Barron's Medical Journal
Friday, October 21, 2016
President Obama’s Legacy Gets A Moonshot Lift With A Song — "Time Is Luck Love With A O"
Wednesday, September 7, 2016
President Obama — Legacy Contribution Is Clearly BlackShear Field
Austin ( BMJSports ) — If You Ever Lived In Prairie View Texas As A Young Man — Where Ever You Go — PV Stays With You : For PVAMU Is A Moveable Feast — Progress In Our Life Time.
President Obama — Legacy Contribution is Clearly BlackShear Field Opening on September 4, 2016 — As The Social Event Of The Year — As Far as you can see smiles of joy and A “Since of Pride ” — You only Witness when there is A Amazing Event — Like The United States Of America Nominates The First African American President. Both Prairie View & Texas Southern Universities Presidents George C. Wright And Dr. Austin A. Lane glowing with “Pride” — BMJSports Caught up with Wright and His Wife walking the Grounds With A Amazement — Much like Denzel Washington winning A Oscar . Had Gumbo in The Press Box Area with Lane and his lovely wife again all this made possible with the leadership from President Obama and His Wife . With His daughter walking on campus Kenny Houston — The Hall Of Fame Football Player From The Washington Redskins. We discussed the shoulders we all where walking on. Prairie Vew’s head coach — Simmons said the “Panthers, who averaged nearly 45 points a game last year, again will play an up-tempo offense and try to snap the ball before the play clock hits 18 seconds.” “We’re going to have to weather the storm early because they are going to be extremely excited, flying around making plays and we’re going to have to play at the same speed,” Haywood said. TSU athletic director Dr. Charles McClelland is banking that Haywood, who has coached under Nick Saban, Mack Brown and Charlie Weis, can match the success of what men’s basketball coach Mike Davis has accomplished for the Tigers. In The Very near future. One thing is for sure The LaborDay Classic Is In Great Hands B Bobby Graham -B .G
Wednesday, July 6, 2016
The Legacy Of President Obama : A Cancer Cure
Monday, March 7, 2016
President #Obama Legacy - The President Obama Legacy - The President Who Developed A Breast Cancer Cure:
“I think to them I looked like a freak,” she recently recalled. “And I felt like a freak.” Her isolation contributed to a kind of bookishness that propelled her toward science. Her upbringing “toughened her up,” said her husband, Jamie Cate. “She can handle a lot of pressure.” These days, that talent is being put to the test.
Three years ago, Dr. Doudna, a biochemist at the University of California, Berkeley, helped make one of the most monumental discoveries in biology: a relatively easy way to alter any organism’s DNA, just as a computer user can edit a word in a document.
The discovery has turned Dr. Doudna (the first syllable rhymes with loud) into a celebrity of sorts, the recipient of numerous accolades and prizes. The so-called Crispr-Cas9 genome editing technique is already widely used in laboratory studies, and scientists hope it may one day help rewrite flawed genes in people, opening tremendous new possibilities for treating, even curing, diseases. But now Dr. Doudna, 51, is battling on two fronts to control what she helped create. While everyone welcomes Crispr-Cas9 as a strategy to treat disease, many scientists are worried that it could also be used to alter genes in human embryos, sperm or eggs in ways that can be passed from generation to generation. The prospect raises fears of a dystopian future in which scientists create an elite population of designer babies with enhanced intelligence, beauty or other traits. Scientists in China reported last month that they had already used the technique in an attempt to change genes in human embryos, though on defective embryos and without real success.
In April 2015 a team of Chinese scientists reported in a little known journal, Protein & Cell, the use of CRISPR/Cas9 to cleave and then repair the HBB gene in nonviable human embryos. The mutated form of HBB causes B-thalassemia, a potentially fatal blood disease. To say the experiment prompted controversy is an understatement. It was published on the heels of two high-profile commentaries in Nature and Science, both of which urged caution about using CRISPR/Cas9 and other technologies to edit the human germline; the Nature authors went so far as to recommend a stop of experiments precisely like the one reported in Protein & Cell. The Liang et al. paper seemed to fly in the face of the recommendations. Though the researchers used triponuclear human embryos (an essential fact missed by some of the breathless reporting in the days after), they designed the experiment as a test of a possible therapeutic strategy. If eventually proven safe, a diseased embryo would be corrected using CRISPR/Cas9 with the intent of eventually making a healthy baby. Importantly, the authors reported notable off-target effects of CRISPR-based gene editing, low efficiency of homologous recombination directed repair (HDR), mosaicism, and unwanted mutations. They concluded: Taken together, our data underscore the need to more comprehensively understand the mechanisms of CRISPR/Cas9-mediated genome editing in human cells, and support the notion that clinical applications of the CRISPR/Cas9 system may be premature at this stage.
Further Genomics Research:
Genomcis and LC (liquid Chromatography) -MS/MS (Tandem Mass) mass spectrometry analysis is What’s Next For A Breast Cancer Cure. Barron Medical Journal has found we now have the know how and the systems to detect breast cancer genes and now at this year’s show BMJ has found one of the major advances in science that have been around for over a Hundred years MS mass Spectrometry (MS) is an analytical technique that produces spectra (singular spectrum) of the masses of the molecules comprising a sample of material. The great news about MS is we can now validate our genomic gene finding. The next step is to get this technology out of the University
centers in to commercial use. Here are some success stories on breast cancer and MS Mass Spectrometry. Barron’s Medical Journal breast cancer focus was amplified right outside of Washington, DC USA Where The National Institute Of Health Director Francis Collins gave the rights and say so of one of the most important genes in the fight for breast cancer. The HSP70 the gene protein cancer cells kept alive…..More on the background for Henrietta Lacks in the next paragraph. Tumor differentiation factor (TDF) is our line of discussion in this article. We now have genomics which tells us that genes GRP78 and HSP70 are key in Indentifying and solving breast cancer. In molecular genomics we also have a tool called Mass spectrometry which allows scientist to verify our gene analysis.
In others words cancer cells taken without consent from A African American Women is used to identify bio Markers used in the scientific puzzle "A Breast Cancer Cure". Henrietta Lacks (August 1, 1920 – October 4, 1951) (sometimes erroneously called Henrietta Lakes, Helen Lane or Helen Larson) was an African-American woman who was the unwitting source of cells (from her cancerous tumor) which were cultured by George Otto Gey to create an immortal cell line for medical research. This is now known as the HeLa cell line. On January 29, 1951, Henrietta went to Johns Hopkins Hospital because she felt a knot inside her. It all started when she asked her cousins to feel her belly, asking if they felt the lump that she did. Her cousins assumed correctly that she was pregnant. But, after giving birth to her fifth child, Joseph, Henrietta started bleeding abnormally and profusely. Her local doctor tested her for syphilis, which came back negative, and referred her to Johns Hopkins.
Johns Hopkins was their only choice for a hospital, since it was the only one in proximity to them that treated black patients. Howard Jones, her new doctor, examined Henrietta and the lump in her cervix. It was like nothing he had ever seen before. He cut off a small part of the tumor and sent it to the pathology lab. Soon after, Jones discovered she had a malignant epidermoid carcinoma of the cervix Stage 1 (cervical cancer). Lacks was treated with radium tube inserts, which were sewn in place. After several days in place, the tubes were removed and she was released from Johns Hopkins with instructions to return for X-ray treatments as a follow-up. During her radiation treatments for the tumor, two samples of Henrietta's cervix were removed— a healthy part and a cancerous part— without her permission.[10] The cells from her cervix were given to Dr. George Otto Gey. These cells would eventually become the HeLa immortal cell line, a commonly used cell line in biomedical research.
In significant pain and without improvement, Lacks returned to Hopkins on August 8th for a treatment session, but asked to be admitted. She remained at the hospital until the day of her death. Though she received treatment and blood transfusions, she died of uremic poisoning on October 4, 1951 at the age of thirty-one. A subsequent partial autopsy showed that the cancer had metastasized throughout her entire body. Henrietta Lacks was buried without a tombstone in a family cemetery in Lackstown, a part of Clover in Halifax County, Virginia. Her exact burial location is not known, although the family believes it is within feet of her mother's gravesite. Lackstown is the name of the land that has been held by the (black) Lacks family since they received it from the (white) Lacks family, who had owned the ancestors of the black Lackses when slavery was legal. Many members of the black Lacks family were also descended from the white Lacks family. A row of boxwoods separates the graves of whites from those of the blacks buried in the family cemetery.For decades, Henrietta Lacks' mother had the only tombstone of the five graves in the family cemetery in Lackstown, and Henrietta's own grave was unmarked. [11][12] In 2010, however, Dr. Roland Pattillo of the Morehouse School of Medicine donated a headstone for Lacks after reading The Immortal Life of Henrietta Lacks. The headstone, which is shaped like a book, reads: Henrietta Lacks, August 01, 1920-October 04, 1951. In loving memory of a phenomenal woman, wife and mother who touched the lives of many. Here lies Henrietta Lacks (HeLa). Her immortal cells will continue to help mankind forever. Eternal Love and Admiration, From Your Family The cells from Henrietta's tumor were given to researcher George Gey, who "discovered that [Henrietta's] cells did something they'd never seen before: They could be kept alive and grow." Before this, cells cultured from other cells would only survive for a few days. Scientists spent more time trying to keep the cells alive than performing actual research on the cells but some cells from Lacks's tumor sample behaved differently than others. George Gey was able to isolate one specific cell, multiply it, and start a cell line. Gey named the sample HeLa, after the initial letters of Henrietta Lacks' name. As the first human cells grown in a lab that were "immortal" (they do not die after a few cell divisions), they could be used for conducting many experiments. This represented an enormous boon to medical and biological research. HeLa by a researcher at the hospital helped answer the demands of the 10,000 who marched for a cure to polio shortly before Lacks' death. By 1954, the HeLa strain of cells was being used by Jonas Salk to develop a vaccine for polio To test Salk's new vaccine, the cells were
In the avalanche of commentary that followed was a blink-and-you-missed-it defense of the decision to publish the paper by Xiaoxue Zhang (2014), the editor of Protein & Cell. The editorial is a fascinating read, encapsulating the social and ethical tensions surrounding germline editing. Perhaps stung by criticism the experiment was unethical , Zhang says, “With extraordinary care, consideration and deliberation, Protein & Cell has decided to publish in this issue a scientific study that reports CRISPR-based gene-editing of human tripronuclear zygotes.” Zhang goes on to justify why the research was published in the first place: The editorial decision to publish this study should not be viewed as an endorsement of this practice nor an encouragement of similar attempts, but rather the sounding of an alarm to draw immediate attention to the urgent need to rein in applications of gene-editing technologies, especially in the human germ cells or embryos.
From an ethics and policy perspective, how should we measure the Protein & Cell experiment and the decision to publish it? A framework for social responsibility such as the model proposed by Sankar and Cho in their target article might help, but would likely need to include more stakeholders than just bench scientists. Decisions to publish do not occur in isolation. Researchers, reviewers, ethics advisors, and editorial boards all have an opportunity to dialogue during the review process, so the responsibilities to publish socially controversial research are shared. In her commentary, Bovenkirk argues for a “thick” accounting of social responsibility in the sciences and this seems to make sense here. With respect to the Protein & Cell publications, it appears that important elements of the Sankar and Cho framework are already in play. Categories of justification, reasoning to identify harms and benefits, reflexivity, and timing—specifically, designing an experiment ostensibly to uncover the risks the authors enumerate in the conclusions—are on full view in both the research paper and in the editor’s justification. Of course we must trust that other stakeholders were part of the “extraordinary care, consideration and deliberation” and that those deliberations would be fully available to outside observers. But there is a nuance about the Protein & Cell example that is worth a closer look. In their commentary, Mertes and Penning argue that because the Liang et al research showed the dangers of any clinical use of the technology, an outcry about whether the research should have been published is misplaced. After all, both the Science and Nature essays called for more research to determine the safety and efficacy of CRISPR/Cas9 for future clinical use. Wasn’t this precisely what the experts ordered?
It would seem so. But an argument could be made—something hinted at but not directly addressed in Greeley and Charo’s lighthearted target article—that the Chinese experiment was frivolous. The results in the Protein & Cell study were anticipated in animal studies and indeed predicted by the Nature commentary. Some CRISPR/Cas9 researchers believe that the experiment provided little scientific insight. The raises the question of whether we should publish the technical feat of human germline editing or work that moves the field forward in significant ways. So what do we do now that the Protein & Cell study is out? Follow-on experiments become increasingly derivative and are worth exponentially less to science. At what point do such experiments become data-gathering exercises rather than answers to fundamental questions about human development and disease? Given the controversial nature of human germline research, what experiments investigating disease type, embryo stage, culture conditions and other incremental advances should go forward? For example, gene-editing technologies can either knock out (cleave a gene of interest) or knock in (insert a gene of interest). The Liang and colleagues experiment was technically a knock out study. The researchers edited the HBB gene and then asked whether genetic repair pathways recruited an endogenous gene, HBD, to replace the cleaved sequence. Suppose the next CRISPR/Cas9 experiment using human embryos attempts a knock in or gene replacement strategy. Does this represent a frivolous or an important use of the technology? There are some pathways to take with respect to this question. In a recent commentary in Nature Biotechnology, we offer examples of in vitro research that is ethically and scientifically justified, such as probing questions of early human development and infertility. Such research is covered under existing oversight mechanisms and regulation.
Tuesday, January 12, 2016
President Obama Legacy Will Include A Breast Cancer Cure
Saturday, October 10, 2015
The New Weapon To Fight Breast Cancer: A ( Breast Cancer Month Special Report)
Brought To You By Woodlands Fashion: 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.”
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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.
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."
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,
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
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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.
“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.
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.
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