scholarly journals Multiple cancer-specific antigens are targeted by a chimeric antibody receptor on a single cancer cell

JCI Insight ◽  
2019 ◽  
Vol 4 (21) ◽  
Author(s):  
Yanran He ◽  
Karin Schreiber ◽  
Steven P. Wolf ◽  
Frank Wen ◽  
Catharina Steentoft ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Chimeric Antibody ◽  
Multiple Cancer ◽  
Specific Antigens ◽  
Single Cancer

scholarly journals Multiple cancer-specific antigens are targeted by a chimeric antigen receptor on a single cancer cell

JCI Insight ◽  
2019 ◽  
Vol 4 (23) ◽  
Author(s):  
Yanran He ◽  
Karin Schreiber ◽  
Steven P. Wolf ◽  
Frank Wen ◽  
Catharina Steentoft ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Chimeric Antigen Receptor ◽  
Antigen Receptor ◽  
Multiple Cancer ◽  
Specific Antigens ◽  
Single Cancer

scholarly journals Investigation of squalene-doxorubicin distribution and interactions within single cancer cell using Raman microspectroscopy

2021 ◽  
pp. 102404
Author(s):  
Hassan Rammal ◽  
Almar Al Assaad ◽  
Franco Dosio ◽  
Barbara Stella ◽  
Andrei Maksimenko ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Raman Microspectroscopy ◽  
Single Cancer

M200, a Chimeric Antibody Against Integrin alpha5 beta1, Inhibits Cancer Cell Growth In Vitro

2004 ◽  
Vol 27 (6) ◽  
pp. S9 ◽  
Author(s):  
Vinay Bhaskar ◽  
Pauline Wales ◽  
Danna Breinberg ◽  
Melvin Fox ◽  
Sun Ho
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Chimeric Antibody ◽  
Cancer Cell Growth

scholarly journals Imaging of cisplatin in single cancer cell and visualizing its mechanism of action by FIB-TOF-SIMS

2019 ◽  
Vol 26 (2) ◽  
pp. 198-199
Author(s):  
Kazuya Tanuma ◽  
Takurou Hasegawa ◽  
Masato Morita ◽  
Kumiko Nagase ◽  
Masatoshi Kakihana ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Mechanism Of Action ◽  
Tof Sims ◽  
Single Cancer

scholarly journals Blocking IL-6/GP130 Signaling Inhibits Cell Viability/Proliferation, Glycolysis, and Colony Forming Activity in Human Pancreatic Cancer Cells

2019 ◽  
Vol 19 (5) ◽  
pp. 417-427 ◽  
Author(s):  
Xiang Chen ◽  
Jilai Tian ◽  
Gloria H. Su ◽  
Jiayuh Lin
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Human Pancreatic Cancer ◽  
Multiple Cancer ◽  
Pancreatic Cancer Cells ◽  
Stat3 Phosphorylation

Background:Elevated production of the pro-inflammatory cytokine interleukin-6 (IL-6) and dysfunction of IL-6 signaling promotes tumorigenesis and are associated with poor survival outcomes in multiple cancer types. Recent studies showed that the IL-6/GP130/STAT3 signaling pathway plays a pivotal role in pancreatic cancer development and maintenance.Objective:We aim to develop effective treatments through inhibition of IL-6/GP130 signaling in pancreatic cancer.Methods:The effects on cell viability and cell proliferation were measured by MTT and BrdU assays, respectively. The effects on glycolysis was determined by cell-based assays to measure lactate levels. Protein expression changes were evaluated by western blotting and immunoprecipitation. siRNA transfection was used to knock down estrogen receptor α gene expression. Colony forming ability was determined by colony forming cell assay.Results:We demonstrated that IL-6 can induce pancreatic cancer cell viability/proliferation and glycolysis. We also showed that a repurposing FDA-approved drug bazedoxifene could inhibit the IL-6/IL-6R/GP130 complexes. Bazedoxifene also inhibited JAK1 binding to IL-6/IL-6R/GP130 complexes and STAT3 phosphorylation. In addition, bazedoxifene impeded IL-6 mediated cell viability/ proliferation and glycolysis in pancreatic cancer cells. Consistently, other IL-6/GP130 inhibitors SC144 and evista showed similar inhibition of IL-6 stimulated cell viability, cell proliferation and glycolysis. Furthermore, all three IL-6/GP130 inhibitors reduced the colony forming ability in pancreatic cancer cells.Conclusion:Our findings demonstrated that IL-6 stimulates pancreatic cancer cell proliferation, survival and glycolysis, and supported persistent IL-6 signaling is a viable therapeutic target for pancreatic cancer using IL-6/GP130 inhibitors.

Highly accurate and label-free discrimination of single cancer cell using a plasmonic oxide-based nanoprobe

2021 ◽  
pp. 113814
Author(s):  
Bao Yue Zhang ◽  
Pengju Yin ◽  
Yihong Hu ◽  
Crispin Szydzik ◽  
Muhammad Waqas Khan ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Label Free ◽  
Single Cancer

scholarly journals Metformin Decreases the Dose of Chemotherapy for Prolonging Tumor Remission in Mouse Xenografts Involving Multiple Cancer Cell Types

2011 ◽  
Vol 71 (9) ◽  
pp. 3196-3201 ◽  
Author(s):  
Dimitrios Iliopoulos ◽  
Heather A. Hirsch ◽  
Kevin Struhl
Keyword(s):  
Cancer Cell ◽  
Cell Types ◽  
Multiple Cancer ◽  
Tumor Remission

scholarly journals Species D Adenoviruses as Oncolytic Viral Vectors

Viruses ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1399
Author(s):  
Brianna L. Bullard ◽  
Brigette N. Corder ◽  
Eric A. Weaver
Keyword(s):  
Blood Coagulation ◽  
Cell Lines ◽  
Cancer Cell ◽  
Neutralizing Antibodies ◽  
Coagulation Factor ◽  
Cancer Cell Lines ◽  
Factor X ◽  
Multiple Cancer ◽  
Iodide Uptake ◽  
Oncolytic Adenoviruses

Oncolytic adenoviruses (Ad) have shown promising results in the therapeutic treatment of cancer. Ad type 5 (Ad5) is the most extensively utilized Ad type. However, several limitations exist to using Ad5 as an oncolytic virus, including high levels of anti-Ad5 neutralizing antibodies in the population, binding of the Ad5 hexon to blood coagulation factor X leading to liver sequestration and toxicity, and reduced expression of the primary receptor CAR on many tumors. Here, we use in vitro methods to explore the oncolytic potential of four alternative Ad types (Ad26, 28, 45, and 48) belonging to the species D Ad subgroup and developed replication-competent species D Ads expressing the human sodium iodide symporter protein (hNIS) for combination radiovirotherapy. We evaluated the species D Ad vectors transduction, replication, cytotoxicity, and gene expression in six different cancer cell lines. Species D Ads showed the greatest transduction and cytotoxic killing in the SKBR3 breast cancer cells, followed by 293, A549, and HepG2 cells, however the cytotoxicity was less than the wild type Ad5 virus. In contrast, species D Ads showed limited transduction and cytotoxicity in the Hela and SKOV3 cancer cell lines. These species D Ad vectors also successfully expressed the hNIS gene during infection leading to increased iodide uptake in multiple cancer cell lines. These results, the low seroprevalence of anti-species D antibodies, and the lack of binding to blood coagulation FX, support further exploration of species D Ads as alternative oncolytic adenoviruses against multiple types of cancer.

A Machine Learning‐Assisted Nanoparticle‐Printed Biochip for Real‐Time Single Cancer Cell Analysis

2020 ◽  
Vol 4 (11) ◽  
pp. 2000160
Author(s):  
Kushal Joshi ◽  
Alireza Javani ◽  
Joshua Park ◽  
Vanessa Velasco ◽  
Binzhi Xu ◽  
...  
Keyword(s):  
Machine Learning ◽  
Real Time ◽  
Cancer Cell ◽  
Cell Analysis ◽  
Single Cancer

Anti-EpCAM XmAb antibodies with improved cytotoxicity

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 12506-12506 ◽  
Author(s):  
O. Vafa ◽  
S. Kharki ◽  
J. Vielmetter ◽  
A. Chamberlain ◽  
P. Hammond ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Clinical Efficacy ◽  
Cancer Cell Lines ◽  
In Vitro Cytotoxicity ◽  
Binding Assays ◽  
Multiple Cancer ◽  
Effector Cells ◽  
Dependent Cell

12506 Background: The epithelial cell adhesion molecule (EpCAM), also known as epithelial protein 2 (EGP-2) or 17–1A antigen, is a trans-membrane protein expressed on the surfaces of most carcinomas, including those of pancreatic, colorectal, prostate, breast, kidney, lung, and ovarian origins. Moderate affinity antibodies (Abs) such as 17–1A (Kd ∼ 10−7 nM) have been safe in humans albeit with limited clinical efficacy. Attempts to improve clinical efficacy by enhancing antigen affinity (Kd ∼ 10−9 nM) have led to serious clinical toxicity, including pancreatitis. These observations raise the question of whether a moderate affinity Ab with enhanced effector function will be both safe and clinically efficacious. Methods: We applied our proprietary XmAb™ technologies to humanize the 17–1A variable domain and engineer a human IgG1 Fc domain to increase affinity for the activating receptor FcγRIIIa. Ab binding to Ep-CAM or to Fc receptors was tested with Biacore and/or AlphaScreen binding assays. In vitro cytotoxic activity against representative cancer cell lines was measured with Antibody Dependent Cell-mediated Cytotoxicity (ADCC) assays, using human PBMC as effector cells. Results: Humanized anti-EpCAM Abs have affinity for EpCAM similar to the parent 17–1A. Affinity for the activating FcγRIIIa was increased 100-fold relative to a control Ab with an IgG1 Fc domain. As expected, these Abs exhibit dramatically enhanced ADCC against multiple cancer cell lines relative to 17–1A and IgG1 control Abs. Despite their moderate affinity for EpCAM, these novel Abs have in vitro cytotoxicity comparable to the high affinity Ab ING-1. CDC activities of these Abs were similar to chimeric 17–1A. Conclusions: We have demonstrated that antibodies with moderate affinity for EpCAM and increased FcγRIIIa affinity exhibit superior cancer cell killing via an ADCC mechanism. The humanized nature and the increased cytotoxicity of anti-EpCAM XmAb™ antibodies make them promising candidates for clinical development of a novel pan-carcinoma Ab that is superior to 17–1A. [Table: see text]

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