Expression of p53 mutant nuclear phosphoprotein in oral carcinoma and potentially malignant oral lesions
Identifieur interne : 000A74 ( Istex/Corpus ); précédent : 000A73; suivant : 000A75Expression of p53 mutant nuclear phosphoprotein in oral carcinoma and potentially malignant oral lesions
Auteurs : K. A. A. S. Warnakulasuriya ; N. W. JohnsonSource :
- Journal of Oral Pathology & Medicine [ 0904-2512 ] ; 1992-10.
English descriptors
- Teeft :
- Allele deletions, Antibody dilution, Breast carcinoma, Carcinoma, Cell carcinoma, Cell carcinomas, Cell proliferation, Colorectal, Colorectal carcinoma adenoma, Deletion, Dental sciences, Early stages, Focal areas, Gene mutations, Gene product, Head neck, Human cancer, Human neoplasms, Immunohistochemical study, Lesion, Malignancy, Malignant, Monoclonal antibodies, Monoclonal antibody, Mutant, Mutant form, Mutant forms, Mutant protein, Mutation, Oncogene, Oral cancer, Oral carcinoma, Oral pathol, Positive nuclei, Protein product, Risk markers, Royal college, Squamous cell carcinomas, Tumor suppressor gene, White caucasoids, Wild type.
Abstract
An immunohistochemical study of primary oral squamous cell carcinomas (n = 37) with a monoclonal antibody (PAb 1801) specific to p53 antioncogene product demonstrated nuclear overexpression of the mutant protein in 35% of cases. Those positive included carcinomas without deep invasion suggesting that p53 mutation may occur in the early stages of progression of a malignancy. This is supported by the observation that mutant protein was detectable in limited amounts in 2 cases of oral mucosal dysplasia (n= 12). None of the normal or reactive oral mucosal tissues (n= 17) were positive for p53. The presence or absence of p53 was not correlated with the site of the lesion or its degree of differentiation. Our data suggest that p53 gene mutations are commonly involved in oral cancer but are neither sufficient nor necessary for the development of malignancy. Nevertheless, as this mutation is the commonest genetic change described so far in cancers in white caucasoids, it is possible that its presence can be used as a marker of risk in a high proportion of malignant and potentially malignant oral lesions.
Url:
DOI: 10.1111/j.1600-0714.1992.tb01028.x
Links to Exploration step
ISTEX:CAD999681CE073AD5E0A39DD88A8CE5CE3064BD0Le document en format XML
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S.</namePart><namePart type="family">Warnakulasuriya</namePart><affiliation>Department of Dental Sciences, Hunterian Institute, Royal College of Surgeons of England, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N. W.</namePart><namePart type="family">Johnson</namePart><affiliation>Department of Dental Sciences, Hunterian Institute, Royal College of Surgeons of England, London, England</affiliation><affiliation>Correspondence address: Newell W. Johnson, Department of Dental Sciences, Royal College of Surgeons of England, Lincoln's Inn Fields, London WC2A 3PN.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1992-10</dateIssued><edition>Accepted for publication April 9, 1992.</edition><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="references">35</extent><extent unit="linksCrossRef">3</extent></physicalDescription><abstract lang="en">An immunohistochemical study of primary oral squamous cell carcinomas (n = 37) with a monoclonal antibody (PAb 1801) specific to p53 antioncogene product demonstrated nuclear overexpression of the mutant protein in 35% of cases. Those positive included carcinomas without deep invasion suggesting that p53 mutation may occur in the early stages of progression of a malignancy. This is supported by the observation that mutant protein was detectable in limited amounts in 2 cases of oral mucosal dysplasia (n= 12). None of the normal or reactive oral mucosal tissues (n= 17) were positive for p53. The presence or absence of p53 was not correlated with the site of the lesion or its degree of differentiation. Our data suggest that p53 gene mutations are commonly involved in oral cancer but are neither sufficient nor necessary for the development of malignancy. Nevertheless, as this mutation is the commonest genetic change described so far in cancers in white caucasoids, it is possible that its presence can be used as a marker of risk in a high proportion of malignant and potentially malignant oral lesions.</abstract><subject lang="en"><genre>keywords</genre><topic>Antioncogene</topic><topic>oncogenes</topic><topic>oral cancer</topic><topic>precancer, oral</topic><topic>p53</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Oral Pathology & Medicine</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0904-2512</identifier><identifier type="eISSN">1600-0714</identifier><identifier type="DOI">10.1111/(ISSN)1600-0714</identifier><identifier type="PublisherID">JOP</identifier><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>404</start><end>408</end><total>5</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Mutations in the p53 gene occur in diverse human tumour types</title></titleInfo><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Nigro</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Baker</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Preisinger</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Nigro JM, Baker SJ, Preisinger AC, et al. Mutations in the p53 gene occur in diverse human tumour types. Nature 1989; 342: 705–8.</note><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>342</number></detail><extent unit="pages"><start>705</start><end>8</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>342</number></detail><extent unit="pages"><start>705</start><end>8</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit2"><titleInfo><title>p53 mutations in human cancers</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Hollstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Sidransky</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Vogelstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CC</namePart><namePart type="family">Harris</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hollstein M, Sidransky D, Vogelstein B, Harris CC. p53 mutations in human cancers. Science 1991: 253: 49–53.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>253</number></detail><extent unit="pages"><start>49</start><end>53</end></extent></part><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>253</number></detail><extent unit="pages"><start>49</start><end>53</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit3"><titleInfo><title>Expression of the p53 protein during cell cycle of human peripheral blood lymphocytes</title></titleInfo><name type="personal"><namePart type="given">WE</namePart><namePart type="family">Mercer</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Baserga</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mercer WE. Baserga A. Expression of the p53 protein during cell cycle of human peripheral blood lymphocytes. Exp Cell Res 1985; 160: 31–46.</note><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>160</number></detail><extent unit="pages"><start>31</start><end>46</end></extent></part><relatedItem type="host"><titleInfo><title>Exp Cell Res</title></titleInfo><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>160</number></detail><extent unit="pages"><start>31</start><end>46</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit4"><titleInfo><title>The role of p53 in normal control of cell proliferation</title></titleInfo><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Milner</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Milner J. The role of p53 in normal control of cell proliferation. Curr Opin Cell Biol 1991; 3: 282–6.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>3</number></detail><extent unit="pages"><start>282</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>Curr Opin Cell Biol</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>3</number></detail><extent unit="pages"><start>282</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit5"><titleInfo><title>The p53 protooncogene can act as a suppressor of transformation</title></titleInfo><name type="personal"><namePart type="given">CA</namePart><namePart type="family">Finlay</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PW</namePart><namePart type="family">Hinds</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AJ</namePart><namePart type="family">Levine</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Finlay CA, Hinds PW, Levine AJ. The p53 protooncogene can act as a suppressor of transformation. Cell 1989; 57: 1083–93.</note><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>57</number></detail><extent unit="pages"><start>1083</start><end>93</end></extent></part><relatedItem type="host"><titleInfo><title>Cell</title></titleInfo><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>57</number></detail><extent unit="pages"><start>1083</start><end>93</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit6"><titleInfo><title>Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas</title></titleInfo><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Baker</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ER</namePart><namePart type="family">Fearon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Nigro</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Baker SJ, Fearon ER, Nigro JM, et al. Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas. Science 1989; 244: 217–21.</note><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>244</number></detail><extent unit="pages"><start>217</start><end>21</end></extent></part><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>244</number></detail><extent unit="pages"><start>217</start><end>21</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit7"><titleInfo><title>p53: oncogene or anti‐oncogene</title></titleInfo><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Lane</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Benchimol</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lane DP. Benchimol S. p53: oncogene or anti‐oncogene Genes Dev 1990; 4: 1–8.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>1</start><end>8</end></extent></part><relatedItem type="host"><titleInfo><title>Genes Dev</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>1</start><end>8</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit8"><titleInfo><title>Expression of the nuclear oncogene p53 in colon tumours</title></titleInfo><name type="personal"><namePart type="given">FM</namePart><namePart type="family">Vanden Berg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AJ</namePart><namePart type="family">Tigges</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MEI</namePart><namePart type="family">Schipper</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">FCA</namePart><namePart type="family">Den Hartog‐Jager</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">WGM</namePart><namePart type="family">Kroes</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JMM</namePart><namePart type="family">Walhoomers</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vanden Berg FM, Tigges AJ, Schipper MEI, Den Hartog‐Jager FCA, Kroes WGM. Walhoomers JMM. Expression of the nuclear oncogene p53 in colon tumours. J Pathol 1989; 157: 193–9.</note><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>157</number></detail><extent unit="pages"><start>193</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>J Pathol</title></titleInfo><part><date>1989</date><detail type="volume"><caption>vol.</caption><number>157</number></detail><extent unit="pages"><start>193</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit9"><titleInfo><title>p53 mutations in colorectal cancer</title></titleInfo><name type="personal"><namePart type="given">NR</namePart><namePart type="family">Rodrigues</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Rowan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MEF</namePart><namePart type="family">Smith</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Rodrigues NR, Rowan A, Smith MEF, et al. p53 mutations in colorectal cancer. Proc Natl Acad Sci (USA) 1990; 87: 7555–9.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><extent unit="pages"><start>7555</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci (USA)</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><extent unit="pages"><start>7555</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit10"><titleInfo><title>p53 expression in colorectal tumours</title></titleInfo><name type="personal"><namePart type="given">CA</namePart><namePart type="family">Purdie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">O'Grady</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Piris</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AH</namePart><namePart type="family">Wyllie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CC</namePart><namePart type="family">Bird</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Purdie CA, O'Grady J, Piris J, Wyllie AH, Bird CC. p53 expression in colorectal tumours. Am J Pathol 1991; 138: 807–13.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>138</number></detail><extent unit="pages"><start>807</start><end>13</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Pathol</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>138</number></detail><extent unit="pages"><start>807</start><end>13</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit11"><titleInfo><title>p53 expression in human breast cancer related to survival and prognostic factors: an immunohistochemical study</title></titleInfo><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Ostrowski</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Sawan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Henry</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ostrowski JL, Sawan A, Henry L, et al. p53 expression in human breast cancer related to survival and prognostic factors: an immunohistochemical study. J Pathol 1991; 164: 75–81.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>164</number></detail><extent unit="pages"><start>75</start><end>81</end></extent></part><relatedItem type="host"><titleInfo><title>J Pathol</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>164</number></detail><extent unit="pages"><start>75</start><end>81</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit12"><titleInfo><title>Maintenance of p53 alterations throughout breast cancer progression</title></titleInfo><name type="personal"><namePart type="given">AM</namePart><namePart type="family">Davidoff</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">BM</namePart><namePart type="family">Kerns</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Iglehart</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JR</namePart><namePart type="family">Marks</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Davidoff AM, Kerns BM, Iglehart JD, Marks JR. Maintenance of p53 alterations throughout breast cancer progression. Cancer Res 1991; 51: 2605–10.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>51</number></detail><extent unit="pages"><start>2605</start><end>10</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Res</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>51</number></detail><extent unit="pages"><start>2605</start><end>10</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit13"><titleInfo><title>p53 expression in breast cancer</title></titleInfo><name type="personal"><namePart type="given">G</namePart><namePart type="family">Cattoretti</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Rilke</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Andreola</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LD</namePart><namePart type="family">Amato</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Delia</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Cattoretti G, Rilke F, Andreola S. Amato LD, Delia D. p53 expression in breast cancer. Int J Cancer 1988; 41: 178–83.</note><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>41</number></detail><extent unit="pages"><start>178</start><end>83</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Cancer</title></titleInfo><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>41</number></detail><extent unit="pages"><start>178</start><end>83</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit14"><titleInfo><title>Increased expression of mutant forms of p53 oncogene in primary lung cancer</title></titleInfo><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Iggo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Gatter</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Bartek</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Lane</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AL</namePart><namePart type="family">Harris</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Iggo R. Gatter K, Bartek J, Lane DP, Harris AL. Increased expression of mutant forms of p53 oncogene in primary lung cancer. Lancet 1990; 335: 675–9.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>335</number></detail><extent unit="pages"><start>675</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Lancet</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>335</number></detail><extent unit="pages"><start>675</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit15"><titleInfo><title>Aberrant expression of the p53 oncoprotein is a common feature of a wide spectrum of human malignancies</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Bartek</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Bartkova</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Vojtesek</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bartek J, Bartkova J. Vojtesek B, et al. Aberrant expression of the p53 oncoprotein is a common feature of a wide spectrum of human malignancies. Oncogene 1991: 6: 1698–1703.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><extent unit="pages"><start>1698</start><end>1703</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogene</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><extent unit="pages"><start>1698</start><end>1703</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit16"><titleInfo><title>Frequent mutation of the p53 gene in human oesophageal cancer</title></titleInfo><name type="personal"><namePart type="given">MC</namePart><namePart type="family">Hollstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Metcalf</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Welsh</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Montessano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CC</namePart><namePart type="family">Harris</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hollstein MC, Metcalf RA, Welsh JA, Montessano R. Harris CC. Frequent mutation of the p53 gene in human oesophageal cancer. Proc Natl Acad Sci (USA) 1990: 87: 9958–61.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><extent unit="pages"><start>9958</start><end>61</end></extent></part><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci (USA)</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>87</number></detail><extent unit="pages"><start>9958</start><end>61</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit17"><titleInfo><title>Mutant p53‐: The commonest genetic abnormality in human cancer</title></titleInfo><name type="corporate"><namePart>Editorial.</namePart></name><genre>journal-article</genre><note type="citation/reference">Editorial. Mutant p53‐: The commonest genetic abnormality in human cancer J Pathol 1990; 162: 5–6.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>162</number></detail><extent unit="pages"><start>5</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>J Pathol</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>162</number></detail><extent unit="pages"><start>5</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit18"><titleInfo><title>Expression of p53 in premalignant and malignant squamous epithelium</title></titleInfo><name type="personal"><namePart type="given">BA</namePart><namePart type="family">Gusterson</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Anbazhagan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Warren</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Gusterson BA. Anbazhagan R. Warren W, et al. Expression of p53 in premalignant and malignant squamous epithelium. Oncogene 1991; 6: 1785–9.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><extent unit="pages"><start>1785</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogene</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>6</number></detail><extent unit="pages"><start>1785</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit19"><titleInfo><title>Elevated p53 expression correlates with a history of heavy smoking in squamous cell carcinoma of the head and neck</title></titleInfo><name type="personal"><namePart type="given">JK</namePart><namePart type="family">Field</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Spadidos</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Malliri</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Field JK, Spadidos A, Malliri A, et al. Elevated p53 expression correlates with a history of heavy smoking in squamous cell carcinoma of the head and neck. Br J Cancer 1991; 64: 573–7.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>64</number></detail><extent unit="pages"><start>573</start><end>7</end></extent></part><relatedItem type="host"><titleInfo><title>Br J Cancer</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>64</number></detail><extent unit="pages"><start>573</start><end>7</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit20"><titleInfo><title>Isolation of human‐p53‐specific monoclonal antibodies and their use in the studies of human p53 expression</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Banks</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Matlashewski</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L.</namePart><namePart type="family">Crawford</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Banks L, Matlashewski G, Crawford L. Isolation of human‐p53‐specific monoclonal antibodies and their use in the studies of human p53 expression. Eur J Biochem 1986: 159: 529–34.</note><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>159</number></detail><extent unit="pages"><start>529</start><end>34</end></extent></part><relatedItem type="host"><titleInfo><title>Eur J Biochem</title></titleInfo><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>159</number></detail><extent unit="pages"><start>529</start><end>34</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit21"><titleInfo><title>The cellular oncogene p53 can be activated by mutagenesis</title></titleInfo><name type="personal"><namePart type="given">JR</namePart><namePart type="family">Jenkins</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Rudge</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Chumakov</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GA</namePart><namePart type="family">Currie</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Jenkins JR, Rudge K. Chumakov P. Currie GA. The cellular oncogene p53 can be activated by mutagenesis. Nature 1985; 317: 816–8.</note><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>317</number></detail><extent unit="pages"><start>816</start><end>8</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>317</number></detail><extent unit="pages"><start>816</start><end>8</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit22"><titleInfo><title>Genetic and immunochemical analysis of mutant p53 in human breast cancer cell lines</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Bartek</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Iggo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Gannon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Lane</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bartek J, Iggo R, Gannon J, Lane DP. Genetic and immunochemical analysis of mutant p53 in human breast cancer cell lines. Oncogene 1990; 5: 893–9.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>893</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogene</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>893</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit23"><titleInfo><title>Activating mutations in p53 produce a common conformational effect. A monoclonal antibody specific for the mutant form</title></titleInfo><name type="personal"><namePart type="given">JV</namePart><namePart type="family">Gannon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Greaves</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Iggo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Lane</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Gannon JV, Greaves R. Iggo R. Lane DP. Activating mutations in p53 produce a common conformational effect. A monoclonal antibody specific for the mutant form. EMBO 1990; 9: 1595–1602.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>1595</start><end>1602</end></extent></part><relatedItem type="host"><titleInfo><title>EMBO</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>1595</start><end>1602</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit24"><titleInfo><title>Different tumour‐derived p53 mutants exhibit distinct biological activities</title></titleInfo><name type="personal"><namePart type="given">O</namePart><namePart type="family">Halevy</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Michalovittz</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Oren</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Halevy O, Michalovittz D. Oren M. Different tumour‐derived p53 mutants exhibit distinct biological activities. Science 1990: 250: 113–6.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>250</number></detail><extent unit="pages"><start>113</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>250</number></detail><extent unit="pages"><start>113</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit25"><titleInfo><title>Asymmetric PCR‐based strategy for genetic analysis of the p53 tumor suppressor gene in cell lines and tumour tissues</title></titleInfo><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Bartek</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Iggo</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Vojtesek</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Lane</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bartek J. Iggo R. Vojtesek B, Lane DP. Asymmetric PCR‐based strategy for genetic analysis of the p53 tumor suppressor gene in cell lines and tumour tissues. Neoplasma 1991; 38: 93–9.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>38</number></detail><extent unit="pages"><start>93</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Neoplasma</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>38</number></detail><extent unit="pages"><start>93</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit26"><titleInfo><title>Mutation and cancer: Statistical study of retinoblastoma</title></titleInfo><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Knudson</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Knudson J. Mutation and cancer: Statistical study of retinoblastoma. Proc Natl Acad Sci (USA) 1971: 68: 820–3.</note><part><date>1971</date><detail type="volume"><caption>vol.</caption><number>68</number></detail><extent unit="pages"><start>820</start><end>3</end></extent></part><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci (USA)</title></titleInfo><part><date>1971</date><detail type="volume"><caption>vol.</caption><number>68</number></detail><extent unit="pages"><start>820</start><end>3</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit27"><titleInfo><title>Inactivation of the p53 oncogene by internal deletion or retroviral integration in erythroleukemic cell lines induced by Friend leukemia virus</title></titleInfo><name type="personal"><namePart type="given">YB</namePart><namePart type="family">David</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">VR</namePart><namePart type="family">Prideaux</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Chow</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Benchimol</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Bernstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">David YB, Prideaux VR. Chow V, Benchimol S, Bernstein A. Inactivation of the p53 oncogene by internal deletion or retroviral integration in erythroleukemic cell lines induced by Friend leukemia virus. Oncogens 1988; 3: 179–85.</note><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>3</number></detail><extent unit="pages"><start>179</start><end>85</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogens</title></titleInfo><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>3</number></detail><extent unit="pages"><start>179</start><end>85</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit28"><titleInfo><title>T‐antigen is bound to host protein in SV40‐transformed cells</title></titleInfo><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Lane</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">LV</namePart><namePart type="family">Crawford</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lane DP, Crawford LV. T‐antigen is bound to host protein in SV40‐transformed cells. Nature 1979; 278: 261–3.</note><part><date>1979</date><detail type="volume"><caption>vol.</caption><number>278</number></detail><extent unit="pages"><start>261</start><end>3</end></extent></part><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1979</date><detail type="volume"><caption>vol.</caption><number>278</number></detail><extent unit="pages"><start>261</start><end>3</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit29"><titleInfo><title>Genetic alterations during colorectal‐tumor development</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Vogelstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ER</namePart><namePart type="family">Fearon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SR</namePart><namePart type="family">Hamilton</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vogelstein B, Fearon ER, Hamilton SR, et al. Genetic alterations during colorectal‐tumor development. N Engl J Med 1988; 319: 527–32.</note><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>319</number></detail><extent unit="pages"><start>527</start><end>32</end></extent></part><relatedItem type="host"><titleInfo><title>N Engl J Med</title></titleInfo><part><date>1988</date><detail type="volume"><caption>vol.</caption><number>319</number></detail><extent unit="pages"><start>527</start><end>32</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit30"><titleInfo><title>Macdonald F, Ford CHJ. Oncogenes and tumor suppressor genes. Oxford : Bios Scientific Publishers, 1991: 33.</title></titleInfo><note type="citation/reference">Macdonald F, Ford CHJ. Oncogenes and tumor suppressor genes. Oxford : Bios Scientific Publishers, 1991: 33.</note><name type="personal"><namePart type="given">F</namePart><namePart type="family">Macdonald</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CHJ</namePart><namePart type="family">Ford</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>book</genre><originInfo><publisher>Bios Scientific Publishers</publisher></originInfo><part><date>1991</date><extent unit="pages"><start>33</start></extent></part></relatedItem><relatedItem type="references" displayLabel="cit31"><titleInfo><title>A genetic model for colorectal tumorigenesis</title></titleInfo><name type="personal"><namePart type="given">ER</namePart><namePart type="family">Fearon</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Vogelstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Fearon ER, Vogelstein B. A genetic model for colorectal tumorigenesis. Cell 1990; 61: 759–67.</note><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>61</number></detail><extent unit="pages"><start>759</start><end>67</end></extent></part><relatedItem type="host"><titleInfo><title>Cell</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>61</number></detail><extent unit="pages"><start>759</start><end>67</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit32"><titleInfo><title>Prognostic value of various molecular and cellular features in oral squamous cell carcinomas: a review</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Bryne</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bryne M. Prognostic value of various molecular and cellular features in oral squamous cell carcinomas: a review. J Oral Pathol Med 1991; 20: 413–20.</note><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>413</start><end>20</end></extent></part><relatedItem type="host"><titleInfo><title>J Oral Pathol Med</title></titleInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>413</start><end>20</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit33"><titleInfo><title>Pindborg JJ. Oral cancer and precancer. Bristol : Wright, 1980: 15.</title></titleInfo><note type="citation/reference">Pindborg JJ. Oral cancer and precancer. Bristol : Wright, 1980: 15.</note><name type="personal"><namePart type="given">JJ</namePart><namePart type="family">Pindborg</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>book</genre><originInfo><publisher>Wright</publisher></originInfo><part><date>1980</date><extent unit="pages"><start>15</start></extent></part></relatedItem><relatedItem type="references" displayLabel="cit34"><titleInfo><title>Advanced methods in the evaluation of premalignant lesions and carcinomas of the oral mucosa</title></titleInfo><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Burkhardt</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Burkhardt A. Advanced methods in the evaluation of premalignant lesions and carcinomas of the oral mucosa. J Oral Pathol 1985; 14: 751–78.</note><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>751</start><end>78</end></extent></part><relatedItem type="host"><titleInfo><title>J Oral Pathol</title></titleInfo><part><date>1985</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>751</start><end>78</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="cit35"><titleInfo><title>Envoi: New knowledge concerning oral cancer and research priorities</title></titleInfo><name type="personal"><namePart type="given">NW</namePart><namePart type="family">Johnson</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>book-chapter</genre><relatedItem type="host"><titleInfo><title>Detection of patients and lesions at risk</title></titleInfo><originInfo><publisher>Cambridge University Press</publisher></originInfo><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>Vol 2</number></detail><extent unit="pages"><start>389</start><end>93</end></extent></part></relatedItem></relatedItem><identifier type="istex">CAD999681CE073AD5E0A39DD88A8CE5CE3064BD0</identifier><identifier type="ark">ark:/67375/WNG-TPG1BMLM-W</identifier><identifier type="DOI">10.1111/j.1600-0714.1992.tb01028.x</identifier><identifier type="ArticleID">JOP404</identifier><accessCondition type="use and reproduction" contentType="copyright">© Wiley. 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