William Gullick

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We have determined the expression of transforming growth factor alpha (TGF alpha), amphiregulin (AR), CRIPTO, the epidermal growth factor receptor (EGFR), erbB-2, erbB-3, and tumor angiogenesis in a series of 195 patients with stage I-IIIA non-small cell lung cancer (NSCLC) treated with radical surgery to define their usefulness as prognostic indicators of(More)
The c-erbB-2 gene codes for a putative transmembrane protein, similar in structure to the epidermal growth factor (EGF) receptor. Amplification of the gene has been described in a variety of human adenocarcinomas and is particularly well documented in breast carcinoma. It has been suggested that amplification is indicative of poor prognosis and, as such, is(More)
Epidermal growth factor receptor (EGF-R) expression was assessed in 63 lung tumour samples with a monoclonal antibody (EGF-R1) by indirect immunoperoxidase staining on cryostat sections. All 15 small cell lung cancer samples were negative whereas over 80% of the 48 non small lung cancer stained positively. In 30 bronchial biopsies two monoclonal antibodies(More)
We have investigated the possibility of a direct regulatory effect of gonadotrophin releasing hormone (GnRH) analogues on prostatic cancer cell growth. Here we report high affinity binding (Kd = 50 nM) of a GnRH analogue resulting in biphasic growth modulation of the human androgen-sensitive prostatic cancer cell line LNCaP. In contrast, the human(More)
We have determined the expression of transforming growth factor a (TGFa), amphiregulin (AR), CRIPTO, the epidermal growth factor receptor (EGFR), erbB-2, erbB-3, and tumor angiogenesis in a series of 195 patients with stage I-lilA non-small cell lung cancer (NSCLC) treated with radical surgery to define their usefulness as prognostic indicators of survival.(More)
Cancer results from cumulative alterations of the genetic make-up of somatic cells that lead to aberrant expression, mutation or deletion of proteins modulating cellular proliferation, differentiation and survival. Through deregulation of intracellular pathways, these defects allow cancer cells to evade signals, which normally keep cell proliferation and(More)
The means by which oncogenes and their products activate malignant transformation are currently under intense investigation. However, published papers on experiments using human tumour material do not always report in detail their methods of collection or storage of the specimens. In order to assess the stability of oncogene encoded proteins following(More)
Over the last 10 years, advances in molecular biology have shed new light on the control of cell growth at the genetic level. Several genes have been identified, called protooncogenes which encode proteins which appear to be involved in regulating cell division. Abnormalities converting them to oncogenes appear to be of fundamental importance in the(More)
The Editor, Marc Lippman, and Associate Editors: Stephen P. Ethier, Kevin S. Hughes, Alberto Montero, Steven A. Narod, and Ben H. Park would like to acknowledge the valuable contributions of the reviewers to the journal. We fully understand the burden and effort that are involved in the reviews. We rely on your expertise to maintain the standards of(More)
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