Molecular support for field cancerization in the head and neck

William Michael Lydiatt, Peter E. Anderson, Tullia Bazzana, Michelle Casale, Christopher J. Hughes, Andrew G. Huvos, Daniel Lydiatt, Stimson P. Schantz

Research output: Contribution to journalArticle

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Abstract

BACKGROUND. Two competing concepts, field cancerization and micrometastatic lesions, have been postulated to account for the high frequency of second primary tumors and multicentric dysplasia in patients with head and neck carcinoma. METHODS. To provide insight into this process, the authors examined histologically normal mucosa and dysplastic tissue adjacent to invasive tumor for loss of heterozygosity (LOH) at three commonly deleted loci. Tissues from 21 patients with carcinoma of the oral cavity and oropharynx were identified and verified by a pathologist to contain histologically normal mucosa, dysplasia, and adjacent invasive squamous cell carcinoma. Each specimen was analyzed for LOH at D9S171 (9p21), D3S1007 (3p21.3-22), and D3S1228 (3p14). RESULTS. Of the 21 patients, 19 had adequate DNA for analysis. Seventeen patients were heterozygous at one or both of the 3p sites and LOH occurred in 6 of 17 invasive tumor specimens, 1 of 17 dysplasia specimens, and in none of the mucosal specimens. LOH at 9p21 occurred in 11 of 13 informative specimens of invasive tumor, 8 of 13 dysplasia specimens, and 6 of 13 normal mucosa specimens. However, one case that did not have 9p deletion in the tumor demonstrated LOH in the mucosa and two cases had LOH in both the tumor and mucosa but with deletion of the opposite allele. CONCLUSIONS. These data suggest that 9p21 but not 3p14 or 3p21 deletions occur in the absence of histologic changes. In two cases preinvasive and invasive lesions that apparently were an example of histologic progression contained disparate genetic events, calling into question the use of adjacent dysplasia as a model for premalignant lesions.

Original languageEnglish (US)
Pages (from-to)1376-1380
Number of pages5
JournalCancer
Volume82
Issue number7
DOIs
StatePublished - Apr 1 1998

Fingerprint

Loss of Heterozygosity
Neck
Head
Mucous Membrane
Neoplasms
Carcinoma
Oropharynx
Mouth
Squamous Cell Carcinoma
Alleles
DNA

Keywords

  • 9p21
  • Dysplasia
  • Head and neck carcinoma
  • Leukeplakia
  • Loss of heterozygosity
  • Premalignant

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Lydiatt, W. M., Anderson, P. E., Bazzana, T., Casale, M., Hughes, C. J., Huvos, A. G., ... Schantz, S. P. (1998). Molecular support for field cancerization in the head and neck. Cancer, 82(7), 1376-1380. https://doi.org/10.1002/(SICI)1097-0142(19980401)82:7<1376::AID-CNCR22>3.0.CO;2-2

Molecular support for field cancerization in the head and neck. / Lydiatt, William Michael; Anderson, Peter E.; Bazzana, Tullia; Casale, Michelle; Hughes, Christopher J.; Huvos, Andrew G.; Lydiatt, Daniel; Schantz, Stimson P.

In: Cancer, Vol. 82, No. 7, 01.04.1998, p. 1376-1380.

Research output: Contribution to journalArticle

Lydiatt, WM, Anderson, PE, Bazzana, T, Casale, M, Hughes, CJ, Huvos, AG, Lydiatt, D & Schantz, SP 1998, 'Molecular support for field cancerization in the head and neck', Cancer, vol. 82, no. 7, pp. 1376-1380. https://doi.org/10.1002/(SICI)1097-0142(19980401)82:7<1376::AID-CNCR22>3.0.CO;2-2
Lydiatt WM, Anderson PE, Bazzana T, Casale M, Hughes CJ, Huvos AG et al. Molecular support for field cancerization in the head and neck. Cancer. 1998 Apr 1;82(7):1376-1380. https://doi.org/10.1002/(SICI)1097-0142(19980401)82:7<1376::AID-CNCR22>3.0.CO;2-2
Lydiatt, William Michael ; Anderson, Peter E. ; Bazzana, Tullia ; Casale, Michelle ; Hughes, Christopher J. ; Huvos, Andrew G. ; Lydiatt, Daniel ; Schantz, Stimson P. / Molecular support for field cancerization in the head and neck. In: Cancer. 1998 ; Vol. 82, No. 7. pp. 1376-1380.
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abstract = "BACKGROUND. Two competing concepts, field cancerization and micrometastatic lesions, have been postulated to account for the high frequency of second primary tumors and multicentric dysplasia in patients with head and neck carcinoma. METHODS. To provide insight into this process, the authors examined histologically normal mucosa and dysplastic tissue adjacent to invasive tumor for loss of heterozygosity (LOH) at three commonly deleted loci. Tissues from 21 patients with carcinoma of the oral cavity and oropharynx were identified and verified by a pathologist to contain histologically normal mucosa, dysplasia, and adjacent invasive squamous cell carcinoma. Each specimen was analyzed for LOH at D9S171 (9p21), D3S1007 (3p21.3-22), and D3S1228 (3p14). RESULTS. Of the 21 patients, 19 had adequate DNA for analysis. Seventeen patients were heterozygous at one or both of the 3p sites and LOH occurred in 6 of 17 invasive tumor specimens, 1 of 17 dysplasia specimens, and in none of the mucosal specimens. LOH at 9p21 occurred in 11 of 13 informative specimens of invasive tumor, 8 of 13 dysplasia specimens, and 6 of 13 normal mucosa specimens. However, one case that did not have 9p deletion in the tumor demonstrated LOH in the mucosa and two cases had LOH in both the tumor and mucosa but with deletion of the opposite allele. CONCLUSIONS. These data suggest that 9p21 but not 3p14 or 3p21 deletions occur in the absence of histologic changes. In two cases preinvasive and invasive lesions that apparently were an example of histologic progression contained disparate genetic events, calling into question the use of adjacent dysplasia as a model for premalignant lesions.",
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AU - Lydiatt, William Michael

AU - Anderson, Peter E.

AU - Bazzana, Tullia

AU - Casale, Michelle

AU - Hughes, Christopher J.

AU - Huvos, Andrew G.

AU - Lydiatt, Daniel

AU - Schantz, Stimson P.

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N2 - BACKGROUND. Two competing concepts, field cancerization and micrometastatic lesions, have been postulated to account for the high frequency of second primary tumors and multicentric dysplasia in patients with head and neck carcinoma. METHODS. To provide insight into this process, the authors examined histologically normal mucosa and dysplastic tissue adjacent to invasive tumor for loss of heterozygosity (LOH) at three commonly deleted loci. Tissues from 21 patients with carcinoma of the oral cavity and oropharynx were identified and verified by a pathologist to contain histologically normal mucosa, dysplasia, and adjacent invasive squamous cell carcinoma. Each specimen was analyzed for LOH at D9S171 (9p21), D3S1007 (3p21.3-22), and D3S1228 (3p14). RESULTS. Of the 21 patients, 19 had adequate DNA for analysis. Seventeen patients were heterozygous at one or both of the 3p sites and LOH occurred in 6 of 17 invasive tumor specimens, 1 of 17 dysplasia specimens, and in none of the mucosal specimens. LOH at 9p21 occurred in 11 of 13 informative specimens of invasive tumor, 8 of 13 dysplasia specimens, and 6 of 13 normal mucosa specimens. However, one case that did not have 9p deletion in the tumor demonstrated LOH in the mucosa and two cases had LOH in both the tumor and mucosa but with deletion of the opposite allele. CONCLUSIONS. These data suggest that 9p21 but not 3p14 or 3p21 deletions occur in the absence of histologic changes. In two cases preinvasive and invasive lesions that apparently were an example of histologic progression contained disparate genetic events, calling into question the use of adjacent dysplasia as a model for premalignant lesions.

AB - BACKGROUND. Two competing concepts, field cancerization and micrometastatic lesions, have been postulated to account for the high frequency of second primary tumors and multicentric dysplasia in patients with head and neck carcinoma. METHODS. To provide insight into this process, the authors examined histologically normal mucosa and dysplastic tissue adjacent to invasive tumor for loss of heterozygosity (LOH) at three commonly deleted loci. Tissues from 21 patients with carcinoma of the oral cavity and oropharynx were identified and verified by a pathologist to contain histologically normal mucosa, dysplasia, and adjacent invasive squamous cell carcinoma. Each specimen was analyzed for LOH at D9S171 (9p21), D3S1007 (3p21.3-22), and D3S1228 (3p14). RESULTS. Of the 21 patients, 19 had adequate DNA for analysis. Seventeen patients were heterozygous at one or both of the 3p sites and LOH occurred in 6 of 17 invasive tumor specimens, 1 of 17 dysplasia specimens, and in none of the mucosal specimens. LOH at 9p21 occurred in 11 of 13 informative specimens of invasive tumor, 8 of 13 dysplasia specimens, and 6 of 13 normal mucosa specimens. However, one case that did not have 9p deletion in the tumor demonstrated LOH in the mucosa and two cases had LOH in both the tumor and mucosa but with deletion of the opposite allele. CONCLUSIONS. These data suggest that 9p21 but not 3p14 or 3p21 deletions occur in the absence of histologic changes. In two cases preinvasive and invasive lesions that apparently were an example of histologic progression contained disparate genetic events, calling into question the use of adjacent dysplasia as a model for premalignant lesions.

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KW - Leukeplakia

KW - Loss of heterozygosity

KW - Premalignant

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