Recessive mechanisms of malignancy

Green, A. R.

doi:10.1038/bjc.1988.176

Cited by 50 publications

(18 citation statements)

References 102 publications

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“…In lung carcinomas, LOH of 3, 13 and 17 is found in the early stage of tumours and amplification of myc family gene is detected in advanced carcinomas (Yokota et al, 1987(Yokota et al, , 1988b. These results support the hypothesis of multistep carcinogenesis including mutation as the first step, loss of heterozygosity at the second step, and oncogene amplification at the final step (Land et al, 1983;Barbacid, 1987;Nicolson et al, 1987;Yokota et al, 1987Yokota et al, , 1988bGreen, 1988). Moreover, our recent results indicate that overexpression of several tumour autocrine growth factors in primary tumours occurs regardless of gene amplifications (Yoshida et al, 1990a,b).…”

Section: Tissuessupporting

confidence: 73%

Alterations of oncogenes in metastatic tumours of human gastric carcinomas

Tsujino

Yoshida²,

Nakayama³

et al. 1990

Br J Cancer

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(Slamon et al., 1987;Varley et al., 1987), and small cell lung carcinomas (Johnson et al., 1988). Moreover, specific chromosome abnormalities have also been found in a number of human cancers (Yokota et al., 1987;Baker et al., 1989;Lee et al., 1989). However, activation of proto-oncogenes in gastric carcinomas is low compared to colonic and pancreatic carcinomas (Forrester et al., 1987;Smit et al., 1988).Loss of chromosomal heterozygosity is also infrequently found in gastric carcinomas even at chromosomal loci frequently deleted in other tumours, and little is known about genetic changes that are associated with metastasis of gastric carcinomas. We have demonstrated previously that amplification of ERBB and ERBB2 genes is detected in 2.7% and 5.4% of primary gastric carcinomas, respectively (Yoshida et al., 1989 Southern blot analysis High molecular weight DNAs were prepared using the phenol-chloroform method after treatment with sodium dodecyl sulphate (SDS) and proteinase K. DNAs were digested with EcoRI or BamHI, and 10 iLg of completely digested DNAs was electrophoresis on 0.8% agarose gel. After electrophoresis, DNAs were denatured, neutralised and transferred to nitrocellulose filters according to the method of Southern (Southern, 1975). The filters were hybridised under stringent conditions with 32P-labelled probes. After hybridisation, filters were washed and exposed to Kodak XAR-5 films. The same filters were hybridised repeatedly with probes for several oncogenes to exclude the possibility that the difference in the intensities of the bands in different lanes was due to difference in the amounts of DNAs loaded on agarose gels. The levels of amplification were determined by densitometry and the sum of the densitometric signals of all the bands was taken.Slot blot analysis DNAs were extracted from formalin-fixed and paraffinembedded tissues of 20 early gastric carcinomas and one advanced gastric carcinoma whose metastatic tumours had amplification of ERBB2, HST1, and INT2 genes. Sections of 20 Itm in thickness were cut from the blocks using a microtome and these sections were collected. DNAs were extracted following the methods of Goelz et al. (1985) or Dubeau et al. (1986). Ten ILg of the DNA was dissolved in 0.4 M sodium hydroxide, and TE (10 mM tris hydroxymethyl aminomethane and 1 mM ethylene diaminetetraacetic acid (EDTA) pH 7.4) was added to make 50 pAl of the solution. The samples were incubated for 10 minutes at 37°C, treated with an equal volume of 2 M ammonium acetate and applied to a nitrocellulose filter. Filters were baked at 80°C for 2 hours under vacuum. The procedure of hybridisation was the same as that of Southern blot analysis as described above. DNA

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Section: Tissuessupporting

confidence: 73%

Alterations of oncogenes in metastatic tumours of human gastric carcinomas

Tsujino

Yoshida²,

Nakayama³

et al. 1990

Br J Cancer

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“…The elevated rate and altered spectrum ofHPRT mutations we observed in WS cells suggest that somatic mutations, and perhaps the preferential accumulation of deletions, may play a role in the pathogenesis of WS and of associated agedependent human disease processes, such as neoplasia and atherosclerosis (35)(36)(37). Deletions could initiate or promote these processes by altering the structure or expression of genes or the structure and mitotic transmission fidelity of chromosomes.…”

Section: Discussionmentioning

confidence: 97%

Mutator phenotype of Werner syndrome is characterized by extensive deletions.

Fukuchi

Martin

Monnat

1989

Proc. Natl. Acad. Sci. U.S.A.

396

241

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“…In his review of recessive mechanisms of malignancy (Green, 1988), Green commences with the statement 'cancer is a genetic disease'. It is certainly true that sequential genetic changes occur as tumours become more malignant and advanced Vogelstein, 1988).…”

mentioning

confidence: 99%

“…It is certainly true that sequential genetic changes occur as tumours become more malignant and advanced Vogelstein, 1988). Many transforming oncogenes have been identified associated with a variety of malignancies including ovarian tumours (Kacinski, 1989;Slamon, 1989); recently however much interest had focused in solid tumours on the role of tumour suppressor genes (Green, 1988;Ponder, 1988) which manifest themselves when loss of function (either by mutation or deletion in both alleles) leads to transformation and tumorigenesis.…”

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confidence: 99%

Overexpression of the p53 protein and allele loss at 17p13 in ovarian carcinoma

Eccles

Brett²,

Lessells³

et al. 1992

Br J Cancer

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Mouse monoclonal antibodies PAb 240 and PAb 1801 which specifically immunoprecipitate p53 protein, were used to examine 27 fresh ovarian tumours (16 serous adenocarcinomas, six endometrioid carcinomas, one mucinous adenocarcinoma, one mucinous borderline tumour and three benign adenomas). Eleven out of 16 (69%) serous adenocarcinomas and one endometrioid tumour showed positive staining with one or both antibodies and none of the mucinous or benign tumours stained with either antibody. DNA from tumour and peripheral blood leukocytes was used to identify allelic deletions on chromosome 17p in tumours. 11/12 positively staining tumours showed less of heterozygosity (LOH) on 17p at the nearest informative locus to the p53 gene. In this series of ovarian tumours, LOH on 17p correlates closely with the aberrant expression of the p53 protein in a high proportion of advanced stage serous adenocarcinomas. This observation suggests that the p53 tumour suppressor gene is involved in the evolution of epithelial ovarian cancer (EOC) and may have prognostic significance. Images Figure 2 Figure 3

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Recessive mechanisms of malignancy

Cited by 50 publications

References 102 publications

Alterations of oncogenes in metastatic tumours of human gastric carcinomas

Alterations of oncogenes in metastatic tumours of human gastric carcinomas

Mutator phenotype of Werner syndrome is characterized by extensive deletions.

Overexpression of the p53 protein and allele loss at 17p13 in ovarian carcinoma

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