2q-, a non-random chromosomal abnormality in human non-small-cell lung cancer

Lu, Yong‐Jie; Dong, Xiang-Yang; Guo, Shu; Zhang, Rugang; Ke, Yang; Zhang, Liang-Ze; Xu, Lihua; Cheng, Shujun

doi:10.1093/carcin/17.8.1589

Cited by 9 publications

(6 citation statements)

References 24 publications

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“…Allelic deletions detected as a loss of heterozygosity (LOH) were reported for multiple chromosomal loci, indicating inactivation of several tumour suppressor genes and finally leading to oncogenesis and progression to lung cancer. Recurrent alterations in tumours at numerous chromosomal loci of any chromosome have been seen in NSCLC at a rate between 8% and 100% (3,7,13,14).…”

Section: Introductionmentioning

confidence: 99%

High rate of molecular alteration in histologically tumour-free bronchial epithelium of NSCLC patients detected by multicolour fluorescence in situ hybridisation

Hilbe

Auberger²,

Dirnhofer³

et al. 2006

Oncol Rep

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Abstract. Detection of molecular abnormalities could provide an essential tool for the diagnosis of non-small cell lung cancer (NSCLC) and defining patients at risk for early relapse. Fluorescence in situ hybridisation (FISH) targeting 17 gene loci was applied to determine the frequency of molecular alteration in NSCLC probes and adjacent tumourfree bronchial epithelium. FISH was performed on fresh frozen specimens from 76 patients with histologically confirmed NSCLC and 54 specimens of adjacent tumour-free tissue. Routine autopsy lung tissue probes from 7 cancer-free patients served as a control group. Locus-specific (3p14.2, 3p21.2, 3p21.3, 3p25.3, 5p15.2, 7p12, 8q24.12, 9p21, 13q14, and 17p13.1) as well as centromere probes (4, 6, 7, 9, 11 and 16) were used. Molecular alterations using FISH on interphase nuclei were detected in 100% of NSCLC tumour specimens and 89% of microscopically tumour-free tissues of NSCLC patients. In histologically 'normal' epithelium, the most frequent alterations were seen with locus-specific probes for 3p14.2, 3p.21, 3p21.3, 3p25.3 and 7p12 and centromerespecific probes 11 and 16 (12-93%). As expected, the majority of genetic alterations seen in 'premalignant' specimens were found in the correlating tumour probes. None of the tested parameters revealed prognostic significance in univariate Cox analysis. FISH analysis, performing multicolour strategies, demonstrated its power in detecting genetic abnormalities in NSCLC specimens and even in tumour-free sections of tumour patients.

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Section: Introductionmentioning

confidence: 99%

High rate of molecular alteration in histologically tumour-free bronchial epithelium of NSCLC patients detected by multicolour fluorescence in situ hybridisation

Hilbe

Auberger²,

Dirnhofer³

et al. 2006

Oncol Rep

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“…2q-has rarely been reported in human lung cancer before. However, we found that 2q-exists in cell line M and two other immortalized human bronchial epithelial cell lines we established [13]. It shows that 2q-is also a frequent genetic alteration in the human bronchial epithelial cell lines.…”

Section: Chromosome Deletion Involved In 3p and 2qmentioning

confidence: 73%

“…Using a chromosome 2-and chromosome 3-specific DNA probe (from American Type Culture Collection, Rockville, MD) combined with DAPI(4*6-diamidino-2-phenylindole) banding, we found 3p-deletion occurred at passage 14 M(p14), and another chromosome abnormality, 2q-, occurred at passage 30 [13]. Cytogenetic analysis has confirmed that lung cancers are associated with multiple genetic alterations.…”

Section: Chromosome Deletion Involved In 3p and 2qmentioning

confidence: 91%

“…In M(p13) SV40 integrated mainly at 12q 23, but in some cells SV40 was also found on other chromosome regions, such as 2p and 5q. In M(p30) and M(p71), the hybridization signal was almost exclusively in 12q [13]. The specific integration site may correlate with the transformation of cell line M, conferring some kind of growth advantage to these cells.…”

Section: Integration Of Sv40 At 12q 23mentioning

confidence: 98%

“…We hope to identify specific biomarkers accompanying the carcinogenesis process in human bronchial epithelial cells. Previous results [12][13][14] are discussed below.…”

Section: Tumorigenicity Assaymentioning

confidence: 99%

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Molecular cytogenetic alterations in the early stage at human bronchial epithelial cell carcinogenesis

Dong¹,

Lu²,

Tong³

et al. 1997

J. Cell. Biochem.

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Lung carcinogenesis is a multi-step process involving activation of oncogenes and inactivation of tumor suppress genes. Many molecular and cytogenetic alterations occur in the early stages of carcinogenesis. We have developed an effective culture system for human bronchial epithelial cells and lung cancer cells. Four immortalized human bronchial epithelial cell lines were established by transfecting the epithelial cells with plasmid DNA containing the early region of SV40. Some molecular and cytogenetic alterations, such as 3p-, 2q-, 9p-, c-myc translocation t(8;14) (q23; q32), were found in one immortalized bronchial epithelial cell line M when approaching malignant transformation. An increase in cell proliferation and decrease of apoptosis were noted in the late passages of the immortalized cell line M. Some molecular cytogenetic alterations were also observed in human primary non-small cell lung cancers. Molecular cytogenetic alterations during the early stage of carcinogenesis of human bronchial epithelial cells may be useful as biomarkers for both diagnosis and intermediate endpoint of chemoprevention of lung cancer. J. Cell. Biochem. Suppls. 28/29:74-80. 1998 Wiley-Liss, Inc. 1998 Wiley-Liss, Inc.*CFE: colony forming efficiency; PD/D: per doubling/day; EGF: epidermal growth factor; MSFM-EGF: deprivation of EGF from MSFM. CFE% and PD/D between M(p16) and M(p71) P Ͻ 0.01; CFE% and PD/D of M(p16) between MSFM and MSFM-EGF, P Ͻ 0.01.

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Allelotyping demonstrates common and distinct patterns of chromosomal loss in human lung cancer types

Virmani

Fong

Kodagoda

et al. 1998

Genes Chromosom. Cancer

166

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Allelic loss is a hallmark of tumor suppressor gene (TSG) inactivation. We have allelotyped 29 paired lymphoblastoid and lung cancer cell lines derived from 11 patients with small cell (SCLC) and 18 patients with non‐small cell lung carcinomas (NSCLC). Statistical analysis indicated that a threshold of 30% separated non‐random allelic loss from the random genetic deletions of malignancy. We have identified non‐random allelic loss at 42 of 54 (78%) specific chromosomal regions examined, with 22 regions (52%) common between the two major lung cancer histologic types. There were 3 regions (7%) with allelic loss specific for SCLC and 17 regions (41%) specific for NSCLC. Furthermore, there were significant differences in loss of heterozygosity (LOH) frequencies between NSCLC and SCLC at 13 regions on eight chromosome arms (3p, 5q, 6q, 9p, 10q, 11p, 13q, and 19p). Eight homozygous deletions were present in seven cell lines at four regions, 3p12, 3p14.2, 9p21, and 10q23–25. We have also identified novel sites of chromosomal deletions. In particular, there was frequent loss at 11p13 in SCLC and loss at 6p21.3 and 13q12.3 in NSCLC. In this study, we demonstrate that a) non‐random allelic losses in lung cancer involve multiple regions; b) some losses are common to both NSCLC and SCLC subtypes, whereas others are subtype specific; c) there are genetic deletions at novel chromosomal regions; and d) several homozygous deletions have been noted. Our studies demonstrate the usefulness of continuous cell lines for detailed allelotyping, for comparing genetic abnormalities between SCLC and NSCLC, and for identifying homozygous deletions. Genes Chromosomes Cancer 21:308–319, 1998. © 1998 Wiley‐Liss, Inc.

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2q-, a non-random chromosomal abnormality in human non-small-cell lung cancer

Cited by 9 publications

References 24 publications

High rate of molecular alteration in histologically tumour-free bronchial epithelium of NSCLC patients detected by multicolour fluorescence in situ hybridisation

High rate of molecular alteration in histologically tumour-free bronchial epithelium of NSCLC patients detected by multicolour fluorescence in situ hybridisation

Molecular cytogenetic alterations in the early stage at human bronchial epithelial cell carcinogenesis

Allelotyping demonstrates common and distinct patterns of chromosomal loss in human lung cancer types

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