RCH-ACV: A lymphoblastic leukemia cell line with chromosome translocation 1;19 and trisomy 8

Jack, Ian; Seshadri, Ram; Garson, Margaret; Michael, P.; Callen, David F.; Zola, Heddy; Morley, Alexander A.

doi:10.1016/0165-4608(86)90055-5

Cited by 48 publications

(22 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A subset of these was transduced on retronectin-coated plates with a retroviral vector containing pMIG_GFP (provided by M. Muschen). Human leukemia cell lines included RCH-ACV (pre-B ALL with an E2A-PBX1 fusion protein22), BV173 (Pre B Ph+ ALL23), SD-1 (pre-B Ph + ALL, DSMZ, Braunschweig, Germany) and RS4;11 (pre-B t(4;11) ALL, ATCC, Manassas, VA).…”

Section: Methodsmentioning

confidence: 99%

Adipocytes Impair Leukemia Treatment in Mice

Behan¹,

Yun²,

Proektor³

et al. 2009

Cancer Research

154

165

View full text Add to dashboard Cite

Obesity is associated with increased cancer incidence and mortality. We have previously found that obesity in children is associated with a 50% increased recurrence of acute lymphoblastic leukemia (ALL) in high-risk patients. We have therefore developed novel in vivo and in vitro preclinical models to study the mechanism(s) of this association. Obesity increased relapse after monotherapy with vincristine (P = 0.03) in obese mice injected with syngeneic ALL cells. This occurred although the drug was dosed proportionally to body weight, equalizing blood and tissue drug levels. In coculture, 3T3-L1 adipocytes significantly impaired the antileukemia efficacy of vincristine, as well as three other chemotherapies (P < 0.05). Interestingly, this protection was independent of cell-cell contact, and it extended to human leukemia cell lines as well. Adipocytes prevented chemotherapy-induced apoptosis, and this was associated with increased expression of the two prosurvival signals Bcl-2 and Pim-2. These findings highlight the role of the adipocyte in fostering leukemia chemotherapy resistance, and may help explain the increased leukemia relapse rate in obese children and adults. Given the growing prevalence of obesity worldwide, these effects are likely to have increasing importance to cancer treatment.

show abstract

Section: Methodsmentioning

confidence: 99%

Adipocytes Impair Leukemia Treatment in Mice

Behan¹,

Yun²,

Proektor³

et al. 2009

Cancer Research

154

165

View full text Add to dashboard Cite

show abstract

“…Positive cell lines included RCH-ACV and HAL-01, which respectively contain balanced (1;19)(q23;p13) and (17;19)(q21;p13) translocations (kindly provided by Drs Ram Seshadri and Kazuma Ohyashiki). 23,24 Negative cell lines were Jurkat, Nalm6, REH and TS-2. TS-2 (kindly provided by Drs Yoshinari and Imaizumi, Tohoku University, Sendai, Japan) contains a t(1;19)(q23;p13), but lacks E2A gene rearrangements and E2A-PBX1 fusion transcripts.…”

Section: Specimensmentioning

confidence: 99%

Detection of E2A translocations in leukemias via fluorescence in situ hybridization

et al. 2001

View full text Add to dashboard Cite

“…We tested two t(1;19) positive pre-B cell lines; Sup-B27 and RCH-ACV (Jack et al, 1986;Nourse et al, 1990, see also Figure 1). We also tested Reh cells and Reh-23s cells.…”

Section: Expression Of G-csfr On T(1;19) Cellsmentioning

confidence: 99%

The gene encoding the granulocyte colony-stimulating factor receptor is a target for deregulation in pre-B ALL by the t(1;19)-specific oncoprotein E2A-Pbx1

Wb¹,

Hurenkamp²,

Berendes

et al. 1998

Oncogene

View full text Add to dashboard Cite

Approximately 25 ± 30% of childhood pre-B cell acute lymphoblastic leukemias (pre-B ALL) is characterized by the presence of a (1;19)(q23;p13.3) translocation. The presence of this translocation is generally accompanied by a poor prognosis. The chimeric gene resulting from this chromosomal rearrangement encodes a hybrid transcription factor, E2A-Pbx1. In an attempt to delineate the genetic cascade initiated by E2A-Pbx1, we sought to identify genes that are deregulated by this transcription factor in t(1;19) pre-B ALL. We show here that the gene encoding the granulocyte colonystimulating factor receptor (G-CSFr) is speci®cally upregulated in pre-B cells expressing E2A-Pbx1. GCSFr is also expressed in cell lines established from t(1;19) pre-B cell leukemia and on primary t(1;19) tumor cells, but not on control cells. These data indicate that G-CSFr gene is a target for deregulation by E2A-Pbx1.

show abstract

RCH-ACV: A lymphoblastic leukemia cell line with chromosome translocation 1;19 and trisomy 8

Cited by 48 publications

References 20 publications

Adipocytes Impair Leukemia Treatment in Mice

Adipocytes Impair Leukemia Treatment in Mice

Detection of E2A translocations in leukemias via fluorescence in situ hybridization

The gene encoding the granulocyte colony-stimulating factor receptor is a target for deregulation in pre-B ALL by the t(1;19)-specific oncoprotein E2A-Pbx1

Contact Info

Product

Resources

About