scholarly journals Relationship of Doxorubicin- and Radiation-Induced Apoptosis with Ki-67 Labeling Index in Human Tumors in vivo.

1999 ◽  
Vol 49 (6) ◽  
pp. 431-435
Author(s):  
Kayoko Hayakawa ◽  
Masatoshi Hasegawa ◽  
Miho Kawashima ◽  
Hisako Toda ◽  
Kazushige Hayakawa ◽  
...  
Keyword(s):  
Human Tumors ◽  
Labeling Index ◽  
Ki 67 ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
Relationship Of

scholarly journals DR5 Knockout Mice Are Compromised in Radiation-Induced Apoptosis

2005 ◽  
Vol 25 (5) ◽  
pp. 2000-2013 ◽  
Author(s):  
Niklas Finnberg ◽  
Joshua J. Gruber ◽  
Peiwen Fei ◽  
Dorothea Rudolph ◽  
Anka Bric ◽  
...  
Keyword(s):  
Cell Death ◽  
Null Mouse ◽  
Organ Specific ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
The Brain ◽  
Necrosis Factor

ABSTRACT DR5 (also called TRAIL receptor 2 and KILLER) is an apoptosis-inducing membrane receptor for tumor necrosis factor-related apoptosis-inducing ligand (also called TRAIL and Apo2 ligand). DR5 is a transcriptional target of p53, and its overexpression induces cell death in vitro. However, the in vivo biology of DR5 has remained largely unexplored. To better understand the role of DR5 in development and in adult tissues, we have created a knockout mouse lacking DR5. This mouse is viable and develops normally with the exception of having an enlarged thymus. We show that DR5 is not expressed in developing embryos but is present in the decidua and chorion early in development. DR5-null mouse embryo fibroblasts expressing E1A are resistant to treatment with TRAIL, suggesting that DR5 may be the primary proapoptotic receptor for TRAIL in the mouse. When exposed to ionizing radiation, DR5-null tissues exhibit reduced amounts of apoptosis compared to wild-type thymus, spleen, Peyer's patches, and the white matter of the brain. In the ileum, colon, and stomach, DR5 deficiency was associated with a subtle phenotype of radiation-induced cell death. These results indicate that DR5 has a limited role during embryogenesis and early stages of development but plays an organ-specific role in the response to DNA-damaging stimuli.

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

Ki-67 Correlates With In Vivo Bromodeoxyuridine Labeling Index in Operable Breast Cancer

2006 ◽  
Vol 24 (23) ◽  
pp. 3809-3809 ◽  
Author(s):  
William H. Goodson ◽  
Dan H. Moore ◽  
Frederick M. Waldman
Keyword(s):  
Breast Cancer ◽  
Operable Breast Cancer ◽  
Labeling Index ◽  
Ki 67

scholarly journals bak deletion stimulates gastric epithelial proliferation and enhances Helicobacter felis-induced gastric atrophy and dysplasia in mice

2015 ◽  
Vol 309 (6) ◽  
pp. G420-G430 ◽  
Author(s):  
C. A. Duckworth ◽  
A. A. Abuderman ◽  
M. D. Burkitt ◽  
J. M. Williams ◽  
L. A. O'Reilly ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Gastric Gland ◽  
Gastric Atrophy ◽  
Colorectal Carcinogenesis ◽  
Ki 67 ◽  
Epithelial Cell Apoptosis ◽  
Mucosal Thickness ◽  
Gastric Corpus ◽  
Induced Apoptosis

Helicobacter infection causes a chronic superficial gastritis that in some cases progresses via atrophic gastritis to adenocarcinoma. Proapoptotic bak has been shown to regulate radiation-induced apoptosis in the stomach and colon and also susceptibility to colorectal carcinogenesis in vivo. Therefore we investigated the gastric mucosal pathology following H. felis infection in bak-null mice at 6 or 48 wk postinfection. Primary gastric gland culture from bak-null mice was also used to assess the effects of bak deletion on IFN-γ-, TNF-α-, or IL-1β-induced apoptosis. bak-null gastric corpus glands were longer, had increased epithelial Ki-67 expression, and contained fewer parietal and enteroendocrine cells compared with the wild type (wt). In wt mice, bak was expressed at the luminal surface of gastric corpus glands, and this increased 2 wk post- H. felis infection. Apoptotic cell numbers were decreased in bak-null corpus 6 and 48 wk following infection and in primary gland cultures following cytokine administration. Increased gastric epithelial Ki-67 labeling index was observed in C57BL/6 mice after H. felis infection, whereas no such increase was detected in bak-null mice. More severe gastric atrophy was observed in bak-null compared with C57BL/6 mice 6 and 48 wk postinfection, and 76% of bak-null compared with 25% of C57BL/6 mice showed evidence of gastric dysplasia following long-term infection. Collectively, bak therefore regulates gastric epithelial cell apoptosis, proliferation, differentiation, mucosal thickness, and susceptibility to gastric atrophy and dysplasia following H. felis infection.

2001 p53-Dependent radiation-induced apoptosis in vivo: Relationship to Bcl-2 and Bax expression

1997 ◽  
Vol 39 (2) ◽  
pp. 241
Author(s):  
Masatoshi Hasegawa ◽  
Yoshiyuki Suzuki ◽  
Masaya Furuta ◽  
Michitaka Yamakawa ◽  
Katsuya Maebayashi ◽  
...  
Keyword(s):  
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
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