✦ LIBER ✦

The paradox of E2F1: Oncogene and tumor suppressor gene

✍ Scribed by David G. Johnson

Publisher: John Wiley and Sons
Year: 2000
Tongue: English
Weight: 100 KB
Volume: 27
Category: Article
ISSN: 0899-1987
DOI: 10.1002/(sici)1098-2744(200003)27:3<151::aid-mc1>3.0.co;2-c

No coin nor oath required. For personal study only.

✦ Synopsis

Cancer cells often contain mutations that lead to the loss of retinoblastoma tumor suppressor (Rb) function and the activation of E2F-dependent transcription. As a result, proliferation is deregulated, and sensitivity to apoptotic stimuli is increased. In cell culture studies, the transcription factor E2F1 has been shown to be equally adept at inducing proliferation and apoptosis. Several groups using mouse models have been examining how these E2F1-regulated processes impact the development of cancer. The conclusion from these studies is that E2F1 can function as both oncogene and tumor suppressor gene and that both positive and negative effects on tumorigenesis can be observed whether E2F1 is absent or overexpressed. These findings are discussed in the context of a model in which pathways controlling cell-cycle progression and apoptosis are intimately linked.

📜 SIMILAR VOLUMES

Analysis of oncogene, tumor suppressor g

Analysis of oncogene, tumor suppressor gene, and chromosomal alterations in HeLa × osteosarcoma somatic cell hybrids

✍ Robert J. Isfort; David B. Cody; Glenda J. Lovell; Daniel Gioeli; Bernard E. Wei 📂 Article 📅 1999 🏛 John Wiley and Sons 🌐 English ⚖ 350 KB 👁 2 views

Using a series of tumorigenic and non-tumorigenic somatic cell hybrids that resulted from the fusion of the human osteosarcoma cell line OHS50-P16T (P16T) with the HeLa cell line D98OR, we investigated the role that genetic mutations, including alterations of oncogenes, tumor suppressor genes, and c

Codeletion of the JUN proto-oncogene and

Codeletion of the JUN proto-oncogene and the CDKN2A tumor-suppressor gene in HRAS-transformed rat embryo fibroblast cell lines

✍ Jian-Nian Zhou; Sofia Ljungdahl; Dan Röhme; Göran Levan; Maria C. Shoshan; Stig 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 English ⚖ 181 KB 👁 1 views

The cyclin kinase inhibitor p16, encoded by the CDKN2A gene, suppresses the transformation of mouse embryonic fibroblasts by oncogenic RAS. In contrast, the c-JUN transcription factor (a major component of AP-1) has been suggested to be required for RAS transformation of rodent fibroblasts. The CDKN

Mutations of p53 tumor-suppressor gene i

Mutations of p53 tumor-suppressor gene in angiosarcoma

✍ Norifumi Naka; Yasuhiko Tomita; Hirofumi Nakanishi; Nobuhito Araki; Tadashi Hong 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 French ⚖ 50 KB 👁 2 views

Transgenic mice deficient for the p53 gene were reported to frequently develop angiosarcoma (AS), suggesting that alterations in the gene are associated with tumorigenesis of AS. However, little is known about genetic changes, including p53 gene alterations, in human AS because of its rarity. We ana

Human E2F5 gene is oncogenic in primary

Human E2F5 gene is oncogenic in primary rodent cells and is amplified in human breast tumors

✍ Jolanta Polanowska; Laurent Le Cam; Béatrice Orsetti; Heléne Vallés; Eric Fabbri 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 English ⚖ 113 KB 👁 1 views

E2F transcription factors (E2F1 to 6) are central players in the control of animal cell proliferation as regulators of genes involved in cell cycle progression and in transformation. In this report, we have investigated the potential involvement of the E2F5 gene in tumorigenesis. We show that E2F5 c

Genomic structure and mutation screening

Genomic structure and mutation screening of the E2F4 gene in human tumors

✍ Sabine Schwemmle; Gerd P. Pfeifer 📂 Article 📅 2000 🏛 John Wiley and Sons 🌐 French ⚖ 232 KB 👁 1 views

E2F4, a member of the E2F family of transcription factors, is abundant in non-proliferating and differentiated cells where it plays an important role in the suppression of proliferation-associated genes. The E2F4 gene spans 6 kb and has 10 exons. It contains a serine (CAG) repeat tract in exon 7, wh

Upstream stimulating factor-1 (USF1) and

Upstream stimulating factor-1 (USF1) and USF2 bind to and activate the promoter of the adenomatous polyposis coli (APC) tumor suppressor gene

✍ Aruna S. Jaiswal; Satya Narayan 📂 Article 📅 2001 🏛 John Wiley and Sons 🌐 English ⚖ 354 KB 👁 2 views