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Analysis of the DMBT1 gene in carcinomas of the respiratory tract
Author(s) -
Petersen Simone,
Rudolf Jacqueline,
Bockmühl Ulrike,
Deutschmann Nicole,
Dietel Manfred,
Petersen Iver
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20001001)88:1<71::aid-ijc11>3.0.co;2-x
Subject(s) - biology , metastasis , comparative genomic hybridization , northern blot , southern blot , gene , cancer research , complementary dna , cancer , chromosome , lung cancer , tumor progression , microbiology and biotechnology , pathology , genetics , medicine
Loss of chromosome 10q is a critical step during the progression and metastasis formation of lung cancer. We recently defined 3 distinct regions of allelic imbalances and considered the DMBT1 gene at 10q25‐q26 an interesting candidate for the most telomeric region. Therefore, we investigated DMBT1 in 25 cancer cell lines and 39 primary tumors of the respiratory tract. The analysis by RT‐PCR and Northern blot hybridization revealed that the gene is expressed in all tumors and cell lines and diminished in the SCLC line H187, indicating that RT‐PCR is critical when used as the single method for the evaluation of gene expression. No mutations were found by SSCP analysis of the cDNA and the partially known genomic sequence. Similarly, Southern blot hybridization was unable to detect homozygous deletions. Allelotyping of the markers D10S587, D10S1708 and D10S1723 located near or within the DMBT1 gene did not reach the peak incidence of the 3 minimally deleted regions that we recently defined. In summary, our data do not confirm previous findings reporting frequent loss of DMBT1 expression in lung cancer. However, they strengthen the notion that the responsible gene on chromosome 10q25‐q26 mediating tumor progression and metastasis formation in respiratory tract cancer remains enigmatic. Int. J. Cancer 88:71–76, 2000. © 2000 Wiley‐Liss, Inc.