IMMUNOREACTIVITY FOR HEPATOCYTE GROWTH FACTOR/SCATTER FACTOR AND ITS RECEPTOR, met, IN HUMAN LUNG CARCINOMAS AND MALIGNANT MESOTHELIOMAS

Harvey, P; Warn, A.; Newman, Piers; Perry, Lynn J. Poole; Ball, R. Y.; Warn, R. M.

doi:10.1002/(sici)1096-9896(199612)180:4<389::aid-path685>3.0.co;2-k

Cited by 70 publications

(42 citation statements)

References 22 publications

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“…The expression of HGF/SF by lung cancer cells in vitro and in vivo has also been reported (Yoshinaga et al, 1992;Tsao et al, 1993;Harvey et al, 1996;Olivero et al, 1996). A recent publication also indicated that high levels of HGF/SF protein content in primary non-small-cell lung carcinoma (NSCLC) was correlated with poor prognosis, suggesting that paracrine and/or autocrine functions of HGF/SF may play important roles in the biology of lung cancer cells (Siegfried et al, 1997).…”

mentioning

confidence: 71%

“…This requires further studies that use techniques to silence the HGF/SF expression and/or function. Recent reports indicated that a significant proportion of primary NSCLC overexpress HGF/SF and Met/HGFR (Harvey et al, 1996;Olivero et al, 1996;Takanami et al, 1996), and high levels of HGF/SF in these tissues may be correlated with a poor overall survival rate (Siegfried et al, 1997). The most important biological process that affects the survival or prognosis of lung cancer patients is metastasis, and cellular motility is one of the critical cellular functions during metastasis.…”

Section: Morphogenic Effect Of Hgf/sfmentioning

confidence: 99%

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Paracrine effects of hepatocyte growth factor/scatter factor on non-small-cell lung carcinoma cell lines

Chen²,

Viallet³

et al. 1998

Br J Cancer

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mentioning

confidence: 71%

Section: Morphogenic Effect Of Hgf/sfmentioning

confidence: 99%

Paracrine effects of hepatocyte growth factor/scatter factor on non-small-cell lung carcinoma cell lines

Chen²,

Viallet³

et al. 1998

Br J Cancer

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“…HGF overexpression is found in NSCLCs but not in SCLCs (Harvey et al 1996;Olivero et al 1996). The HGF receptor, c-Met, however, is expressed in both NSCLC and SCLC.…”

Section: Deregulating Growth Factors Via Autocrine/ Paracrine Loopsmentioning

confidence: 93%

Mouse models for human lung cancer

Meuwissen

Berns²

2005

Genes Dev.

270

243

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In recent years several new mouse models for lung cancer have been described. These include models for both non-small-cell lung cancer (NSCLC) and small-cell lung cancer (SCLC). Tumorigenesis in these conditional mouse tumor models can be initiated in adult mice through Cre-recombinase-induced activation of oncogenic mutations in a subset of the cells. They present a marked improvement over mouse models that depend on carcinogen induction of tumors. These models permit us to study the consecutive steps involved in initiation and progression and allow us to address questions like the cell of origin, and the role of cancer stem cells in the maintenance of these tumors. They now need to be validated as suitable preclinical models for intervention studies in which questions with respect to therapy response and resistance can be addressed.During the last decades lung cancer has become the leading cause of cancer deaths in the world, accounting for even more solid tumor deaths than breast, pancreatic, prostate, and colorectal combined (Landis et al. 1999). More then 170,000 new cases are being diagnosed each year in the United States alone, of whom ∼160,000 will eventually die, representing 28% of all cancer deaths (Jemal et al. 2004). Worldwide more than a million deaths are due to lung cancer. Tobacco smoking is the major causal agent, being responsible for ∼85% of the lung cancer incidence. Other respiratory exposure to occupational or environmental carcinogens, such as asbestos or radon, and yet unknown genetic factors contribute to the remaining 15% . Although smoking cessation before the age of 30 does substantially reduce the risk of lung cancer, this is significantly less for those who stop smoking at 50 or 60 yr (Peto et al. 2000;Doll et al. 2004). Interestingly, nearly 50% of all first diagnosed lung cancers in the United States are from people who stopped smoking at least 5 or more years ago (Peto and Lopez 2001). This indicates that extensive damage to the respiratory tract can persist over many years. Indeed, recent studies (Mao 2002;Pfeifer et al. 2002;Wistuba et al. 2002) showed the presence of multiple genetic lesions, often manifested in clonal patches of cells in respiratory epithelium of current and former smokers.Lung cancer can be divided into two major histopathological groups: non-small-cell lung cancer (NSCLC) (Van Zandwijk et al. 1995) SCLC and NSCLC show major differences in histopathologic characteristics that can be explained by the distinct patterns of genetic lesions found in both tumor classes . Responsiveness to treatment with chemotherapy and/or radiation also differs significantly between NSCLC and SCLC and has a dramatic effect on clinical treatment outcome. The overall 5-yr survival rate for lung cancer is ∼14% (Travis et al. 1995); for SCLC alone it is even worse, ∼5% (Worden and Kalemkerian 2000).Spontaneous lung tumors in mice are similar in morphology, histopathology, and molecular characteristics to human adenocarcinomas. Mouse models for lung cancer can thus serve as a valua...

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“…Moreover, as recently shown, the requirement of CD44 for hepatocyte growth factor (HGF)/c-Met signalling has been recently demonstrated (Orian-Rousseau et al, 2002). Interestingly, HGF/c-Met has been considered as an autocrine loop in the control of MM cell proliferation (Harvey et al, 1996;Klominek et al, 1998). Hence, NF2 appears to be possibly associated with pathways regulating proliferation of MM cells.…”

Section: Introductionmentioning

confidence: 97%

Hemizygosity of Nf2 is associated with increased susceptibility to asbestos-induced peritoneal tumours

et al. 2003

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Biallelic NF2 gene inactivation is frequently found in human malignant mesothelioma. In order to assess whether NF2 hemizygosity may enhance susceptibility to asbestos fibres, we investigated the Nf2 status in mesothelioma developed in mice presenting a heterozygous mutation of the Nf2 gene (Nf2 KO3/ þ ), after intraperitoneal inoculation of crocidolite fibres. Asbestos-exposed Nf2 KO3/ þ mice developed tumoural ascites and mesothelioma at a higher frequency than their wild-type (WT) counterparts (Po0.05). Six out of seven mesothelioma cell lines established from neoplastic ascitic fluids of Nf2 KO3/ þ mice exhibited loss of the WT Nf2 allele and no neurofibromatosis type 2 protein expression was found in these cells. The results show the importance of the NF2 gene in mesothelial oncogenesis, the potential association of asbestos exposure and tumour suppressor gene inactivation, and suggest that NF2 gene mutation may be a susceptibility factor to asbestos.

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IMMUNOREACTIVITY FOR HEPATOCYTE GROWTH FACTOR/SCATTER FACTOR AND ITS RECEPTOR, met, IN HUMAN LUNG CARCINOMAS AND MALIGNANT MESOTHELIOMAS

Cited by 70 publications

References 22 publications

Paracrine effects of hepatocyte growth factor/scatter factor on non-small-cell lung carcinoma cell lines

Paracrine effects of hepatocyte growth factor/scatter factor on non-small-cell lung carcinoma cell lines

Mouse models for human lung cancer

Hemizygosity of Nf2 is associated with increased susceptibility to asbestos-induced peritoneal tumours

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