The combine therapy with IFN α+HREC TNF α and 5-FU in patients with pancreatic cancer after total resection

1995 ◽  
Vol 121 (S1) ◽  
pp. A52-A52
Author(s):  
R. Braczkowski ◽  
Z. Cieślik ◽  
M. Muc-Wierzgoń ◽  
B. Zubelewicz ◽  
W. Romanowski
Keyword(s):  
Pancreatic Cancer ◽  
Combine Therapy ◽  
Total Resection ◽  
Tnf Α

scholarly journals Mesothelin confers pancreatic cancer cell resistance to TNF-α-induced apoptosis through Akt/PI3K/NF-κB activation and IL-6/Mcl-1 overexpression

2011 ◽  
Vol 10 (1) ◽  
pp. 106 ◽  
Author(s):  
Uddalak Bharadwaj ◽  
Christian Marin-Muller ◽  
Min Li ◽  
Changyi Chen ◽  
Qizhi Yao
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Cell Resistance ◽  
Tnf Α ◽  
Induced Apoptosis

Salicylates Inhibit NF-κB Activation and Enhance TNF-α-Induced Apoptosis in Human Pancreatic Cancer Cells

1999 ◽  
Vol 83 (1) ◽  
pp. 56-61 ◽  
Author(s):  
Theodore P. McDade ◽  
Richard A. Perugini ◽  
Frank J. Vittimberga ◽  
Rebecca C. Carrigan ◽  
Mark P. Callery
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Pancreatic Cancer Cells ◽  
Tnf Α ◽  
Induced Apoptosis

Phase I Study of Capecitabine With Concomitant Radiotherapy for Patients With Locally Advanced Pancreatic Cancer: Expression Analysis of Genes Related to Outcome

2005 ◽  
Vol 23 (34) ◽  
pp. 8679-8687 ◽  
Author(s):  
M. Wasif Saif ◽  
Mohammaed A. Eloubeidi ◽  
Suzanne Russo ◽  
Adam Steg ◽  
Jennifer Thornton ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Dihydropyrimidine Dehydrogenase ◽  
Locally Advanced ◽  
Three Dimensional ◽  
Advanced Pancreatic Cancer ◽  
Needle Aspiration ◽  
Mrna Levels ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Grade 3

Purpose To establish the feasibility of capecitabine with concurrent radiotherapy (XRT) in patients with locally advanced (LA) pancreatic cancer and evaluate the effect of XRT on thymidine phosphorylase (TP), dihydropyrimidine dehydrogenase (DPD), and tumor necrosis factor-alpha (TNF-α). Patients and Methods Fifteen patients with LA pancreatic cancer received three-dimensional conformal XRT to a dose of 50.4 Gy with capecitabine at escalating doses from 600 to 1,250 mg/m2 bid (Monday through Friday). Following chemo-XRT, stable and responding patients were treated with capecitabine 2,000 mg/m2 orally bid for 14 days every 21 days. Tumor specimens were procured with endoscopic ultrasound–guided fine-needle aspiration 1 week before and 2 weeks after chemo-XRT to evaluate TP, DPD, and TNF-α mRNA levels. Results Dose-limiting grade 3 diarrhea was observed in two of six patients treated at a capecitabine dose of 1,000 mg/m2 with XRT. Three patients (20%) achieved partial response. Mean percent difference in TP pre- and post-XRT was 119.2% (P = .1934). There was no significant differences in mean TNF-α, or DPD levels pre- and post-XRT (P = .1934 and .4922, respectively). TP and TNF-α levels were not significantly correlated both at pre- and post-XRT (P = .670 and P < .154, respectively). Median value of TP:DPD ratios at baseline was 2.65 (range, 0.36 to 11.08). No association between TP:DPD ratio and efficacy of capecitabine or severity of toxicities was identified. Conclusion The recommended dose for phase II evaluation is capecitabine 800 mg/m2 bid (Monday through Friday) with concurrent XRT. This approach offers an easy alternative to intravenous fluorouracil as a radiosensitizer in these patients. Role of TP and TP:DPD ratio warrants further investigation in a larger clinical trial.

CMTM5 induces apoptosis of pancreatic cancer cells and has synergistic effects with TNF-α

2009 ◽  
Vol 387 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Xiaohuan Guo ◽  
Ting Li ◽  
Yu Wang ◽  
Luning Shao ◽  
Yingmei Zhang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Synergistic Effects ◽  
Pancreatic Cancer Cells ◽  
Tnf Α

TNF-α, IFN-α and Tegafur Combination Therapy for Advanced Pancreatic Cancer

1993 ◽  
pp. 774-776
Author(s):  
Noriaki Tanaka ◽  
Hiromasa Kasino ◽  
Akira Gouchi ◽  
Akio Hizuta ◽  
Yoshio Naomoto ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Combination Therapy ◽  
Advanced Pancreatic Cancer ◽  
Tnf Α

Association of interleukin-6 levels and neutropenia during gemcitabine monotherapy for advanced pancreatic cancer.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 178-178 ◽  
Author(s):  
H. Okuyama ◽  
S. Mitsunaga ◽  
K. Nakachi ◽  
I. Ohno ◽  
S. Shimizu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Inflammatory Cytokines ◽  
Performance Status ◽  
Advanced Pancreatic Cancer ◽  
Serum Levels ◽  
Severe Neutropenia ◽  
Ecog Performance Status ◽  
Tnf Α ◽  
Low Serum ◽  
Pro Inflammatory Cytokines

178 Background: Neutropenia is an important dose-limiting toxicity of gemcitabine (GEM) in patients with advanced pancreatic cancer (PC). Serum haptoglobin, regulated by pro-inflammatory cytokines, is a predictor of neutropenia in PC patients under treatment with GEM. We conducted this study with the aim of identifying the association between serum levels of haptoglobin and cytokines and the risk of development of neutropenia in advanced PC patients receiving GEM therapy. Methods: Serum levels of haptoglobin and pro-inflammatory cytokines (GM-CSF, IFN-γ, IL-1β, IL-2β, IL-6, IL-8, IL-10, IL-12, TNF-α) were measured in 55 patients with advanced PC. All patients (median age: 67 years, male/female: 26/29, ECOG performance status: 0/1/2: 32/21/2,) received GEM monotherapy as the initial treatment for PC. The severity of neutropenia within the first 90 days of the GEM treatment was graded according to the NCI Common Terminology Criteria for Adverse Events, version 3.0. Categorical or and noncategorical data were compared using Student's t test. Multivariate regression analysis was performed using logistic regression modeling. The significance level was set at p<0.05. Results: Grade 0 to 2 (G0/1/2) and grade 3 to 4 (G3/4) neutropenia were observed in 32 patients (58.2%) and 23 patients (41.8%), respectively. The G3/4 neutropenia group showed low serum levels of haptoglobin (mean 144.4 mg/dl vs. 186.7 mg/dl, p=0.097), IL-1β (mean 0.07 pg/ml vs. 0.24 pg/ml, p=0.044), IL-6 (mean 1.13 pg/ml vs. 6.43 pg/ml, p=0.002), IL-8 (mean 18.4 pg/ml vs. 44.8 pg/ml, p=0.015), and TNF-α (mean 6.28 pg/ml vs. 8.86 pg/ml, p=0.017) as compared to the G0/1/2 neutropenia group. Multivariate analysis revealed that only low serum IL-6 was significantly associated with the development of G3/4 neutropenia (OR=0.081, p=0.0011). Conclusions: Low serum IL-6 level was associated with severe neutropenia. Thus, circulating IL- 6 levels may be a predictor of the development of severe neutropenia in advanced PC patients receiving GEM therapy. No significant financial relationships to disclose.

scholarly journals Involvement of COX-2/PGE2Pathway in the Upregulation of MMP-9 Expression in Pancreatic Cancer

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Xianmin Bu ◽  
Chenghai Zhao ◽  
Xianwei Dai
Keyword(s):  
Pancreatic Cancer ◽  
Mrna Level ◽  
Strong Expression ◽  
Tnf Α ◽  
Cox 2 ◽  
Cox 2 Inhibitors

COX-2 and MMP-9 have been reported to show an overexpression in pancreatic cancer, and thus an attempt to explore the correlation between them has become a target of this study. Besides, PGE2, a product of COX-2, was also under research as to whether it is involved in the upregulation of MMP-9 expression by COX-2. Expression of COX-2 and MMP-9 mRNA varied in pancreatic adenocarcinomas, and the mRNA level of COX-2 was correlated positively with MMP-9. Both BxPC-3 and Capan-1 cells had strong expression of COX-2 and MMP-9. MMP-9 expression was downregulated significantly in BxPC-3 and Capan-1 cells after treatment with COX-2 inhibitors or COX-2 siRNA plasmids, and upregulated in BxPC-3 significantly by exogenous TNF-α, LPS or PGE2. The upregulation of MMP-9 by TNF-α or LPS was inhibited by COX-2 inhibitor NS398. There was a significant increase in the migration of BxPC-3 cells with TNF-α, LPS, or PGE2treatment; however, the increase caused by TNF-α or LPS was also inhibited remarkably by NS398. Our findings demonstrated that COX-2 upregulates MMP-9 expression in pancreatic cancer, and PGE2may be involved in it.

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