scholarly journals Chromosome 8 copy numbers and the c-myc gene amplification in non-small cell lung cancer. Analysis by interphase cytogenetics.

1999 ◽  
Vol 66 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Hirotoshi Kubokura ◽  
Kiyoshi Koizumi ◽  
Mitsunobu Yamamoto ◽  
Shigeo Tanaka
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Chromosome 8 ◽  
Small Cell Lung ◽  
Interphase Cytogenetics ◽  
Copy Numbers ◽  
Myc Gene

scholarly journals Multiple mechanisms for transcriptional regulation of the myc gene family in small-cell lung cancer.

1988 ◽  
Vol 8 (8) ◽  
pp. 3373-3381 ◽  
Author(s):  
G Krystal ◽  
M Birrer ◽  
J Way ◽  
M Nau ◽  
E Sausville ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Promoter Activity ◽  
Small Cell ◽  
Mrna Levels ◽  
Small Cell Lung ◽  
Myc Gene

The molecular mechanisms reported to regulate the expression of myc family genes are multiple and complex and include gene amplification, transcriptional activation, transcriptional attenuation, and mRNA stability. We have investigated which of these mechanisms are responsible for the extreme variation in myc gene family mRNA levels observed in human small-cell lung cancer cell lines. In addition to gene amplification, a block to nascent mRNA chain elongation, causing attenuation of transcription, is an important regulatory mechanism controlling the steady-state levels of c-myc and L-myc mRNA. The loss of transcriptional attenuation is correlated with overexpression of these two genes in cell lines which do not show gene amplification. Expression of c-myc mRNA appears to be dependent on promoter activity and attenuator function. In contrast, regulation of expression of the N-myc gene does not involve transcriptional attenuation; steady-state mRNA levels are correlated with promoter activity as well as gene amplification. We conclude that transcriptional regulation of each member of the myc gene family is accomplished by a different assortment of complex mechanisms, including gene copy number, promoter activation, and transcriptional attenuation. Interference at multiple points in this complex regulatory process appears to be an important mechanism by which small-cell lung cancer and other human tumors evade growth control.

Multiple mechanisms for transcriptional regulation of the myc gene family in small-cell lung cancer

1988 ◽  
Vol 8 (8) ◽  
pp. 3373-3381
Author(s):  
G Krystal ◽  
M Birrer ◽  
J Way ◽  
M Nau ◽  
E Sausville ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Family ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Promoter Activity ◽  
Small Cell ◽  
Mrna Levels ◽  
Small Cell Lung ◽  
Myc Gene

The molecular mechanisms reported to regulate the expression of myc family genes are multiple and complex and include gene amplification, transcriptional activation, transcriptional attenuation, and mRNA stability. We have investigated which of these mechanisms are responsible for the extreme variation in myc gene family mRNA levels observed in human small-cell lung cancer cell lines. In addition to gene amplification, a block to nascent mRNA chain elongation, causing attenuation of transcription, is an important regulatory mechanism controlling the steady-state levels of c-myc and L-myc mRNA. The loss of transcriptional attenuation is correlated with overexpression of these two genes in cell lines which do not show gene amplification. Expression of c-myc mRNA appears to be dependent on promoter activity and attenuator function. In contrast, regulation of expression of the N-myc gene does not involve transcriptional attenuation; steady-state mRNA levels are correlated with promoter activity as well as gene amplification. We conclude that transcriptional regulation of each member of the myc gene family is accomplished by a different assortment of complex mechanisms, including gene copy number, promoter activation, and transcriptional attenuation. Interference at multiple points in this complex regulatory process appears to be an important mechanism by which small-cell lung cancer and other human tumors evade growth control.

Structure and expression of the human L-myc gene reveal a complex pattern of alternative mRNA processing

1988 ◽  
Vol 8 (1) ◽  
pp. 186-195
Author(s):  
F Kaye ◽  
J Battey ◽  
M Nau ◽  
B Brooks ◽  
E Seifter ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Lung Cancer ◽  
Cancer Cell Lines ◽  
Small Cell ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Myc Gene

We analyzed in detail the structure of the L-myc gene isolated from human placental DNA and characterized its expression in several small-cell lung cancer cell lines. The gene is composed of three exons and two introns spanning 6.6 kilobases in human DNA. Several distinct mRNA species are produced in all small-cell lung cancer cell lines that express L-myc. These transcripts are generated from a single gene by alternative splicing of introns 1 and 2 and by use of alternative polyadenylation signals. In some mRNAs there is a long open reading frame with a predicted translated protein of 364 residues. Amino acid sequence comparison with c-myc and N-myc demonstrated multiple discrete regions with extensive homology. In contrast, other mRNA transcripts, generated by alternative processing, could encode a truncated protein with a novel carboxy-terminal end.

Intrachromosomal rearrangements fusing L-myc and rlf in small-cell lung cancer

1991 ◽  
Vol 11 (8) ◽  
pp. 4015-4021
Author(s):  
T P Mäkelä ◽  
J Kere ◽  
R Winqvist ◽  
K Alitalo
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Human Cancer ◽  
Small Cell ◽  
Chromosome 1 ◽  
Small Cell Lung ◽  
Amino Terminal ◽  
Myc Gene ◽  
Intrachromosomal Rearrangements

Chromosomal abnormalities affecting proto-oncogenes are frequently detected in human cancer. Oncogenes of the myc family are activated in several types of tumors as a result of gene amplification or chromosomal translocation. We have recently found the L-myc gene involved in a gene fusion in small-cell lung cancer (SCLC). This results in a chimeric protein with amino-terminal sequences from a novel gene named rif joined to L-myc. Here we present a preliminary structural characterization of the rlf-L-myc fusion gene, which has been found only in cells with an amplified L-myc gene. In addition, we have used somatic cell hybrids to assign the normal rlf locus to the same chromosome (chromosome 1) on which L-myc resides. Finally, we have been able to establish a physical linkage between rif and L-myc with pulsed-field gel electrophoresis. Our results demonstrate that normal rlf and L-myc genes are separated by less than 800 kb of DNA. Thus, the rlf-L-myc gene fusions are due to similar but not identical intrachromosomal rearrangements at 1p32. The presence of independent genetic lesions that cause the formation of identical chimeric rlf-L-myc proteins suggests a role for the fusion protein in the development of these tumors.

O-191 HER1-HER2-HER3 gene amplification and akt activation inpatients with advanced non-small cell lung cancer (NSCLC) treated with gefitinib

Lung Cancer ◽  
2005 ◽  
Vol 49 ◽  
pp. S63-S64
Author(s):  
F. Cappuzzo ◽  
M. Varella-Garcia ◽  
L. Toschi ◽  
I. Domenichini ◽  
G. Ceresoli ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Akt Activation

scholarly journals High MET Receptor Expression But Not Gene Amplification in ALK 2p23 Rearrangement Positive Non–Small-Cell Lung Cancer

2014 ◽  
Vol 9 (5) ◽  
pp. 646-653 ◽  
Author(s):  
Yan Feng ◽  
Eugen C. Minca ◽  
Christopher Lanigan ◽  
Angen Liu ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Receptor Expression ◽  
Small Cell Lung ◽  
Met Receptor

scholarly journals Intrachromosomal rearrangements fusing L-myc and rlf in small-cell lung cancer.

1991 ◽  
Vol 11 (8) ◽  
pp. 4015-4021 ◽  
Author(s):  
T P Mäkelä ◽  
J Kere ◽  
R Winqvist ◽  
K Alitalo
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Human Cancer ◽  
Small Cell ◽  
Chromosome 1 ◽  
Small Cell Lung ◽  
Amino Terminal ◽  
Myc Gene ◽  
Intrachromosomal Rearrangements

Chromosomal abnormalities affecting proto-oncogenes are frequently detected in human cancer. Oncogenes of the myc family are activated in several types of tumors as a result of gene amplification or chromosomal translocation. We have recently found the L-myc gene involved in a gene fusion in small-cell lung cancer (SCLC). This results in a chimeric protein with amino-terminal sequences from a novel gene named rif joined to L-myc. Here we present a preliminary structural characterization of the rlf-L-myc fusion gene, which has been found only in cells with an amplified L-myc gene. In addition, we have used somatic cell hybrids to assign the normal rlf locus to the same chromosome (chromosome 1) on which L-myc resides. Finally, we have been able to establish a physical linkage between rif and L-myc with pulsed-field gel electrophoresis. Our results demonstrate that normal rlf and L-myc genes are separated by less than 800 kb of DNA. Thus, the rlf-L-myc gene fusions are due to similar but not identical intrachromosomal rearrangements at 1p32. The presence of independent genetic lesions that cause the formation of identical chimeric rlf-L-myc proteins suggests a role for the fusion protein in the development of these tumors.

Gene amplification is a relatively frequent event leading toZBTB7A(Pokemon) overexpression in non-small cell lung cancer

2007 ◽  
Vol 213 (3) ◽  
pp. 294-302 ◽  
Author(s):  
K Apostolopoulou ◽  
IS Pateras ◽  
K Evangelou ◽  
PK Tsantoulis ◽  
M Liontos ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gene Amplification ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Frequent Event
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