Effects of Capecitabine and Celecoxib in Experimental Pancreatic Cancer

Pancreatology ◽  
2010 ◽  
Vol 10 (5) ◽  
pp. 641-647 ◽  
Author(s):  
Álvaro Arjona-Sánchez ◽  
Juan Ruiz-Rabelo ◽  
María D. Perea ◽  
Reyes Vázquez ◽  
Adolfo Cruz ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Experimental Pancreatic Cancer

scholarly journals DNA Ploidy and Markovian Analysis of Neoplastic Progression in Experimental Pancreatic Cancer

2003 ◽  
Vol 51 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Russell G. Postier ◽  
Megan R. Lerner ◽  
Stan A. Lightfoot ◽  
Rick Vannarath ◽  
Mary M. Lane ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Pancreatic Adenocarcinoma ◽  
Dna Ploidy ◽  
Computer Assisted ◽  
Nuclear Morphology ◽  
Neoplastic Progression ◽  
Atypical Cell ◽  
Atypical Cells ◽  
Experimental Pancreatic Cancer ◽  
Markovian Analysis

Computer-assisted analysis of DNA ploidy and nuclear morphology were used to elucidate changes in the cell nucleus that occur during the development of experimental pancreatic cancer. Ductal pancreatic adenocarcinoma was induced in 49 Syrian hamsters by SC injection of N-nitrosobis (2-oxopropyl) amine; twenty hamsters served as controls. Groups of animals were sacrificed every 4 weeks for 20 weeks and adjacent sections of pancreatic tissue were H&E and Feulgen-stained for light microscopy and computer assisted cytometry. Pancreatic ductal cells were classified as normal, atypical, or malignant; tissue inflammation (pancreatitis) was also noted when present. DNA ploidy and nuclear morphology evaluation (Markovian analysis) identified an atypical cell stage clearly distinguishable from either normal or malignant cells; pancreatitis preceded this atypia. The DNA ploidy histogram of these atypical cells revealed a major diploid peak and a minor aneuploid peak. The receiver operator characteristic curve areas for a logistic regression model of normal vs atypical cells was 0.94 and for atypical vs malignant was 0.98, numbers indicative of near-perfect discrimination among these three cell types. The ability to identify an atypical cell population should be useful in establishing the role of these cells in the progression of human pancreatic adenocarcinoma.

Experimental pancreatic cancer in the rat treated by photodynamic therapy

1994 ◽  
Vol 81 (8) ◽  
pp. 1185-1189 ◽  
Author(s):  
S. Evrard ◽  
P. Keller ◽  
A. Hajri ◽  
G. Balboni ◽  
L. Mendoza-Burgos ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Photodynamic Therapy ◽  
Experimental Pancreatic Cancer

PCL20-116: Can Antisense Oligonucleotides Targeted to K-Ras Gene Inhibit the Tumor Growth, Invasiveness and Expression of MMP-2 and MMP-9 In Vitro and In Vivo in Hamster Experimental Pancreatic Cancer Model?

2020 ◽  
Vol 18 (3.5) ◽  
pp. PCL20-116
Author(s):  
Cintia Yoko Morioka ◽  
Marcel Cerqueira Cesar Machado ◽  
Jose Pinhata Otoch ◽  
Luma Princess Schneider ◽  
Edgard Mesquita Rodrigues Lima ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Antisense Oligonucleotides ◽  
Cancer Model ◽  
Ras Gene ◽  
Experimental Pancreatic Cancer

Experimental Pancreatic Cancer Model Using PGHAM-1 Cells: Characteristics and Experimental Therapeutic Trials

2008 ◽  
Vol 75 (6) ◽  
pp. 325-331 ◽  
Author(s):  
Eiji Uchida ◽  
Akira Matsushita ◽  
Ken Yanagi ◽  
Makoto Hiroi ◽  
Takayuki Aimoto ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Model ◽  
Therapeutic Trials ◽  
Experimental Pancreatic Cancer

Comparative benefits of nab-paclitaxel over gemcitabine or polysorbate-based docetaxel in experimental pancreatic cancer.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 192-192
Author(s):  
Niranjan Awasthi ◽  
Katherine T Ostapoff ◽  
Changhua Zhang ◽  
Margaret A. Schwarz ◽  
Roderich Schwarz
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Growth ◽  
Single Agent ◽  
Nuclear Antigen ◽  
In Vivo Model ◽  
Tumor Growth Inhibition ◽  
Multiple Tumor ◽  
Animal Survival ◽  
Experimental Pancreatic Cancer

192 Background: Gemcitabine (Gem), a standard cytotoxic therapy for pancreatic cancer, has shown limited clinical benefits. Nanoparticle albumin-bound (nab) paclitaxel (NPT), an approved treatment for breast cancer, has shown efficacy as mono- and combination therapy in multiple tumor types including pancreatic, lung and ovarian cancer. We evaluated the NPT treatment benefits compared with Gem or solvent-based taxane docetaxel (DT) in experimental pancreatic cancer. Methods: In vitro cell proliferation and protein expression were measured by WST-1 assay and immunoblotting. Tumor growth and animal survival studies were performed in murine xenografts. Intratumoral proliferative activity was measured using Ki67 nuclear antigen staining. Results: For AsPC-1, BxPC-3, MIA PaCa-2 and Panc-1 cells in vitro, Gem IC50 levels were 23.9 mM, 506 nM, 332 nM and 14.5 nM; DT IC50 levels were 30 nM, 4.6 nM, 37.5 nM and 27 nM; and NPT IC50 levels were 7.6 mM, 208 nM, 519 nM and 526 nM. NPT addition decreased Gem IC50 to 1.7 mM, 189 nM, 123 nM and 913 nM; DT addition decreased Gem IC50 to 436 nM, 470 nM, 124 nM and 0.2 nM in AsPC-1, BxPC-3, MIA PaCa-2 and Panc-1 cells, respectively. NPT and DT treatment increased stathmin phosphorylation and decreased tubulin expression in vitro. In a heterotopic in vivo model, net tumor growth inhibition after Gem, DT and NPT was 67, 31 and 72 percent, while intratumoral proliferative index inhibition was 41, 53 and 68 percent, respectively. In an intraperitoneal model, median animal survival was significantly longer in the NPT treatment group (41 days, p<0.002 vs. control and Gem) compared to Gem (32 days, p=0.005 vs. control), DT (32 days, p=0.005 vs. control) and controls (20 days). Animal survival in NPT-Gem and DT-Gem sequential treatment groups was 43 and 40 days, and thus not superior to NPT alone. Conclusions: Nab-paclitaxel has significantly superior antitumor activity as a single agent in experimental pancreatic cancer compared with gemcitabine or docetaxel. These findings provide a strong rationale for considering nab-paclitaxel as first-line monotherapy in patients with pancreatic cancer.

An antiendothelial combination therapy strategy to increase survival in experimental pancreatic cancer

Surgery ◽  
2009 ◽  
Vol 146 (2) ◽  
pp. 241-249 ◽  
Author(s):  
Roderich E. Schwarz ◽  
Srivani Konduri ◽  
Niranjan Awasthi ◽  
Danielle Cafasso ◽  
Margaret A. Schwarz
Keyword(s):  
Pancreatic Cancer ◽  
Combination Therapy ◽  
Therapy Strategy ◽  
Experimental Pancreatic Cancer
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