Mutations in Tumor suppressor TP53 Gene in Formalin- Fixed, Paraffin Embedded Tissues of Squamous Cell Carcinoma (SCC) of Lung Cancer

Mohammadi, Abbas; Gohar, Ali Vaziri; Shakibaie, Mohamad Reza

doi:10.3844/ajbbsp.2008.1.6

Cited by 11 publications

(8 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tissue fragments were deparaffinized with xylene, ethanol and washed with PBS buffer ( pH 7.4; 1.7 mM KH 2 PO 4 , 5.2 mM Na 2 HPO 4 , 150 mM NaCl) two times. For digestion, lysis buffer (1M Tris, 0.5M EDTA, SDS 10% w/v and proteinase K (20 mg.ml -1 )) were added to each microtube and incubated 16 h at 55ºC and DNA was extracted by phenol-chloroform extraction method (12)(13)(14).…”

Section: Genomic Dna Extraction and Pcr Amplificationmentioning

confidence: 99%

Association of Two Polymorphic Codons in P53 and ABCC1 Promoter with Prostate Cancer

et al. 2015

View full text Add to dashboard Cite

Section: Genomic Dna Extraction and Pcr Amplificationmentioning

confidence: 99%

Association of Two Polymorphic Codons in P53 and ABCC1 Promoter with Prostate Cancer

et al. 2015

View full text Add to dashboard Cite

“…It has been reported that smoking induces mutations in exons 5 to 8 of p53 gene in laryngeal cancer (21). Scientific evidence shows that cancer of the oral cavity, larynx and esophagus are directly associated with smoking.…”

Section: Tobacco and Larynx Cancermentioning

confidence: 99%

“…It is observed that PAH, a well-known chemical in cigarette, increases the frequency of thymine and guanine replacement in this gene. Likewise, a certain nitrosamine in cigarette smoke, Nicotinderived nitrosamine ketone (NNK), has been shown to elevate substitution of guanine to adenine in exon 5 of p53 gene in lung cancer, highlighting the importance of this chemical in lung carcinogenesis (21). As another mechanism, it is known that cigarette smoke is a rich source of free radicals and reactive oxygen species (ROS).…”

Section: Tobacco and Genetic Changesmentioning

confidence: 99%

See 1 more Smart Citation

The Molecular Mechanisms of Tobacco in Cancer Pathogenesis

et al. 2017

View full text Add to dashboard Cite

Context: Studies have shown that cancer is a multi-factorial disease in its pathogenesis, in addition to genetic disorders, the effect of environmental factors can also be pointed. Among all environmental factors, tobacco that is considered as the leading cause of respiratory and cardiovascular disease plays a key role in cancer pathogenesis and progression. More than 5,000 chemicals and 62 carcinogenes have been detected in tobacco, which could contribute to tumorgenesis through activating oncogenes, inhibition of tumor suppressor genes, genetic and epigenetic changes, alteration of growth pathways, angiogenesis and metastasis. Evidence Acquisition: To access the articles, we used valid external and internal databases. In order to set the search formula with maximum collectivity, at the first step, the main keywords were characterized and then equivalent terms were identified using various sources. In order to retrieve the last research papers, searches were conducted constantly from 1970 until 2015. The obtained results were screened in terms of relevance and quality indicators such as proper research design, control groups, inclusion and exclusion criteria, and also the statistical analysis. Accordingly, 150 articles were obtained and finally 64 articles which were eligible and had high relevance to the topic were selected and reviewed. Results: This review explains the association between tobacco smoking and the incidence of different human cancers; also it focuses on molecular mechanisms through which carcinogenic chemicals in tobacco smoke promote cancer progression. Among multiple components of tobacco smoke, three carcinogens, including polycyclic aromatic hydrocarbons (PAH), nictotine and nicotin-derived nitrosamine ketone (NNK) convincingly play major roles in the pathogenesis of a wide range of cancers. In fact, these toxic and carcinogenic agents alter the expression of oncogenes, tumor suppressors, DNA repair, and last but not least, apoptosis-related genes through several mechanisms, such as point mutations, deletions, translocations and gene recombination. Moreover, implication of different tumorgenic signal transduction pathways, such as PI3K/AKT, STAT3, ERK1/2 and COX-2 in tobacco-induced tumorgenesis should not be underestimated. Conclusions: Although many facts about the carcinogenic character of tobacco are yet unknown, understanding the molecular mechanisms of cancer development associated with smoking could be promising for early detection, treatment, and reducing metastasis of tobacco-related cancers.

show abstract

“…In addition, hypermethylation of histone proteins causes changes in the chromatin configuration, predisposing cells to allelic loss at a specific locus in the chromosomes [18]. Such genetic and epigenetic alterations in growth-control genes such as DNA-repair genes, tumor suppressor genes, oncogenes, apoptotic genes, combine to determine the cellular phenotype and differentiation [13,19].…”

Section: Introductionmentioning

confidence: 99%

A Review on Epigenetic Effect of Heavy Metal Carcinogens on Human Health~!2010-01-27~!2010-02-09~!2010-06-09~!

Mishra¹,

Dwivedi²,

Singh³

2010

TONUTRAJ

View full text Add to dashboard Cite

Cancer is a leading cause of morbidity, mortality, and premature death worldwide. Certain strategies for minimizing carcinogenic factors' exposure can reduce the risk of most cancer types in human. Millions of people around the world get exposed to high levels of heavy metals in the drinking-water. Therefore, quality control in drinking-water and detection of its heavy metals is extremely critical issue in maintaining the human health. The carcinogenicity of aluminum, arsenic, chromium, nickel and selenium has been documented previously, but in scattered fashion. Trace amount of these elements entering the body via various routes can induce genetic and epigenetic alteration in different cancer related genes of somatic and stem cells, thus involving in cancer stem cell formation. Epigenetic variations in the etiology of cancer have led to increasing of cancer research studies in last recent years. Although epigenetic effects of these elements have more prominent role than their genetics effects, these elements are able to alter the pattern of cancerrelated genes' expression profiles, too. Therefore, an understanding of the underlying epigenetically mechanisms of these trace elements and the compounds, which could reduce their toxicities or the number of cancer cases due to these elements in the areas that are contaminated with these metals. Perhaps the toxic effects of these elements in many regions are predictable, but antioxidant supplements may eliminate the reactive oxygen species as leading effects of these elements. The present review article is the compilation of various studies dealt with epigenetic effects of carcinogens on human health.

show abstract

Mutations in Tumor suppressor TP53 Gene in Formalin- Fixed, Paraffin Embedded Tissues of Squamous Cell Carcinoma (SCC) of Lung Cancer

Cited by 11 publications

References 30 publications

Association of Two Polymorphic Codons in P53 and ABCC1 Promoter with Prostate Cancer

Association of Two Polymorphic Codons in P53 and ABCC1 Promoter with Prostate Cancer

The Molecular Mechanisms of Tobacco in Cancer Pathogenesis

A Review on Epigenetic Effect of Heavy Metal Carcinogens on Human Health~!2010-01-27~!2010-02-09~!2010-06-09~!

Contact Info

Product

Resources

About