Whole genome microarray analysis in non-small cell lung cancer

@article{AlZeyadi2015WholeGM,
  title={Whole genome microarray analysis in non-small cell lung cancer},
  author={Mohammad Mohawsh Al Zeyadi and Ivanka Dimova and Vladislav Ranchich and Blaga Rukova and Desislava N Nesheva and Zora Hamude and Sevdalin Georgiev and Danail B. Petrov and Draga Toncheva},
  journal={Biotechnology, Biotechnological Equipment},
  year={2015},
  volume={29},
  pages={111 - 118}
}
Lung cancer is a serious health problem, since it is one of the leading causes for death worldwide. Molecular–cytogenetic studies could provide reliable data about genetic alterations which could be related to disease pathogenesis and be used for better prognosis and treatment strategies. We performed whole genome oligonucleotide microarray-based comparative genomic hybridization in 10 samples of non-small cell lung cancer. Trisomies were discovered for chromosomes 1, 13, 18 and 20. Chromosome… 

Whole genome copy number analyses reveal a highly aberrant genome in TP53 mutant lung adenocarcinoma tumors

The genomic architecture in NSCLC tumors is complex, and particularly TP53-mutated lung adenocarcinomas displayed highly aberrant copy number profiles, and it is suggested to always include TP 53-mutation status when studying copy number aberrations in NS CLC tumors.

Transcriptome of Breast Tumors With Different Amplification Status of the Long Arm of Chromosome 8

It was shown that in 65% of cases, amplification of 8q was preserved in the tumour after neoadjuvant chemotherapy (NAC), and NAC significantly enhanced the heterogeneity of the transcriptome between tumours with and without amplification of 7q.

Suppression of CEP 55 reduces cell viability and induces apoptosis in human lung cancer

The crucial role of CEP55 in promoting lung cancer cell proliferation in vitro and its inhibition may be a novel therapeutic strategy for lung cancer are highlighted.

Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis

The transcriptomic analysis suggests that cancer has an important coregulatory network of transcription factors related to the acquisition of the hallmarks of cancer.

Suppression of CEP55 reduces cell viability and induces apoptosis in human lung cancer.

The crucial role of CEP55 in promoting lung cancer cell proliferation in vitro and its inhibition may be a novel therapeutic strategy for lung cancer are highlighted.

Identification of candidate biomarkers and pathways associated with SCLC by bioinformatics analysis

The present study can shed new light on the understanding of molecular mechanisms of SCLC and may provide molecular targets and diagnostic biomarkers for the treatment and early diagnosis of SclC.

Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer

A therapeutic model based on an ING2 biomarker-guided strategy is proposed based on existing public databases and known pharmacological properties of HDAC inhibitors in NSCLC.

Integrated bioinformatics analysis reveals CDK1 and PLK1 as potential therapeutic targets of lung adenocarcinoma

Kaplan–Meier analysis indicated that the expressions of CDK1 and PLK1 in LUAD patients were associated with overall survival and disease-free survival and may be used as potential biomarkers and therapeutic targets for LUAD.

Crosstalk in competing endogenous RNA network reveals the complex molecular mechanism underlying lung cancer

Two novel pathways, olfactory transduction and neuroactive ligand-receptor interactions, were significantly enriched by differentially expressed genes and may explore new mechanism of lung cancer and aid the development of novel therapy.

References

SHOWING 1-10 OF 22 REFERENCES

Chromosomal aberrations and gene expression profiles in non-small cell lung cancer.

DNA profiling by array comparative genomic hybridization (CGH) of peripheral blood mononuclear cells (PBMC) and tumor tissue cell in non-small cell lung cancer (NSCLC)

The results of this study highlighted the connection between PBMC and tumor cell genomic DNA in lung cancer patients and the application of these studies to cancer prognosis may pose a challenge due to the large amount of information contained in genetic predisposition and family history.

Frequent allelic imbalance suggests involvement of a tumor suppressor gene at 1p36 in the pathogenesis of human lung cancers

The present study identified the shortest region of overlap between D1S507 and TP73, which included the most frequently affected marker, D1 S508 at 1p36, and identified the putative tumor suppressor gene(s) at 1 p36 to gain a better understanding of the molecular pathogenesis of lung cancer.

High resolution chromosome 3p allelotyping of human lung cancer and preneoplastic/preinvasive bronchial epithelium reveals multiple, discontinuous sites of 3p allele loss and three regions of frequent breakpoints.

It is concluded that 3p allele loss is nearly universal in lung cancer pathogenesis; involves multiple, discrete, 3p LOH sites that often show a "discontinuous LOH" pattern in individual tumors; occurs in preneoplastic/preinvasive lesions in smokers with and without lung cancer (multiple lesions often lose the same parental allele).

Molecular and Genetic Aspects of Lung Cancer

Knowledge of the genetic aspects will aid the understanding of the essence of lung carcinogenesis in the search for appropriate markers for early diagnosis and adequate treatment.

Molecular and genetic aspects of lung cancer.

The role of p53 as the Guardian of the Genome and Protector of the Lung from Environmental Carcinogens and the role of Activated Oncogenic ras in the Genesis of Lung Cancer are discussed.

Non-small cell lung cancer: epidemiology, risk factors, treatment, and survivorship.

The introduction of angiogenesis, epidermal growth factor receptor inhibitors, and other new anti-cancer agents is changing the present and future of this disease and will certainly increase the number of lung cancer survivors.