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By contrast, a kinase domain deletion mutant EtkΔK, functioning as a dominant-negative mutant, ameliorates EGF-induced Stat1 activation and apoptosis in MDA-MB-468 cells.

Title from cover Issue for June 1994 numbered v.19, no.5, but constitutes v.17,no.5Issue for July 1997 lacks numbering, but constitutes v.20, no.6; issue for April 1998 lacks numbering, but constitutes, v.21, no.3Vol.

22, no.3 omitted from numbering; March-April 1999 each numbered v.22, no.4Issues for Sept-Dec 2002 lack vol.

Overexpression of EGF receptor is common among human epithelial malignancies (Merlino et al., 1985; Derynck et al., 1987; Costa et al., 1988; Sainsbury et al., 1988; Kikuchi et al., 1990; Ibrahim et al., 1997).

Amplification and mutation of the EGFR locus have also been found in a variety of tumors including glioblastoma (Xu et al., 1984; Wong et al., 1987; Ro et al., 1988; Ekstrand et al., 1991; Garcia de Palazzo et al., 1993).

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Etk/Bmx, a member of the Tec family of tyrosine kinases, mediates various signaling pathways and confers several cellular functions.