scholarly journals Mouse Tumor Gene Index

2020 ◽  
Author(s):  
Keyword(s):  
Mouse Tumor ◽  
Tumor Gene ◽  
Gene Index

scholarly journals Human Tumor Gene Index

2020 ◽  
Author(s):  
Keyword(s):  
Human Tumor ◽  
Tumor Gene ◽  
Gene Index

Electron Microscopy of the Nucleic Acid of Mouse Mammary Tumor Virus

1968 ◽  
Vol 26 ◽  
pp. 22-23
Author(s):  
N. H. Sarkar ◽  
Dan H. Moore
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Ammonium Acetate ◽  
Dry Weight ◽  
Mouse Tumor ◽  
Mammary Tumor Virus ◽  
Rna Molecules ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
The Subject

Mouse mammary tumor virus (MTV) is believed to contain about 0.8% single stranded ribonucleic acid (RNA). This value of RNA content was estimated on a dry weight basis. The subject of this report is an attempt to visualize the RNA molecules of MTV particles.MTV particles were isolated from RIII mouse (tumor incidence approximately 80%) milk according to the method described by Lyons and Moore. Purified virions from 5 ml of milk were finally suspended in 0.2 ml of PBS, pH 7.4 and was mixed with an equal volume of pronase (5 mg/ml). This mixture was incubated at 37°C for an hour. RNA was extracted three times using freshly prepared cold phenol. It was then treated three times with cold ethyl ether to remove any trace of phenol. The RNA thus extracted was divided into two parts. One part was diluted four fold with 8M urea to avoid aggregation of the molecules. The other part was left untreated. Both samples were then mixed with an equal volume of 1M ammonium acetate, adjusted to pH 8.0 with NH3 containing chymotrypsin at a concentration of 0.01%.

Identification of circulating microrna pattern alteration during the tumor development using C38/C57BL/6 mouse tumor model

2012 ◽  
Vol 50 (05) ◽  
Author(s):  
Z Nagy ◽  
B Barták ◽  
S Spisák ◽  
B Wichmann ◽  
A Kalmár ◽  
...  
Keyword(s):  
Tumor Development ◽  
Tumor Model ◽  
Circulating Microrna ◽  
Mouse Tumor ◽  
Mouse Tumor Model

Photodynamic Therapy using a Diode Laser with NPe6 for Implanted Mouse Tumor.

1994 ◽  
Vol 15 (Supplement) ◽  
pp. 37-40
Author(s):  
Toichiro Katsumi ◽  
Katsuo Aizawa ◽  
Yukari Kuroiwa ◽  
Kouichi Saito ◽  
Hiroshi Shibuya ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Diode Laser ◽  
Mouse Tumor

Trojan horse at cellular level for tumor gene therapies

Gene ◽  
2013 ◽  
Vol 525 (2) ◽  
pp. 208-216 ◽  
Author(s):  
Guillaume Collet ◽  
Catherine Grillon ◽  
Mahdi Nadim ◽  
Claudine Kieda
Keyword(s):  
Cellular Level ◽  
Trojan Horse ◽  
Gene Therapies ◽  
Tumor Gene

scholarly journals Monocytic MDSC mobilization promotes tumor recurrence after liver transplantation via CXCL10/TLR4/MMP14 signaling

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Hui Liu ◽  
Chang Chun Ling ◽  
Wai Ho Oscar Yeung ◽  
Li Pang ◽  
Jiang Liu ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Tumor Recurrence ◽  
Ischemia Reperfusion Injury ◽  
Therapeutic Potential ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
Liver Graft ◽  
Mouse Tumor ◽  
Hepatic Ischemia ◽  
Tlr4 Signaling

AbstractTumor recurrence is the major obstacle for pushing the envelope of liver transplantation for hepatocellular carcinoma (HCC) patients. The inflammatory cascades activated by acute liver graft injury promote tumor recurrence. We aimed to explore the role and mechanism of myeloid-derived suppressor cell (MDSC) mobilization induced by liver graft injury on tumor recurrence. By analyzing 331 HCC patients who received liver transplantation, the patients with graft weight ratio (GWR, the weight of liver graft divided by the estimated standard liver weight of recipient) <60% had higher tumor recurrence than GWR ≥60% ones. MDSCs and CXCL10/TLR4 levels were significantly increased in patients with GWR <60% or tumor recurrence. These findings were further validated in our rat orthotopic liver transplantation model. In CXCL10−/− and TLR4−/− mice of hepatic ischemia/reperfusion injury plus major hepatectomy (IRH) model, monocytic MDSCs, instead of granulocytic MDSCs, were significantly decreased. Importantly, CXCL10 deficiency reduced the accumulation of TLR4+ monocytic MDSCs, and CXCL10 increased MDSC mobilization in the presence of TLR4. Moreover, MMP14 was identified as the key molecule bridging CXCL10/TLR4 signaling and MDSC mobilization. Knockout or inhibition of CXCL10/TLR4 signaling significantly reduced the tumor growth with decreased monocytic MDSCs and MMP14 in the mouse tumor recurrent model. Our data indicated that monocytic MDSCs were mobilized and recruited to liver graft during acute phase injury, and to promote HCC recurrence after transplantation. Targeting MDSC mobilization via CXCL10/TLR4/MMP14 signaling may represent the therapeutic potential in decreasing post-transplant liver tumor recurrence.

Ultrasound molecular imaging-guided tumor gene therapy through dual-targeted cationic microbubbles

2021 ◽  
Vol 9 (7) ◽  
pp. 2454-2466
Author(s):  
Yingying Liu ◽  
Yuli Zhou ◽  
Jinfeng Xu ◽  
Hui Luo ◽  
Yao Zhu ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Molecular Imaging ◽  
Transfection Efficiency ◽  
Gene Transfection ◽  
Tumor Gene Therapy ◽  
Ultrasound Molecular Imaging ◽  
Tumor Gene

A novel dual-targeted cationic microbubbles help to improve gene transfection efficiency.

705 Anti-tumor activity of CB-668, a potent, selective and orally bioavailable small-molecule inhibitor of the immuno-suppressive enzyme Interleukin 4 (IL-4)-Induced Gene 1 (IL4I1)

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A747-A747
Author(s):  
Andrew MacKinnon ◽  
Deepthi Bhupathi ◽  
Jason Chen ◽  
Tony Huang ◽  
Weiqun Li ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Tumor Microenvironment ◽  
Immune Cell ◽  
Interleukin 4 ◽  
Mouse Tumor ◽  
Syngeneic Mouse ◽  
Molecule Inhibitor ◽  
Anti Tumor Activity ◽  
Mouse Tumor Models

BackgroundTumors evade destruction by the immune system through multiple mechanisms including altering metabolism in the tumor microenvironment. Metabolic control of immune responses occurs through depletion of essential nutrients or accumulation of toxic metabolites that impair immune cell function and promote tumor growth. The secreted enzyme interleukin 4 (IL-4)-induced gene 1 (IL4I1) is an L-phenylalanine oxidase that catabolizes phenylalanine and produces phenyl-pyruvate and hydrogen peroxide. IL4I1 regulates several aspects of adaptive immunity in mice, including inhibition of cytotoxic T cells through its production of hydrogen peroxide (reviewed in1). In human tumors, IL4I1 expression is significantly elevated relative to normal tissues and is notably high in ovarian tumors and B cell lymphomas. Motivated by the hypothesis that IL4I1 is an immuno-metabolic enzyme that suppresses anti-tumor immunity, we discovered CB-668, the first known small-molecule inhibitor of IL4I1.MethodsIL4I1 enzymatic activity was measured using an HRP-coupled enzyme assay. RNA in-situ hybridization was carried out on the RNAScope platform. Syngeneic mouse tumor models were used to evaluate the anti-tumor activity of CB-668. The level of phenyl-pyruvate in tumor homogenates was measured by LC/MS.ResultsOur clinical candidate, CB-668 is a potent and selective non-competitive inhibitor of IL4I1 (IC50 = 15 nM). CB-668 has favorable in vitro ADME properties and showed low clearance and high oral bioavailability in rodents. Twice-daily oral administration of CB-668 was well-tolerated in mice and resulted in single-agent anti-tumor activity in the syngeneic mouse tumor models B16-F10, A20, and EG7. Oral CB-668 administration reduced the levels of phenyl-pyruvate in the tumor, consistent with inhibition of IL4I1 enzymatic activity. Anti-tumor activity of CB-668 was immune cell-mediated since efficacy was abrogated in CD8-depleted mice, and CB-668 treatment caused increased expression of pro-inflammatory immune genes in the tumor. Moreover, CB-668 had no direct anti-proliferative activity on tumor cells grown in vitro (IC50 > 50 µM). CB-668 also favorably combined with anti-PD-L1 therapy to reduce tumor growth in the B16-F10 tumor model.ConclusionsThese data support an immune-mediated anti-tumor effect of IL4I1 inhibition by CB-668, and suggest inhibition of IL4I1 represents a novel strategy for cancer immuno-therapy.ReferencesMolinier-Frenkel V, Prévost-Blondel A, and Castellano F. The IL4I1 Enzyme: A New Player in the Immunosuppressive Tumor Microenvironment. Cells 2019;8:1–9.

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