chloroquine has been researched along with Cancer of Pancreas in 46 studies
Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.
chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Utilizing an orthotopic murine PDA model in C57/Bl6 mice and patient correlative samples, we studied the role of NETs in PDA hypercoagulability and targeted this pathway through treatment with the NET inhibitor chloroquine." | 7.88 | Chloroquine reduces hypercoagulability in pancreatic cancer through inhibition of neutrophil extracellular traps. ( Boone, BA; Doerfler, WR; Ellis, JT; Liang, X; Lotze, MT; Miller-Ocuin, J; Murthy, P; Neal, MD; Ross, MA; Sperry, JL; Wallace, CT; Zeh, HJ, 2018) |
| "MiaPaCa2 (non-metastatic) and S2VP10 (metastatic) cell lines were treated with 25 and 50 µM chloroquine for 24 and 48 hours in normoxia and hypoxia (5-10% O₂)." | 7.80 | Chloroquine-mediated cell death in metastatic pancreatic adenocarcinoma through inhibition of autophagy. ( Frieboes, HB; Huang, JS; McNally, LR; Yin, WC, 2014) |
| "We observed that bortezomib-induced protective autophagy in cultured PANC-1 pancreatic cancer cells and HT-29 colorectal cancer cells." | 7.80 | Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells. ( Chen, ZR; Huang, M; Min, H; Xu, M; Zheng, K; Zhou, JD; Zou, XP, 2014) |
| "Utilizing an orthotopic murine PDA model in C57/Bl6 mice and patient correlative samples, we studied the role of NETs in PDA hypercoagulability and targeted this pathway through treatment with the NET inhibitor chloroquine." | 3.88 | Chloroquine reduces hypercoagulability in pancreatic cancer through inhibition of neutrophil extracellular traps. ( Boone, BA; Doerfler, WR; Ellis, JT; Liang, X; Lotze, MT; Miller-Ocuin, J; Murthy, P; Neal, MD; Ross, MA; Sperry, JL; Wallace, CT; Zeh, HJ, 2018) |
| "MiaPaCa2 (non-metastatic) and S2VP10 (metastatic) cell lines were treated with 25 and 50 µM chloroquine for 24 and 48 hours in normoxia and hypoxia (5-10% O₂)." | 3.80 | Chloroquine-mediated cell death in metastatic pancreatic adenocarcinoma through inhibition of autophagy. ( Frieboes, HB; Huang, JS; McNally, LR; Yin, WC, 2014) |
| "We observed that bortezomib-induced protective autophagy in cultured PANC-1 pancreatic cancer cells and HT-29 colorectal cancer cells." | 3.80 | Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells. ( Chen, ZR; Huang, M; Min, H; Xu, M; Zheng, K; Zhou, JD; Zou, XP, 2014) |
| "In 2020, GLOBOCAN reported that pancreatic cancer accounts for 4." | 2.82 | Pharmacological Modulation of Apoptosis and Autophagy in Pancreatic Cancer Treatment. ( Islam, MK; Lian, HK; Lim, JCW; Sagineedu, SR; Selvarajoo, N; Stanslas, J, 2022) |
| "Approaches to improve pancreatic cancer therapy are essential as this disease has a very bleak outcome." | 1.91 | Effects of chloroquine and hydroxychloroquine on the sensitivity of pancreatic cancer cells to targeted therapies. ( Abrams, SL; Cervello, M; Follo, MY; Manzoli, L; Martelli, AM; McCubrey, JA; Ratti, S, 2023) |
| "Hydroxychloroquine (HCQ) has been the subject of multiple recent preclinical and clinical studies for its beneficial use in the combination treatments of different types of cancers." | 1.72 | Polymeric Chloroquine as an Effective Antimigration Agent in the Treatment of Pancreatic Cancer. ( Bennett, RG; Ding, L; Kapoor, E; Khan, R; Oupický, D; Panja, S; Tang, S; Tang, W, 2022) |
| "Pterostilbene is a stilbenoid chemically related to resveratrol, and has potential for the treatment of cancers." | 1.62 | Chloroquine Potentiates the Anticancer Effect of Pterostilbene on Pancreatic Cancer by Inhibiting Autophagy and Downregulating the RAGE/STAT3 Pathway. ( Chen, RJ; Chen, YY; Ho, YS; Lee, YC; Lyu, YJ; Pan, MH; Wang, YJ, 2021) |
| "Penfluridol treatment induced apoptosis and inhibited the growth of Panc-1, BxPC-3 and AsPC-1, pancreatic cancer cells with IC50 ranging between 6-7 μM after 24 h of treatment." | 1.43 | Penfluridol suppresses pancreatic tumor growth by autophagy-mediated apoptosis. ( Ranjan, A; Srivastava, SK, 2016) |
| "The role of autophagy in pancreatic cancer is still not clear." | 1.40 | Autophagy is needed for the growth of pancreatic adenocarcinoma and has a cytoprotective effect against anticancer drugs. ( Bläuer, M; Hashimoto, D; Hirota, M; Ikonen, NH; Laukkarinen, J; Sand, J, 2014) |
| "Pancreatic cancer is an aggressive disease with a poor prognosis." | 1.40 | Combination of chloroquine and GX15-070 (obatoclax) results in synergistic cytotoxicity against pancreatic cancer cells. ( Chen, S; Cui, L; Cui, X; Edwards, H; Ge, Y; Wang, G, 2014) |
| "Moreover, pancreatic cancer aggressiveness is closely related to high levels of pro-survival mediators, which can ultimately lead to rapid disease progression, resistance and metastasis." | 1.39 | Calix[6]arene bypasses human pancreatic cancer aggressiveness: downregulation of receptor tyrosine kinases and induction of cell death by reticulum stress and autophagy. ( de Fátima, A; de Jesus, MB; Ferreira-Halder, CV; Nakamura, CV; Pelizzaro-Rocha, KJ; Reis, FS; Ruela-de-Sousa, RR, 2013) |
| "We evaluated these compounds in pancreatic cancer cells in vitro and observed specific antagonism of CXCR4-mediated signaling and cell proliferation." | 1.38 | Identification of anti-malarial compounds as novel antagonists to chemokine receptor CXCR4 in pancreatic cancer cells. ( Heinrich, EL; Hsin, LY; Kim, J; Labarge, S; Lee, W; Li, H; Lu, J; Shen, X; Vaidehi, N; Yip, ML, 2012) |
| "Here we show that pancreatic cancers have a distinct dependence on autophagy." | 1.37 | Pancreatic cancers require autophagy for tumor growth. ( Bardeesy, N; Bause, A; Contino, G; Dell'antonio, G; Doglioni, C; Haigis, M; Kimmelman, AC; Li, Y; Liesa, M; Mautner, J; Sahin, E; Shirihai, OS; Stommel, JM; Tonon, G; Wang, X; Yang, S; Ying, H, 2011) |
| "Cholecystokinin is thought to be an important factor regulating the growth of human pancreatic cancers." | 1.29 | Loxiglumide (CR1505), a cholecystokinin antagonist, specifically inhibits the growth of human pancreatic cancer lines xenografted into nude mice. ( Fukumoto, M; Hayashi, H; Imamura, M; Kawabata, K; Manabe, T; Masai, Y; Morimoto, H; Nio, Y; Tsubono, M, 1993) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 3 (6.52) | 18.7374 |
| 1990's | 2 (4.35) | 18.2507 |
| 2000's | 2 (4.35) | 29.6817 |
| 2010's | 28 (60.87) | 24.3611 |
| 2020's | 11 (23.91) | 2.80 |
| Authors | Studies |
|---|---|
| Chen, Y | 1 |
| Lopez-Sanchez, M | 1 |
| Savoy, DN | 1 |
| Billadeau, DD | 1 |
| Dow, GS | 1 |
| Kozikowski, AP | 1 |
| Li, J | 1 |
| Seupel, R | 1 |
| Bruhn, T | 2 |
| Feineis, D | 2 |
| Kaiser, M | 2 |
| Brun, R | 2 |
| Mudogo, V | 2 |
| Awale, S | 2 |
| Bringmann, G | 2 |
| Tshitenge, DT | 1 |
| Schmidt, D | 1 |
| Würthner, F | 1 |
| Chen, RJ | 1 |
| Lyu, YJ | 1 |
| Chen, YY | 1 |
| Lee, YC | 1 |
| Pan, MH | 1 |
| Ho, YS | 1 |
| Wang, YJ | 1 |
| Stalnecker, CA | 2 |
| Coleman, MF | 1 |
| Bryant, KL | 3 |
| Selvarajoo, N | 1 |
| Stanslas, J | 1 |
| Islam, MK | 1 |
| Sagineedu, SR | 1 |
| Lian, HK | 1 |
| Lim, JCW | 1 |
| Zhou, R | 1 |
| Kusaka, E | 1 |
| Wang, Y | 2 |
| Zhang, J | 1 |
| Webb, A | 1 |
| Carrico-Moniz, D | 1 |
| Zhou, Z | 1 |
| Dong, Y | 1 |
| Li, N | 1 |
| Niu, M | 1 |
| Wang, S | 1 |
| Zhou, Y | 1 |
| Sun, Z | 1 |
| Chu, P | 1 |
| Tang, Z | 1 |
| McCubrey, JA | 1 |
| Abrams, SL | 1 |
| Follo, MY | 1 |
| Manzoli, L | 1 |
| Ratti, S | 1 |
| Martelli, AM | 1 |
| Cervello, M | 1 |
| Khan, R | 1 |
| Panja, S | 1 |
| Ding, L | 1 |
| Tang, S | 1 |
| Tang, W | 1 |
| Kapoor, E | 1 |
| Bennett, RG | 1 |
| Oupický, D | 2 |
| Silvis, MR | 1 |
| Silva, D | 1 |
| Rohweder, R | 1 |
| Schuman, S | 1 |
| Gudipaty, S | 1 |
| Truong, A | 2 |
| Yap, J | 1 |
| Affolter, K | 1 |
| McMahon, M | 2 |
| Kinsey, C | 1 |
| Pan, H | 1 |
| Zhu, S | 1 |
| Gong, T | 1 |
| Wu, D | 1 |
| Zhao, Y | 1 |
| Yan, J | 1 |
| Dai, C | 1 |
| Huang, Y | 1 |
| Yang, Y | 1 |
| Guo, Y | 1 |
| Yamamoto, K | 1 |
| Venida, A | 1 |
| Yano, J | 1 |
| Biancur, DE | 1 |
| Kakiuchi, M | 1 |
| Gupta, S | 1 |
| Sohn, ASW | 1 |
| Mukhopadhyay, S | 1 |
| Lin, EY | 1 |
| Parker, SJ | 1 |
| Banh, RS | 1 |
| Paulo, JA | 1 |
| Wen, KW | 1 |
| Debnath, J | 1 |
| Kim, GE | 1 |
| Mancias, JD | 1 |
| Fearon, DT | 1 |
| Perera, RM | 1 |
| Kimmelman, AC | 4 |
| Chang, WH | 1 |
| Nguyen, TT | 1 |
| Hsu, CH | 1 |
| Kim, HJ | 1 |
| Ying, H | 3 |
| Erickson, JW | 1 |
| Der, CJ | 2 |
| Cerione, RA | 1 |
| Antonyak, MA | 1 |
| Sleightholm, R | 1 |
| Yang, B | 1 |
| Yu, F | 1 |
| Xie, Y | 1 |
| Samaras, P | 1 |
| Tusup, M | 1 |
| Nguyen-Kim, TDL | 1 |
| Seifert, B | 1 |
| Bachmann, H | 1 |
| von Moos, R | 1 |
| Knuth, A | 1 |
| Pascolo, S | 1 |
| Fu, Z | 1 |
| Cheng, X | 1 |
| Kuang, J | 1 |
| Feng, H | 2 |
| Chen, L | 1 |
| Liang, J | 1 |
| Shen, X | 2 |
| Yuen, S | 1 |
| Peng, C | 1 |
| Shen, B | 1 |
| Jin, Z | 1 |
| Qiu, W | 1 |
| Monma, H | 1 |
| Iida, Y | 1 |
| Moritani, T | 1 |
| Okimoto, T | 1 |
| Tanino, R | 1 |
| Tajima, Y | 1 |
| Harada, M | 1 |
| Boone, BA | 1 |
| Murthy, P | 1 |
| Miller-Ocuin, J | 1 |
| Doerfler, WR | 1 |
| Ellis, JT | 1 |
| Liang, X | 1 |
| Ross, MA | 1 |
| Wallace, CT | 1 |
| Sperry, JL | 1 |
| Lotze, MT | 1 |
| Neal, MD | 1 |
| Zeh, HJ | 1 |
| Vidoni, C | 1 |
| Ferraresi, A | 1 |
| Seca, C | 1 |
| Secomandi, E | 1 |
| Isidoro, C | 1 |
| Wei, DM | 1 |
| Jiang, MT | 1 |
| Lin, P | 1 |
| Yang, H | 1 |
| Dang, YW | 1 |
| Yu, Q | 1 |
| Liao, DY | 1 |
| Luo, DZ | 1 |
| Chen, G | 1 |
| Kinsey, CG | 1 |
| Camolotto, SA | 1 |
| Boespflug, AM | 1 |
| Guillen, KP | 1 |
| Foth, M | 1 |
| Schuman, SS | 1 |
| Shea, JE | 1 |
| Seipp, MT | 1 |
| Yap, JT | 1 |
| Burrell, LD | 1 |
| Lum, DH | 1 |
| Whisenant, JR | 1 |
| Gilcrease, GW | 1 |
| Cavalieri, CC | 1 |
| Rehbein, KM | 1 |
| Cutler, SL | 1 |
| Affolter, KE | 1 |
| Welm, AL | 1 |
| Welm, BE | 1 |
| Scaife, CL | 1 |
| Snyder, EL | 1 |
| Zeitouni, D | 1 |
| Klomp, JE | 1 |
| Peng, S | 1 |
| Tikunov, AP | 1 |
| Gunda, V | 1 |
| Pierobon, M | 1 |
| Waters, AM | 1 |
| George, SD | 1 |
| Tomar, G | 1 |
| Papke, B | 1 |
| Hobbs, GA | 1 |
| Yan, L | 1 |
| Hayes, TK | 1 |
| Diehl, JN | 1 |
| Goode, GD | 1 |
| Chaika, NV | 1 |
| Zhang, GF | 1 |
| Witkiewicz, AK | 1 |
| Knudsen, ES | 1 |
| Petricoin, EF | 1 |
| Singh, PK | 1 |
| Macdonald, JM | 1 |
| Tran, NL | 1 |
| Lyssiotis, CA | 1 |
| Cox, AD | 1 |
| Elliott, IA | 1 |
| Dann, AM | 1 |
| Xu, S | 1 |
| Kim, SS | 1 |
| Abt, ER | 1 |
| Kim, W | 1 |
| Poddar, S | 1 |
| Moore, A | 1 |
| Zhou, L | 1 |
| Williams, JL | 1 |
| Capri, JR | 1 |
| Ghukasyan, R | 1 |
| Matsumura, C | 1 |
| Tucker, DA | 1 |
| Armstrong, WR | 1 |
| Cabebe, AE | 1 |
| Wu, N | 1 |
| Li, L | 1 |
| Le, TM | 1 |
| Radu, CG | 1 |
| Donahue, TR | 1 |
| Yan, Z | 1 |
| Ohuchida, K | 2 |
| Fei, S | 1 |
| Zheng, B | 2 |
| Guan, W | 1 |
| Kibe, S | 1 |
| Ando, Y | 1 |
| Koikawa, K | 2 |
| Abe, T | 2 |
| Iwamoto, C | 2 |
| Shindo, K | 1 |
| Moriyama, T | 2 |
| Nakata, K | 2 |
| Miyasaka, Y | 2 |
| Ohtsuka, T | 2 |
| Mizumoto, K | 2 |
| Hashizume, M | 2 |
| Nakamura, M | 2 |
| Pelizzaro-Rocha, KJ | 1 |
| de Jesus, MB | 1 |
| Ruela-de-Sousa, RR | 1 |
| Nakamura, CV | 1 |
| Reis, FS | 1 |
| de Fátima, A | 1 |
| Ferreira-Halder, CV | 1 |
| Hashimoto, D | 1 |
| Bläuer, M | 1 |
| Hirota, M | 1 |
| Ikonen, NH | 1 |
| Sand, J | 1 |
| Laukkarinen, J | 1 |
| Frieboes, HB | 1 |
| Huang, JS | 1 |
| Yin, WC | 1 |
| McNally, LR | 1 |
| Balic, A | 1 |
| Sørensen, MD | 1 |
| Trabulo, SM | 1 |
| Sainz, B | 1 |
| Cioffi, M | 1 |
| Vieira, CR | 1 |
| Miranda-Lorenzo, I | 1 |
| Hidalgo, M | 1 |
| Kleeff, J | 1 |
| Erkan, M | 1 |
| Heeschen, C | 1 |
| Min, H | 1 |
| Xu, M | 1 |
| Chen, ZR | 1 |
| Zhou, JD | 1 |
| Huang, M | 1 |
| Zheng, K | 1 |
| Zou, XP | 1 |
| Wang, G | 1 |
| Chen, S | 1 |
| Edwards, H | 1 |
| Cui, X | 1 |
| Cui, L | 1 |
| Ge, Y | 1 |
| Kim, SE | 1 |
| Park, HJ | 1 |
| Jeong, HK | 1 |
| Kim, MJ | 1 |
| Kim, M | 1 |
| Bae, ON | 1 |
| Baek, SH | 1 |
| Ranjan, A | 1 |
| Srivastava, SK | 1 |
| Loncle, C | 1 |
| Molejon, MI | 1 |
| Lac, S | 1 |
| Tellechea, JI | 1 |
| Lomberk, G | 1 |
| Gramatica, L | 1 |
| Fernandez Zapico, MF | 1 |
| Dusetti, N | 1 |
| Urrutia, R | 1 |
| Iovanna, JL | 1 |
| Endo, S | 1 |
| Takesue, S | 1 |
| Nakayama, H | 1 |
| Okumura, T | 1 |
| Sada, M | 1 |
| Horioka, K | 1 |
| Mizuuchi, Y | 1 |
| Murata, M | 1 |
| Oda, Y | 1 |
| Yang, S | 2 |
| Wang, X | 1 |
| Contino, G | 1 |
| Liesa, M | 1 |
| Sahin, E | 1 |
| Bause, A | 1 |
| Li, Y | 1 |
| Stommel, JM | 1 |
| Dell'antonio, G | 1 |
| Mautner, J | 1 |
| Tonon, G | 1 |
| Haigis, M | 1 |
| Shirihai, OS | 1 |
| Doglioni, C | 1 |
| Bardeesy, N | 1 |
| Jenks, S | 1 |
| Larsen, CJ | 1 |
| Kim, J | 1 |
| Yip, ML | 1 |
| Li, H | 1 |
| Hsin, LY | 1 |
| Labarge, S | 1 |
| Heinrich, EL | 1 |
| Lee, W | 1 |
| Lu, J | 1 |
| Vaidehi, N | 1 |
| Nio, Y | 1 |
| Tsubono, M | 1 |
| Morimoto, H | 1 |
| Kawabata, K | 1 |
| Masai, Y | 1 |
| Hayashi, H | 1 |
| Manabe, T | 1 |
| Imamura, M | 1 |
| Fukumoto, M | 1 |
| Gibson, GA | 1 |
| Hill, WG | 1 |
| Weisz, OA | 1 |
| Svoboda, M | 1 |
| Dupuche, MH | 1 |
| Lambert, M | 1 |
| Bui, D | 1 |
| Christophe, J | 1 |
| Zeilhofer, HU | 1 |
| Mollenhauer, J | 1 |
| Brune, K | 1 |
| Göke, R | 1 |
| Richter, G | 1 |
| Göke, B | 1 |
| Trautmann, M | 1 |
| Arnold, R | 1 |
| Hutton, JC | 1 |
| Davidson, HW | 1 |
| Grimaldi, KA | 1 |
| Peshavaria, M | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Multicenter, Open-label, ExploRatory Platform Trial to EValuate ImmunOtherapy Combinations With Chemotherapy for the Treatment of Patients With PreviousLy UnTreated MetastatIc Pancreatic AdenOcarciNoma (REVOLUTION)[NCT04787991] | Phase 1 | 45 participants (Anticipated) | Interventional | 2021-08-09 | Active, not recruiting | ||
| Phase I/II Study of Preoperative Gemcitabine in Combination With Oral Hydroxychloroquine (GcHc) in Subjects With High Risk Stage IIb or III Adenocarcinoma of the Pancreas[NCT01128296] | Phase 1/Phase 2 | 35 participants (Actual) | Interventional | 2010-10-31 | Completed | ||
| Randomized Phase II Trial of Pre-Operative Gemcitabine and Nab Paclitacel With or With Out Hydroxychloroquine[NCT01978184] | Phase 2 | 104 participants (Actual) | Interventional | 2013-11-30 | Completed | ||
| Stereotactic Body Radiation Therapy Plus Pembrolizumab and Trametinib vs. Stereotactic Body Radiation Therapy Plus Gemcitabine for Locally Recurrent Pancreatic Cancer After Surgical Resection: an Open-label, Randomized, Controlled, Phase 2 Trial[NCT02704156] | Phase 2 | 170 participants (Actual) | Interventional | 2016-10-31 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Median number of months of disease-free survival for participants receiving study treatment. (NCT01128296)
Timeframe: Up to 30 months
| Intervention | months (Median) |
|---|---|
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (1200 mg/Day) | 11.97 |
Number of Participants at each dose level of HCQ that experienced a Dose Limiting Toxicity (DLT). (NCT01128296)
Timeframe: Up to 31 days
| Intervention | participants (Number) |
|---|---|
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (200 mg/Day) | 0 |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (400 mg/Day) | 0 |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (600 mg/Day) | 0 |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (800 mg/Day) | 0 |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (1000 mg/Day) | 0 |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (1200 mg/Day) | 0 |
Median number of months of overall survival for participants receiving study treatment. (NCT01128296)
Timeframe: Up to 35 months
| Intervention | months (Median) |
|---|---|
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 34.83 |
Number of participants that underwent a resection with microscopically margin-negative resection in which no gross or microscopic tumor remains in the primary tumor bed (24) / number of that completed treatment (31) (NCT01128296)
Timeframe: Up to 30 months
| Intervention | percentage of participants (Number) |
|---|---|
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 77 |
Median number of months of disease-free survival for participants who experienced Ca 19-9 (surrogate biomarker) response (either an increase or decrease in Ca 19-9), or no Ca 19-9 response. Per participant increases in Ca 19-9 ranged from >0 to 225%. Per participant decreases in Ca 19-9 ranged from >0 to 100%. (NCT01128296)
Timeframe: Up to 30 months
| Intervention | months (Median) | |
|---|---|---|
| Ca 19-9 Response | No Ca 19-9 Response | |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 21.4 | 6.9 |
Median number of months of disease-free survival in participants who did and did not experience response to HCQ treatment. Patients who had >51 % increase in their LC3-II staining were classified as having a response to HCQ. (NCT01128296)
Timeframe: Up to 30 months
| Intervention | months (Median) | |
|---|---|---|
| Response to HQC treatment | No response to HQC treatment | |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 15.03 | 6.9 |
(NCT01128296)
Timeframe: Up to 35 months
| Intervention | months (Median) | |
|---|---|---|
| p53 WT | p53 Mutant | |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 21.4 | 11.8 |
Median number of months of overall survival for participants who experienced Ca 19-9 (surrogate biomarker) response (either an increase or decrease in Ca 19-9), or, no Ca 19-9 response. Per participant increases in Ca 19-9 ranged from >0 to 225%. Per participant decreases in Ca 19-9 ranged from >0 to 100%. (NCT01128296)
Timeframe: Up to 35 months
| Intervention | months (Median) | |
|---|---|---|
| Ca 19-9 Response (increase or decrease) | No Ca 19-9 Response | |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 34.8 | 8.8 |
(NCT01128296)
Timeframe: Up to 35 months
| Intervention | months (Median) | |
|---|---|---|
| p53 WT | p53 Mutant | |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | NA | 26.1 |
Median number of months of overall survival in participants who did and did not experience response to HCQ treatment. Patients who had >51 % increase in their LC3-II staining were classified as having a response to HCQ. (NCT01128296)
Timeframe: Up to 35 months
| Intervention | months (Median) | |
|---|---|---|
| Response to HQC treatment | No response to HQC treatment | |
| Preoperative Gemcitabine (1500 mg/m^2) + HCQ (≤1200 mg/Day) | 34.83 | 10.83 |
The mean age of patients at the time of diagnosis of disease (as a variable in the proportional odds logistic regression, secondary analysis of Evans Grade). (NCT01978184)
Timeframe: Baseline - At the time of diagnosis, prior to treatment
| Intervention | years (Mean) |
|---|---|
| Gemcitabine + Abraxane | 63.6 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 66.1 |
Levels of Carbohydrate antigen 19-9 (CA19-9) response to pre-operative gemcitabine/ nab-paclitaxel measured in the serum (original scale) (NCT01978184)
Timeframe: Prior to treatment (average 73.3 +/- 9.9 days prior to surgery)
| Intervention | units per milliliter (U/mL) (Mean) |
|---|---|
| Gemcitabine + Abraxane | 351.820 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 1534.633 |
Levels of Carbohydrate antigen 19-9 (CA19-9) response to pre-operative gemcitabine/ nab-paclitaxel measured in the serum (original scale). (NCT01978184)
Timeframe: After treatment (50-67 days post treatment/surgery)
| Intervention | units per milliliter (U/mL) (Mean) |
|---|---|
| Gemcitabine + Abraxane | 319.079 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 1696.710 |
Tumor size as measured via computerized tomography (CT) scan (as a variable in the proportional odds logistic regression, secondary analysis of Evans Grade). (NCT01978184)
Timeframe: Baseline - At the time of diagnosis, prior to treatment
| Intervention | centimeters (Mean) |
|---|---|
| Gemcitabine + Abraxane | 2.562069 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 2.543056 |
The proportion of participants with positive (disease) lymph nodes involvement. (NCT01978184)
Timeframe: At the time of surgery (≥2 weeks and ≤6 weeks post chemotherapy)
| Intervention | proportion of participants (Number) |
|---|---|
| Gemcitabine + Abraxane | 0.8 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 0.561 |
The proportion of participants having resection for cure or complete remission, in which the surgical margins are negative for tumor cells. R0 resection indicates a microscopically margin-negative resection, in which no gross or microscopic tumor remains in the primary tumor bed. (NCT01978184)
Timeframe: At the time of surgery (≥2 weeks and ≤6 weeks post chemotherapy)
| Intervention | proportion of participants (Mean) |
|---|---|
| Gemcitabine + Abraxane | 0.7 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 0.829 |
The Charlson Comorbidity Index is a method of categorizing comorbidities of patients based on the International Classification of Diseases (ICD) diagnosis codes found in administrative data, such as hospital abstracts data. Each comorbidity category has an associated weight (from 1 to 6), based on the adjusted risk of mortality or resource use, and the sum of all the weights results in a single comorbidity score for a patient. A score of zero indicates that no comorbidities were found. The higher the score, the more likely the predicted outcome will result in mortality or higher resource use. Up to 12 comorbidities with various weightings can result in a maximum score of 24. The minimum score is zero. (NCT01978184)
Timeframe: Prior to treatment
| Intervention | Participants (Count of Participants) | ||||||
|---|---|---|---|---|---|---|---|
| Age-Adjusted CCI=2 | Age-Adjusted CCI=3 | Age-Adjusted CCI=4 | Age-Adjusted CCI=5 | Age-Adjusted CCI=6 | Age-Adjusted CCI=7 | Age-Adjusted CCI=8 | |
| Gemcitabine + Abraxane | 3 | 5 | 7 | 8 | 5 | 2 | 0 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 1 | 2 | 11 | 15 | 8 | 2 | 2 |
"The number of participants in cancer diagnosis stage groups. Stage 0: cancer hasn't spread to nearby tissues/located in the same of origin.Stage I: cancers hasn't grown deeply into nearby tissues or spread to lymph nodes or other parts of the body. Stage II and III: cancers have grown more deeply into nearby tissues (may have metastasized to lymph nodes but not other parts of the body). Stage IV: most advanced stage (metastatic cancer) ; cancer has spread to other parts of the body. Stages subdivided further into the categories A (less agressive disease) and B (more advanced cancer). Example: stage IIA is less aggressive than stage IIB, but stage IIIA is more aggressive than stage IIB. (Stage variable used in the proportional odds logistic regression, secondary analysis of Evans Grade)." (NCT01978184)
Timeframe: Baseline - At the time of diagnosis, prior to treatment
| Intervention | Participants (Count of Participants) | ||||
|---|---|---|---|---|---|
| IA | IB | IIA | IIB | Not Available | |
| Gemcitabine + Abraxane | 0 | 5 | 6 | 19 | 0 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 2 | 1 | 11 | 20 | 7 |
The number of patients who exhibited an Evans grade Histologic response (I, IIA, IIB, or III) to pre-operative gemcitabine / nab-paclitaxel. Histological response validated scoring system by Evans is as follows: Grade I: 1-9% tumor destruction, Grade II: 10 - 90%, Grade III: >90% tumor destruction (Grade IIA = 10-50% of tumor cells destroyed; Grade IIB = 50-90% of tumor cells destroyed), Grade IV: Absence of viable tumor cells. (NCT01978184)
Timeframe: Up to 4 years
| Intervention | number of participants (Number) | |||
|---|---|---|---|---|
| Evans grade - I | Evans grade - IIA | Evans grade - IIB | Evans grade - III | |
| Gemcitabine + Abraxane | 10 | 17 | 3 | 0 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 7 | 12 | 13 | 9 |
The number of participants who had robotic resection surgery. (Robotic surgery variable used in the proportional odds logistic regression, secondary analysis of Evans Grade). (NCT01978184)
Timeframe: At the time of surgery (≥2 weeks and ≤6 weeks post chemotherapy)
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| Yes - robotic surgical resection procedure | No - not robotic surgical resection procedure | |
| Gemcitabine + Abraxane | 8 | 22 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 10 | 31 |
The number of participants in having each type of surgical resection procedure: Celiac Axis Resection With Distal Pancreatectomy (DPCAR) (Modified Appleby), Distal Pancreatectomy, Total Pancreatectomy, or Whipple. (Operation variable used in the proportional odds logistic regression, secondary analysis of Evans Grade). (NCT01978184)
Timeframe: At the time of surgery (≥2 weeks and ≤6 weeks post chemotherapy)
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| DPCAR | Distal Pancreatectomy | Total Pancreatectomy | Whipple | |
| Gemcitabine + Abraxane | 2 | 3 | 1 | 24 |
| Gemcitabine + Abraxane and Hydroxychloroquine | 0 | 5 | 0 | 36 |
The time from the start of treatment until documentation of any clinical or radiological disease progression or death, whichever occurred first. Progression is assessed by the Response Evaluation Criteria in Solid Tumors (RECIST; version 1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT02704156)
Timeframe: 3 years
| Intervention | months (Median) |
|---|---|
| SBRT Plus Gemcitabine | 5.4 |
| SBRT Plus Pembrolizumab and Trametinib | 8.2 |
The time from the start of treatment to death (NCT02704156)
Timeframe: 3 years
| Intervention | months (Median) |
|---|---|
| SBRT Plus Gemcitabine | 12.8 |
| SBRT Plus Pembrolizumab and Trametinib | 14.9 |
The number of patients alive at 1 year and 2 years. (NCT02704156)
Timeframe: 2 year
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| 1-year OS rate | 2-year OS rate | |
| SBRT Plus Gemcitabine | 48 | 0 |
| SBRT Plus Pembrolizumab and Trametinib | 53 | 2 |
The proportion of patients without disease progressions at 1 year and 2 years. (NCT02704156)
Timeframe: 2 years
| Intervention | Participants (Count of Participants) | |
|---|---|---|
| 1-year PFS rate | 2-year PFS rate | |
| SBRT Plus Gemcitabine | 7 | 0 |
| SBRT Plus Pembrolizumab and Trametinib | 18 | 0 |
The analysis of quality of life is based on European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (QLQ-C30). All scales and subscales range from 0 to 100. Regarding physical functioning, role functioning, emotional functioning, cognitive functioning, social functioning and global health, higher scores may indicate better outcomes. In the case of fatigue, nausea and vomitting, pain, dyspnea, insomina, appetite loss, constipation, diarrhea and financial difficulties, lower scores may indicate better outcomes. Scales of all items are independent and not combined to compute a total score. (NCT02704156)
Timeframe: 3 years
| Intervention | units on a scale (Mean) | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Physical functioning | Role functioning | Emotional functioning | Cognitive functioning | Social functioning | Global health | Fatigue | Nausea and vomitting | Pain | Dyspnea | Insomina | Appetite loss | Constipation | Diarrhea | Financial difficulties | |
| SBRT Plus Gemcitabine | 86.2 | 81.8 | 73.9 | 84.7 | 85.5 | 83.6 | 29.6 | 29.4 | 23.9 | 16.1 | 14.9 | 31.0 | 14.5 | 15.7 | 16.8 |
| SBRT Plus Pembrolizumab and Trametinib | 83.7 | 84.5 | 72.1 | 83.3 | 84.1 | 83.2 | 26.6 | 28.8 | 26.5 | 13.7 | 17.6 | 33.3 | 16.5 | 15.7 | 17.2 |
Treatment-related adverse effects are determined by National Cancer Institute Common Toxicity Criteria for Adverse Events (CTCAE) version 4.0. (NCT02704156)
Timeframe: 3 years
| Intervention | Participants (Count of Participants) | |||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Grade 3 pyrexia | Grade 3 vomitting | Grade 3 and 4 increased ALT or AST | Grade 3 stomatitis | Grade 3 rash | Grade 3 and 4 neutropenia | Grade 3 thrombocytopenia | Grade 3 increased blood bilirubin | Grade 3 hypokalemia | Grade 3 hyponatremia | Grade 3 pneumonia | Grade 3 hypertension | |
| SBRT Plus Gemcitabine | 0 | 2 | 6 | 0 | 0 | 9 | 4 | 0 | 0 | 0 | 0 | 0 |
| SBRT Plus Pembrolizumab and Trametinib | 2 | 1 | 10 | 1 | 2 | 1 | 1 | 4 | 1 | 3 | 1 | 2 |
1 review available for chloroquine and Cancer of Pancreas
| Article | Year |
|---|---|
Pharmacological Modulation of Apoptosis and Autophagy in Pancreatic Cancer Treatment.
Topics: Antineoplastic Agents; Apoptosis; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB | 2022 |
Pharmacological Modulation of Apoptosis and Autophagy in Pancreatic Cancer Treatment.
Topics: Antineoplastic Agents; Apoptosis; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB | 2022 |
Pharmacological Modulation of Apoptosis and Autophagy in Pancreatic Cancer Treatment.
Topics: Antineoplastic Agents; Apoptosis; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB | 2022 |
Pharmacological Modulation of Apoptosis and Autophagy in Pancreatic Cancer Treatment.
Topics: Antineoplastic Agents; Apoptosis; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB | 2022 |
1 trial available for chloroquine and Cancer of Pancreas
| Article | Year |
|---|---|
Phase I study of a chloroquine-gemcitabine combination in patients with metastatic or unresectable pancreatic cancer.
Topics: Aged; Antimalarials; Antimetabolites, Antineoplastic; Chloroquine; Deoxycytidine; Female; Gemcitabin | 2017 |
44 other studies available for chloroquine and Cancer of Pancreas
| Article | Year |
|---|---|
A series of potent and selective, triazolylphenyl-based histone deacetylases inhibitors with activity against pancreatic cancer cells and Plasmodium falciparum.
Topics: Animals; Antimalarials; Antineoplastic Agents; Cell Line, Tumor; Drug Resistance; Drug Screening Ass | 2008 |
Jozilebomines A and B, Naphthylisoquinoline Dimers from the Congolese Liana Ancistrocladus ileboensis, with Antiausterity Activities against the PANC-1 Human Pancreatic Cancer Cell Line.
Topics: Algorithms; Alkaloids; Animals; Antimalarials; Antineoplastic Agents, Phytogenic; Congo; Drug Screen | 2017 |
Ealamines A-H, a Series of Naphthylisoquinolines with the Rare 7,8'-Coupling Site, from the Congolese Liana
Topics: Animals; Antineoplastic Agents, Phytogenic; Antiprotozoal Agents; Caryophyllales; Drug Screening Ass | 2019 |
Chloroquine Potentiates the Anticancer Effect of Pterostilbene on Pancreatic Cancer by Inhibiting Autophagy and Downregulating the RAGE/STAT3 Pathway.
Topics: Antigens, Neoplasm; Antineoplastic Agents; Autophagy; Carcinoma, Pancreatic Ductal; Cell Proliferati | 2021 |
Susceptibility to autophagy inhibition is enhanced by dual IGF1R and MAPK/ERK inhibition in pancreatic cancer.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Humans; Pancreatic Neoplasms | 2022 |
Susceptibility to autophagy inhibition is enhanced by dual IGF1R and MAPK/ERK inhibition in pancreatic cancer.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Humans; Pancreatic Neoplasms | 2022 |
Susceptibility to autophagy inhibition is enhanced by dual IGF1R and MAPK/ERK inhibition in pancreatic cancer.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Humans; Pancreatic Neoplasms | 2022 |
Susceptibility to autophagy inhibition is enhanced by dual IGF1R and MAPK/ERK inhibition in pancreatic cancer.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Humans; Pancreatic Neoplasms | 2022 |
Isoprenylated Coumarin Exhibits Anti-proliferative Effects in Pancreatic Cancer Cells Under Nutrient Starvation by Inhibiting Autophagy.
Topics: Adenocarcinoma; Autophagy; Cell Line, Tumor; Chloroquine; Coumarins; Glucose; Humans; Nutrients; Pan | 2022 |
Isoprenylated Coumarin Exhibits Anti-proliferative Effects in Pancreatic Cancer Cells Under Nutrient Starvation by Inhibiting Autophagy.
Topics: Adenocarcinoma; Autophagy; Cell Line, Tumor; Chloroquine; Coumarins; Glucose; Humans; Nutrients; Pan | 2022 |
Isoprenylated Coumarin Exhibits Anti-proliferative Effects in Pancreatic Cancer Cells Under Nutrient Starvation by Inhibiting Autophagy.
Topics: Adenocarcinoma; Autophagy; Cell Line, Tumor; Chloroquine; Coumarins; Glucose; Humans; Nutrients; Pan | 2022 |
Isoprenylated Coumarin Exhibits Anti-proliferative Effects in Pancreatic Cancer Cells Under Nutrient Starvation by Inhibiting Autophagy.
Topics: Adenocarcinoma; Autophagy; Cell Line, Tumor; Chloroquine; Coumarins; Glucose; Humans; Nutrients; Pan | 2022 |
An oleanolic acid derivative, K73-03, inhibits pancreatic cancer cells proliferation in vitro and in vivo via blocking EGFR/Akt pathway.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB Receptors; | 2022 |
An oleanolic acid derivative, K73-03, inhibits pancreatic cancer cells proliferation in vitro and in vivo via blocking EGFR/Akt pathway.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB Receptors; | 2022 |
An oleanolic acid derivative, K73-03, inhibits pancreatic cancer cells proliferation in vitro and in vivo via blocking EGFR/Akt pathway.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB Receptors; | 2022 |
An oleanolic acid derivative, K73-03, inhibits pancreatic cancer cells proliferation in vitro and in vivo via blocking EGFR/Akt pathway.
Topics: Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Chloroquine; ErbB Receptors; | 2022 |
Effects of chloroquine and hydroxychloroquine on the sensitivity of pancreatic cancer cells to targeted therapies.
Topics: Animals; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Hydroxychloroquine; Mice; Mito | 2023 |
Effects of chloroquine and hydroxychloroquine on the sensitivity of pancreatic cancer cells to targeted therapies.
Topics: Animals; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Hydroxychloroquine; Mice; Mito | 2023 |
Effects of chloroquine and hydroxychloroquine on the sensitivity of pancreatic cancer cells to targeted therapies.
Topics: Animals; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Hydroxychloroquine; Mice; Mito | 2023 |
Effects of chloroquine and hydroxychloroquine on the sensitivity of pancreatic cancer cells to targeted therapies.
Topics: Animals; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Hydroxychloroquine; Mice; Mito | 2023 |
Polymeric Chloroquine as an Effective Antimigration Agent in the Treatment of Pancreatic Cancer.
Topics: Antineoplastic Agents; Chloroquine; Humans; Hydroxychloroquine; Pancreatic Neoplasms; Polymers | 2022 |
Polymeric Chloroquine as an Effective Antimigration Agent in the Treatment of Pancreatic Cancer.
Topics: Antineoplastic Agents; Chloroquine; Humans; Hydroxychloroquine; Pancreatic Neoplasms; Polymers | 2022 |
Polymeric Chloroquine as an Effective Antimigration Agent in the Treatment of Pancreatic Cancer.
Topics: Antineoplastic Agents; Chloroquine; Humans; Hydroxychloroquine; Pancreatic Neoplasms; Polymers | 2022 |
Polymeric Chloroquine as an Effective Antimigration Agent in the Treatment of Pancreatic Cancer.
Topics: Antineoplastic Agents; Chloroquine; Humans; Hydroxychloroquine; Pancreatic Neoplasms; Polymers | 2022 |
MYC-mediated resistance to trametinib and HCQ in PDAC is overcome by CDK4/6 and lysosomal inhibition.
Topics: Carcinoma, Pancreatic Ductal; Chloroquine; Cyclin-Dependent Kinase 4; Humans; Hydroxychloroquine; Ly | 2023 |
MYC-mediated resistance to trametinib and HCQ in PDAC is overcome by CDK4/6 and lysosomal inhibition.
Topics: Carcinoma, Pancreatic Ductal; Chloroquine; Cyclin-Dependent Kinase 4; Humans; Hydroxychloroquine; Ly | 2023 |
MYC-mediated resistance to trametinib and HCQ in PDAC is overcome by CDK4/6 and lysosomal inhibition.
Topics: Carcinoma, Pancreatic Ductal; Chloroquine; Cyclin-Dependent Kinase 4; Humans; Hydroxychloroquine; Ly | 2023 |
MYC-mediated resistance to trametinib and HCQ in PDAC is overcome by CDK4/6 and lysosomal inhibition.
Topics: Carcinoma, Pancreatic Ductal; Chloroquine; Cyclin-Dependent Kinase 4; Humans; Hydroxychloroquine; Ly | 2023 |
Matrix stiffness triggers chemoresistance through elevated autophagy in pancreatic ductal adenocarcinoma.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Cell Proliferation; Chloroquine; Deoxycyt | 2023 |
Matrix stiffness triggers chemoresistance through elevated autophagy in pancreatic ductal adenocarcinoma.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Cell Proliferation; Chloroquine; Deoxycyt | 2023 |
Matrix stiffness triggers chemoresistance through elevated autophagy in pancreatic ductal adenocarcinoma.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Cell Proliferation; Chloroquine; Deoxycyt | 2023 |
Matrix stiffness triggers chemoresistance through elevated autophagy in pancreatic ductal adenocarcinoma.
Topics: Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Cell Proliferation; Chloroquine; Deoxycyt | 2023 |
Autophagy promotes immune evasion of pancreatic cancer by degrading MHC-I.
Topics: Adenocarcinoma; Animals; Antigen Presentation; Autophagy; Carcinoma, Pancreatic Ductal; CD8-Positive | 2020 |
KRAS-dependent cancer cells promote survival by producing exosomes enriched in Survivin.
Topics: Cell Communication; Cell Line, Tumor; Cell Survival; Chloroquine; Exosomes; Extracellular Vesicles; | 2021 |
Chloroquine-Modified Hydroxyethyl Starch as a Polymeric Drug for Cancer Therapy.
Topics: Cell Line, Tumor; Cell Movement; Chloroquine; Drug Screening Assays, Antitumor; Humans; Hydroxyethyl | 2017 |
CQ sensitizes human pancreatic cancer cells to gemcitabine through the lysosomal apoptotic pathway via reactive oxygen species.
Topics: Animals; Apoptosis; Cell Line, Tumor; Chloroquine; Deoxycytidine; Gemcitabine; Humans; Lysosomes; Ma | 2018 |
Chloroquine augments TRAIL-induced apoptosis and induces G2/M phase arrest in human pancreatic cancer cells.
Topics: Animals; Apoptosis; Apoptosis Regulatory Proteins; Autophagy; Cell Line, Tumor; Chloroquine; Drug Sy | 2018 |
Chloroquine reduces hypercoagulability in pancreatic cancer through inhibition of neutrophil extracellular traps.
Topics: Adenocarcinoma; Animals; Chloroquine; DNA; Extracellular Traps; Female; Humans; Hydrolases; Hydroxyc | 2018 |
Chloroquine reduces hypercoagulability in pancreatic cancer through inhibition of neutrophil extracellular traps.
Topics: Adenocarcinoma; Animals; Chloroquine; DNA; Extracellular Traps; Female; Humans; Hydrolases; Hydroxyc | 2018 |
Chloroquine reduces hypercoagulability in pancreatic cancer through inhibition of neutrophil extracellular traps.
Topics: Adenocarcinoma; Animals; Chloroquine; DNA; Extracellular Traps; Female; Humans; Hydrolases; Hydroxyc | 2018 |
Chloroquine reduces hypercoagulability in pancreatic cancer through inhibition of neutrophil extracellular traps.
Topics: Adenocarcinoma; Animals; Chloroquine; DNA; Extracellular Traps; Female; Humans; Hydrolases; Hydroxyc | 2018 |
Methods for Monitoring Macroautophagy in Pancreatic Cancer Cells.
Topics: Animals; Autophagosomes; Autophagy; Autophagy-Related Proteins; Carcinogenesis; Cell Culture Techniq | 2019 |
Potential ceRNA networks involved in autophagy suppression of pancreatic cancer caused by chloroquine diphosphate: A study based on differentially‑expressed circRNAs, lncRNAs, miRNAs and mRNAs.
Topics: Adult; Aged; Autophagy; Cell Line, Tumor; Chloroquine; Female; Gene Expression Regulation, Neoplasti | 2019 |
Protective autophagy elicited by RAF→MEK→ERK inhibition suggests a treatment strategy for RAS-driven cancers.
Topics: Animals; Autophagy; CA-19-9 Antigen; Cell Line, Tumor; Chloroquine; Humans; MAP Kinase Signaling Sys | 2019 |
Protective autophagy elicited by RAF→MEK→ERK inhibition suggests a treatment strategy for RAS-driven cancers.
Topics: Animals; Autophagy; CA-19-9 Antigen; Cell Line, Tumor; Chloroquine; Humans; MAP Kinase Signaling Sys | 2019 |
Protective autophagy elicited by RAF→MEK→ERK inhibition suggests a treatment strategy for RAS-driven cancers.
Topics: Animals; Autophagy; CA-19-9 Antigen; Cell Line, Tumor; Chloroquine; Humans; MAP Kinase Signaling Sys | 2019 |
Protective autophagy elicited by RAF→MEK→ERK inhibition suggests a treatment strategy for RAS-driven cancers.
Topics: Animals; Autophagy; CA-19-9 Antigen; Cell Line, Tumor; Chloroquine; Humans; MAP Kinase Signaling Sys | 2019 |
Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer.
Topics: Animals; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; Drug Synergism; HEK293 Cells; | 2019 |
Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer.
Topics: Animals; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; Drug Synergism; HEK293 Cells; | 2019 |
Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer.
Topics: Animals; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; Drug Synergism; HEK293 Cells; | 2019 |
Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer.
Topics: Animals; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; Drug Synergism; HEK293 Cells; | 2019 |
Lysosome inhibition sensitizes pancreatic cancer to replication stress by aspartate depletion.
Topics: Animals; Aspartic Acid; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroquine; Female; Humans; | 2019 |
Inhibition of ERK1/2 in cancer-associated pancreatic stellate cells suppresses cancer-stromal interaction and metastasis.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Cell Communication; Cell Line, Tumor; Cell Movemen | 2019 |
Calix[6]arene bypasses human pancreatic cancer aggressiveness: downregulation of receptor tyrosine kinases and induction of cell death by reticulum stress and autophagy.
Topics: Apoptosis; Autophagy; Calixarenes; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferation; Cel | 2013 |
Autophagy is needed for the growth of pancreatic adenocarcinoma and has a cytoprotective effect against anticancer drugs.
Topics: Adenocarcinoma; Androstadienes; Antineoplastic Agents; Autophagy; Cell Line, Tumor; Cell Proliferati | 2014 |
Chloroquine-mediated cell death in metastatic pancreatic adenocarcinoma through inhibition of autophagy.
Topics: Adenocarcinoma; Apoptosis; Autophagy; Cell Death; Cell Line, Tumor; Cell Survival; Chloroquine; Dose | 2014 |
Chloroquine targets pancreatic cancer stem cells via inhibition of CXCR4 and hedgehog signaling.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Cell Movement; Cell Proliferation; Chloroquine; He | 2014 |
Bortezomib induces protective autophagy through AMP-activated protein kinase activation in cultured pancreatic and colorectal cancer cells.
Topics: Adenine; AMP-Activated Protein Kinases; Antineoplastic Agents; Autophagy; Boronic Acids; Bortezomib; | 2014 |
Combination of chloroquine and GX15-070 (obatoclax) results in synergistic cytotoxicity against pancreatic cancer cells.
Topics: Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Autophagy; bcl-X Protein; Cell Line, Tumo | 2014 |
Autophagy sustains the survival of human pancreatic cancer PANC-1 cells under extreme nutrient deprivation conditions.
Topics: Amino Acid Chloromethyl Ketones; Amino Acids; AMP-Activated Protein Kinases; Androstadienes; Apoptos | 2015 |
Penfluridol suppresses pancreatic tumor growth by autophagy-mediated apoptosis.
Topics: Animals; Antineoplastic Agents; Apoptosis; Autophagy; Cell Line, Tumor; Chloroquine; Disease Models, | 2016 |
The pancreatitis-associated protein VMP1, a key regulator of inducible autophagy, promotes Kras(G12D)-mediated pancreatic cancer initiation.
Topics: Animals; Autophagy; Carcinoma, Ductal; Cell Line, Tumor; Cell Proliferation; Cell Survival; Chloroqu | 2016 |
Autophagy Is Required for Activation of Pancreatic Stellate Cells, Associated With Pancreatic Cancer Progression and Promotes Growth of Pancreatic Tumors in Mice.
Topics: Animals; Autophagy; Cell Line, Tumor; Cell Movement; Cell Proliferation; Chloroquine; Disease Progre | 2017 |
Pancreatic cancers require autophagy for tumor growth.
Topics: Animals; Antineoplastic Agents; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Chloroqui | 2011 |
A critical role for autophagy in pancreatic cancer.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Chloroquine; Humans; Models, Biological; Pancreati | 2011 |
AACR highlights: promise for treating pancreatic cancer.
Topics: Albumin-Bound Paclitaxel; Albumins; Anilides; Animals; Antineoplastic Agents; Antineoplastic Combine | 2011 |
[Autophagy: a necessary allied in the growth of pancreatic adenocarcinoma].
Topics: Adenocarcinoma; Animals; Autophagy; Cell Line, Tumor; Cell Proliferation; Chloroquine; Humans; Immun | 2011 |
Identification of anti-malarial compounds as novel antagonists to chemokine receptor CXCR4 in pancreatic cancer cells.
Topics: Antimalarials; Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Chloroquine; Drug Discov | 2012 |
Loxiglumide (CR1505), a cholecystokinin antagonist, specifically inhibits the growth of human pancreatic cancer lines xenografted into nude mice.
Topics: Animals; Cell Division; Chloroquine; Cholecystokinin; DNA; Esters; Gabexate; Guanidines; Humans; Mic | 1993 |
Evidence against the acidification hypothesis in cystic fibrosis.
Topics: Acids; Adenocarcinoma; Adenoviridae; Animals; Biological Transport; Cell Compartmentation; Cell Line | 2000 |
Internalization-sequestration and degradation of cholecystokinin (CCK) in tumoral rat pancreatic AR 4-2 J cells.
Topics: Animals; Arsenicals; Binding, Competitive; Cell Membrane; Chloroquine; Cholecystokinin; Cytochalasin | 1990 |
Selective growth inhibition of ductal pancreatic adenocarcinoma cells by the lysosomotropic agent chloroquine.
Topics: Auranofin; Carcinoma, Intraductal, Noninfiltrating; Cell Division; Chloroquine; Humans; Pancreatic N | 1989 |
Internalization of glucagon-like peptide-1(7-36)amide in rat insulinoma cells.
Topics: Adenoma, Islet Cell; Animals; Chloroquine; Chromatography, High Pressure Liquid; Glucagon; Glucagon- | 1989 |
Biosynthesis of betagranin in pancreatic beta-cells. Identification of a chromogranin A-like precursor and its parallel processing with proinsulin.
Topics: Animals; Chemical Precipitation; Chloroquine; Chromogranin A; Chromogranins; Electrophoresis, Polyac | 1987 |