Establishment of a rhabdoid tumor cell line with a specific chromosomal abnormality, 46,XY,t(11;22)(p15.5;q11.23)

Karnes, Pamela S.; Tran, Tuan N.; Cui, M.Y.; Bogenmann, Emil; Shimada, Hiroyuki; Ying, K.L.

doi:10.1016/0165-4608(91)90359-3

Cited by 46 publications

(28 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is tempting to Versteege et al, 1998). TTC549, TTC642, TM87-16, and G401 have been described in more detail elsewhere (Garvin et al, 1993;Karnes et al, 1991;Ota et al, 1993;Peebles et al, 1978;Suzuki et al, 1997). Cells were maintained in RPMI 1640 supplemented with 10% fetal bovine serum at 378C in 5% CO 2 .…”

Section: Discussionmentioning

confidence: 99%

Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1arrest associated with induction of p16ink4a and activation of RB

et al. 2002

View full text Add to dashboard Cite

Truncating mutations and homozygous deletions in the hSNF5/INI1/BAF47 subunit of human SWI/SNF complexes occur in most malignant rhabdoid tumors and some other malignancies. How loss of hSNF5 contributes to tumorigenesis remains unknown. Because the SWI/ SNF subunit BRG1 is required for RB-mediated cell cycle arrest, we hypothesized that hSNF5 deficiency disrupts RB signaling. Here we demonstrate that unlike BRG1, hSNF5 deficient cells retain functional RB since ectopic expression of either p16ink4a or a constitutively active form of RB (PSM -RB) led to cell cycle arrest. To determine how hSNF5 loss might contribute to tumorigenesis, we used a retrovirus to introduce hSNF5 into multiple deficient cell lines. In all cases, re-expression inhibited colony formation and induced cell cycle arrest characterized by a flattened morphology. Flow cytometry revealed that these cells accumulated in G 0 /G 1 . Importantly, arrested cells exhibited strong induction of p16ink4a, hypophosphorylated RB, and down-regulation of cyclin A, suggesting that hSNF5 signals upstream of RB to induce growth arrest. Co-expression of SV40 T/t abolished hSNF5-induced G 1 arrest and activation of RB. Likewise, HPV-16 E7 was sufficient to partially overcome cell cycle arrest. These results suggest that hSNF5 loss is not equivalent to BRG1/ BRM loss in human tumor cell lines. Furthermore, hSNF5-induced cell cycle arrest of deficient cells is mediated in part through activation of p16ink4a expression. These findings provide insight into mechanisms of hSNF5-mediated tumor suppression.

show abstract

Section: Discussionmentioning

confidence: 99%

Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1arrest associated with induction of p16ink4a and activation of RB

et al. 2002

View full text Add to dashboard Cite

show abstract

“…Two of these cell lines (BT-12 and BT-16) were derived from atypical teratoid/rhabdoid tumors. STM-91-01 cells were derived from a lung metastasis in a child with a renal malignant rhabdoid tumor (36), whereas TM-87-16 cells were isolated from a malignant pleural effusion in a patient with a retroperitoneal mass (37). Each cell line was exposed to live or UV-inactivated-DV VSV DM51 (1 MOI) or MV (10 MOI), cultured for 72 h, and then examined for evidence of viral infection.…”

Section: Vsvmentioning

confidence: 99%

Oncolytic Efficacy of Recombinant Vesicular Stomatitis Virus and Myxoma Virus in Experimental Models of Rhabdoid Tumors

Lun

Zhou

et al. 2008

Clinical Cancer Research

View full text Add to dashboard Cite

Purpose: Rhabdoid tumors are highly aggressive pediatric tumors that are usually refractory to available treatments. The purpose of this study was to evaluate the therapeutic potential of two oncolytic viruses, myxoma virus (MV) and an attenuated vesicular stomatitis virus (VSV : 25 days versus 21days, log-rank test, P = 0.0036; MV: median survival not reached versus 21 days, log-rank test, P = 0.0007). Most of the MV-treated animals (4 of 6; 66.7%) were alive and apparently ''cured'' when the experiment was arbitrarily ended (>180 days). Conclusions: These results suggest that VSV DM51 and MV could be novel effective therapies against human rhabdoid tumor.

show abstract

“…Tm87-16 was established from malignant pleural effusion in a 21-month-old boy with a retroperitoneal mass, which was in fact extrarenal MRT (12). STM91-01 was established from pulmonary metastasis in an 8-month-old boy with a left renal MRT (13).…”

Section: Cell Culturementioning

confidence: 99%

Subcellular Distribution of Cytokeratin and Vimentin in Malignant Rhabdoid Tumor: Three-Dimensional Imaging with Confocal Laser Scanning Microscopy and Double Immunofluorescence

et al. 2001

View full text Add to dashboard Cite

show abstract

Establishment of a rhabdoid tumor cell line with a specific chromosomal abnormality, 46,XY,t(11;22)(p15.5;q11.23)

Cited by 46 publications

References 16 publications

Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1arrest associated with induction of p16ink4a and activation of RB

Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1arrest associated with induction of p16ink4a and activation of RB

Oncolytic Efficacy of Recombinant Vesicular Stomatitis Virus and Myxoma Virus in Experimental Models of Rhabdoid Tumors

Subcellular Distribution of Cytokeratin and Vimentin in Malignant Rhabdoid Tumor: Three-Dimensional Imaging with Confocal Laser Scanning Microscopy and Double Immunofluorescence

Contact Info

Product

Resources

About