hydroxychloroquine has been researched along with Cancer of Pancreas in 22 studies
Hydroxychloroquine: A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970)
hydroxychloroquine : An aminoquinoline that is chloroquine in which one of the N-ethyl groups is hydroxylated at position 2. An antimalarial with properties similar to chloroquine that acts against erythrocytic forms of malarial parasites, it is mainly used as the sulfate salt for the treatment of lupus erythematosus, rheumatoid arthritis, and light-sensitive skin eruptions.
| Excerpt | Relevance | Reference |
|---|---|---|
| "In this phase 1/2 trial, we examined treatment with hydroxychloroquine (HCQ) and gemcitabine for patients with pancreatic adenocarcinoma." | 9.20 | Safety and Biologic Response of Pre-operative Autophagy Inhibition in Combination with Gemcitabine in Patients with Pancreatic Adenocarcinoma. ( Bahary, N; Bao, P; Bartlett, DL; Boone, BA; Espina, V; Liotta, LA; Lotze, MT; Loughran, P; Moser, AJ; Normolle, DP; Singhi, AD; Wu, WC; Zeh, HJ; Zureikat, AH, 2015) |
| "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) |
| " We evaluated hydoxychloroquine (HCQ), an inhibitor of autophagy, in patients with pancreatic cancer and analyzed pharmacodynamic markers in treated patients and mice." | 6.79 | Phase II and pharmacodynamic study of autophagy inhibition using hydroxychloroquine in patients with metastatic pancreatic adenocarcinoma. ( Chan, JA; Cleary, JM; Enzinger, PC; Fuchs, CS; Killion, L; Kimmelman, AC; Mamon, H; McCleary, NJ; Meyerhardt, JA; Ng, K; Rubinson, DA; Schrag, D; Sikora, AL; Spicer, BA; Wang, X; Wolpin, BM, 2014) |
| " Trametinib in combination with hydroxychloroquine (HCQ) or CDK4/6 inhibitors for pancreatic adenocarcinoma showed promising efficacy in preclinical studies." | 5.91 | A real-world analysis of trametinib in combination with hydroxychloroquine or CDK4/6 inhibitor as third- or later-line therapy in metastatic pancreatic adenocarcinoma. ( Bai, C; Cheng, Y; Ge, Y; Li, X; Tang, H; Wang, Y; You, T, 2023) |
| "In this phase 1/2 trial, we examined treatment with hydroxychloroquine (HCQ) and gemcitabine for patients with pancreatic adenocarcinoma." | 5.20 | Safety and Biologic Response of Pre-operative Autophagy Inhibition in Combination with Gemcitabine in Patients with Pancreatic Adenocarcinoma. ( Bahary, N; Bao, P; Bartlett, DL; Boone, BA; Espina, V; Liotta, LA; Lotze, MT; Loughran, P; Moser, AJ; Normolle, DP; Singhi, AD; Wu, WC; Zeh, HJ; Zureikat, AH, 2015) |
| "Hydroxychloroquine (HCQ) is an autophagy inhibitor that has been used for the treatment of many diseases, such as malaria, rheumatoid arthritis, systemic lupus erythematosus, and cancer." | 4.12 | Quantitative Proteomics Explore the Potential Targets and Action Mechanisms of Hydroxychloroquine. ( Chen, K; Hou, W; Huang, H; Jiang, Y; Liu, G; Liu, H; Liu, K; Ren, X; Zhao, J; Zhao, Z, 2022) |
| "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) |
| "Hydroxychloroquine (HCQ) is an autophagy inhibitor." | 3.01 | SMAD4 loss is associated with response to neoadjuvant chemotherapy plus hydroxychloroquine in patients with pancreatic adenocarcinoma. ( Bahary, N; Boone, BA; Fei, N; Hogg, ME; Lotze, MT; Ramanathan, R; Singhi, AD; Wen, S; Zeh, HJ; Zureikat, AH, 2021) |
| "Hydroxychloroquine sulfate (HCQ) is an inhibitor of autophagy that inhibits the fusion of the autophagosome to the lysosome." | 2.90 | Effect of Gemcitabine and nab-Paclitaxel With or Without Hydroxychloroquine on Patients With Advanced Pancreatic Cancer: A Phase 2 Randomized Clinical Trial. ( Amaravadi, RK; Borazanci, E; Burrell, JA; De Jesus-Acosta, A; Drebin, JA; Karasic, TB; Laheru, DA; Loaiza-Bonilla, A; O'Dwyer, PJ; O'Hara, MH; Redlinger, C; Reiss, KA; Teitelbaum, UR; Von Hoff, DD, 2019) |
| " We evaluated hydoxychloroquine (HCQ), an inhibitor of autophagy, in patients with pancreatic cancer and analyzed pharmacodynamic markers in treated patients and mice." | 2.79 | Phase II and pharmacodynamic study of autophagy inhibition using hydroxychloroquine in patients with metastatic pancreatic adenocarcinoma. ( Chan, JA; Cleary, JM; Enzinger, PC; Fuchs, CS; Killion, L; Kimmelman, AC; Mamon, H; McCleary, NJ; Meyerhardt, JA; Ng, K; Rubinson, DA; Schrag, D; Sikora, AL; Spicer, BA; Wang, X; Wolpin, BM, 2014) |
| "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) |
| " Trametinib in combination with hydroxychloroquine (HCQ) or CDK4/6 inhibitors for pancreatic adenocarcinoma showed promising efficacy in preclinical studies." | 1.91 | A real-world analysis of trametinib in combination with hydroxychloroquine or CDK4/6 inhibitor as third- or later-line therapy in metastatic pancreatic adenocarcinoma. ( Bai, C; Cheng, Y; Ge, Y; Li, X; Tang, H; Wang, Y; You, T, 2023) |
| " Collectively, these results indicated that the lysosome‑targeted drug combination induces multiple organelle dysfunction and exerts a marked cytotoxic effect in PDAC cells." | 1.72 | Lysosome‑targeted drug combination induces multiple organelle dysfunctions and non‑canonical death in pancreatic cancer cells. ( Hiramoto, M; Hirota, A; Kazama, H; Miyazaki, M; Miyazawa, K; Ogawa, M; Ota, K; Suzuki, S; Takano, N, 2022) |
| "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) |
| "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) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 8 (36.36) | 24.3611 |
| 2020's | 14 (63.64) | 2.80 |
| Authors | Studies |
|---|---|
| AlMasri, SS | 1 |
| Zenati, MS | 1 |
| Desilva, A | 1 |
| Nassour, I | 1 |
| Boone, BA | 5 |
| Singhi, AD | 4 |
| Bartlett, DL | 3 |
| Liotta, LA | 2 |
| Espina, V | 3 |
| Loughran, P | 2 |
| Lotze, MT | 5 |
| Paniccia, A | 1 |
| Zeh, HJ | 5 |
| Zureikat, AH | 4 |
| Bahary, N | 4 |
| Jiang, H | 1 |
| Courau, T | 1 |
| Borison, J | 1 |
| Ritchie, AJ | 1 |
| Mayer, AT | 1 |
| Krummel, MF | 1 |
| Collisson, EA | 1 |
| Stalnecker, CA | 1 |
| Grover, KR | 1 |
| Edwards, AC | 1 |
| Coleman, MF | 1 |
| Yang, R | 1 |
| DeLiberty, JM | 1 |
| Papke, B | 1 |
| Goodwin, CM | 1 |
| Pierobon, M | 1 |
| Petricoin, EF | 1 |
| Gautam, P | 1 |
| Wennerberg, K | 1 |
| Cox, AD | 1 |
| Der, CJ | 1 |
| Hursting, SD | 1 |
| Bryant, KL | 1 |
| Suzuki, S | 1 |
| Ogawa, M | 1 |
| Miyazaki, M | 1 |
| Ota, K | 1 |
| Kazama, H | 1 |
| Hirota, A | 1 |
| Takano, N | 1 |
| Hiramoto, M | 1 |
| Miyazawa, K | 1 |
| Hoque, MM | 1 |
| Iida, Y | 1 |
| Kotani, H | 1 |
| Kartika, ID | 1 |
| Harada, M | 1 |
| Zhao, J | 1 |
| Zhao, Z | 1 |
| Hou, W | 1 |
| Jiang, Y | 1 |
| Liu, G | 1 |
| Ren, X | 1 |
| Liu, K | 1 |
| Liu, H | 1 |
| Chen, K | 1 |
| Huang, H | 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 | 1 |
| Silvis, MR | 1 |
| Silva, D | 1 |
| Rohweder, R | 1 |
| Schuman, S | 1 |
| Gudipaty, S | 1 |
| Truong, A | 1 |
| Yap, J | 1 |
| Affolter, K | 1 |
| McMahon, M | 1 |
| Kinsey, C | 1 |
| Tang, H | 1 |
| Ge, Y | 1 |
| You, T | 1 |
| Li, X | 1 |
| Wang, Y | 2 |
| Cheng, Y | 1 |
| Bai, C | 1 |
| Chen, X | 1 |
| Yu, Q | 1 |
| Liu, Y | 1 |
| Sheng, Q | 1 |
| Shi, K | 1 |
| Li, M | 1 |
| Zhang, Z | 1 |
| He, Q | 1 |
| Miller-Ocuin, JL | 1 |
| Normolle, DP | 2 |
| Hogg, ME | 2 |
| Lee, KK | 1 |
| Tsung, A | 1 |
| Marsh, JW | 1 |
| Murthy, P | 2 |
| Tang, D | 1 |
| Seiser, N | 1 |
| Amaravadi, RK | 2 |
| Liotta, L | 1 |
| Ji, Y | 1 |
| Liu, X | 1 |
| Li, J | 1 |
| Xie, X | 1 |
| Huang, M | 1 |
| Jiang, J | 1 |
| Liao, YP | 1 |
| Donahue, T | 1 |
| Meng, H | 1 |
| Xavier, CB | 1 |
| Marchetti, KR | 1 |
| Castria, TB | 1 |
| Jardim, DLF | 1 |
| Fernandes, GS | 1 |
| Fei, N | 1 |
| Wen, S | 1 |
| Ramanathan, R | 1 |
| Miller-Ocuin, J | 1 |
| Doerfler, WR | 1 |
| Ellis, JT | 1 |
| Liang, X | 1 |
| Ross, MA | 1 |
| Wallace, CT | 1 |
| Sperry, JL | 1 |
| Neal, MD | 1 |
| Karasic, TB | 1 |
| O'Hara, MH | 1 |
| Loaiza-Bonilla, A | 1 |
| Reiss, KA | 1 |
| Teitelbaum, UR | 1 |
| Borazanci, E | 1 |
| De Jesus-Acosta, A | 1 |
| Redlinger, C | 1 |
| Burrell, JA | 1 |
| Laheru, DA | 1 |
| Von Hoff, DD | 1 |
| Drebin, JA | 1 |
| O'Dwyer, PJ | 1 |
| Rosenfeldt, MT | 1 |
| O'Prey, J | 1 |
| Morton, JP | 1 |
| Nixon, C | 1 |
| MacKay, G | 1 |
| Mrowinska, A | 1 |
| Au, A | 1 |
| Rai, TS | 1 |
| Zheng, L | 1 |
| Ridgway, R | 1 |
| Adams, PD | 1 |
| Anderson, KI | 1 |
| Gottlieb, E | 1 |
| Sansom, OJ | 1 |
| Ryan, KM | 1 |
| Wolpin, BM | 1 |
| Rubinson, DA | 1 |
| Wang, X | 1 |
| Chan, JA | 1 |
| Cleary, JM | 1 |
| Enzinger, PC | 1 |
| Fuchs, CS | 1 |
| McCleary, NJ | 1 |
| Meyerhardt, JA | 1 |
| Ng, K | 1 |
| Schrag, D | 1 |
| Sikora, AL | 1 |
| Spicer, BA | 1 |
| Killion, L | 1 |
| Mamon, H | 1 |
| Kimmelman, AC | 2 |
| Yang, A | 1 |
| Moser, AJ | 1 |
| Wu, WC | 1 |
| Bao, P | 1 |
| Kim, J | 1 |
| Yip, ML | 1 |
| Shen, X | 1 |
| Li, H | 1 |
| Hsin, LY | 1 |
| Labarge, S | 1 |
| Heinrich, EL | 1 |
| Lee, W | 1 |
| Lu, J | 1 |
| Vaidehi, N | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| 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 | ||
| A Phase I/II/Pharmacodynamic Study of Hydroxychloroquine in Combination With Gemcitabine/Abraxane to Inhibit Autophagy in Pancreatic Cancer[NCT01506973] | Phase 1/Phase 2 | 119 participants (Actual) | Interventional | 2011-12-31 | Completed | ||
| Phase II Study of Hydroxychloroquine in Previously Treated Patients With Metastatic Pancreatic Cancer[NCT01273805] | Phase 2 | 20 participants (Actual) | Interventional | 2011-01-31 | 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 |
2-month progression-free survival rate was defined as the percentage of patients absent progression (PD) or death before 2 months. Patients were considered to have experienced PD if they demonstrated either clinical deterioration resulting in withdrawal or PD per RECIST 1.0 criteria: At least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. (NCT01273805)
Timeframe: Disease was evaluated radiologically at baseline and at the first restaging at 2 months.
| Intervention | percentage of patients (Number) |
|---|---|
| Hydroxychloroquine 400 mg b.i.d. | 10 |
| Hydroxychloroquine 600 mg b.i.d. | 10 |
All grade 4-5 adverse events with treatment attribution of possibly, probably or definite based on CTCAEv3 as reported on case report forms. (NCT01273805)
Timeframe: Adverse events were assessed each cycle throughout treatment. Participants were followed for the duration of treatment, an average of 34 days for this study population.
| Intervention | Participants (Count of Participants) |
|---|---|
| Hydroxychloroquine 400 mg b.i.d. | 0 |
| Hydroxychloroquine 600 mg b.i.d. | 0 |
Overall survival estimated using Kaplan-Meier (KM) methods is defined as the time from study entry to death or date last known alive. (NCT01273805)
Timeframe: All patients were followed until death. Median survival follow-up in this study cohort was 60 days (95% CI: 40-184).
| Intervention | days (Median) |
|---|---|
| Hydroxychloroquine 400 mg b.i.d. | 51.5 |
| Hydroxychloroquine 600 mg b.i.d. | 83 |
Progression-free survival based on the Kaplan-Meier method is defined as the duration of time from study entry to time of objective progression on CT scan or the time of death for patients with clinical deterioration resulting in withdrawal from the trial. Per RECIST 1.0 criteria: progressive disease (PD) is at least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. Patients without an event were censored at date of last disease evaluation. (NCT01273805)
Timeframe: Disease was evaluated radiologically at baseline and every 2 months on treatment. Median PFS follow-up in this study cohort was 46.5 days (95% CI 33-61).
| Intervention | days (Median) |
|---|---|
| Hydroxychloroquine 400 mg b.i.d. | 51.5 |
| Hydroxychloroquine 600 mg b.i.d. | 44.5 |
Tumor response rate is the percentage of patients achieving complete or partial response on treatment based on RECIST 1.0 criteria. For target lesions, complete response (CR) is disappearance of all target lesions and partial response (PR) is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. CR for the evaluation of non-target lesions is the disappearance of non-target lesions and normalization of tumor marker level. Appearance of one or more new lesions is classified as progression of non-target lesions. CR or PR confirmation is required >/= 4 weeks. (NCT01273805)
Timeframe: Disease was evaluated radiologically at baseline and every 2 months on treatment. Median duration of treatment for this study cohort was 34 days.
| Intervention | percentage of patients (Number) |
|---|---|
| Hydroxychloroquine 400 mg b.i.d. | 0 |
| Hydroxychloroquine 600 mg b.i.d. | 0 |
1 review available for hydroxychloroquine and Cancer of Pancreas
5 trials available for hydroxychloroquine and Cancer of Pancreas
| Article | Year |
|---|---|
A Randomized Phase II Preoperative Study of Autophagy Inhibition with High-Dose Hydroxychloroquine and Gemcitabine/Nab-Paclitaxel in Pancreatic Cancer Patients.
Topics: Adult; Aged; Aged, 80 and over; Albumins; Antineoplastic Combined Chemotherapy Protocols; Autophagy; | 2020 |
SMAD4 loss is associated with response to neoadjuvant chemotherapy plus hydroxychloroquine in patients with pancreatic adenocarcinoma.
Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Autophagy; Carcinoma, Pancreatic Ductal; Disea | 2021 |
Effect of Gemcitabine and nab-Paclitaxel With or Without Hydroxychloroquine on Patients With Advanced Pancreatic Cancer: A Phase 2 Randomized Clinical Trial.
Topics: Adult; Aged; Aged, 80 and over; Albumins; Antineoplastic Agents; Antineoplastic Combined Chemotherap | 2019 |
Phase II and pharmacodynamic study of autophagy inhibition using hydroxychloroquine in patients with metastatic pancreatic adenocarcinoma.
Topics: Adenocarcinoma; Animals; Antineoplastic Combined Chemotherapy Protocols; Autophagy; Disease-Free Sur | 2014 |
Safety and Biologic Response of Pre-operative Autophagy Inhibition in Combination with Gemcitabine in Patients with Pancreatic Adenocarcinoma.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antirheumatic Agent | 2015 |
Safety and Biologic Response of Pre-operative Autophagy Inhibition in Combination with Gemcitabine in Patients with Pancreatic Adenocarcinoma.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antirheumatic Agent | 2015 |
Safety and Biologic Response of Pre-operative Autophagy Inhibition in Combination with Gemcitabine in Patients with Pancreatic Adenocarcinoma.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antirheumatic Agent | 2015 |
Safety and Biologic Response of Pre-operative Autophagy Inhibition in Combination with Gemcitabine in Patients with Pancreatic Adenocarcinoma.
Topics: Adenocarcinoma; Adult; Aged; Aged, 80 and over; Antimetabolites, Antineoplastic; Antirheumatic Agent | 2015 |
16 other studies available for hydroxychloroquine and Cancer of Pancreas
| Article | Year |
|---|---|
Activating Immune Recognition in Pancreatic Ductal Adenocarcinoma via Autophagy Inhibition, MEK Blockade, and CD40 Agonism.
Topics: Animals; Autophagy; Azetidines; Carcinoma, Pancreatic Ductal; CD40 Antigens; Cell Line, Tumor; Drug | 2022 |
Concurrent Inhibition of IGF1R and ERK Increases Pancreatic Cancer Sensitivity to Autophagy Inhibitors.
Topics: Animals; Apoptosis; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Drug Synergism; Enzym | 2022 |
Lysosome‑targeted drug combination induces multiple organelle dysfunctions and non‑canonical death in pancreatic cancer cells.
Topics: Aminopyridines; Antineoplastic Agents; Benzimidazoles; Carcinoma, Pancreatic Ductal; Cell Line, Tumo | 2022 |
Hydroxychloroquine Promotes Bcl-xL Inhibition-induced Apoptosis in BxPC-3 Human Pancreatic Cancer Cells.
Topics: Animals; Apoptosis; Humans; Hydroxychloroquine; Mice; Pancreatic Neoplasms; Proto-Oncogene Proteins | 2022 |
Hydroxychloroquine Promotes Bcl-xL Inhibition-induced Apoptosis in BxPC-3 Human Pancreatic Cancer Cells.
Topics: Animals; Apoptosis; Humans; Hydroxychloroquine; Mice; Pancreatic Neoplasms; Proto-Oncogene Proteins | 2022 |
Hydroxychloroquine Promotes Bcl-xL Inhibition-induced Apoptosis in BxPC-3 Human Pancreatic Cancer Cells.
Topics: Animals; Apoptosis; Humans; Hydroxychloroquine; Mice; Pancreatic Neoplasms; Proto-Oncogene Proteins | 2022 |
Hydroxychloroquine Promotes Bcl-xL Inhibition-induced Apoptosis in BxPC-3 Human Pancreatic Cancer Cells.
Topics: Animals; Apoptosis; Humans; Hydroxychloroquine; Mice; Pancreatic Neoplasms; Proto-Oncogene Proteins | 2022 |
Quantitative Proteomics Explore the Potential Targets and Action Mechanisms of Hydroxychloroquine.
Topics: Antirheumatic Agents; Arthritis, Rheumatoid; Galectins; Humans; Hydroxychloroquine; Lupus Erythemato | 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 |
A real-world analysis of trametinib in combination with hydroxychloroquine or CDK4/6 inhibitor as third- or later-line therapy in metastatic pancreatic adenocarcinoma.
Topics: Adenocarcinoma; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cyclin-Depend | 2023 |
A real-world analysis of trametinib in combination with hydroxychloroquine or CDK4/6 inhibitor as third- or later-line therapy in metastatic pancreatic adenocarcinoma.
Topics: Adenocarcinoma; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cyclin-Depend | 2023 |
A real-world analysis of trametinib in combination with hydroxychloroquine or CDK4/6 inhibitor as third- or later-line therapy in metastatic pancreatic adenocarcinoma.
Topics: Adenocarcinoma; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cyclin-Depend | 2023 |
A real-world analysis of trametinib in combination with hydroxychloroquine or CDK4/6 inhibitor as third- or later-line therapy in metastatic pancreatic adenocarcinoma.
Topics: Adenocarcinoma; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Cyclin-Depend | 2023 |
Synergistic cytotoxicity and co-autophagy inhibition in pancreatic tumor cells and cancer-associated fibroblasts by dual functional peptide-modified liposomes.
Topics: Animals; Antineoplastic Agents; Autophagy; Cancer-Associated Fibroblasts; Carcinoma, Pancreatic Duct | 2019 |
Use of ratiometrically designed nanocarrier targeting CDK4/6 and autophagy pathways for effective pancreatic cancer treatment.
Topics: Animals; Apoptosis; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Cyclin-Dependent Kina | 2020 |
Trametinib and Hydroxychloroquine (HCQ) Combination Treatment in KRAS-Mutated Advanced Pancreatic Adenocarcinoma: Detailed Description of Two Cases.
Topics: Aged, 80 and over; Antineoplastic Combined Chemotherapy Protocols; Autophagy; CA-19-9 Antigen; Carci | 2021 |
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 |
p53 status determines the role of autophagy in pancreatic tumour development.
Topics: Alleles; Animals; Autophagy; Autophagy-Related Protein 5; Autophagy-Related Protein 7; Carcinoma, Pa | 2013 |
Inhibition of autophagy attenuates pancreatic cancer growth independent of TP53/TRP53 status.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Disease Models, Animal; Humans; | 2014 |
Inhibition of autophagy attenuates pancreatic cancer growth independent of TP53/TRP53 status.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Disease Models, Animal; Humans; | 2014 |
Inhibition of autophagy attenuates pancreatic cancer growth independent of TP53/TRP53 status.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Disease Models, Animal; Humans; | 2014 |
Inhibition of autophagy attenuates pancreatic cancer growth independent of TP53/TRP53 status.
Topics: Animals; Autophagy; Carcinoma, Pancreatic Ductal; Cell Line, Tumor; Disease Models, Animal; Humans; | 2014 |
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 |