Archive for the ‘Gene Therapy Research’ Category

PUBLIC RELEASE DATE:

12-Dec-2013

Contact: Jim Ritter jritter@lumc.edu 708-216-2445 Loyola University Health System

MAYWOOD, IL. A newly improved internet research tool is helping cancer researchers and physicians make sense out of a deluge of genetic data from nearly 100,000 patients and more than 50,000 mice.

The tool, called the Gene Expression Barcode 3.0, is proving to be a vital resource in the new era of personalized medicine, in which cancer treatments are tailored to the genetic makeup of an individual patient's tumor.

Significant new improvements in the Gene Expression Barcode 3.0 are reported in the January issue of the journal Nucleic Acids Research, published online ahead of print.

Senior author is Michael J. Zilliox of Loyola University Chicago Stritch School of Medicine. Zilliox is co-inventor of the Gene Expression Barcode.

"The tool has two main advantages," Zilliox said. "It's fast and it's free."

The Gene Expression Barcode is available at a website http://barcode.luhs.org/ designed and hosted by Loyola University Chicago Stritch School of Medicine. The website is receiving 1,600 unique visitors per month.

Knowing how a patient's cancer genes are expressed can help a physician devise an individualized treatment. In a tumor cell, for example, certain genes are turned on (expressed) while other genes are turned off (unexpressed). Also, different types of cancer cells have different patterns of gene expression. Genes are expressed through RNA, a nucleic acid that acts as a messenger to carry out instructions from DNA for making proteins.

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Helping cancer researchers make sense of the deluge of genetic data

Dec. 11, 2013 There may be a better way to analyze the genetic causes of cutaneous melanoma (CM) according to a study published in Human Genetics conducted by researchers Yale and Dartmouth. A statistical analysis using the natural and orthogonal interaction (NOIA) model showed increased power over existing approaches for detecting genetic effects and interactions when applied to the genome-wide melanoma dataset.

The gene-gene interactions underlying CM had not been fully explored. The usual functional model uses substitution of alleles for estimating genetic effects but the estimators are confounded. The NOIA model estimates population effects of alleles and the resulting estimators are orthogonal and no longer confounded. In simulation studies, the NOIA model had higher power for finding interactions and main effects than the usual model.

"We confirmed the previously identified significant associated genes HERC2, MC1R, and CDKN2A using a NOIA one-locus statistical model," said Christopher I. Amos, PhD, associate director for Population Sciences, Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, a corresponding author of the study. "When compared to the usual one-locus model we found that the HERC2 signal was detected more clearly by the NOIA model" The NOIA model also identified an additional potential interaction between the rs1129038 of HERC2 gene and a region at chromosome 5. The SNPs that interact with HERC2 to increase melanoma risk are located in the IL31RA gene, which is involved in STAT3 signaling and upregulated in activated monocytes.

The first author Feifei Xiao, a postdoctoral associate of Yale University, concluded that the power of the NOIA model was better for detecting genetic effects when interactions are tested. When main and interaction effects between two loci were modeled, the usual functional model was less powerful.

CM is highly aggressive and accounts for the majority of deaths from skin cancer. Prior genome-wide association studies have identified multiple genetic factors for the illness, including MC1R, HERC2, and CDKN2A. This study provides new insights for understanding the influence of gene-gene interactions on melanoma risk.

The NOIA framework was developed for modeling gene-gene interactions in the analysis of quantitative traits, to allow for reduced genetic models, dichotomous traits, and gene-environment interactions. The NOIA statistical model can be used for additive, dominant, and recessive genetic models as well as for a binary environmental exposures. It is an easily implemented approach that improves estimation of genetic effects that include interactions.

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More powerful approach to analyze melanoma's genetic causes

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Newswise MAYWOOD, IL. A newly improved internet research tool is helping cancer researchers and physicians make sense out of a deluge of genetic data from nearly 100,000 patients and more than 50,000 mice.

The tool, called the Gene Expression Barcode 3.0, is proving to be a vital resource in the new era of personalized medicine, in which cancer treatments are tailored to the genetic makeup of an individual patients tumor.

Significant new improvements in the Gene Expression Barcode 3.0 are reported in the January issue of the journal Nucleic Acids Research, published online ahead of print. Senior author is Michael J. Zilliox of Loyola University Chicago Stritch School of Medicine. Zilliox is co-inventor of the Gene Expression Barcode.

The tool has two main advantages, Zilliox said. Its fast and its free. The Gene Expression Barcode is available at a website http://barcode.luhs.org/ designed and hosted by Loyola University Chicago Stritch School of Medicine. The website is receiving 1,600 unique visitors per month.

Knowing how a patients cancer genes are expressed can help a physician devise an individualized treatment. In a tumor cell, for example, certain genes are turned on (expressed) while other genes are turned off (unexpressed). Also, different types of cancer cells have different patterns of gene expression. Genes are expressed through RNA, a nucleic acid that acts as a messenger to carry out instructions from DNA for making proteins.

Research institutions have made public genetic data from nearly 100,000 patients, most of whom had cancer, and more than 50,000 laboratory mice. In raw form, however, these data are too unwieldy to be of much practical use for most researchers. The Gene Expression Barcode applies advanced statistical techniques to make this mass of data much more user-friendly to researchers.

The barcode algorithm is designed to estimate which genes are expressed and which are unexpressed. Like a supermarket barcode, the Gene Expression Barcode is binary, meaning it consists of ones and zeros -- the expressed genes are ones and the unexpressed genes are zeroes.

Zilliox co-invented the Gene Expression Barcode, along with Rafael Irizarry, PhD. (At the time, Zilliox and Irizarry were at Johns Hopkins University.) Zilliox joined Loyola in 2012, and Irizarry now is at the Dana Farber Cancer Institute. Zilliox and Irizarry first reported the Gene Expression Barcode in 2007. In 2011, they reported an improved 2.0 version. The Barcode already has been cited in more than 120 scientific papers, and the new 3.0 version will make it even easier and faster for researchers to use, Zilliox said.

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Helping Cancer Researchers Make Sense of a Deluge of Genetic Data

Dec. 12, 2013 Scientists have discovered a second code hiding within DNA. This second code contains information that changes how scientists read the instructions contained in DNA and interpret mutations to make sense of health and disease.

A research team led by Dr. John Stamatoyannopoulos, University of Washington associate professor of genome sciences and of medicine, made the discovery. The findings are reported in the Dec. 13 issue of Science. The work is part of the Encyclopedia of DNA Elements Project, also known as ENCODE. The National Human Genome Research Institute funded the multi-year, international effort. ENCODE aims to discover where and how the directions for biological functions are stored in the human genome.

Since the genetic code was deciphered in the 1960s, scientists have assumed that it was used exclusively to write information about proteins. UW scientists were stunned to discover that genomes use the genetic code to write two separate languages. One describes how proteins are made, and the other instructs the cell on how genes are controlled. One language is written on top of the other, which is why the second language remained hidden for so long.

"For over 40 years we have assumed that DNA changes affecting the genetic code solely impact how proteins are made," said Stamatoyannopoulos. "Now we know that this basic assumption about reading the human genome missed half of the picture. These new findings highlight that DNA is an incredibly powerful information storage device, which nature has fully exploited in unexpected ways."

The genetic code uses a 64-letter alphabet called codons. The UW team discovered that some codons, which they called duons, can have two meanings, one related to protein sequence, and one related to gene control. These two meanings seem to have evolved in concert with each other. The gene control instructions appear to help stabilize certain beneficial features of proteins and how they are made.

The discovery of duons has major implications for how scientists and physicians interpret a patient's genome and will open new doors to the diagnosis and treatment of disease.

"The fact that the genetic code can simultaneously write two kinds of information means that many DNA changes that appear to alter protein sequences may actually cause disease by disrupting gene control programs or even both mechanisms simultaneously," said Stamatoyannopoulos.

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Scientists discover double meaning in genetic code

Genetics and genomics laboratory - Royal Brompton Hospital
The cardiovascular genetics and genomics laboratory is based in Sydney Wing, Royal Brompton Hospital. The laboratory, led by Professor Stuart Cook, is a join...

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Genetics Vocabulary
Genetics Vocabulary.

By: Lauren Snyder

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Heather Smith carries a recessive gene for a rare sex-linked primary immune deficiency disease that kills most boys before they are 1 year old, and she passed it on to her two sons.

Her oldest, Brandon, behaved like a normal, healthy baby until he was about six months old and couldn't fight off his first cold. He had trouble eating, he developed a rash on his face and thrush in his mouth, and his fingernails turned blue.

'Bubble Boy' legislation to create home treatment program

Brandon died within three weeks of being hospitalized in 1993 of severe combined immunodeficiency, or SCID-X1, commonly known as "bubble boy disease." It was so named for David Vetter, a Texas child with SCID-X1, who died in 1984 after living for 12 years in a germ-free plastic bubble.

Courtesy Heather Smith

Brandon Dahley died at the age of seven months from SCID-X1 or "bubble boy" disease.

"I had seen the movie ["The Boy in the Plastic Bubble"] with John Travolta, but I never dreamed I would someday lose my first-born child to this devastating disease," said Smith, founder of SCID-Angels for Life, which successfully pushed for mandatory screening of all newborns for the disease in her home state of Florida.

"[A bone transplant] wasn't even an option presented to us for consideration," she said. "Instead, we were told that we had to say goodbye to our only child and turn off the machines."

After genetic testing, Smith's son Taylor was born in 1995, and because of early detection, he received the first-ever in-utero bone marrow cell transplant, previously only done on sheep. Today, at 18, he is "thriving," according to his mother and leads a normal life. He's now preparing to go to college.

Taylor receives infusions of gamma globulin, a blood product that helps his immune system fight off infection.

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'Bubble Boy' Disease, Nearly Always Fatal, Could Have Cure

In one of the biggest advances against leukemia and other blood cancers in many years, doctors are reporting unprecedented success by using gene therapy to transform patients' blood cells into soldiers that seek and destroy cancer.

A few patients with one type of leukemia were given this one-time, experimental therapy several years ago and some remain cancer-free today. Now, at least six research groups have treated more than 120 patients with many types of blood and bone marrow cancers, with stunning results.

"It's really exciting," said Dr. Janis Abkowitz, blood diseases chief at the University of Washington in Seattle and president of the American Society of Hematology. "You can take a cell that belongs to a patient and engineer it to be an attack cell."

In one study, all five adults and 19 of 22 children with acute lymphocytic leukemia, or ALL, had a complete remission, meaning no cancer could be found after treatment, although a few have relapsed since then.

These were gravely ill patients out of options. Some had tried multiple bone marrow transplants and up to 10 types of chemotherapy or other treatments.

Cancer was so advanced in 8-year-old Emily Whitehead of Philipsburg, Pa., that doctors said her major organs would fail within days. She was the first child given the gene therapy and shows no sign of cancer today, nearly two years later.

Results on other patients with myeloma, lymphoma and chronic lymphocytic leukemia, or CLL, will be reported at the hematology group's conference that starts Saturday in New Orleans.

Doctors say this has the potential to become the first gene therapy approved in the United States and the first for cancer worldwide. Only one gene therapy is approved in Europe, for a rare metabolic disease.

The treatment involves filtering patients' blood to remove millions of white blood cells called T-cells, altering them in the lab to contain a gene that targets cancer, and returning them to the patient in infusions over three days.

"What we are giving essentially is a living drug" permanently altered cells that multiply in the body into an army to fight the cancer, said Dr. David Porter, a University of Pennsylvania scientist who led one study.

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Doctors say gene therapy helping fight cancer

Dec. 10, 2013 Researchers at the UNC School of Medicine and the Medical College of Wisconsin found that a new kind of gene therapy led to a dramatic decline in bleeding events in dogs with naturally occurring hemophilia A, a serious and costly bleeding condition that affects about 50,000 people in the United States and millions more around the world.

Before the gene treatment, the animals experienced about five serious bleeding events a year. After receiving the novel gene therapy, though, they experienced substantially fewer bleeding events over three years, as reported in the journal Nature Communications.

"The promise and the hope for gene therapy is that people with hemophilia would be given a single therapeutic injection and then would express the protein they are missing for an extended period of time, ideally for years or even their entire lifetimes," said Tim Nichols, director of the Francis Owen Blood Research Laboratory at UNC and co-author of the paper. The hope is that after successful gene therapy, people with hemophilia would experience far fewer bleeding events because their blood would clot better.

People with hemophilia A lack the coagulation factor VIII in their blood plasma -- the liquid in which red, white, and platelet cells are suspended.

"Bleeding events in hemophilia are severe, and without prompt factor VIII replacement, the disease can be crippling or fatal," said Nichols, a professor of medicine and pathology. "The random and spontaneous nature of the bleeding is a major challenge for people with hemophilia and their families."

In underdeveloped countries, people with hemophilia and many undiagnosed people typically die from bleeding in their late teens or early 20s. In developed countries, patients usually live fairly normal lives, as long as they receive preventive injections of recombinant protein therapy a few times a week. The disease requires life-long management that is not without health risks. The annual cost of medications alone is about $200,000 a year.

However, about 35 percent of people with hemophilia A develop an antibody response that blocks the factor VIII therapy. They require continuous infusions of various protein factors and they face a higher mortality rate. Also, the cost of treatment can easily rise to $2 million or more a year per patient.

Nichols and David Wilcox from the Medical College of Wisconsin figured out a potential way around the antibody response in dogs with naturally occurring hemophilia A.

Using a plasmapheresis machine and a blood-enrichment technique, the research team isolated specific platelet precursor cells from three dogs that have hemophilia A. The team then engineered those platelet precursor cells to incorporate a gene therapy vector that expresses factor VIII. The researchers put those engineered platelet precursors back into the dogs. As the cells proliferated and produced new platelets, more and more were found to express factor VIII.

Then, nature took over. Platelets naturally discharge their contents at sites of vascular injury and bleeding. In this experiment, the contents included factor VIII.

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New gene therapy proves promising as hemophilia treatment

Originally published December 7, 2013 at 3:18 PM | Page modified December 7, 2013 at 8:18 PM

In one of the biggest advances against leukemia and other blood cancers in many years, doctors are reporting unprecedented success by using gene therapy to transform patients blood cells into soldiers that seek and destroy cancer.

A few patients with one type of leukemia were given this one-time, experimental therapy several years ago, and some remain cancer-free. At least six research groups have treated more than 120 patients with many types of blood and bone-marrow cancers, with stunning results.

Its really exciting, said Dr. Janis Abkowitz, blood-diseases chief at the University of Washington in Seattle and president of the American Society of Hematology. You can take a cell that belongs to a patient and engineer it to be an attack cell.

In one study, all five adults and 19 of 22 children with acute lymphocytic leukemia, or ALL, had complete remission, meaning no cancer could be found after treatment, although a few have relapsed since then.

These were gravely ill patients out of options. Some had tried multiple bone-marrow transplants and as many as 10 types of chemotherapy or other treatments.

Cancer was so advanced in Emily Whitehead, 8, of Philipsburg, Pa., that doctors said her major organs would fail within days. She was the first child given the gene therapy and shows no sign of cancer nearly two years later.

Results on other patients with myeloma, lymphoma and chronic lymphocytic leukemia, or CLL, will be reported at the hematology groups conference that started Saturday in New Orleans.

Doctors say this has the potential to become the first gene therapy approved in the United States and the first for cancer worldwide. Only one gene therapy is approved in Europe, for a rare metabolic disease.

The treatment involves filtering patients blood to remove millions of white blood cells called T-cells, altering them in the lab to contain a gene that targets cancer, and returning them to the patient in infusions over three days.

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Gene therapy makes advances in blood-cancer treatment

Gene therapy breakthrough in cancer treatment
An experimental gene therapy is showing high rates of success with cancer patients who have failed to respond to traditional treatments. Jim Axelrod reports.

By: CBS Evening News

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Gene therapy breakthrough in cancer treatment - Video

Theme: Uncover the potential that lies within the cell

Zhe Sha, Harvard Medical School, USA

Its my real honor to be part of this great conference. I had a truly rewarding experience meeting with many experts in the field.

Ramin Lotfi, University Hospital Ulm, Germany

It was my pleasure to participate in the meeting and present my talk.

Barbara Carletti, Childrens Hospital Bambino Gesu, Italy

Thank you very much for the opportunity, it will be a pleasure for me to participate to the next meetings and give my contribution.

Welcome Message

3rd InternationalConferenceand Exhibition on Cell & Gene Therapyto be held during October 27-29, 2014 at Las Vegas, USA. Cell Therapy-2014 is a remarkable event which brings together a unique and International mix of leading oncologists, academic scientists, industry researchers and scholars to exchange and share their experiences and research results about all aspects, making the Congress a perfect platform to share experience and which paves a way to gather visionaries through the research talks and presentations and put forward many thought provoking strategies in emerging cell & gene therapies.The scientific program will include workshops, symposia and poster sessions on a wide collection of Cell & Gene Therapy topics.

The previous conferences were 2ndInternationalConferenceand Exhibition on Cell & Gene Therapywas held during October 23-25 2013, at Orlando-FL, USA with the theme Innovative Strategies in Cell & Gene Therapies & International Conference on Emerging Cell Therapies was held during the October 1-3, 2012 at DoubleTree by Hilton Chicago-North Shore, USA with the theme Evolving Technology in Cell Therapy and its Future Perspectives". Brought together the International blend of people from Evolving Cell Therapies making it the largest endeavor from OMICS Group. All the papers presented at this conference were published in special issues of Journal of Cell Science & Therapy. Cell & Gene Therapy conferences opened up new vistas and fostered collaborations in the industry and academia.

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Cell & Gene Therapy International Conference 2014 | Las Vegas ...

Human genetic engineering is the alteration of an individual's genotype with the aim of choosing the phenotype of a newborn or changing the existing phenotype of a child or adult.[1]

It holds the promise of curing genetic diseases like cystic fibrosis. Gene therapy has been successfully used to treat multiple diseases, including X-linked SCID,[2]chronic lymphocytic leukemia (CLL),[3] and Parkinson's disease.[4] In 2012, Glybera became the first gene therapy treatment to be approved for clinical use in either Europe or the United States after its endorsement by the European Commission.[5][6]

It is speculated that genetic engineering could be used to change physical appearance, metabolism, and even improve physical capabilities and mental faculties like memory and intelligence, although for now these uses are limited to science fiction.

Gene therapy trials on humans began in 2004 on patients with severe combined immunodeficiency (SCID). In 2000, the first gene therapy "success" resulted in SCID patients with a functional immune system. These trials were stopped when it was discovered that two of ten patients in one trial had developed leukemia resulting from the insertion of the gene-carrying retrovirus near an oncogene. In 2007, four of the ten patients had developed leukemia.[7] Work is now focusing on correcting the gene without triggering an oncogene. Since 1999, gene therapy has restored the immune systems of at least 17 children with two forms (ADA-SCID and X-SCID) of the disorder.[citation needed]

Human genetic engineering is already being used on a small scale to allow infertile women with genetic defects in their mitochondria to have children.[8] The technique, known as ooplasmic transfer, is used to inject the mitochondria from the donor's egg cell into the egg of the infertile woman. In vitro fertilization is performed on the egg. [9] Healthy human eggs from a second mother are used. The first mother thus contributes the 23 chromosomes of the nuclear genome, which contain the majority of the child's genetic information, while the second mother contributes the mitochondrial genome, which contains 37 genes. The child produced this way has genetic information from two mothers and one father.[8] The changes made are germline changes and will likely be passed down from generation to generation, and, thus, are a permanent change to the human genome.[8]

Other forms of human genetic engineering are still theoretical. Recombinant DNA research is usually performed to study gene expression and various human diseases. This includes the creation of transgenic animals, such as mice.

Genetic engineering can be broken down into two applications, somatic and germline. Both processes involve changing the genes in a cell through the use of a vector carrying the gene of interest. The new gene may be integrated into the cells genetic material through recombination, or may remain separate from the genome, such as in the form of a plasmid. If integrated into the genome, it may recombine at a random location or at a specific location (site-specific recombination) depending on the technology used.

As the name suggests, somatic cell therapy alters the genome of somatic cells. This process targets specific organs and tissues in a person. The aim of this technique is to correct a mutation or provide a new function in human cells. If successful, somatic cell therapy has the potential to treat genetic disorders with few therapeutic options. This process does not affect the genetics of gametic cells within the same body. Any genetic modifications are restricted to a patient individually and cannot be passed on to their offspring.

Several somatic cell gene transfer experiments are currently in clinical trials with varied success. Over 600 clinical trials utilizing somatic cell therapy are underway in the United States. Most of these trials focus on treating severe genetic disorders, including immunodeficiencies, haemophilia, thalassaemia, and cystic fibrosis. These disorders are good candidates for somatic cell therapy because they are caused by single gene defects. While somatic cell therapy is promising for treatment, a complete correction of a genetic disorder or the replacement of multiple genes in somatic cells is not yet possible. Only a few of the many clinical tries are in the advanced stages.[10]

Germline cell therapy alters the genome of germinal cells. Specifically, it targets eggs, sperm, and very early embryos. Genetic changes made to germline cells affect every cell in the resulting individuals body and can also be passed on to their offspring. The practice of germline cell therapy is currently banned in several countries, but has not been banned in the US.

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Human genetic engineering - Wikipedia, the free encyclopedia

Medelian Genetics 1
In this video we cover the first half of our lecture on Medelian Genetics. We look at who Mendel was, what he did and, how he began to investigate the pricip...

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California Lightworks 800W Solarstorm - exoticgenetix (Afterlife OG) / DNA Genetics (Tangie) Day 43
Holy shit these need to be transplanted!

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Caf scientifique - heart genetics: predicting the future? (audio only)
Caf scientifique Heart genetics: Predicting the future? Caf scientifique at Royal Brompton Harefield NHS Foundation Trust discussing research on how gene...

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Genetics Practice Problems

You may type in your own answers, then check to see if you were right. If youre totally stumped, you can tell the computer to show you the answer to a particular question.

Monohybrid Cross:

In humans, brown eyes (B) are dominant over blue (b)*. A brown-eyed man marries a blue-eyed woman and they have three children, two of whom are brown-eyed and one of whom is blue-eyed. Draw the Punnett square that illustrates this marriage. What is the mans genotype? What are the genotypes of the children?

(* Actually, the situation is complicated by the fact that there is more than one gene involved in eye color, but for this example, well consider only this one gene.)

Testcross:

In dogs, there is an hereditary deafness caused by a recessive gene, d. A kennel owner has a male dog that she wants to use for breeding purposes if possible. The dog can hear, so the owner knows his genotype is either DD or Dd. If the dogs genotype is Dd, the owner does not wish to use him for breeding so that the deafness gene will not be passed on. This can be tested by breeding the dog to a deaf female (dd). Draw the Punnett squares to illustrate these two possible crosses. In each case, what percentage/how many of the offspring would be expected to be hearing? deaf? How could you tell the genotype of this male dog? Also, using Punnett square(s), show how two hearing dogs could produce deaf offspring.

Incomplete Dominance:

Note: at least one textbook Ive seen also uses this as an example of pleiotropy (one gene multiple effects), though to my mind, the malaria part of this is not a direct effect of the gene.

For many genes, such as the two mentioned above, the dominant allele codes for the presence of some characteristic (like, B codes for make brown pigment in someones eyes), and the recessive allele codes for something along the lines of, I dont know how to make that, (like b codes for the absence of brown pigment in someones eyes, so by default, the eyes turn out blue). If someone is a heterozygote (Bb), that person has one set of instructions for make brown and one set of instructions for, I dont know how to make brown, with the result that the person ends up with brown eyes. There are, however, some genes where both alleles code for something. One classic example is that in many flowering plants such as roses, snapdragons, and hibiscus, there is a gene for flower color with two alleles: red and white. However, in that case, white is not merely the absence of red, but that allele actually codes for, make white pigment. Thus the flowers on a plant that is heterozygous have two sets of instructions: make red, and make white, with the result that the flowers turn out mid-way in between; theyre pink.

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Genetics Practice Problems - University of Cincinnati

Population genetics is the study of allele frequency distribution and change under the influence of the four main evolutionary processes: natural selection, genetic drift, mutation and gene flow. It also takes into account the factors of recombination, population subdivision and population structure. It attempts to explain such phenomena as adaptation and speciation.

Population genetics was a vital ingredient in the emergence of the modern evolutionary synthesis. Its primary founders were Sewall Wright, J. B. S. Haldane and R. A. Fisher, who also laid the foundations for the related discipline of quantitative genetics.

Traditionally a highly mathematical discipline, modern population genetics encompasses theoretical, lab and field work. Computational approaches, often using coalescent theory, have played a central role since the 1980s.

Biston betularia f. carbonaria is the black-bodied form of the peppered moth.

Population genetics is the study of the frequency and interaction of alleles and genes in populations.[1] A sexual population is a set of organisms in which any pair of members can breed together. This implies that all members belong to the same species and live near each other.[2]

For example, all of the moths of the same species living in an isolated forest are a population. A gene in this population may have several alternate forms, which account for variations between the phenotypes of the organisms. An example might be a gene for coloration in moths that has two alleles: black and white. A gene pool is the complete set of alleles for a gene in a single population; the allele frequency for an allele is the fraction of the genes in the pool that is composed of that allele (for example, what fraction of moth coloration genes are the black allele). Evolution occurs when there are changes in the frequencies of alleles within a population; for example, the allele for black color in a population of moths becoming more common.

Natural selection will only cause evolution if there is enough genetic variation in a population. Before the discovery of Mendelian genetics, one common hypothesis was blending inheritance. But with blending inheritance, genetic variance would be rapidly lost, making evolution by natural selection implausible. The HardyWeinberg principle provides the solution to how variation is maintained in a population with Mendelian inheritance. According to this principle, the frequencies of alleles (variations in a gene) will remain constant in the absence of selection, mutation, migration and genetic drift.[3] The HardyWeinberg "equilibrium" refers to this stability of allele frequencies over time.

A second component of the HardyWeinberg principle concerns the effects of a single generation of random mating. In this case, the genotype frequencies can be predicted from the allele frequencies. For example, in the simplest case of a single locus with two alleles: the dominant allele is denoted A and the recessive a and their frequencies are denoted by p and q; freq(A)=p; freq(a)=q; p+q=1. If the genotype frequencies are in HardyWeinberg proportions resulting from random mating, then we will have freq(AA)=p2 for the AA homozygotes in the population, freq(aa)=q2 for the aa homozygotes, and freq(Aa)=2pq for the heterozygotes.

Natural selection is the fact that some traits make it more likely for an organism to survive and reproduce. Population genetics describes natural selection by defining fitness as a propensity or probability of survival and reproduction in a particular environment. The fitness is normally given by the symbol w=1-s where s is the selection coefficient. Natural selection acts on phenotypes, or the observable characteristics of organisms, but the genetically heritable basis of any phenotype which gives a reproductive advantage will become more common in a population (see allele frequency). In this way, natural selection converts differences in fitness into changes in allele frequency in a population over successive generations.

Before the advent of population genetics, many biologists doubted that small differences in fitness were sufficient to make a large difference to evolution.[4] Population geneticists addressed this concern in part by comparing selection to genetic drift. Selection can overcome genetic drift when s is greater than 1 divided by the effective population size. When this criterion is met, the probability that a new advantageous mutant becomes fixed is approximately equal to 2s.[5][6] The time until fixation of such an allele depends little on genetic drift, and is approximately proportional to log(sN)/s.[7]

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Population genetics - Wikipedia, the free encyclopedia

Cell therapy hope for rare diseases
Cell therapy hope for rare diseases UK cell therapy trial for rare diseases A trial has begun of a new cell therapy has begun in the UK, and the BBCs Fergus ...

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The Human Genome Project (HGP) is an international scientific research project with a primary goal of determining the sequence of chemical base pairs which make up human DNA, and of identifying and mapping the total genes of the human genome from both a physical and functional standpoint.[1] It remains the largest collaborative biological project.[2]

The first official funding for the Project originated with the US Department of Energys Office of Health and Environmental Research, headed by Charles DeLisi, and was in the Reagan Administrations 1987 budget submission to the Congress.[3] It subsequently passed both Houses. The Project was planned for 15 years.[4]

In 1990, the two major funding agencies, DOE and NIH, developed a memorandum of understanding in order to coordinate plans, and set the clock for initiation of the Project to 1990.[5] At that time David Galas was Director of the renamed Office of Biological and Environmental Research in the U.S. Department of Energys Office of Science, and James Watson headed the NIH Genome Program. In 1993 Aristides Patrinos succeeded Galas, and Francis Collins succeeded James Watson, and assumed the role of overall Project Head as Director of the U.S. National Institutes of Health (NIH) National Human Genome Research Institute. A working draft of the genome was announced in 2000 and a complete one in 2003, with further, more detailed analysis still being published.

A parallel project was conducted outside of government by the Celera Corporation, or Celera Genomics, which was formally launched in 1998. Most of the government-sponsored sequencing was performed in universities and research centres from the United States, the United Kingdom, Japan, France, Germany, Spain and China.[6] Researchers continue to identify protein-coding genes and their functions; the objective is to find disease-causing genes and possibly use the information to develop more specific treatments. It also may be possible to locate patterns in gene expression, which could help physicians glean insight into the body's emergent properties.

The Human Genome Project originally aimed to map the nucleotides contained in a human haploid reference genome (more than three billion). Several groups have announced efforts to extend this to diploid human genomes including the International HapMap Project, Applied Biosystems, Perlegen, Illumina, J. Craig Venter Institute, Personal Genome Project, and Roche-454.

The "genome" of any given individual is unique; mapping "the human genome" involves sequencing multiple variations of each gene.[7] The project did not study the entire DNA found in human cells; some heterochromatic areas (about 8% of the total genome) remain unsequenced.

The project began with the culmination of several years of work supported by the US Department of Energy, in particular workshops in 1984[8] of the US Department of Energy.[9] This 1987 report stated boldly, "The ultimate goal of this initiative is to understand the human genome" and "knowledge of the human is as necessary to the continuing progress of medicine and other health sciences as knowledge of human anatomy has been for the present state of medicine." The proposal was made by Dr. Alvin Trivelpiece and was approved by Deputy Secretary William Flynn Martin. This chart[10] was used in the Spring of 1986 by Trivelpiece, then Director of the Office of Energy Research in the Department of Energy, to brief Martin and Under Secretary Joseph Salgado regarding his intention to reprogram $4 million to initiate the project with the approval of Secretary Herrington. This reprogramming was followed by a line item budget of $16 million the following year. Candidate technologies were already being considered for the proposed undertaking at least as early as 1985.[11]

James D. Watson was head of the National Center for Human Genome Research at the National Institutes of Health in the United States starting from 1988. Largely due to his disagreement with his boss, Bernadine Healy, over the issue of patenting genes, Watson was forced to resign in 1992. He was replaced by Francis Collins in April 1993, and the name of the Centre was changed to the National Human Genome Research Institute (NHGRI) in 1997.

The $3-billion project was formally founded in 1990 by the US Department of Energy and the National Institutes of Health, and was expected to take 15 years.[12] In addition to the United States, the international consortium comprised geneticists in the United Kingdom, France, Australia, Japan and myriad other spontaneous relationships.[13]

Due to widespread international cooperation and advances in the field of genomics (especially in sequence analysis), as well as major advances in computing technology, a 'rough draft' of the genome was finished in 2000 (announced jointly by U.S. President Bill Clinton and the British Prime Minister Tony Blair on June 26, 2000).[14] This first available rough draft assembly of the genome was completed by the Genome Bioinformatics Group at the University of California, Santa Cruz, primarily led by then graduate student Jim Kent. Ongoing sequencing led to the announcement of the essentially complete genome in April 2003, 2 years earlier than planned.[15] In May 2006, another milestone was passed on the way to completion of the project, when the sequence of the last chromosome was published in the journal Nature.[16]

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Human Genome Project - Wikipedia, the free encyclopedia

The science of indirectly manipulating an organism's genes using techniques like molecular cloning and transformation to alter the structure and nature of genes is called genetic engineering. Genetic engineering can bring about a great amount of transformation in the characteristics of an organism by the manipulation of DNA, which is like the code inscribed in every cell determining how it functions. Like any other science, genetic engineering also has pros and cons. Let us look at some of them.

Pros of Genetic Engineering

Better Taste, Nutrition and Growth Rate Crops like potato, tomato, soybean and rice are currently being genetically engineered to obtain new strains with better nutritional qualities and increased yield. The genetically engineered crops are expected to have the capacity to grow on lands that are presently not suitable for cultivation. The manipulation of genes in crops is expected to improve their nutritional value as also their rate of growth. Biotechnology, the science of genetically engineering foods, can be used to impart a better taste to food.

Pest-resistant Crops and Longer Shelf life Engineered seeds are resistant to pests and can survive in relatively harsh climatic conditions. The plant gene At-DBF2, when inserted in tomato and tobacco cells is seen to increase their endurance to harsh soil and climatic conditions. Biotechnology can be used to slow down the process of food spoilage. It can thus result in fruits and vegetables that have a greater shelf life.

Genetic Modification to Produce New Foods Genetic engineering in food can be used to produce totally new substances such as proteins and other food nutrients. The genetic modification of foods can be used to increase their medicinal value, thus making homegrown edible vaccines available.

Modification of Genetic Traits in Humans Genetic engineering has the potential of succeeding in case of human beings too. This specialized branch of genetic engineering, which is known as human genetic engineering is the science of modifying genotypes of human beings before birth. The process can be used to manipulate certain traits in an individual.

Boost Positive Traits, Suppress Negative Ones Positive genetic engineering deals with enhancing the positive traits in an individual like increasing longevity or human capacity while negative genetic engineering deals with the suppression of negative traits in human beings like certain genetic diseases. Genetic engineering can be used to obtain a permanent cure for dreaded diseases.

Modification of Human DNA If the genes responsible for certain exceptional qualities in individuals can be discovered, these genes can be artificially introduced into genotypes of other human beings. Genetic engineering in human beings can be used to change the DNA of individuals to bring about desirable structural and functional changes in them.

Cons of Genetic Engineering

May Hamper Nutritional Value Genetic engineering in food involves the contamination of genes in crops. Genetically engineered crops may supersede natural weeds. They may prove to be harmful for natural plants. Undesirable genetic mutations can lead to allergies in crops. Some believe that genetic engineering in foodstuffs can hamper their nutritional value while enhancing their taste and appearance.

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Pros and Cons of Genetic Engineering - Buzzle

Bookshelf

A collection of biomedical books that can be searched directly or from linked data in other NCBI databases. The collection includes biomedical textbooks, other scientific titles, genetic resources such as GeneReviews, and NCBI help manuals.

A resource to provide a public, tracked record of reported relationships between human variation and observed health status with supporting evidence. Related information intheNIH Genetic Testing Registry (GTR),MedGen,Gene,OMIM,PubMedand other sources is accessible through hyperlinks on the records.

An archive and distribution center for the description and results of studies which investigate the interaction of genotype and phenotype. These studies include genome-wide association (GWAS), medical resequencing, molecular diagnostic assays, as well as association between genotype and non-clinical traits.

An open, publicly accessible platform where the HLA community can submit, edit, view, and exchange data related to the human major histocompatibility complex. It consists of an interactive Alignment Viewer for HLA and related genes, an MHC microsatellite database, a sequence interpretation site for Sequencing Based Typing (SBT), and a Primer/Probe database.

A searchable database of genes, focusing on genomes that have been completely sequenced and that have an active research community to contribute gene-specific data. Information includes nomenclature, chromosomal localization, gene products and their attributes (e.g., protein interactions), associated markers, phenotypes, interactions, and links to citations, sequences, variation details, maps, expression reports, homologs, protein domain content, and external databases.

A collection of expert-authored, peer-reviewed disease descriptions on the NCBI Bookshelf that apply genetic testing to the diagnosis, management, and genetic counseling of patients and families with specific inherited conditions.

Summaries of information for selected genetic disorders with discussions of the underlying mutation(s) and clinical features, as well as links to related databases and organizations.

A voluntary registry of genetic tests and laboratories, with detailed information about the tests such as what is measured and analytic and clinical validity. GTR also is a nexus for information about genetic conditions and provides context-specific links to a variety of resources, including practice guidelines, published literature, and genetic data/information. The initial scope of GTR includes single gene tests for Mendelian disorders, as well as arrays, panels and pharmacogenetic tests.

A database of known interactions of HIV-1 proteins with proteins from human hosts. It provides annotated bibliographies of published reports of protein interactions, with links to the corresponding PubMed records and sequence data.

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Attackaratus by PlantBot Genetics
Attackaratus http://www.monsantra.com This PlantBot is so fierce and hardy that PlantBot Genetic scientists find one they immediately (at great risks to themselves) try to contain it in a sealed...

By: Wendy DesChene

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Attackaratus by PlantBot Genetics - Video

"Genetics", The Nucleus

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"Genetics", The Nucleus - Video