Differences in C‐myc and pvt‐1 amplification in sewa sarcoma sublines selected for adherent or non‐adherent growth

Abstract

Conversion of solid sarcomas and carcinomas into ascites tumors depends on the in vivo selection of phenotypically altered tumor cell variants that can grow in the dissociated form. Once selected, they retain this property even after prolonged s.c. growth as solid tumors. From an s.c.-passaged subline of an ascites-converted murine sarcoma (SEWA-AS12), we were able to separate cells adapted to the ascites form of growth from cells that can only grow in the solid form on the basis of their differential adherence to plastic. Both c-myc and pvt-1 were amplified approximately 63- to 77-fold in the nonadherent subline (SEWA-AS12-NA), but only 5- to 8-fold in the adherent subline (SEWA-AS12-ADH). This suggests that c-myc and/or pvt-1 amplification may provide a selective advantage to cells that can grow in the dissociated form.

α2, 6 sialylation of N‐acetyllactosaminic sequences in human colorectal cancer cell lines. Relationship with non‐adherent growth

“…Owing to the heterogeneity of the tumor-cell population, solid tumors may often include a minority of cells expressing this property at an extreme level, being able to grow in nonadherent or ascites form. Cells expressing this property, which has been related to over-expression of "nuclear type" oncogenes such as c-myb in colon cancer cells (Alitalo et al, 1984) or c-myc in sarcoma cells (Minarovits et al, 1990), may be selected in vivo or in vitro according to the conditions of growth. COLO 205 cells, which were isolated from the ascitic fluid of a colon cancer patient, may be considered a case of in vivo selection.…”

The 8q24 Gene Desert: An Oasis of Non-Coding Transcriptional Activity

“…In addition, to GWAS linkage, there are several other cancer-associated features of this region of chr.8q24 (128.0–130.0 Mb) that serve to further establish the significance of 8q24 in driving tumor development that also complicates its’ study as well. While MYC is recognized to be the most frequently amplified protein-coding gene across all cancer types (Beroukhim et al, 2010), the fact that increased copies of MYC are often accompanied by co-amplification of an adjacent non-coding locus, PVT1 is not fully appreciated nor understood (Asker et al, 1988; Shtivelman and Bishop, 1989; Bakkus et al, 1990; Minarovits et al, 1990; Figure 1). Furthermore, chromosomal translocations that appear to target MYC are often found in Burkitt’s lymphoma (BL) and other non-Hodgkin’s lymphoma types, but a subset of these lymphomas (15–20%) exhibiting breakpoints as far as 300–400 kb downstream of MYC on 8q24, is a feature that complicates the hypothesis that singular MYC is always the intended target.…”

Amplified extrachromosomal elements containing c-Myc and Pvt 1 in a mouse plasmacytoma

“…c-Myc is assumed to be a principal target of such gene amplification. However, neighboring loci are coamplified to varying levels, suggesting that the amplicon extends beyond the limits of the c-Myc gene locus (Mengle-Gaw and Rabbitts 1987;Bakkus et al 1990;Asker et al 1988;Minarovits et al 1990;Heerdt et al 1991;Shtivelman and Bishop 1989;Huppi et al 1993). Amplification of loci on distinct chromosomes is also observed in conjunction with c -M y c amplification and implies that multiple factors may be associated with a growth advantage in cultured cells (for review see Alitalo and Schwab 1986;Stark 1993).…”

“…In detailed studies of cells with c -M y c amplification, we and others have found that the c-Myc amplicon appears to consist primarily of c -M y c and Pvt I (plasmacytoma variant translocation gene; Bakkus et al 1990;Asker et al 1988;Minarovits et al 1990;Heerdt et al 1991 ;Huppi et al 1993). The inclusion of Pvt I in the amplicon is particularly intriguing since (i) Pvt I is found 260 kilobases downstream of c -M y c and is transcriptionally active (Shtivelman and Bishop 1990;Huppi et al 1990); (ii) both c -M y c and Pvt I associated chromosomal translocations are major lesions found in lymphoid neoplasms, such as Burkitt's lymphoma, HIV lymphomas, and plasmacytomas (1972).…”