The New Weapon To Fight Breast Cancer: A ( Breast Cancer Month Special Report) – The Winner Is: TP53 And Noninherited (Somatic) Mutations .
Houston ( AP ) -- Its Breast Cancer Month, Barron’s Medical Journal love to see all of the organizations and individuals coming together to end breast cancer. Our sister division BMJSports reports 100% of the NFL Teams in the United States will wear pink apparel. Houston's Own Carolyn Farb Who's Giving to so many causes including Breast Cancer and The Community Artists' Collective. One must think With all of the effort and inference to October as Breast Cancer Month, We would like to offer a Report Card on what is The Best Science has to offer in A Cure. A 2015 Answer which addresses this awful disease.
The breast cancer buzz is The ( TP53 ) What is the official name of the TP53 gene? The official name of this gene is “tumor protein p53.”
TP53 is the gene's official symbol. The TP53. The TP53 gene provides instructions for making a protein called tumor protein p53 (or p53).
This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way.
This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way.
The p53 protein is located in the nucleus of cells throughout the body, where it attaches (binds) directly to DNA. When the DNA in a cell becomes damaged by agents such as toxic chemicals, radiation, or ultraviolet (UV) rays from sunlight, this protein plays a critical role in determining whether the DNA will be repaired or the damaged cell will self-destruct (undergo apoptosis). If the DNA can be repaired,
p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. By stopping cells with mutated or damaged DNA from dividing, p53 helps prevent the development of tumors. Because p53 is essential for regulating cell division and preventing tumor formation, it has been nicknamed the "guardian of the genome."
p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. By stopping cells with mutated or damaged DNA from dividing, p53 helps prevent the development of tumors. Because p53 is essential for regulating cell division and preventing tumor formation, it has been nicknamed the "guardian of the genome."
Noninherited (somatic) mutations in the TP53 gene are much more common than inherited mutations, occurring in 20 to 40 percent of all breast cancers. These somatic mutations are acquired during a person's lifetime and are present only in cells that become cancerous. The cancers associated with 
somatic mutations do not occur as part of a cancer syndrome. Most of these mutations change single protein building blocks (amino acids) in the p53 protein, which reduces or eliminates the protein's tumor suppressor function. Because the altered protein is less able to regulate cell growth and division, DNA damage can accumulate. This damage may contribute to the development of a cancerous tumor by allowing cells to grow and divide in an uncontrolled way. polygenic trait is one whose phenotype is
influenced by more than one gene. Traits that display a continuous distribution, such as height or skin color,
somatic mutations do not occur as part of a cancer syndrome. Most of these mutations change single protein building blocks (amino acids) in the p53 protein, which reduces or eliminates the protein's tumor suppressor function. Because the altered protein is less able to regulate cell growth and division, DNA damage can accumulate. This damage may contribute to the development of a cancerous tumor by allowing cells to grow and divide in an uncontrolled way. polygenic trait is one whose phenotype is
influenced by more than one gene. Traits that display a continuous distribution, such as height or skin color,
A single nucleotide polymorphism, also known as simple nucleotide polymorphism, (SNP, pronounced snip; plural snips) is a DNA sequence variation occurring commonly within a population (e.g. 1%) in which a single nucleotide — A, T, C or G — in the genome (or other shared sequence) differs between members of a biological
Germline mutations in the TP53 gene are associated with Li-Fraumeni syndrome (LFS), a rare inherited cancer predisposition syndrome that significantly increases a person’s risk of developing breast cancer and many other types of cancer. LFS affects between one in 5,000 and one in 20,000 people.
People with LFS have up to a 50% risk of developing cancer by age 30, and up to a 93% chance of developing cancer in their lifetime. Breast cancer is the most common cancer diagnosed in women with a TP53gene mutation. Most individuals with LFS inherited the TP53 mutation from a parent, though an estimated 7-20% are the first in their family to have a TP53 gene mutation.
People with LFS have up to a 50% risk of developing cancer by age 30, and up to a 93% chance of developing cancer in their lifetime. Breast cancer is the most common cancer diagnosed in women with a TP53gene mutation. Most individuals with LFS inherited the TP53 mutation from a parent, though an estimated 7-20% are the first in their family to have a TP53 gene mutation.
“These findings suggest that we have been identifying only the most clinically affected LFS families, and raises the concern that we have overestimated cancer risks for them,” said Judy Garber, MD, MPH, Director, Center for Cancer Genetics and Prevention, Dana Farber Cancer Institute in Boston, and one of the study’s authors.
“The findings make the collection and analysis of unselected data more important than ever, and the kind of data that panels can provide essential to that work.” For the study, researchers reviewed data from 25,182 patients that underwent TP53testing conducted at Ambry. Among those positive for a TP53 mutation, personal and family cancer histories were examined to identify specific patterns and to determine whether any National Comprehensive Cancer Network (NCCN) testing criteria were met, including Classic criteria, Chompret criteria, and breast cancer diagnosis before age 36 years.
“The findings make the collection and analysis of unselected data more important than ever, and the kind of data that panels can provide essential to that work.” For the study, researchers reviewed data from 25,182 patients that underwent TP53testing conducted at Ambry. Among those positive for a TP53 mutation, personal and family cancer histories were examined to identify specific patterns and to determine whether any National Comprehensive Cancer Network (NCCN) testing criteria were met, including Classic criteria, Chompret criteria, and breast cancer diagnosis before age 36 years.
In total, 187 patients (0.74%) tested positive for TP53 mutations. These results came from single gene testing (118/2956, 3.99%) and from MGPT (69/22,226, 0.31%). Of all those tested, 95% who underwent single gene testing (SGT) had a cancer diagnosis, versus 82% of patients who had MGPT.
A Cool software --canEvolve that will be based on cloud computing. Cloud computing can accelerate the processing time by providing on-demand resources for queries and Hadoop-based distributed computing for running analysis. Currently we are redesigning some of the processing and visualization pipelines to use R with the Hadoop framework. The next version of canEvolve will better integrate regulatory and protein-protein interaction information.
It will also allow researchers to analyze their own datasets in light of current knowledge, stored analysis results and state-of-the-art methodologies available at the portal in the form of automated workflows.
It will also allow researchers to analyze their own datasets in light of current knowledge, stored analysis results and state-of-the-art methodologies available at the portal in the form of automated workflows.
Neurogenesis and Epidermal Growth Factor Receptor genes can partner with , Genomics and President Obama Brain Acivity Mapping all working hand in hand will look for tumors identified recurrent genomic aberrations in each molecular subtype. The classical subtype was characterised by frequent EGFR amplification and EGFRvIII mutations, CDKN2A deletion, and a lack of TP53mutations, whereas the mesenchymal subtype was characterised by NF1,
TP53, and PTEN mutations. Consensus neuropathological review of a subset of TCGA cases has shown that the proneural, classical, and mesenchymal subtypes are enriched for GBM with oligodendroglial features, small-cell GBM, and gliosarcoma (a morphological variant of GBM with mesenchymal differentiation (Miller and Perry, 2007)), respectively (Cameron Brennan, personal communication). Moreover, pseudopalisading necrosis and to a lesser extent florid microvascular proliferation are frequent in mesenchymal GBM, but the proneural subtype typically lacks necrosis. These findings suggest that mesenchymal GBM may be uniquely susceptible to angiogenesis inhibitors, a hypothesis currently being tested in the RTOG 0825 trial discussed below. The proneural subtype, which like previous studies (Phillips et al, 2006; Lee et al, 2008) was found in younger patients, harboured frequent PDGFRAamplification and mutations in IDH1, TP53, andPIK3CA/PIK3R1, suggesting susceptibility to PDGFRA- and PI3K-targeted therapies. A recent proteomic analysis confirmed protein- and phosphorylation-level signalling abnormalities in the EGFR, PDGFR, and NF1 pathways in classical, proneural, and mesenchymal subtypes of GBM, respectively, further suggesting that these GBM subtypes may be uniquely susceptible to targeted agents (Brennan et al, 2009). It is a great day for Science and News organization around The World
TP53, and PTEN mutations. Consensus neuropathological review of a subset of TCGA cases has shown that the proneural, classical, and mesenchymal subtypes are enriched for GBM with oligodendroglial features, small-cell GBM, and gliosarcoma (a morphological variant of GBM with mesenchymal differentiation (Miller and Perry, 2007)), respectively (Cameron Brennan, personal communication). Moreover, pseudopalisading necrosis and to a lesser extent florid microvascular proliferation are frequent in mesenchymal GBM, but the proneural subtype typically lacks necrosis. These findings suggest that mesenchymal GBM may be uniquely susceptible to angiogenesis inhibitors, a hypothesis currently being tested in the RTOG 0825 trial discussed below. The proneural subtype, which like previous studies (Phillips et al, 2006; Lee et al, 2008) was found in younger patients, harboured frequent PDGFRAamplification and mutations in IDH1, TP53, andPIK3CA/PIK3R1, suggesting susceptibility to PDGFRA- and PI3K-targeted therapies. A recent proteomic analysis confirmed protein- and phosphorylation-level signalling abnormalities in the EGFR, PDGFR, and NF1 pathways in classical, proneural, and mesenchymal subtypes of GBM, respectively, further suggesting that these GBM subtypes may be uniquely susceptible to targeted agents (Brennan et al, 2009). It is a great day for Science and News organization around The World
