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The genetic mutations that accompany aging lead to cancer

Posted by star on 2019-03-27 23:19:47

As people age, they show signs of aging, such as chloasma on the skin and greyish hair. These are just phenotypes, and the root cause is genomic change. Errors introduced during DNA damage and replication accumulate, making the genome different in each cell. As cells divide, the changes continue to be passed on, with more and more effects. If the change - known as a mutation - shuts off the system that controls cell proliferation and survival, it could lead to cancer.
Cancer has familial components, and cancer-susceptible genes, such as BRCA1 and TP53, are involved in coordinating the cell's response to DNA damage. A defect in the BRCA1 gene increases a woman's risk of developing breast and ovarian cancer. In addition, the DNA repair mechanism collapsed, damaged cells can accumulate mutations, the occurrence of cancer is inevitable. In addition to genetics, environmental and lifestyle factors can also influence cancer risk.

Lung cancer patients who compared smokers with non-smokers had different mutation patterns, because chemicals in cigarette smoke attack DNA. One of the most common mutations in cancer or normal cells is the methylated DNA reaction. DNA methylation is a small chemical modification that helps control the opening and closing of genes. This small change is crucial for normal development, but methylation also makes DNA more vulnerable to damage.

Although the occurrence of cancer is directly related to the accumulation of DNA damage, our immune system also plays an important role.

Lifestyle differences, such as stress, diet and so on will also produce certain risks.

The results suggest that some people accumulate more DNA damage than others, and measuring these differences may help reduce risk.

Identify the invasive breast cancer candidate gene CBX2

Posted by star on 2019-03-25 19:01:11

Hundreds of oncogenes have been identified in the human genome through genetic mutations. Most oncogenes, however, are found in people with a particular type of cancer. Jess Mar, an assistant professor at the Australian institute of bioengineering and nanotechnology, says these genes are not the whole story. He believes that gene activity is different in patients of the same or subspecies, and that it is difficult to compare the level of gene activity in a group of patients by looking at data on the molecular makeup of cancer.

A new statistical method, called Oncomix, identifies oncogene candidates (OCs) in RNA-seq data. The principle of this method is to identify OCs by detecting low expression in normal tissues and overexpression in patient tumor subsets. Patients were grouped according to the expression of OC. To demonstrate the usefulness of Oncomix, Dr Mar and his colleagues applied the Oncomix approach to RNA-seq data from the cancer genome atlas (TCGA) breast cancer cohort and identified a set of five OCs (CBX2, NELL2, EPYC, SLC24A2 and LAG3). Chromobox 2 (CBX2) was associated with poor clinical outcomes, according to calculations and experimental evidence, and Mar suggested that this may be a driving factor for breast cancer and should be further explored as a potential drug target for invasive breast cancer. This finding underscores the value of the Oncomix approach. Finding hidden, specific oncogenes could lead to new treatments for cancer.

Khorana's studies also identified three chain termination signals. The existence of one of these signals became evident when a polyribonucleotide with a repeating GAUA sequence (GAUAGAUAGAUA……..) was studied. Instead of directing the synthesis of a polypeptide, this polyribonucleotide directs the synthesis of a tripeptide with the sequence lle-Asp-Arg. the UAG codon acts as a chain termination signal. Two other codons, UAA and UGA, also were shown to be termination codons. The finding of three stop codons fit nicely with the available genetic evidence. Working independently, the laboratories of Seymour Benzer and Syd-ney Brenner had demonstrated that some gene mutations cause the gene product to be much shorter than normal. They explained the production of the truncated polypeptides by proposing that the mutations change normal codons into stop codons. Mutations that change a normal codon into a stop codon are termed nonsense mutations because they change a triplet from one that specifies an aminoacid to one that does not. Three different types of nonsense mutation were shown to exist and geneticists named them amber, ochre, and opal. These names, which have no physiological significance, were coined in a rather lighthearted spirit. The amber codon is UAG; the ochre codon is UAA; and the opal codon is UGA.

Long-term smoking can damage the body ability to fight skin cancer

Posted by star on 2019-03-22 00:19:06

Smoking may weaken the body's immune response to melanoma, according to a study published in the journal Cancer Research. The scientists found that long-term smokers had a 40 percent lower survival rate than non-smokers with melanoma. Among 156 patients with the most genetic markers of immune cells, smokers were about 4.5 times less likely to survive cancer than never-smokers.
The researchers found the drop in survival was most pronounced among smokers in the group with the highest number of immune-cell markers, suggesting that smoking may have a direct effect on the rapid proliferation of cancer cells.
Scientists believe that smoking may have an effect on the body's immune system, altering its ability to fight skin cancer. Smokers can still boost the immune response to try to destroy melanoma, but it seems to be less effective than nonsmokers, and smokers are less likely to survive cancer. Therefore, people diagnosed with melanoma should be strongly advised to quit smoking.
Dr Julie sharp, director of health information at cancer research UK, said: "taken together, these results suggest that smoking may reduce the survival rate of melanoma patients, so it is particularly important for their health to stop smoking."

The structural basis for pre-and post-transfer editing has been elucidated for the bacterial IIe-tRNA synthetase. The Rossman-fold domain of this enzyme has a polypeptide with it. This insert, which is approximately 200 residues long, it called connective polypeptide 1 (CP1). Three different kinds of experiments show that CP1 forms the editing domain. First, mutations that alter residues in CP1 block the editing function. Second, the CP1 fragment hydrolyzes Val-tRNAwithout the assistance of any other part of the synthetase. Third, structural studies performed by Shigeyuki Yokoyama and coworkers in 1998 show that valine binds to both the Rossman-fold and the CP1 domain in IIe-tRNA synthetase from the gram-negative bacterial Thermus thermophilus, whereas isoleucine binds to only the former. The double-sieve model predicts this binding difference between the two amino acids. The Rossman-fold domain acts as the coarse sieve that accommodates both amino acids, whereas CP1 (the editing site) acts as the fine sieve that accommodates only valine.
Ile-tRNA synthetase’s aminoacylation and editing sites are more than 25 Á apart, raising the issue of how the 3’-end of a misacylated tRNA moves from the aminoacylation to the editing site. Structural studies performed by Thomas Steitz and his coworkers show that when Ile-tRNA synthetase forms a complex with tRNAIIe and mupirocin ( an antibiotic inhibitor that binds to the aminoacylation site ), the 3'-terminal of tRNAIIe is located in the CP1 domain. This observation suggests that when valine attaches to tRNAIIe, the tRNA’s acceptor stem flips from the aminoacylation site to editing site while the rest of the RNA molecule remains in place.
CP1 also catalyzes the hydrolysis of valyl-AMP that is mistakenly formed at Ile-tRNA synthetase’s aminoacylation site. Many, but probably not all of the CP1 residues that participate in editing Val-tRNAIIe al......

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