Nano-sheets of graphene oxide enhances the combined effect of hyperthermia and radiation treatment in pancreatic cancer cell lines.

2021 ◽  
Vol 16 ◽  
Author(s):  
Mohammad H. Haqiqian ◽  
Dariush Sardari ◽  
Mohammad Houshyari ◽  
R. Moghadasali

Background: Pancreatic cancer leaves little hope for survival among patients. This is due to its cancerous cell resistance to radiation and chemicals. Objective: Synergistic effect between three modalities of pancreatic cancer treatment is investigated. These are radiation therapy, Hyperthermia and graphene oxide nanosheets. The aim is to overcome resistance of pancreatic cancer cell against radiation therapy. Methods: Cancerous cell lines were treated by each one of three modalities separately. Other samples were treated with various combinations of these modalities. Hyperthermia accomplished with placing cell lines for 15 min in 42°C. In the course of radiation therapy, the cancerous cells were irradiated by 6 MV Linac for two cases of 2 Gy and 3 Gy. The cell line viability was readout by MTT assay in 24 hours and 48 hours after treatment. Results: In single modality treatment it was shown that 24h after the treatment, the group treated by RT 3 Gy had the highest cell killing result. Following up the result in 48h readout, hyperthermia and 3 Gy radiotherapy had similar result. In double modality treatment, for both 24h and 48h viability readout, the group graphene-oxide plus 2 Gy radiotherapy showed cell survival amounting to 69% and 43% respectively being the lowest cell survival among all double combinations. Conclusion: In triple modality treatment, the cell viability for 24h showed no significant improvement but in 48h the hyperthermia plus Graphene-oxide and 3 Gy radiotherapy had very low cell viability. Significant sensitizing effect for GO when combined by radiation therapy was observed.

Oncotarget ◽  
2017 ◽  
Vol 8 (45) ◽  
pp. 78556-78572 ◽  
Author(s):  
Trevor J. Grant ◽  
Anita K. Mehta ◽  
Anamika Gupta ◽  
Ahmad A.D. Sharif ◽  
Kshitij S. Arora ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 563 ◽  
Author(s):  
Robert G. Goetze ◽  
Soeren M. Buchholz ◽  
Ning Ou ◽  
Qinrong Zhang ◽  
Shilpa Patil ◽  
...  

Background: Pancreatic ductal adenocarcinoma (PDAC) is highly resistant to standard chemo- and radiotherapy. Recently, a new class of non-platinum-based halogenated molecules (called FMD compounds) was discovered that selectively kills cancer cells. Here, we investigate the potential of 1,2-Diamino-4,5-dibromobenzene (2Br-DAB) in combination with standard chemotherapy and radiotherapy in murine and human PDAC. Methods: Cell viability and colony formation was performed in human (Panc1, BxPC3, PaTu8988t, MiaPaCa) and three murine LSL-KrasG12D/+;LSL-Trp53R172H/+;Pdx-1-Cre (KPC) pancreatic cancer cell lines. In vivo, preclinical experiments were conducted in LSL-KrasG12D/+;p48-Cre (KC) and KPC mice using 2Br-DAB (7 mg/kg, i.p.), +/- radiation (10 × 1.8 Gy), gemcitabine (100 mg/kg, i.p.), or a combination. Tumor growth and therapeutic response were assessed by high-resolution ultrasound and immunohistochemistry. Results: 2Br-DAB significantly reduced cell viability in human and murine pancreatic cancer cell lines in a dose-dependent manner. In particular, colony formation in human Panc1 cells was significantly decreased upon 25 µM 2Br-DAB + radiation treatment compared with vehicle control (p = 0.03). In vivo, 2Br-DAB reduced tumor frequency in KC mice. In the KPC model, 2Br-DAB or gemcitabine monotherapy had comparable therapeutic effects. Furthermore, the combination of gemcitabine and 2Br-DAB or 2Br-DAB and 18 Gy irradiation showed additional antineoplastic effects. Conclusions: 2Br-DAB is effective in killing pancreatic cancer cells in vitro. 2Br-DAB was not toxic in vivo, and additional antineoplastic effects were observed in combination with irradiation.


1996 ◽  
Vol 270 (5) ◽  
pp. R1078-R1084 ◽  
Author(s):  
J. P. Smith ◽  
A. Shih ◽  
Y. Wu ◽  
P. J. McLaughlin ◽  
I. S. Zagon

The gastrointestinal peptides gastrin and cholecystokinin (CCK) stimulate growth of human pancreatic cancer through a CCK-B/gastrin- like receptor. In the present study we evaluated whether growth of human pancreatic cancer is endogenously regulated by gastrin. Immunohistomical examination of BxPC-3 cells and tumor xenografts revealed specifc gastrin immunoreactivity. Gastrin was detected by radioimmunoassay in pancreatic cancer cell extracts and in pancreatic cancer cell extracts and in the growth media. With use of reverse-transcriptase polymerase chain reaction gastrin gene expression was detected in both cultured BxPC-3 cancer cells and transplanted tumors, as well as seven addition human pancreatic cancer cell lines. Growth of BxPC-3 human pancreatic cancer cell in serum-free medium was inhibited by the addition of the CCK-B/gastrin receptor antagonist L-365,260, and gastrin treatment reversed the inhibitory effect of the antagonist. A selective gastrin antibody (Ab repressed growth of BxPC-3 cells. Gastrin immunoreactivity was detected in fresh human pancreatic cancer specimens but not in normal human pancreatic tissue. These data provide the first evidence that growth of a human pancreatic cancer is tonically stimulated by the autocrine production of gastrin. Evidence for the ubiquity of this system was provided by the detection of gastrin gene expression in multiple human pancreatic cancer cell lines and detection of gastrin in cell lines and fresh pancreatic tumors.


2011 ◽  
Vol 43 (7) ◽  
pp. 565-574 ◽  
Author(s):  
Jonathan P. Celli ◽  
Nicolas Solban ◽  
Alvin Liang ◽  
Stephen P. Pereira ◽  
Tayyaba Hasan

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