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Transcription factors and recessive oncogenes in the pathogenesis of human lung cancer

✍ Scribed by John D. Minna; Jochen Schütte; Jean Viallet; François Thomas; Frederic J. Kaye; Takashi Takahashi; Marion Nau; Jacqueline Whang-Peng; Michael Birrer; Adi F. Gazdar

Publisher
John Wiley and Sons
Year
1989
Tongue
French
Weight
421 KB
Volume
44
Category
Article
ISSN
0020-7136

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✦ Synopsis

Expression of the jun family of transcription factorslproto-oncogenes in lung cancer

From recent studies it is now clear that the product of the cellular counterpart of the oncogene jun (Maki et al., 1987) is one of the proteins making up the transcription-factor preparation AP-1 (Angel et al., 1988a;Bohmann et al., 1987). The expression ofjun and AP-1 activity can be increased by growth-factor stimulation (Quantin and Breathnack, 1988;Ryder and Nathans, 1988) and phorbol esters (Lamph et al., 1988) leading to the model that the transcription of genes regulated by growth factors and tumor promoters is mediated through the expression and/or activity of jun. These include several genes that could influence tumor behavior, such as those for metallothionein 11, , collagenase, and stromelysin. In addition, other members of the jun family such as jun-B and jun-D are also early-response genes with sequence similarity to c-jun and, like jun-A, may also form transcription complexes with the fos protein (

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