Novel promoter upstream of the human c-myc gene and regulation of c-myc expression in B-cell lymphomas.

Bentley, David L.; Groudine, Mark

doi:10.1128/mcb.6.10.3481

Cited by 172 publications

(98 citation statements)

References 44 publications

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“…This would suggest a block to elongation at the exon 1/intron 1 boundary which prevents complete c-myc gene transcription in nonactivated lymphocytes. Similar results were obtained with HL-60 and 54cl2 {3T3) cells [24,30,33,34] which, however, possess amplified c-myc genes. Nuclear run-on analyses also showed a significant transcription of RNA complementary to c-myc mRNA, again only in nonactivated cells (Fig.…”

Section: Discussionsupporting

confidence: 76%

Kinetics of cellular oncogene expression in mouse lymphocytes II. Regulation of c‐fos and c‐myc gene expression

Schneider‐Schaulies¹,

Schimpl²,

Wecker³

1987

Eur J Immunol

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Newly isolated lymphocytes from mouse spleens express the c‐fos oncogene even in the absence of mitogen with maximal mRNA levels 60 min post preparation of single cell suspension, whereas c‐myc mRNA levels increase only after mitogenic stimulation with maximal mRNA levels 6 h post stimulation. The half‐lives of c‐fos mRNA are generally very short; they increase from 14 min (after 30 min of culture) to 70 min (after 2 h of culture). The half‐lives of c‐myc mRNA decrease from 50 min (at 2 and 6 h post stimulation with concanavalin A) to 12 min (at 48 h post stimulation). The c‐fos gene transcription is already turned on in time‐0 lymphocytes 10 min after disruption of the organ structure of the spleens and is down‐regulated after 2 h and later. In nuclear run‐on experiments with nonstimulated lymphocytes there is already significant transcription of the first exon of c‐myc, but almost no elongation of the transcript to exon 2 and 3. In concanavalin A‐treated lymphocytes elongation is stimulated about 5‐fold within 6 h and returns to background levels at 48 h post stimulation. The nuclear run‐on analyses of nonactivated lymphocytes showed a signal for RNA complementary to c‐myc mRNA detected with a probe specific for the exon 1/intron 1 boundary of c‐myc, which disappeared with increasing time of concanavalin A stimulation. This anti‐sense transcription may play a role in regulating the elongation of c‐myc transcripts.

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Section: Discussionsupporting

confidence: 76%

Kinetics of cellular oncogene expression in mouse lymphocytes II. Regulation of c‐fos and c‐myc gene expression

Schneider‐Schaulies¹,

Schimpl²,

Wecker³

1987

Eur J Immunol

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“…The reason for the absence of this RNA is different in the two cases: tumor LU-954 is monosomic for chromosome 7, whereas tumor BWH-42 contains unrearranged DNA for JAZF1 on the allele not broken by the t(7;17), as demonstrated by Southern blot analysis. Failure to detect RNA in the latter case may therefore be due to transcriptional silencing of the normal copy of JAZF1, as has been noted in the unrearranged alleles of MYC and BCL2 in some tumors bearing chromosomal translocations with breakpoints in or near these genes (33,34). Loss of expression for normal versions of JAZF1 in multiple tumors suggests a possible role of this gene as a tumor suppressor, similar to the situation observed for TEL, which is involved in chromosomal translocations and has tumor suppressor activity in some acute lymphoblastic leukemias (35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Frequent fusion of the JAZF1 and JJAZ1 genes in endometrial stromal tumors

Koontz

Soreng

Nucci

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

353

259

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Endometrial stromal tumors are divided into three types: benign stromal nodules, endometrial stromal sarcomas, and undifferentiated endometrial sarcomas. A variety of cytogenetic abnormalities involving chromosome 7 have been reported in endometrial stromal sarcomas, including a recurrent t(7;17)(p15;q21). We have identified two zinc finger genes, which we have termed JAZF1 and JJAZ1, at the sites of the 7p15 and 17q21 breakpoints. Analyses of tumor RNA indicate that a JAZF1͞JJAZ1 fusion is present in all types of endometrial stromal tumors; however, the fusion appears to be rarer among endometrial stromal sarcomas that would be considered high-grade according to certain classification schemes. These findings suggest that the less malignant endometrial stromal tumors may evolve toward more malignant types, but that some endometrial stromal sarcomas with relatively abundant mitotic activity may compose a biologically distinct group.

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“…There is low homology around DNase I hypersensitivity site 1I2 (46) and the PO promoter (3). These regions have also been shown to lack sequence homology between mouse and human sequences (3,8); however, Fahrlander et al (16) have shown that there is a region in the murine c-myc which shows a DNase hypersensitivity pattern similar to that of DNase I hypersensitivity site II2.…”

Section: Methodsmentioning

confidence: 99%

6;7 chromosomal translocation in spontaneously arising rat immunocytomas: evidence for c-myc breakpoint clustering and correlation between isotypic expression and the c-myc target.

Pear¹,

Wahlström²,

Nelson³

et al. 1988

Mol. Cell. Biol.

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Our previous studies have shown that spontaneously arising immunocytomas in the LOU/Wsl strain of rats contain a t(6;7) chromosomal translocation in all seven tumors studied (F. Wiener, M. Babonits, J. Spira, G. Klein, and H. Bazin, Int. J. Cancer 29:431-437, 1982). We have also shown that the c-myc is located on chromosome 7 (J. Sumegi, J. Spira, H. Bazin, J. Szpirer, G. Levan, and G. Klein, Nature (London) 306: [497][498][499] 1983) and the immunoglobulin H cluster on chromosome 6 (W. S. Pear, G. Wahistrom, J. Szpirer, G. Levan, G. Klein, and J. Sumegi, Immunogenetics 23:393-395, 1986). We now report a detailed cytogenetic and molecular analysis of nine additional rat immunocytomas. The t(6;7) chromosomal translocation is found in all tumors. Mapping of the c-myc breakpoints showed that in 10 of 14 tumors, the c-myc breakpoints are clustered in a 1.5-kilobase region upstream of exon 1. In contrast with sporadic Burkitt's lymphoma and mouse plasmacytoma, only 1 of 14 tumors contains the c-myc breakpoints in either exon 1 or intron 1. Analysis of the sequences juxtaposed to the c-myc show that immunoglobulin H switch regions are the targets in at least five tumors and that there is a strong correlation between the secreted immunoglobulin and the c-myc target. Unlike sporadic Burkitt's lymphoma and mouse plasmacytoma, at least two rat immunocytomas show recombination of the c-myc with sequences distinct from immunoglobulin switch regions.Consistent chromosomal translocations are thought to play an important role in the development of certain neoplasms (10, 21). The role of specific translocations has been extensively studied in two B-cell tumors, Burkitt's lymphoma (BL) and mouse plasmacytoma (MPC), and chromosomal translocations have been identified in 100% of the former and 95% of the latter type of tumor (22). BL and MPC represent different stages of B-cell maturation; however, the chromosome translocation in both tumors involves the chromosomes containing one of the immunoglobulin loci and the c-myc cellular oncogene (23). The translocation is believed to act by constitutive activation of c-myc (9). Recent facsimile experiments have shown that constitutively activated c-myc genes can induce tumors in an appropriate host environment (1,24,27

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Novel promoter upstream of the human c-myc gene and regulation of c-myc expression in B-cell lymphomas.

Cited by 172 publications

References 44 publications

Kinetics of cellular oncogene expression in mouse lymphocytes II. Regulation of c‐fos and c‐myc gene expression

Kinetics of cellular oncogene expression in mouse lymphocytes II. Regulation of c‐fos and c‐myc gene expression

Frequent fusion of the JAZF1 and JJAZ1 genes in endometrial stromal tumors

6;7 chromosomal translocation in spontaneously arising rat immunocytomas: evidence for c-myc breakpoint clustering and correlation between isotypic expression and the c-myc target.

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