scholarly journals Zooming in on single tumor cells

2016 ◽  
Vol 13 (5) ◽  
pp. 395-395
Keyword(s):  
Tumor Cells ◽  
Single Tumor

scholarly journals Multiple Mutation Analyses in Single Tumor Cells with Improved Whole Genome Amplification

1999 ◽  
Vol 154 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Wolfgang Dietmaier ◽  
Arndt Hartmann ◽  
Sabine Wallinger ◽  
Ernst Heinmöller ◽  
Thomas Kerner ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Whole Genome Amplification ◽  
Whole Genome ◽  
Genome Amplification ◽  
Multiple Mutation ◽  
Single Tumor ◽  
Mutation Analyses

scholarly journals Imaging Single Tumor Cells in Mice Using Multimodal Correlative Microscopy

2016 ◽  
Vol 22 (S5) ◽  
pp. 30-31 ◽  
Author(s):  
M.A. Karreman ◽  
L. Mercier ◽  
N.L. Schieber ◽  
G. Solecki ◽  
G. Allio ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Correlative Microscopy ◽  
Single Tumor

585 Intralesional injection of rose bengal improves the efficacy of gemcitabine chemotherapy against pancreatic cancer

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A620-A620
Author(s):  
Patrick Innamarato ◽  
Shari Pilon-Thomas ◽  
Jennifer Morse ◽  
Sarah Asby ◽  
Amy Mackay ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Cells ◽  
Rose Bengal ◽  
Tumor Model ◽  
Standard Of Care ◽  
Pancreatic Tumors ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns ◽  
Panc02 Tumor ◽  
Single Tumor

BackgroundChemotherapy regimens that include gemcitabine are considered standard of care in patients with advanced pancreatic ductal adenocarcinoma (PDAC). However, most patients with PDAC die within 2 years of diagnosis, even with these standard of care regimens. In this study, we explored the ability of intratumoral injections of PV-10, a 10% solution of rose bengal, to induce lesion-specific ablation and control of metastatic pancreatic tumors in a murine model.MethodsPV-10 was cultured with human pancreatic cancer cell lines overnight and cell death was measured via Annexin-V and DAPI staining. Murine pancreatic tumor cells (Panc02) were injected subcutaneously in one flank to establish a single tumor model; to establish a bilateral tumor model, Panc02 tumor cells were implanted in the opposite flanks. On day 7, a single tumor was treated with intralesional PV-10. Gemcitabine (60 mg/kg) was injected intraperitoneally twice per week for 2 weeks. These experiments were repeated using Panc02 cells modified to overexpress the neoantigen ovalbumin (OVA). Control mouse tumor were directly injected with PBS. Tumor growth of PV-10 injected tumors and non-injected bystander tumors on the opposite flank were measured. Damage associated molecular patterns (DAMPs) in serum and immune cell frequencies within the spleens of tumor-bearing mice were measured to identify an associated systemic response with tumor lytic treatment regimen.ResultsWe established that less than 50% of human and murine pancreatic cells were alive after a 24 hour incubation with 200µM PV-10 in vitro. The combination of intralesional PV-10 with the systemic administration of gemcitabine delayed the growth treated tumors and non-injected distal tumors. In contrast, gemcitabine monotherapy failed to delay tumor growth in bilateral Panc02 tumor models. We observed that this treatment strategy was markedly more successful in immunogenic Panc02OVA tumors resulting in lesion-specific ablation in 5/8 mice compared to 0/8 mice that were treated with gemcitabine monotherapy. This suggests that the combination therapy enhanced the immune-mediated clearance of tumors. Moreover, regression of tumors in mice that received PV-10 in combination with gemcitabine was associated with the depletion of splenic CD11b+Gr-1+ cells and increases in damage associated molecular patterns HMGB1, S100A8, and IL-1α.ConclusionsTogether, these results demonstrate that intralesional therapy with PV-10 can enhance the efficacy gemcitabine against pancreatic tumors.Ethics ApprovalStudies were performed under approved Institutional Review Board (IRB) laboratory protocols at the H. Lee Moffitt Cancer Center (Tampa, FL).

scholarly journals Oncolytic viruses for therapy of malignant glioma

2016 ◽  
Vol 62 (4) ◽  
pp. 376-390 ◽  
Author(s):  
A.O. Sosnovtceva ◽  
N.F. Grinenko ◽  
A.V. Lipatova ◽  
P.M. Chumakov ◽  
V.P. Chekhonin
Keyword(s):  
Clinical Trials ◽  
Tumor Cells ◽  
Disease Recurrence ◽  
Oncolytic Viruses ◽  
High Rate ◽  
Glial Tumor ◽  
Viral Therapy ◽  
The Brain ◽  
Virus Strains ◽  
Single Tumor

Effective treatment of malignant brain tumors is still an open problem. Location of tumor in vital areas of the brain significantly limits capasities of surgical treatment. The presence of tumor stem cells resistant to radiation and anticancer drugs in brain tumor complicates use of chemoradiotherapy and causes a high rate of disease recurrence. A technological improvement in bioselection and production of recombinant resulted in creation of viruses with potent oncolytic properties against glial tumors. Recent studies, including clinical trials, showed, that majority of oncolytic viruses are safe. Despite the impressive results of the viral therapy in some patients, the treatment of other patients is not effective; therefore, further improvement of the methods of oncolytic virotherapy is necessary. High genetic heterogeneity of glial tumor cells even within a single tumor determines differences in individual sensitivity of tumor cells to oncolytic viruses. This review analyses the most successful oncolytic virus strains, including those which had reached clinical trials, and discusses the prospects for new approaches to virotherapy of gliomas.

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