Proteomic Analysis of Pancreatic Ductal Carcinoma Cells after Combined Treatment with Gemcitabine and Trichostatin A

2005 ◽  
Vol 4 (6) ◽  
pp. 1909-1916 ◽  
Author(s):  
Daniela Cecconi ◽  
Massimo Donadelli ◽  
Aldo Scarpa ◽  
Alberto Milli ◽  
Marta Palmieri ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Ductal Carcinoma ◽  
Trichostatin A ◽  
Combined Treatment ◽  
Carcinoma Cells ◽  
Pancreatic Ductal Carcinoma

Proteomic analysis of pancreatic ductal carcinoma cells treated with 5-aza-2'-deoxycytidine

2003 ◽  
Vol 24 (24) ◽  
pp. 4291-4303 ◽  
Author(s):  
Daniela Cecconi ◽  
Hubert Astner ◽  
Massimo Donadelli ◽  
Marta Palmieri ◽  
Edoardo Missiaglia ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Ductal Carcinoma ◽  
Carcinoma Cells ◽  
Pancreatic Ductal Carcinoma

Combined treatment with immunotherapy and chemotherapy using endoscopic ultrasonography guided injection for locally advanced pancreatic carcinoma

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 13503-13503
Author(s):  
K. Nonogaki ◽  
Y. Hirooka ◽  
A. Itoh ◽  
H. Kawashima ◽  
N. Ohmiya ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Peripheral Blood ◽  
Ductal Carcinoma ◽  
Combined Treatment ◽  
Locally Advanced ◽  
Hematological Toxicity ◽  
Pancreatic Ductal Carcinoma ◽  
Cell Mediated Immunity ◽  
Locally Advanced Pancreatic Carcinoma ◽  
Advanced Pancreatic Carcinoma

13503 Background: Dendritic cells (DCs) play a pivotal role in T cell-mediated immunity. Usually, mature DCs were cultured using resected tumor tissue, but for inoperable cases, this method is impractical. The injection of immature DCs into the tumor after appropriate chemotherapy is reasonable, if DCs come to maturity capturing the specific cancer antigen . The aim of this study is to assess the toxicity and efficacy of combined treatment with immunotherapy and chemotherapy for locally advanced pancreatic carcinoma. Methods: Five patients with pathologically confirmed pancreatic ductal carcinoma using EUS-FNA were enrolled, median age 56 years (range, 46–70 years). All cases without distant metastasis were diagnosed as surgically unresectable . Patients underwent leukapheresis, immature DCs were prepared from peripheral blood by a culture with granulocyte macrophage colony-stimulating factor and interleukin 4. Lymphokine-activated killer (LAK) were also prepared from peripheral blood. Immature DCs were injected biweekly in the mass by endoscopic ultrasound-guided fine needle injection (EUS-FNI), LAK were administered intravenously. Patients received the treatment of gemcitabine 1000 mg / m2 by intravenous injection 3 days before the immunotherapy. One course with 6 times combined therapy was continued until the judgment of progressive diseases (PD) was given. The toxicity and efficacy of this treatment were assessed. We also assessed whether tumor associated antigen (TAA)-specific IFN-?producing cells increase after treatment. Results: Hematological toxicity occurred in one case, leucopenia of grade 2. No severe toxicities of grade 3 to 4 occurred. One had a partial response (PR), stable disease (SD) was observed in 2 patients for more than 6 months (long-term SD). PR patient could undergo curative operation after this therapy. The number of TAA-specific IFN-?producing cells in PR patient increased 12-fold higher than that seen before treatments. Conclusions: These results support the safety and efficacy of combined treatment with immunotherapy and chemotherapy for locally advanced pancreatic ductal carcinoma. This treatment may be a useful for the treatment of pancreatic ductal carcinoma. No significant financial relationships to disclose.

scholarly journals The Sustained Induction of c-MYC Drives Nab-Paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells

2019 ◽  
Vol 17 (9) ◽  
pp. 1815-1827 ◽  
Author(s):  
Erika Parasido ◽  
George S. Avetian ◽  
Aisha Naeem ◽  
Garrett Graham ◽  
Michael Pishvaian ◽  
...  
Keyword(s):  
Ductal Carcinoma ◽  
Carcinoma Cells ◽  
Pancreatic Ductal Carcinoma ◽  
Paclitaxel Resistance

Proteomic profiling of pancreatic ductal carcinoma cell lines treated with trichostatin-A

2003 ◽  
Vol 24 (11) ◽  
pp. 1871-1878 ◽  
Author(s):  
Daniela Cecconi ◽  
Aldo Scarpa ◽  
Massimo Donadelli ◽  
Marta Palmieri ◽  
Mahmoud Hamdan ◽  
...  
Keyword(s):  
Cell Lines ◽  
Ductal Carcinoma ◽  
Carcinoma Cell ◽  
Trichostatin A ◽  
Pancreatic Ductal Carcinoma ◽  
Proteomic Profiling ◽  
Carcinoma Cell Lines

scholarly journals Ca2+ Signaling and Its Potential Targeting in Pancreatic Ductal Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3085
Author(s):  
Louay Bettaieb ◽  
Maxime Brulé ◽  
Axel Chomy ◽  
Mel Diedro ◽  
Malory Fruit ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Exocrine Pancreas ◽  
Ductal Carcinoma ◽  
Ductal Adenocarcinoma ◽  
Molecular Devices ◽  
Pancreatic Ductal Carcinoma ◽  
Aberrant Expression ◽  
Common Cause ◽  
Cancer Hallmarks ◽  
Cancer Mutations

Pancreatic cancer (PC) is a major cause of cancer-associated mortality in Western countries (and estimated to be the second cause of cancer deaths by 2030). The main form of PC is pancreatic adenocarcinoma, which is the fourth most common cause of cancer-related death, and this situation has remained virtually unchanged for several decades. Pancreatic ductal adenocarcinoma (PDAC) is inherently linked to the unique physiology and microenvironment of the exocrine pancreas, such as pH, mechanical stress, and hypoxia. Of them, calcium (Ca2+) signals, being pivotal molecular devices in sensing and integrating signals from the microenvironment, are emerging to be particularly relevant in cancer. Mutations or aberrant expression of key proteins that control Ca2+ levels can cause deregulation of Ca2+-dependent effectors that control signaling pathways determining the cells’ behavior in a way that promotes pathophysiological cancer hallmarks, such as enhanced proliferation, survival and invasion. So far, it is essentially unknown how the cancer-associated Ca2+ signaling is regulated within the characteristic landscape of PDAC. This work provides a complete overview of the Ca2+ signaling and its main players in PDAC. Special consideration is given to the Ca2+ signaling as a potential target in PDAC treatment and its role in drug resistance.

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