a novel tumor suppressor Lefty. ( Azuma, T; Hibi, T; Higuchi, H; Hozawa, S; Igarashi, T; Kabashima, A; Miyata, N; Saeki, K; Yokoyama, A, 2012) |
| "To develop a molecular therapy for pancreatic cancer, the insulin-like growth factor-I (IGF-I) signaling pathway was analyzed." | 1.36 | Insulin-like growth factor-I receptor in proliferation and motility of pancreatic cancer. ( Shinozaki, F; Sueishi, M; Sugiyama, T; Tomizawa, M; Yamamoto, S; Yoshida, T, 2010) |
| "We have previously demonstrated that in pancreatic cancer ErbB3 is the preferred dimerization partner of EGFR, ErbB3 protein expression level directly correlates with the anti-proliferative effect of erlotinib (an EGFR-specific tyrosine kinase inhibitor), and transient knockdown of ErbB3 expression results in acquired resistance to EGFR-targeted therapy." | 1.36 | ErbB3 expression promotes tumorigenesis in pancreatic adenocarcinoma. ( Arnoletti, JP; Frolov, A; Heslin, MJ; Howard, JH; Kossenkov, AV; Kulesza, P; Liles, JS; Tzeng, CW, 2010) |
| "Chemoresistance is a serious problem in pancreatic cancer, but the mechanism of resistance and strategies against the resistance have not been elucidated." | 1.35 | Modulating effect of the PI3-kinase inhibitor LY294002 on cisplatin in human pancreatic cancer cells. ( Fujiwara, M; Hossain, MA; Izuishi, K; Kimura, S; Masaki, T; Sano, T; Suzuki, Y, 2008) |
| "We hypothesize that pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies." | 1.35 | Pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies. ( Dixon, J; Holcomb, B; Kennard, J; Mahomed, J; Matos, JM; Schmidt, CM; Sebolt-Leopold, J; Shanmugam, R; Yip-Schneider, MT, 2008) |
| " The effects of PD98059, LY294002, rapamycin and its analogue CCI-779 were tested in dose-response experiments." | 1.33 | Inhibition of different intracellular signal cascades in human pancreatic cancer cells. ( Axelson, J; Hörlin, K; Lindell, M; Ohlsson, B, 2005) |
| "We identified five human pancreatic cancer cell lines that express the GLP-1R and analyzed cell growth and survival in response to GLP-1R activation." | 1.33 | Activation of glucagon-like peptide-1 receptor signaling does not modify the growth or apoptosis of human pancreatic cancer cells. ( Drucker, DJ; Koehler, JA, 2006) |
| "In PK-45H pancreatic cancer cells, the growth-inhibitory and apoptosis-inducing effects of LY294002, a PI3K inhibitor, were detected in a concentration-dependent manner, followed by the reduction of phosphorylated Akt levels." | 1.32 | Phosphorylated Akt/PKB controls cell growth and apoptosis in intraductal papillary-mucinous tumor and invasive ductal adenocarcinoma of the pancreas. ( Kimura, W; Moriya, T; Semba, S; Yamakawa, M, 2003) |
| "Pancreatic cancer is resistant to almost all cytotoxic drugs." | 1.32 | Role of NF-kappaB and Akt/PI3K in the resistance of pancreatic carcinoma cell lines against gemcitabine-induced cell death. ( Arlt, A; Fölsch, UR; Gehrz, A; Kruse, ML; Müerköster, S; Schäfer, H; Vorndamm, J, 2003) |
| "Flow cytometric analysis revealed that pancreatic cancer cells treated with 50 micromol/L LY294002 underwent G1 arrest, which was associated with dephosphorylation of the ppRB protein, a decrease in the protein expression of cyclin D and E, and their activating partners Cdk2, 4, and 6 with simultaneous accumulation of P27/Kip1." | 1.32 | Role of the phosphatidylinositol 3'-kinase-Akt signal pathway in the proliferation of human pancreatic ductal carcinoma cell lines. ( Adachi, K; Honjo, S; Ito, H; Osaki, M; Takeda, A, 2004) |
| "Genetic mutations found in pancreatic cancer (K-ras, p16, p53) lead to inappropriate cellular proliferation." | 1.31 | Pancreatic cancer cell proliferation is phosphatidylinositol 3-kinase dependent. ( Callery, MP; McDade, TP; Perugini, RA; Vittimberga, FJ, 2000) |
| "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) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 17 (48.57) | 29.6817 |
| 2010's | 17 (48.57) | 24.3611 |
| 2020's | 1 (2.86) | 2.80 |
| Authors | Studies |
|---|---|
| Xu, Y | 1 |
| Tan, M | 1 |
| Tian, X | 1 |
| Zhang, J | 2 |
| Chen, J | 1 |
| Xu, W | 1 |
| Sheng, H | 1 |
| Li, W | 3 |
| Wang, Z | 1 |
| Xiao, X | 1 |
| Han, L | 3 |
| Wu, Z | 1 |
| Ma, Q | 3 |
| Cao, L | 1 |
| Ma, J | 2 |
| Li, B | 1 |
| Liu, J | 2 |
| Xu, Q | 2 |
| Duan, W | 2 |
| Yu, S | 1 |
| Wang, F | 1 |
| Wu, E | 2 |
| Peng, B | 1 |
| Li, J | 1 |
| Chen, C | 2 |
| Laporte, K | 1 |
| Li, Z | 1 |
| Djukom, C | 1 |
| Porro, LJ | 1 |
| Mrazek, A | 1 |
| Townsend, CM | 1 |
| Hellmich, MR | 1 |
| Chao, C | 1 |
| Zhao, H | 1 |
| Wang, L | 1 |
| Wei, R | 1 |
| Xiu, D | 1 |
| Tao, M | 1 |
| Ke, J | 1 |
| Liu, Y | 1 |
| Yang, J | 1 |
| Hong, T | 1 |
| Bai, R | 1 |
| Ding, T | 1 |
| Zhao, J | 1 |
| Liu, S | 1 |
| Zhang, L | 1 |
| Lan, X | 1 |
| Yu, Y | 1 |
| Yin, L | 1 |
| Wang, MC | 1 |
| Jiao, M | 1 |
| Wu, T | 1 |
| Jing, L | 1 |
| Cui, J | 1 |
| Guo, H | 1 |
| Tian, T | 1 |
| Ruan, ZP | 1 |
| Wei, YC | 1 |
| Jiang, LL | 1 |
| Sun, HF | 1 |
| Huang, LX | 1 |
| Nan, KJ | 1 |
| Li, CL | 1 |
| Mao, Y | 1 |
| Xi, L | 1 |
| Li, Q | 1 |
| Cai, Z | 1 |
| Lai, Y | 1 |
| Zhang, X | 1 |
| Yu, C | 1 |
| Wang, Y | 2 |
| Kuramitsu, Y | 1 |
| Baron, B | 1 |
| Kitagawa, T | 1 |
| Tokuda, K | 1 |
| Akada, J | 1 |
| Maehara, SI | 1 |
| Maehara, Y | 1 |
| Nakamura, K | 1 |
| Fujiwara, M | 1 |
| Izuishi, K | 2 |
| Sano, T | 1 |
| Hossain, MA | 1 |
| Kimura, S | 1 |
| Masaki, T | 1 |
| Suzuki, Y | 1 |
| Shen, X | 1 |
| Artinyan, A | 1 |
| Jackson, D | 1 |
| Thomas, RM | 1 |
| Lowy, AM | 1 |
| Kim, J | 1 |
| Han, F | 1 |
| Zhu, HG | 1 |
| Tomizawa, M | 1 |
| Shinozaki, F | 1 |
| Sugiyama, T | 1 |
| Yamamoto, S | 1 |
| Sueishi, M | 1 |
| Yoshida, T | 1 |
| Xu, Z | 1 |
| Zhang, Y | 1 |
| Jiang, J | 1 |
| Yang, Y | 1 |
| Shi, R | 1 |
| Hao, B | 1 |
| Zhang, Z | 1 |
| Huang, Z | 1 |
| Kim, JW | 1 |
| Zhang, G | 1 |
| Liles, JS | 1 |
| Arnoletti, JP | 1 |
| Tzeng, CW | 1 |
| Howard, JH | 1 |
| Kossenkov, AV | 1 |
| Kulesza, P | 1 |
| Heslin, MJ | 1 |
| Frolov, A | 1 |
| Bharadwaj, U | 1 |
| Marin-Muller, C | 1 |
| Li, M | 1 |
| Yao, Q | 1 |
| Miyata, N | 1 |
| Azuma, T | 1 |
| Hozawa, S | 1 |
| Higuchi, H | 1 |
| Yokoyama, A | 1 |
| Kabashima, A | 1 |
| Igarashi, T | 1 |
| Saeki, K | 1 |
| Hibi, T | 1 |
| Ke, XY | 1 |
| Xie, ZQ | 1 |
| Liu, ZQ | 1 |
| Zhang, CF | 1 |
| Zhao, Q | 1 |
| Yang, DL | 1 |
| Bondar, VM | 1 |
| Sweeney-Gotsch, B | 1 |
| Andreeff, M | 1 |
| Mills, GB | 1 |
| McConkey, DJ | 1 |
| Matsumoto, J | 1 |
| Kaneda, M | 1 |
| Tada, M | 1 |
| Hamada, J | 1 |
| Okushiba, S | 1 |
| Kondo, S | 1 |
| Katoh, H | 1 |
| Moriuchi, T | 1 |
| Semba, S | 1 |
| Moriya, T | 1 |
| Kimura, W | 1 |
| Yamakawa, M | 1 |
| Arlt, A | 1 |
| Gehrz, A | 1 |
| Müerköster, S | 1 |
| Vorndamm, J | 1 |
| Kruse, ML | 1 |
| Fölsch, UR | 1 |
| Schäfer, H | 1 |
| Yokoi, K | 1 |
| Fidler, IJ | 1 |
| Takeda, A | 1 |
| Osaki, M | 1 |
| Adachi, K | 1 |
| Honjo, S | 1 |
| Ito, H | 1 |
| Beeharry, N | 1 |
| Chambers, JA | 1 |
| Green, IC | 1 |
| Mirza, AM | 1 |
| Gysin, S | 1 |
| Malek, N | 1 |
| Nakayama, K | 1 |
| Roberts, JM | 1 |
| McMahon, M | 1 |
| Axelson, J | 1 |
| Lindell, M | 1 |
| Hörlin, K | 1 |
| Ohlsson, B | 1 |
| Sarinella, F | 1 |
| Calistri, A | 1 |
| Sette, P | 1 |
| Palù, G | 1 |
| Parolin, C | 1 |
| Koehler, JA | 1 |
| Drucker, DJ | 1 |
| Reichert, M | 1 |
| Saur, D | 1 |
| Hamacher, R | 1 |
| Schmid, RM | 1 |
| Schneider, G | 1 |
| Holcomb, B | 1 |
| Yip-Schneider, MT | 1 |
| Matos, JM | 1 |
| Dixon, J | 1 |
| Kennard, J | 1 |
| Mahomed, J | 1 |
| Shanmugam, R | 1 |
| Sebolt-Leopold, J | 1 |
| Schmidt, CM | 1 |
| Perugini, RA | 1 |
| McDade, TP | 1 |
| Vittimberga, FJ | 1 |
| Callery, MP | 1 |
| Tsao, MS | 1 |
| Chow, S | 1 |
| Hedley, DW | 1 |
| Kato, K | 1 |
| Ogura, T | 1 |
| Kinoshita, T | 1 |
| Esumi, H | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| 1911GCCC:Two Parallel, Single-arm, Open Label, Phase 2 Trials of Galeterone Alone or Galeterone Combined With Gemcitabine for Patients With Metastatic Pancreatic Adenocarcinoma Refractory to Standard Chemotherapy[NCT04098081] | Phase 2 | 58 participants (Anticipated) | Interventional | 2019-12-12 | Recruiting | ||
| The Effects of Exercise Training on Tumor Vascularity and Response to Neoadjuvant Therapy in Operable Breast Cancer: A Phase I-II Study[NCT00405678] | Phase 1/Phase 2 | 23 participants (Actual) | Interventional | 2006-09-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
35 other studies available for 2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one and Pancreatic Neoplasms
| Article | Year |
|---|---|
Leptin receptor mediates the proliferation and glucose metabolism of pancreatic cancer cells via AKT pathway activation.
Topics: Cell Line, Tumor; Cell Proliferation; Chromones; Gene Silencing; Glucose; Glucose Transporter Type 1 | 2020 |
Curcumin attenuates hyperglycemia-driven EGF-induced invasive and migratory abilities of pancreatic cancer via suppression of the ERK and AKT pathways.
Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chromones; Curcumin; Epi | 2019 |
Resveratrol inhibits the epithelial-mesenchymal transition of pancreatic cancer cells via suppression of the PI-3K/Akt/NF-κB pathway.
Topics: Antineoplastic Agents; Cadherins; Cell Line, Tumor; Cell Movement; Chromones; Epithelial-Mesenchymal | 2013 |
Indometacin ameliorates high glucose-induced proliferation and invasion via modulation of e-cadherin in pancreatic cancer cells.
Topics: Cadherins; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chromones; Down-Regulation; Glucose; | 2013 |
Dual inhibition of PI3K and mTOR signaling pathways decreases human pancreatic neuroendocrine tumor metastatic progression.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Blotting, Western; Cell Line, Tumor; Cell P | 2014 |
Activation of glucagon-like peptide-1 receptor inhibits tumourigenicity and metastasis of human pancreatic cancer cells via PI3K/Akt pathway.
Topics: Androstadienes; Animals; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chromones; Diabetes Me | 2014 |
The effect of PI3K inhibitor LY294002 and gemcitabine hydrochloride combined with ionizing radiation on the formation of vasculogenic mimicry of Panc-1 cells in vitro and in vivo.
Topics: Antineoplastic Agents; Apoptosis; Chromones; Deoxycytidine; Gemcitabine; Humans; Morpholines; Neovas | 2016 |
Polycomb complex protein BMI-1 promotes invasion and metastasis of pancreatic cancer stem cells by activating PI3K/AKT signaling, an ex vivo, in vitro, and in vivo study.
Topics: AC133 Antigen; Adult; Aged; Animals; Cell Line, Tumor; Cell Movement; Chromones; Enzyme Activation; | 2016 |
Regulation of cell apoptosis and proliferation in pancreatic cancer through PI3K/Akt pathway via Polo-like kinase 1.
Topics: Animals; Apoptosis; bcl-2-Associated X Protein; Caspase 3; Cell Cycle Proteins; Cell Line, Tumor; Ce | 2016 |
PI3K inhibitor LY294002, as opposed to wortmannin, enhances AKT phosphorylation in gemcitabine-resistant pancreatic cancer cells.
Topics: Androstadienes; Cell Line, Tumor; Cell Survival; Chromones; Deoxycytidine; Drug Resistance, Neoplasm | 2017 |
Modulating effect of the PI3-kinase inhibitor LY294002 on cisplatin in human pancreatic cancer cells.
Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Cell Proliferation; Chromones; C | 2008 |
Chemokine receptor CXCR4 enhances proliferation in pancreatic cancer cells through AKT and ERK dependent pathways.
Topics: Animals; Butadienes; Cell Line, Tumor; Cell Proliferation; Chemokine CXCL12; Chromones; Enzyme Inhib | 2010 |
Caveolin-1 regulating the invasion and expression of matrix metalloproteinase (MMPs) in pancreatic carcinoma cells.
Topics: Carcinoma; Caveolin 1; Cell Line, Tumor; Chromones; Epithelial Cells; Extracellular Signal-Regulated | 2010 |
Insulin-like growth factor-I receptor in proliferation and motility of pancreatic cancer.
Topics: Animals; Apoptosis; Cell Line, Tumor; Cell Proliferation; Chromones; Enzyme Inhibitors; Gene Express | 2010 |
Epidermal growth factor induces HCCR expression via PI3K/Akt/mTOR signaling in PANC-1 pancreatic cancer cells.
Topics: Animals; Antibodies; Blotting, Western; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chromon | 2010 |
ErbB3 expression promotes tumorigenesis in pancreatic adenocarcinoma.
Topics: Adenocarcinoma; Animals; Blotting, Western; Cell Line, Tumor; Cell Proliferation; Chromones; Dose-Re | 2010 |
Mesothelin confers pancreatic cancer cell resistance to TNF-α-induced apoptosis through Akt/PI3K/NF-κB activation and IL-6/Mcl-1 overexpression.
Topics: Antineoplastic Agents; Apoptosis; Apoptosis Regulatory Proteins; Caspase 3; Cell Line, Tumor; Cell S | 2011 |
Transforming growth factor β and Ras/MEK/ERK signaling regulate the expression level of a novel tumor suppressor Lefty.
Topics: Butadienes; Cell Line, Tumor; Cell Proliferation; Chromones; Extracellular Signal-Regulated MAP Kina | 2012 |
LY294002 enhances inhibitory effect of gemcitabine on proliferation of human pancreatic carcinoma PANC-1 cells.
Topics: Adult; Antimetabolites, Antineoplastic; Cell Proliferation; Chromones; Deoxycytidine; Dose-Response | 2013 |
Inhibition of the phosphatidylinositol 3'-kinase-AKT pathway induces apoptosis in pancreatic carcinoma cells in vitro and in vivo.
Topics: Androstadienes; Animals; Apoptosis; Carcinoma; Chromones; Collagen; Dose-Response Relationship, Drug | 2002 |
Differential mechanisms of constitutive Akt/PKB activation and its influence on gene expression in pancreatic cancer cells.
Topics: Chromones; Enzyme Activation; Gene Expression; Genes, p53; Genes, ras; Humans; MAP Kinase Kinase 1; | 2002 |
Phosphorylated Akt/PKB controls cell growth and apoptosis in intraductal papillary-mucinous tumor and invasive ductal adenocarcinoma of the pancreas.
Topics: Adenocarcinoma; Adenocarcinoma, Mucinous; Aged; Apoptosis; Carcinoma, Pancreatic Ductal; Carcinoma, | 2003 |
Role of NF-kappaB and Akt/PI3K in the resistance of pancreatic carcinoma cell lines against gemcitabine-induced cell death.
Topics: Adenocarcinoma; Antimetabolites, Antineoplastic; Apoptosis; Chromones; Deoxycytidine; Dose-Response | 2003 |
Hypoxia increases resistance of human pancreatic cancer cells to apoptosis induced by gemcitabine.
Topics: Antimetabolites, Antineoplastic; Antineoplastic Agents; Apoptosis; Blotting, Western; Butadienes; Ce | 2004 |
Role of the phosphatidylinositol 3'-kinase-Akt signal pathway in the proliferation of human pancreatic ductal carcinoma cell lines.
Topics: Apoptosis; Carcinoma, Pancreatic Ductal; Cell Cycle; Cell Cycle Proteins; Cell Division; Cell Line, | 2004 |
Fatty acid protection from palmitic acid-induced apoptosis is lost following PI3-kinase inhibition.
Topics: Androstadienes; Animals; Apoptosis; Cell Death; Cell Line, Tumor; Cell Survival; Chromones; Enzyme I | 2004 |
Cooperative regulation of the cell division cycle by the protein kinases RAF and AKT.
Topics: Animals; Benzamides; Blotting, Western; Butadienes; Cell Cycle; Cell Cycle Proteins; Cell Division; | 2004 |
Inhibition of different intracellular signal cascades in human pancreatic cancer cells.
Topics: Antibiotics, Antineoplastic; Carcinoma, Pancreatic Ductal; Cell Division; Chromones; Culture Media, | 2005 |
Oncolysis of pancreatic tumour cells by a gamma34.5-deleted HSV-1 does not rely upon Ras-activation, but on the PI 3-kinase pathway.
Topics: Adenocarcinoma; Cell Line, Tumor; Chromones; Flavonoids; Gene Deletion; Genes, ras; Genetic Therapy; | 2006 |
Activation of glucagon-like peptide-1 receptor signaling does not modify the growth or apoptosis of human pancreatic cancer cells.
Topics: Apoptosis; Cell Division; Cell Line, Tumor; Cell Survival; Cholera Toxin; Chromones; Cycloheximide; | 2006 |
Phosphoinositide-3-kinase signaling controls S-phase kinase-associated protein 2 transcription via E2F1 in pancreatic ductal adenocarcinoma cells.
Topics: Carcinoma, Pancreatic Ductal; Cell Cycle; Cell Growth Processes; Chromones; E2F1 Transcription Facto | 2007 |
Pancreatic cancer cell genetics and signaling response to treatment correlate with efficacy of gemcitabine-based molecular targeting strategies.
Topics: Adenocarcinoma; Antimetabolites, Antineoplastic; Antineoplastic Agents; Blotting, Western; Cell Prol | 2008 |
Pancreatic cancer cell proliferation is phosphatidylinositol 3-kinase dependent.
Topics: Cell Cycle; Cell Division; Chromones; Flavonoids; Humans; Mitogen-Activated Protein Kinases; Morphol | 2000 |
Inhibition of phosphatidylinositide 3-kinase enhances gemcitabine-induced apoptosis in human pancreatic cancer cells.
Topics: Adenocarcinoma; Androstadienes; Antimetabolites, Antineoplastic; Apoptosis; Chromones; Deoxycytidine | 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 |