The p53 tumor suppressor gene in anticancer agent-induced apoptosis and chemosensitivity of human gastrointestinal cancer cell lines

1999 ◽  
Vol 43 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Manabu Yamamoto ◽  
Yoshihiko Maehara ◽  
Shinya Oda ◽  
Yuji Ichiyoshi ◽  
Tetsuya Kusumoto ◽  
...  
2015 ◽  
Vol 139 (1) ◽  
pp. 194 ◽  
Author(s):  
Alexandre Buckley de Meritens ◽  
Ayesha Joshi ◽  
Christopher Miller ◽  
Lora Hedrick Ellenson ◽  
Divya Gupta

1970 ◽  
Vol 40 (6) ◽  
pp. 653-658
Author(s):  
Weon Seon Hong ◽  
Seok Il Hong ◽  
Dong Soon Lee ◽  
Young Sook Son ◽  
Choon Taek Lee

Oncogene ◽  
2004 ◽  
Vol 23 (22) ◽  
pp. 4037-4040 ◽  
Author(s):  
Julian Carretero ◽  
Pedro P Medina ◽  
Ruben Pio ◽  
Luis M Montuenga ◽  
Montserrat Sanchez-Cespedes

Blood ◽  
1994 ◽  
Vol 83 (1) ◽  
pp. 191-198 ◽  
Author(s):  
MM Farrugia ◽  
LJ Duan ◽  
MD Reis ◽  
BY Ngan ◽  
NL Berinstein

Abstract Diffuse large cell lymphomas are aggressive tumors of B-cell origin. In some cases they arise from low-grade follicular lymphomas carrying the t(14;18) translocation, an event that leads to the overexpression of the BCL-2 gene product. More frequently, however, they lack the t(14;18) translocation. Rearrangements of the c-MYC proto-oncogene and mutations of the p53 tumor suppressor gene have also been documented in these lymphomas. This study examines the extent to which alterations in the BCL-2, c-MYC, and p53 genes co-exist within individual lymphomas. Eight diffuse large cell lymphoma cell lines and 11 diffuse large cell lymphoma tumors were assessed for genetic alterations in these three genes. Our results indicate that there is a heterogeneity in the oncogene/suppressor gene profile among diffuse large cell lymphomas. Two cell lines and one tumor carried alterations in all three genes, one cell line carried alterations of c-MYC and p53, and one primary tumor and one cell line carried p53 mutations and the t(14;18). Single alterations of BCL-2 and p53 were also observed. Another cell line had no alterations in any of these genes. The heterogeneity indicates that varied mechanisms may be involved in the generation of diffuse large cell lymphomas.


Blood ◽  
1994 ◽  
Vol 83 (1) ◽  
pp. 191-198 ◽  
Author(s):  
MM Farrugia ◽  
LJ Duan ◽  
MD Reis ◽  
BY Ngan ◽  
NL Berinstein

Diffuse large cell lymphomas are aggressive tumors of B-cell origin. In some cases they arise from low-grade follicular lymphomas carrying the t(14;18) translocation, an event that leads to the overexpression of the BCL-2 gene product. More frequently, however, they lack the t(14;18) translocation. Rearrangements of the c-MYC proto-oncogene and mutations of the p53 tumor suppressor gene have also been documented in these lymphomas. This study examines the extent to which alterations in the BCL-2, c-MYC, and p53 genes co-exist within individual lymphomas. Eight diffuse large cell lymphoma cell lines and 11 diffuse large cell lymphoma tumors were assessed for genetic alterations in these three genes. Our results indicate that there is a heterogeneity in the oncogene/suppressor gene profile among diffuse large cell lymphomas. Two cell lines and one tumor carried alterations in all three genes, one cell line carried alterations of c-MYC and p53, and one primary tumor and one cell line carried p53 mutations and the t(14;18). Single alterations of BCL-2 and p53 were also observed. Another cell line had no alterations in any of these genes. The heterogeneity indicates that varied mechanisms may be involved in the generation of diffuse large cell lymphomas.


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