545 Poster In vivo imaging of radiation-induced apoptosis by 99mTc-Annexin-V scintigraphy in follicular lymphoma patients

2002 ◽  
Vol 64 ◽  
pp. S171
Keyword(s):  
Follicular Lymphoma ◽  
In Vivo Imaging ◽  
Annexin V ◽  
Radiation Induced ◽  
Induced Apoptosis

In vivo imaging of radiation-induced apoptosis in follicular lymphoma patients

2004 ◽  
Vol 59 (3) ◽  
pp. 782-787 ◽  
Author(s):  
Rick L.M Haas ◽  
Daphne de Jong ◽  
Renato A Valdés Olmos ◽  
Cees A Hoefnagel ◽  
Iris van Den Heuvel ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
In Vivo Imaging ◽  
Radiation Induced ◽  
Induced Apoptosis

710 In vivo assessment of radiation induced apoptosis in follicular lymphoma patients by 99mTc-Annexin V scintigraphy

2003 ◽  
Vol 1 (5) ◽  
pp. S214
Author(s):  
R.L.M. Haas ◽  
R.A. Valdés-Olmos ◽  
D. de Jong ◽  
S.F. Zerp ◽  
I. van den Heuvel ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
Annexin V ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
In Vivo Assessment

In-vivo visualization of radiation-induced apoptosis using 125I-annexin V

2006 ◽  
Vol 27 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Hiroshige Watanabe ◽  
Yuji Murata ◽  
Masahiko Miura ◽  
Masatoshi Hasegawa ◽  
Tadafumi Kawamoto ◽  
...  
Keyword(s):  
Annexin V ◽  
Radiation Induced ◽  
Induced Apoptosis

In Vivo Imaging of Radiation Induced Apoptosis

2009 ◽  
Vol 75 (3) ◽  
pp. S535
Author(s):  
J. Wang ◽  
F. Xu ◽  
M. Guo ◽  
L. Guo ◽  
Y. Shen ◽  
...  
Keyword(s):  
In Vivo Imaging ◽  
Radiation Induced ◽  
Induced Apoptosis

scholarly journals Preclinical Evaluation of the HDAC Inhibitor Chidamide in Transformed Follicular Lymphoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Mengya Zhong ◽  
Jinshui Tan ◽  
Guangchao Pan ◽  
Yuelong Jiang ◽  
Hui Zhou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Follicular Lymphoma ◽  
Single Agent ◽  
Hdac Inhibitors ◽  
Treatment Strategies ◽  
Annexin V ◽  
Gene Encoding ◽  
New Treatment ◽  
Transformed Follicular Lymphoma

The key factors leading to transformed follicular lymphoma (t-FL) include the aberrations of epigenetic modifiers as early and driving events, especially mutations in the gene encoding for histone acetyltransferase. Therefore, reversal of this phenomenon by histone deacetylase (HDAC) inhibitors is essential for the development of new treatment strategies in t-FL. Several t-FL cell lines were treated with various doses of chidamide and subjected to cell proliferation, apoptosis and cell cycle analyses with CCK-8 assay, Annexin V/PI assay and flow cytometry, respectively. Chidamide dose-dependently inhibited cell proliferation, caused G0/G1 cycle arrest and triggered apoptosis in t-FL cells. In addition, the effects of chidamide on tumor growth were evaluated in vivo in xenograft models. RNA-seq analysis revealed gene expression alterations involving the PI3K-AKT signaling pathway might account for the mechanism underlying the antitumor activity of chidamide as a single agent in t-FL. These findings provide a basis for further clinical exploration of chidamide as a promising treatment for FL.

scholarly journals The use of technetium tc 99m annexin V for in vivo imaging of apoptosis during cardiac allograft rejection

1998 ◽  
Vol 116 (5) ◽  
pp. 844-853 ◽  
Author(s):  
Patrick W. Vriens ◽  
Francis G. Blankenberg ◽  
Jan H. Stoota ◽  
Katsuichi Ohtsuki ◽  
Gerald J. Berry ◽  
...  
Keyword(s):  
In Vivo Imaging ◽  
Allograft Rejection ◽  
Annexin V ◽  
Cardiac Allograft ◽  
Cardiac Allograft Rejection

scholarly journals A Higher Frequency Administration of the Nontoxic Cycloartane-Type Triterpene Argentatin A Improved Its Anti-Tumor Activity

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1780 ◽  
Author(s):  
Zaira Tavarez-Santamaría ◽  
Nadia J. Jacobo-Herrera ◽  
Leticia Rocha-Zavaleta ◽  
Alejandro Zentella-Dehesa ◽  
Beatriz del Carmen Couder-García ◽  
...  
Keyword(s):  
Waste Product ◽  
Industrial Process ◽  
Annexin V ◽  
Control Group ◽  
Healthy Control ◽  
Hct 116 ◽  
Hct 116 Cells ◽  
Induced Apoptosis

Parthenium argentatum (Gray), commonly known as guayule, has been used to obtain natural rubber since the beginning of the 20th century. Additionally, the so called “resin” is a waste product derived from the industrial process. The cycloartane-type triterpene Argentatin A (AA) is one of the main constituents of the industrial waste resin. In this study we evaluated the AA anticancer activity both in vitro and in vivo in the HCT116 colon cancer cells. The apoptosis promotion of AA was assessed by the annexin V/propidium iodide (PI) assay. The senescence was evaluated for SA-β-galactosidase, and PCNA was used as a marker of proliferation. Its antitumor activity was evaluated using a xenograft mouse model. The results indicated that AA-induced apoptosis in HCT-116 cells and was positively stained for SA-β-galactosidase. In the xenografted mice test, the administration of AA at the dose of 250 mg/kg three times a week for 21 days reduced tumor growth by 78.1%. A comparable tumor reduction was achieved with cisplatin at the dose of 2 mg/kg administered three times a week for 21 days. However, nude mice treated with AA did not lose weight, as they did remarkably when treated with cisplatin. Furthermore, the animals treated with AA showed similar blood profiles as the healthy control group. These data indicate the low toxicity of AA compared to that shown by cisplatin.

scholarly journals A Novel High-Throughput Technique for Identifying Monoclonal Antibodies capable of Death Receptor Induced Apoptosis

2009 ◽  
Vol 2 ◽  
pp. JCD.S3660
Author(s):  
Hang Fai Kwok ◽  
Julie A. Gormley ◽  
Christopher J. Scott ◽  
James A. Johnston ◽  
Shane A. Olwill
Keyword(s):  
Cell Death ◽  
High Throughput ◽  
High Throughput Screening ◽  
False Negative ◽  
Death Receptor ◽  
Annexin V ◽  
Fas Receptor ◽  
Induced Apoptosis

The study of death receptor family induced apoptosis has gained momentum in recent years with the knowledge that therapeutic antibodies targeting DR4 and DR5 (death receptor's 4 and 5) have proved efficacious in multiple clinical trials. The therapeutic rationale is based on targeting and amplifying a tumour tissues normal cell death programme (apoptosis). While advances in the targeting of DR4 and DR5 have been successful the search for an agonistic antibody to another family member, the Fas receptor, has proven more elusive. This is partly due to the differing in vitro and in vivo characteristics of individual antibodies. In order to induce Fas targeted cell death an antibody must be capable of binding to and trimerising the receptor. It has been shown that antibodies capable of performing this function in vivo, with the assistance of tumour associated cells, do not always induce apoptosis in vitro. As a result the use of current methodologies to detect functional antibodies in vitro may have dismissed potential therapeutic candidates ('false negative'). Here we report a novel high throughput screening technique which artificially cross-links antibodies bound to the Fas receptor. By combining this process with Annexin-V and Prodidium Iodide (PI) staining we can select for antibodies which have the potential to induce apoptosis in vivo.

scholarly journals Anti-apoptotic effects of 3,5,3′-tri-iodothyronine in mouse hepatocytes

2006 ◽  
Vol 191 (2) ◽  
pp. 447-458 ◽  
Author(s):  
O A Sukocheva ◽  
D O Carpenter
Keyword(s):  
Early Stage ◽  
Dose Range ◽  
Annexin V ◽  
Intracellular Camp ◽  
Camp Content ◽  
Mouse Hepatocytes ◽  
Induced Apoptosis ◽  
Apoptotic Effects ◽  
Intracellular Alkalinization

The present study demonstrates that 3,5,3′-tri-iodothyronine (T3) in physiological dose range inhibits tumor necrosis factor α(TNFα)/Fas-induced apoptosis in mouse hepatocytes. T3 pretreatment prevented Fas-induced early stage of apoptosis signs assessed by flow cytometry analysis of the annexin V positive cell population. T3 attenuated TNFα/Fas-induced cleavage of caspase-8 and DNA fragmentation. We found that T3 exerted its anti-apoptotic effects by mobilization of several non-genomic mechanisms independent of transcriptional activity. Inhibition of protein kinase A (PKA), extracellular signal-regulated kinase (ERK), and Na+/H+ exchanger blocked T3-dependent anti-apoptotic effects indicating an involvement of these intracellular targets into T3-induced signaling cascade. Furthermore, physiological concentrations of T3, but not reverse T3, caused increases in intracellular cAMP content and activated PKA. T3 markedly induced phosphorylation of ERK. We also detected T3-dependent intracellular alkalinization that abolished TNFα-induced acidification. PKA inhibitor KT-5720 blocked T3-induced activation of ERK and intracellular alkalinization confirming the upstream position of PKA signaling. We further detected that hepatocytes from hypothyroid mice are more sensitive to TNFα/Fas-induced apoptosis than euthyroid animals in vivo. Together, these findings imply that T3 triggers PKA- and ERK-regulated intracellular pathways capable of driving and ensuring hepatocytes survival in the presence of death receptor ligand-induced damage under chronic inflammatory conditions.

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