Alliance for Cancer Gene Therapy (ACGT) Thanks Dr. Savio L.C. Woo For His Service; Names Dr. Joseph Glorioso …

Stamford, CT (PRWEB) February 20, 2015

World-renowned scientist and University of Pittsburgh School of Medicine genetics and biochemistry professor Joseph Glorioso III, PhD has been named Chairman of the Scientific Advisory Council at Alliance for Cancer Gene Therapy.

Glorioso, known for his work on the molecular and genetic aspects of the herpes simplex virus and how to better engineer this organism as a vector for transporting therapeutic genes, will take the helm from Dr. Savio L.C. Woo, the founding Chairman of ACGTs Scientific Advisory Council; Dr. Woo has also been named Chairman Emeritus of the Council.

Savio has been a remarkable and dynamic leader who has steered the Council from the beginning to focus on young investigators and groundbreaking clinical translation, Glorioso said. This work has resulted in ACGT pioneering breakthroughs in gene and cell therapy treatments for cancer. We now look forward, to expanding our vision to include later-stage research, which will be very exciting.

Glorioso received his bachelors degree and doctorate from Louisiana State University before joining the University of Michigan Medical School in the late 1970s. He attained the rank of professor and assistant dean for research and graduate studies there, and then joined the University of Pittsburgh School of Medicine in 1989. At Pittsburgh, Glorioso served as Professor and Chair of the Department of Molecular Genetics and Biochemistry, as well as the McEllroy Professorship in Biochemistry until 2009. He continues his groundbreaking work in the development of herpes viral vectors for the treatment of cancer, chronic pain and diseases of the central nervous system. Glorioso has served on ACGTs Scientific Advisory Council since 2005.

Joe has been a valuable member of our Scientific Advisory Council and has made tremendous strides in his own work to improve the quality of life for patients fighting cancer and other diseases; that same vision will advance ACGTs own pursuit of effective cell and gene therapy treatments, said Barbara Netter, President and Co-founder of ACGT.

ACGTs Scientific Advisory Council, composed of preeminent physicians and researchers in cell and gene therapy, serves without remuneration and establishes the scientific criteria for the review of all grants. Council members are also tasked with developing strict accountability guidelines requiring periodic progress reports. At present, the Council is composed of 15 members, including Glorioso.

Based in Stamford, Connecticut, ACGT funds top physicians and researchers at medical institutions in the U.S. and Canada. The Foundation supports a number of gene and cell therapy treatments, including immunotherapy, which activates patients own immune systems to battle cancerous cells. In 2014, the FDA granted fast-track status to 2 immunotherapy treatments for leukemia, for which ACGT provided critical early funding.

About Alliance for Cancer Gene Therapy (ACGT): Established in 2001, ACGT (http://www.acgtfoundation.org) is the nations only not-for-profit dedicated exclusively to cell and gene therapy treatments for all types of cancer. One-hundred percent of contributions go directly to research. ACGT has funded 46 grants in the U.S. and Canada since its founding in 2001 by Barbara Netter, President, and her late husband, Edward, to conduct and accelerate critically needed innovative research. Since its inception, ACGT has awarded 31 grants to Young Investigators and 15 grants to Clinical Investigators, totaling more than $25 million in funding. ACGT is located at 96 Cummings Point Road, Stamford, CT 06902.

ACGT on Facebook: http://www.facebook.com/ACGTfoundation ACGT on Twitter: http://www.twitter.com/ACGTfoundation ACGT on YouTube: http://www.youtube.com/user/ACGTfoundation

See the original post here:

Alliance for Cancer Gene Therapy (ACGT) Thanks Dr. Savio L.C. Woo For His Service; Names Dr. Joseph Glorioso ...

The Clinical Promise of the Gene Therapy from Harrison’s Principles of IM, 19th Edition – Video


The Clinical Promise of the Gene Therapy from Harrison #39;s Principles of IM, 19th Edition
Dr. J. Larry Jameson, editor for Harrison #39;s Principles of Internal Medicine, discusses the clinical promise of the gene therapy. Visit http://www.HarrisonsIM.com to watch more videos of Dr. J. Larry...

By: McGrawHIllPro

The rest is here:

The Clinical Promise of the Gene Therapy from Harrison's Principles of IM, 19th Edition - Video

Gene study finds link with implications for melanoma therapy

Lawrence, KS (PRWEB) February 18, 2015

Pediatric and Developmental Pathology An odd-looking or changing mole or birthmark is always worrisome, particularly on a child. While most are benign, cancer jumps into every parents mind. Gene studies and potential related therapies are just one front in the wide-ranging battle against melanoma.

An analysis in the new issue of the journal Pediatric and Developmental Pathology looks at the link between the typical clinical features of two diseases and the status of two genes. In their study, researchers confirmed that a mutation of the BRAF gene affects people with large or giant birthmarks known as congenital melanocytic nevi (CMNs) and, for the first time, they also found this mutation present in neurocutaneous melanocytosis, a rare neurological disorder associated with Large/Giant CMNs. They suggest that it may be possible to target the BRAF gene during therapy.

CMNs are literally birthmarks, developing in the womb as a fetus grows. Such a dark-colored, sometimes hairy, patch of skin can continue to develop as the child grows, and if it reaches 20 cm or more, it is classified as large or giant. Although usually benign at birth, they can associate with a range of other problems, from decreased sweating and tissue growth to a greater likelihood of melanoma, a skin cancer that is becoming increasingly common worldwide among adults and even teenagers. Neurocutaneous melanocytosis, in which the pigment cells rapidly spread across the brain, spinal cord and meninges, can also develop.

The current study collected pigmented tissue from 66 patients with Large/Giant CMN. The authors first looked for the more commonly mutated NRAS gene and then evaluated those tissues without NRAS mutation for BRAF mutation.

The authors found a new link between BRAF mutations and aggressive disease pattern. They learned of a definite association between the BRAF gene and large or giant CMNs. They also discovered, for the first time, that some patients with neurocutaneous melanocytosis had BRAF but not NRAS mutation. Race was a factor in the appearance of a mutational group, with Asians less likely to show the BRAF mutation.

Surprisingly, more nodules were found in the pigmented skin among people who had the BRAF mutation than among those with the NRAS mutation. Less hair was also found with the BRAF mutation.

The authors concluded that not only NRAS mutations can occur in the studied conditions. They also learned that BRAF mutations may be responsible for more serious disease than previously thought. They said that this means it may be possible to use BRAF inhibitors to target the mutated BRAF gene when treating patients with large or giant CMNs.

Full text of the article BRAF mutations are also associated with neurocutaneous melanocytosis and large/giant congenital melanocytic nevi, Pediatric and Developmental Pathology, Vol. 18, No. 1, 2014, is now available.

###

See original here:

Gene study finds link with implications for melanoma therapy

Synthetic biology yields new approach to gene therapy

10 hours ago by Amanda Siegfried Dr. Leonidas Bleris (left), assistant professor of bioengineering at UT Dallas,and Richard Taplin Moore MS11 helped create a new delivery system that may change gene therapy.

Bioengineers at The University of Texas at Dallas have created a novel gene-delivery system that shuttles a gene into a cell, but only for a temporary stay, providing a potential new gene-therapy strategy for treating disease.

The approach offers distinct advantages over other types of gene therapies under investigation, said Richard Taplin Moore MS'11, a doctoral student in bioengineering in the Erik Jonsson School of Engineering and Computer Science. He is lead author of a study describing the new technique in the Jan. 30 issue of the journal Nucleic Acids Research.

"In other gene therapy approaches, the therapeutic genetic messages being delivered can persist for a long time in the patient, potentially lasting for the patient's entire lifetime," Moore said. "This irreversibility is one reason gene therapies are so difficult to get approved."

The UT Dallas study describes proof-of-concept experiments in which a gene carrying instructions for making a particular protein is ordered to self-destruct once the cell has "read" the instructions and made a certain quantity of the protein. In its experiments with isolated human kidney cells, the research team successfully deliveredand then destroyeda test gene that makes a red fluorescent protein.

More research is needed to determine whether and how well the system might work in living organisms. But Moore said the ultimate goal is to refine the method to deliver genes that produce therapeutic proteins or drugs. The nature of the gene delivery system offers more control over how much protein the gene produces in cells or tissues. Because it does not alter the cell permanently, the method also sidesteps potential health problems that can occur if a gene is delivered to the wrong place in a cell's genome.

"Our goal was to create a delivery system for therapeutic genes that would self-destruct, giving us more control over the delivered DNA by limiting the time it resides in cells," Moore said.

Located in the nucleus of each human cell, genes are made of DNA and contain instructions for making proteins. Machinery inside each cell "reads" the instructions and builds those proteins, which then carry out various functions needed to sustain life. Defective or mutated genes can result in malfunctioning or missing proteins, leading to disease.

Gene therapy aims to replace defective genes with healthy versions. Typically the good genes are packaged with a delivery mechanism called a vector, which transports the genetic material inside cells. With traditional approaches, once in the cell, the gene permanently integrates itself into the cell's DNA.

Although promising, this type of gene therapy also has risks. If a therapeutic gene is inserted in the wrong place in the cell's DNA, such as too close to a cancer-related gene, the process could activate additional disease-causing genes, resulting in lifelong health problems for the patient. While many gene therapy clinical trials are underway worldwide, the Food and Drug Administration has not approved for sale any human gene therapy product in the U.S.

Visit link:

Synthetic biology yields new approach to gene therapy

Cancer gene therapy advances

Flow chart of one method of engineering T cells to fight cancer.

Tough blood cancers are responding to treatment with the patient's own genetically engineered immune cells, according to a cancer specialist who is helping test the bold -- and risky -- approach.

The treatment has produced complete remissions in large percentages of patients treated, up to 90 percent in one group of 30 patients. Moreover, these are all extremely sick patients, whose cancer has resisted other therapies, leaving them with virtually no options. The longest survivor has been in complete remission for more than 4 years, said Dr. David Porter of the University of Pennsylvania.

Porter spoke Sunday at the 35th Annual Conference on Clinical Hematology & Oncology, held in La Jolla by Scripps Health. Speakers like Porter came from around the country to discuss advances in their field, part of a continuing medical education program to keep doctors up to date with the latest medical advances. The conference continues through Tuesday.

Dr. David Porter / University of Pennsylvania

Porter works with Dr. Carl June and other colleagues to hone the effectiveness of using T cells genetically programmed to attack malignant B cells. B cell malignancies cause such cancers as chronic lymphocytic leukemia, or CLL; acute lymphoblastic leukemia, or ALL, and non-Hodgkin's lymphoma.

The genetically altered T cells are given an artificially created gene to produce a chimeric antigen receptor. This receptor recognizes the protein CD19, produced almost exclusively on B cells. The T cells hone in on this protein and kill the B cells. When the cancer is knocked down, some of the T cells remain behind, ready to pounce on any recurrence.

The trials are now expanding to include myloma, Porter said. For more information on the university's T cell-based clinical trials, go to http://www.penncancer.org/tcelltherapy.

June's team began testing the therapy in 2010 in CLL patients and then in those with ALL. These were all patients with relapsed cancers that had become resistant to other therapies. The therapy has been progressively refined, Porter said. Other centers have developed their own versions of this therapy.

In October, 2014, the University of Pennsylvania and Children's Hospital of Philadelphia announced that 27 out of 30 patients with relapsed ALL achieved a complete remission within one month of treatment, and 23 were still alive 6 months after treatment. As of October, 19 of the patients remained in remission. Most treated, 25 out of 30, were children. The response rate with CLL is about 47 percent, Porter said.

Read more:

Cancer gene therapy advances

Genetic counseling: DNA testing for the patient

Proc (Bayl Univ Med Cent). 2005 Apr; 18(2): 134137.

1From the Department of Pathology, The University of Texas Southwestern Medical Center, Dallas, Texas.

Presented at the Department of Pathology Fall Symposium, Baylor University Medical Center, November 23, 2004.

Genetic counseling deals with the human problems associated with the occurrence, or the risk of occurrence, of a genetic disorder in the family (1). Genetic counseling is essentially a communication processabout medical facts, the contribution of heredity to certain conditions, the interpretation of test results, and the options available. It also involves supportive counseling to enable patients to make decisions and to make the best possible adjustment to the presence or risk of genetic disease. Genetic counselors have master's degrees from certified programs and are certified by either the American Board of Medical Genetics or the American Board of Genetic Counseling.

This article reviews several case scenarios in order to highlight some themes and lessons from genetic counseling.

In recent years, obstetricians have begun offering cystic fibrosis carrier screening to all couples either planning a pregnancy or in the early stages of pregnancy. The incidence of cystic fibrosis in Caucasians is about 1 in 2500. Caucasian men and women with no family history of cystic fibrosis would each have a 1 in 25 chance of being a carrier, i.e., of having one of over 1300 different mutations in the CFTR gene. The screening test usually includes analysis for only 23 to 25 of the most common mutations. At this time, sequencing the gene from beginning to end to search for a mutation would be too expensive and time consuming as a screening test.

The decision to undergo carrier screening is a personal one. Some people consider cystic fibrosis a serious disorder appropriate for screening, and others do not. Those who do not may focus on the fact that half of those with the disease survive until the age of 30 or 31, and cystic fibrosis does not involve mental retardation or birth defects. A couple may opt for screening for one or several reasons: because the chance of being a carrier seems high to them, because they would consider prenatal diagnosis if they were shown to be carriers, or because results are usually reassuring. Similarly, those who don't feel the odds of being a carrier are high enough may not be interested in the screening test. Others may not be interested because the cost is not covered by their insurance, the test is imperfect and will not identify all carriers, or they would rather not have the information. Indeed, getting information can provoke anxiety, and some patients prefer not to go down that path.

Some practitioners discourage screening unless the patient plans to pursue prenatal diagnosis. However, my experience has shown that people often change their minds. Some come in with very set ideas about what they would and would not do; until they're faced with a particular circumstance, they may not re-ally know. The point is, options need to be made available.

We will discuss a case in which the woman was screened and found to have mutation G542X (Figure ). This means that in the 542 amino acid position, glycine has been converted to a stop codon. She is a cystic fibrosis carrier. Since cystic fibrosis is an autosomal recessive disorder, this should not affect her health. However, her husband was subsequently screened, and he was shown to have the most common mutation, F508, a deletion of phenylalanine at position 508. Even though they have different mutations, the mutations are in the same gene. The child now has a 1 in 4 risk of inheriting both mutations and therefore having cystic fibrosis.

Pedigree of a couple presenting for carrier screening for cystic fibrosis. (See discussion in the text.) Squares represent males, circles represent females, diamonds are used when the gender is unknown or unspecified, and a P within ...

Read this article:

Genetic counseling: DNA testing for the patient

LYSOGENE, UMM and AU Collaborate To Develop IND-supporting Preclinical Studies In GM1-gangliosidosis

Collaboration entails development of gene therapy treatment for severe neurodegenerative disease GM1-gangliosidosis

LYSOGENE, a leading, clinical stage gene therapy biotechnology company committed to the development and commercialization of breakthrough treatments for severe orphan pathologies affecting the central nervous system (CNS), recently announced that it has entered into a strategic collaboration with the University of Massachusetts Medical School (UMMS) in Worcester, Massachusetts, and Auburn University (AU) in Auburn, Alabama. Through the collaboration, LYSOGENE, UMMS and AU will develop IND-supporting preclinical studies in GM1-gangliosidosis, a rare, inherited disorder characterized by severe neurological impairment, using adeno-associated virus (AAV) gene therapy technology.

The collaboration will combine LYSOGENEs outstanding translational and clinical expertise in gene therapy for CNS disorders with the unique preclinical expertise and infrastructure of UMMS and AU to design and test innovative AAV-based gene therapy approaches to treat GM1-gangliosidosis.

The development of a potential treatment for GM1-gangliosidosis using AAV gene therapy was initiated in 2005 by Miguel Sena-Esteves, PhD, associate professor in the Neurology Department and the Gene Therapy Center at UMMS, and Douglas R. Martin, PhD, associate professor in the Scott-Ritchey Research Center and Department of Anatomy, Physiology & Pharmacology at AU. The approach developed by the investigators uses AAV vectors to treat the entire brain and spinal cord after injection of only a few intracranial sites. Preclinical studies demonstrated a remarkable extension in lifespan from 8 months in untreated GM1 cats to greater than 4.5 years in AAV-treated cats, with dramatic improvements in quality of life. Results were published in Science Translational Medicine in 2014 (McCurdy, V.J., et al., Sustained normalization of neurological disease after intracranial gene therapy in a feline model. Science Translational Medicine, 2014. 6(231): p. 231ra48).

We are thrilled by our collaboration with University of Massachusetts Medical School and Auburn University, which constitutes a significant step towards the development of a treatment for patients affected with GM1-gangliosidosis, a severely debilitating disease. For each of these patients and their families, there is currently no option and an urgent need for a safe and effective therapy, said Karen Aiach, founding president and CEO of LYSOGENE. AAV-based therapies are particularly suitable for inherited disorders of the CNS. In this new program, LYSOGENE will leverage its unique capacity to develop these therapies and bring them to patients with unmet needs. We will also reinforce our scientific and technology base through our collaboration with leaders in the field.

Collaborating with LYSOGENE will allow us to leverage their clinical and translational expertise and advance the development of a gene transfer therapy for treating patients affected with GM1-gangliosidosis, said Sena-Esteves. In our minds, what ultimately matters is the ability to deliver a potential treatment to the children suffering from this horrible disease. Ultimately, thats what drives us all.

About Gangliosidosis with GM1 GM1-gangliosidosis is a rare inherited neurodegenerative disorder characterized by severe cognitive and motor developmental delays resulting in death of most patients at a very young age.

It is caused by mutations in the GLB1 gene, which encodes an enzyme called beta-galactosidase necessary for recycling of a molecule (GM1-ganglioside) in neurons. This brain lipid is indispensable for normal function, but its overabundance causes neurodegeneration, resulting in the severe neurological symptoms of GM1-gangliosidosis.

GM1 affects 1 in 100,000 - 200,000 newborns and is inherited in an autosomal recessive pattern. GM1-gangliosidosis can be classified into three major clinical phenotypes according to the age of onset and severity of symptoms: Type I (infantile), Type II (late infantile/juvenile) and Type III (adult). There is currently no treatment for this disease.

About LYSOGENE LYSOGENE is a clinical stage biotechnology company committed to the development and commercialization of innovative therapies for patients affected with rare disorders and high unmet medical needs. LYSOGENEs team translated its rAAVrh10 lead product for Sanfilippo from bench to bedside in an unprecedented fashion over the last years. Its lead product is for Sanfilippo syndrome, a neurodegenerative lysosomal storage disorder considered to be a perfect model for gene therapy. LYSOGENE is currently expanding its pipeline to additional diseases with high unmet medical needs. Lysogene was launched in 2009. It completed a Series A financing in May 2014 with leading life sciences investors Sofinnova Partners, BPI Innobio and Novo AIS.

View original post here:

LYSOGENE, UMM and AU Collaborate To Develop IND-supporting Preclinical Studies In GM1-gangliosidosis

Precise gene transfer into therapy relevant cells after vector injection into blood

10.02.2015 - (idw) Paul-Ehrlich-Institut - Bundesinstitut fr Impfstoffe und biomedizinische Arzneimittel

Therapeutic gene transfer is considered as a promising novel strategy to treat genetic disorders and cancer. So far, target cells are often isolated from patients for this purpose, and re-administered after gene transfer. In collaboration with colleagues from the Universities of Cologne and Zurich, researchers at the Paul-Ehrlich-Institut have succeeded in developing gene transfer vehicles that target the therapy relevant cell type directly in the organism. The resulting gene transfer occurs with an extremely high degree of selectivity. A report on the research results can be found in Nature Communications in its online edition of 10.02.2015. Vectors derived from adeno-associated viruses (AAV) were used as vehicles for targeted gene transfer by the research group of Professor Christian J. Buchholz, Principal Investigator at the LOEWE Centre for Cell and Gene Therapy at Frankfurt am Main and head of the Section Molecular Biotechnology and Gene Therapy of the President of the Paul-Ehrlich-Institut. AAV is a non-pathogenic parvovirus. The only gene therapy medicinal product authorised in Europe so far, is also based on AAV gene vectors and intended for the treatment of a rare metabolic disorder.

The strategy for the generation of the new precision gene vectors was developed and implemented jointly with Dr Hildegard Bning, head of the AAV Vector Development Research Group at the ZMMK (Zentrum fr Molekulare Medizin Kln, Center for Molecular Medicine Cologne) of the University of Cologne: Through exchange of two amino acids, AAV lost its ability to bind to its natural receptor and became thereby unable to penetrate its broad range of natural target cells. Novel target structures (DARPins, designed ankyrin repeat proteins) were then attached to the surface of the modified vector particles. These structures were developed at Zurich University. The structures can be selected in such a way that they mediate a selective binding of the DARPin-containing AAV vector particles to the therapy relevant cell type only. This is what enables the AAV vector to attach to and penetrate the desired target cell. The paper referenced here reports on the use of three different DARPins, which equipped AAV vectors either with a specificity for Her2/neu, a tumour marker in breast cancer, for EpCAM, an epithelial surface protein, or for a marker of particular blood cells (CD4 on the surface of lymphocytes with distinct immunological functions).

The desired goal of a cell type specific in vivo gene transfer was also achieved with the blood cell targeted vector: AAV transferred the gene only into lymphocytes present in spleen carrying the CD4 protein target structure.

The method developed by us jointly is a very promising tool both in fundamental research and for the targeted gene transfer in medicine, explained Dr Buchholz with regard to the current research results.

Original Publication

Mnch RC, Muth A, Muik A, Friedel T, Schmatz J, Dreier B, Trkola A, Plckthun A, Bning H, Buchholz CJ (2015): Off-target-free gene delivery by affinity-purified receptor-targeted viral vectors. Nat Commun Feb 10 [Epub ahead of print]. http://www.nature.com/ncomms/2015/150210/ncomms7246/full/ncomms7246.html

The Paul-Ehrlich-Institut, Federal Institute for Vaccines and Biomedicines in Langen near Frankfurt/Main, is a senior federal authority reporting to the Federal Ministry of Health (Bundesministerium fr Gesundheit, BMG). It is responsible for the research, assessment, and marketing authorisation of biomedicines for human use and veterinary vaccines. Its remit also includes the authorisation of clinical trials and pharmacovigilance, i.e. recording and evaluation of potential adverse effects. Other duties of the institute include official batch control, scientific advice and inspections. In-house experimental research in the field of biomedicines and life science form an indispensable basis for the varied and many tasks performed at the institute. The PEI, with its roughly 800 staff, also has advisory functions at a national level (federal government, federal states (Lnder)), and at an international level (World Health Organisation, European Medicines Agency, European Commission, Council of Europe etc.). Weitere Informationen:http://www.pei.de

Follow this link:

Precise gene transfer into therapy relevant cells after vector injection into blood

How Origami is Inspiring Scientific Creativity, with BYU and Origami Artist Robert Lang – Video


How Origami is Inspiring Scientific Creativity, with BYU and Origami Artist Robert Lang
Ancient origami inspires surprising modern innovations like solar arrays for NASA and a microscopic nanoinjector that can be used in gene therapy. These origami-inspired designs from Brigham...

By: BYU

Follow this link:

How Origami is Inspiring Scientific Creativity, with BYU and Origami Artist Robert Lang - Video

David Baltimore (Cal Tech) Part 2: Why Gene Therapy Might be a Reasonable Tool for Attacking HIV – Video


David Baltimore (Cal Tech) Part 2: Why Gene Therapy Might be a Reasonable Tool for Attacking HIV
http://www.ibiology.org/ibioseminars/microbiology/david-baltimore-part-2.html Lecture Overview: In this set of lectures, I describe the threat facing the wor...

By: iBiology

Follow this link:

David Baltimore (Cal Tech) Part 2: Why Gene Therapy Might be a Reasonable Tool for Attacking HIV - Video

The Basics on Genes and Genetic Disorders

Have people ever said to you, "It's in your genes"? They were probably talking about a physical characteristic, personality trait, or talent that you share with other members of your family.

We know that genes play an important role in shaping how we look and act and even whether we get sick. Now scientists are trying to use that knowledge in exciting new ways, such as treating health problems.

To understand how genes work, let's review some biology basics. Most living organisms are made up of cells that contain a substance called deoxyribonucleic (pronounced: dee-AHK-see-rye-bow-noo-KLEE-ik) acid (DNA).

DNA contains four chemicals (adenine, thymine, cytosine, and guanine called A, T, C, and G for short) that are strung in patterns on extremely thin, coiled strands in the cell. How thin? Cells are tiny invisible to the naked eye and each cell in your body contains about 6 feet of DNA thread, for a total of about 3 billion miles of DNA inside you!

So where do genes come in? Genes are made of DNA, and different patterns of A, T, G, and C code for the instructions for making things your body needs to function (like the enzymes to digest food or the pigment that gives your eyes their color). As your cells duplicate, they pass this genetic information to the new cells.

DNA is wrapped together to form structures called chromosomes. Most cells in the human body have 23 pairs of chromosomes, making a total of 46. Individual sperm and egg cells, however, have just 23 unpaired chromosomes. You received half of your chromosomes from your mother's egg and the other half from your father's sperm cell. A male child receives an X chromosome from his mother and a Y chromosome from his father; females get an X chromosome from each parent.

Genes are sections or segments of DNA that are carried on the chromosomes and determine specific human characteristics, such as height or hair color. Because you have a pair of each chromosome, you have two copies of every gene (except for some of the genes on the X and Y chromosomes in boys, because boys have only one of each).

Some characteristics come from a single gene, whereas others come from gene combinations. Because every person has about 25,000 different genes, there is an almost endless number of possible combinations!

Original post:

The Basics on Genes and Genetic Disorders