In vitro transformation by the SV40 ‘early region’ of cells from a human benign salivary gland tumor with a12q13→q15 rearrangement

Kazmierczak, Bernd; Bartnitzke, Sabine; Hartl, Markus; Bullerdiek, Jörn

doi:10.1159/000132891

Cited by 30 publications

(21 citation statements)

References 10 publications

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“…The present study demonstrates that the chromosomal region affected by these translocations is on the long arm of chromosome 19, between the border of 19q 13.3 and 19ql3.4 and proximal to TRPT. It also confirms that the transfection procedures previously re ported by Kazmierczak et al ( 1990Kazmierczak et al ( ,1994 for pleomorphic ade nomas and mesenchymal tumors are similarly suited for ob taining cell lines from thyroid tumors that retain specific deriv ative chromosomes.…”

Section: I'isii Studiessupporting

confidence: 69%

FISH analyses of a newly established thyroid tumor cell line showing a t(1;19)(p35 or p36.1;q13) reveal that the breakpoint lies between 19q13.3–13.4 and 19q13.4

Belge

García²,

Jong³

et al. 1995

Cytogenet Genome Res

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Translocations involving the long arm of human chromosome 19 are specific chromosomal alterations found in a subset of benign thyroid tumors. In the present communication we describe the establishment of an SV40-transformed cell line derived from a thyroid adenoma with a t(1;19)(p35 or p36.1;q13). Cytogenetic studies were carried out on this cell line, using a series of cosmids mapping along the long arm of chromosome 19. In situ hybridization with probes for RYR1, ATP1A3, BCKDHA, ERCCl, POLDl, and TRPT revealed that only TRPT mapped distal to the breakpoint of the translocation. The results indicated that the breakpoint is located between POLD1 and TRPT at the boundary between chromosome bands 19q13.3 and 19q13.4.

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Section: I'isii Studiessupporting

confidence: 69%

FISH analyses of a newly established thyroid tumor cell line showing a t(1;19)(p35 or p36.1;q13) reveal that the breakpoint lies between 19q13.3–13.4 and 19q13.4

Belge

García²,

Jong³

et al. 1995

Cytogenet Genome Res

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“…The origin, chromosome aberrations, and growth conditions of these cell lines have been described before (51,52). The primary parosteal lipoma was kindly provided by Prof. J. Bridge (University of Nebraska Medical Center, Omaha, NE).…”

Section: Lipoma Cell Lines and Primary Lipomasmentioning

confidence: 99%

Transactivation Functions of the Tumor-Specific HMGA2/LPP Fusion Protein Are Augmented by Wild-Type HMGA2

Crombez

Vanoirbeek

Ven

et al. 2005

Molecular Cancer Research

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The gene encoding the architectural transcription factor HMGA2 is frequently rearranged in several benign tumors of mesenchymal origin. The lipoma preferred partner (LPP) gene is the most frequent translocation partner of HMGA2 in a subgroup of lipomas, which are benign tumors of adipose tissue. In these lipomas, HMGA2/LPP fusion transcripts are expressed, which encode for the three AT-hooks of HMGA2 followed by the two most carboxyl-terminal LIM domains (protein-protein interaction domains) of LPP. Identical fusion transcripts are also expressed in other benign mesenchymal tumors. Previous studies revealed that the LIM domains of LPP have transcriptional activation capacity in GAL4-based luciferase reporter assays. Here, we show that the HMGA2/LPP fusion protein retains the transactivation functions of the LPP LIM domains and thus functions as transcription factor. The HMGA2/LPP fusion protein activates transcription from the well-characterized PRDII element, which is a part of the IFN-B B enhancer and which is known to bind to HMGA2. We also show that HMGA2/LPP activates transcription from the BAT-1 element of the rhodopsin promoter, a HMGA1-binding element. HMGA1 is a closely related family member of HMGA2. Finally, in a number of lipomas, HMGA2/LPP and HMGA2 are coexpressed, and HMGA2 augments the transactivation functions of HMGA2/LPP. These results support the concept that the transactivation functions of the novel HMGA2/LPP transcription factor contribute to lipomagenesis.

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“…1). Using a were G-banded in order to identify the two derivative chromomethod previously outlined in detail (Kazmierczak et al, 1990), tumor cells were transfected by the SV40 large T-antigen and a cell line was established, which retained the derivative chromosomes from the complex translocation as well as the normal chromosome 6. Metaphase preparations from this cell line were hybridized with a PAC clone containing the HMGI(Y) gene, which was obtained by polymerase chain reaction (PCR) screening of a human PAC library (Genome Systems Library Screening Service, St. Louis, MO).…”

mentioning

confidence: 99%

PAC clone containing the HMGI(Y) gene spans the breakpoint of a 6p21 translocation in a uterine leiomyoma cell line

Kazmierczak

Bol

Wanschura

et al. 1996

Genes Chromosomes & Cancer

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In vitro transformation by the SV40 ‘early region’ of cells from a human benign salivary gland tumor with a12q13→q15 rearrangement

Cited by 30 publications

References 10 publications

FISH analyses of a newly established thyroid tumor cell line showing a t(1;19)(p35 or p36.1;q13) reveal that the breakpoint lies between 19q13.3–13.4 and 19q13.4

FISH analyses of a newly established thyroid tumor cell line showing a t(1;19)(p35 or p36.1;q13) reveal that the breakpoint lies between 19q13.3–13.4 and 19q13.4

Transactivation Functions of the Tumor-Specific HMGA2/LPP Fusion Protein Are Augmented by Wild-Type HMGA2

PAC clone containing the HMGI(Y) gene spans the breakpoint of a 6p21 translocation in a uterine leiomyoma cell line

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