Correlative Patterns between Cellular DNA Content, N-myc Oncogene Amplification, and Karyotypic Abnormalities in Human Neuroblastomas.

1993 ◽  
Vol 677 (1 Clinical Flow) ◽  
pp. 450-453
Author(s):  
BARRY T. SHANNON ◽  
STEPHEN J. QUALMAN ◽  
DEBRA JACOBS
1988 ◽  
Vol 139 (3) ◽  
pp. 659-659 ◽  
Author(s):  
A. Nakagawara ◽  
K. Ikeda ◽  
T. Tsuda ◽  
K. Higashi

1988 ◽  
Vol 57 (5) ◽  
pp. 503-508 ◽  
Author(s):  
JPA Baak ◽  
NW Schipper ◽  
ECM Wisse-Brekelmans ◽  
T Ceelen ◽  
FT Bosman ◽  
...  

1987 ◽  
Vol 5 (10) ◽  
pp. 1690-1703 ◽  
Author(s):  
D E Merkel ◽  
L G Dressler ◽  
W L McGuire

The use of flow cytometry to analyze the cellular DNA content of human malignancies has become increasingly commonplace. The relationship between abnormalities in DNA content or proliferative characteristics and prognosis is becoming clear for a variety of malignancies in part through new techniques that permit analysis of archival material. High- and low-risk groups of patients with early breast and bladder carcinomas, non-small-cell lung cancer, and colorectal, ovarian, and cervical carcinoma can be distinguished on the basis of abnormal stemline DNA content. In several hematologic and common pediatric malignancies, the prognostic relevance of DNA content flow cytometry has been similarly established. Though the interpretation of tumor cell cycle analyses is less certain, this characteristic may also be prognostically important. However, generalizations cannot be made when applying flow cytometric DNA analysis to clinical decision making. The prognostic importance of an abnormal DNA histogram for an individual patient must be assessed on the basis of the relevant data base for that particular tumor type. The current extent of this data base for various malignancies is reviewed.


1990 ◽  
Vol 5 (4) ◽  
pp. 223-227 ◽  
Author(s):  
A. Schillaci ◽  
D. D. Tirindelli ◽  
M. Ferri ◽  
L. Teodori ◽  
F. Mauro ◽  
...  

Cell Cycle ◽  
2011 ◽  
Vol 10 (10) ◽  
pp. 1669-1678 ◽  
Author(s):  
Anna Kozarova ◽  
John W. Hudson ◽  
Panayiotis O. Vacratsis

2005 ◽  
Vol 53 (6) ◽  
pp. 725-733 ◽  
Author(s):  
You-Jun Shen ◽  
Cynthia J. DeLong ◽  
Francois Tercé ◽  
Timothy Kute ◽  
Mark C. Willingham ◽  
...  

Polyploidy is a profound phenotype found in tumors and its mechanism is unknown. We report here that when B-cell lymphoma gene-2 (Bcl-2) was overexpressed in a Chinese hamster ovary cell line that was deficient in CTP:phosphocholine cytidylyltransferase (CT), cellular DNA content doubled. The higher DNA content was due to a permanent conversion from diploid cells to tetraploid cells. The mechanism of polyploid formation could be attributed to the duplication of 18 parental chromosomes. The rate of conversion from diploid to tetraploid was Bcl-2 dose dependent. The diploid genome was not affected by Bcl-2 expression or by CT deficiency alone. Endogenous CT or expression of recombinant rat liver CTα prior to Bcl-2 expression prevented the formation of polyploid cells. This conversion was irreversible even when both initiating factors were removed. In this study, we have identified Bcl-2 as a positive regulator and CTα as a negative regulator of polyploid formation.


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