Archive for the ‘Gene Therapy Research’ Category

ScienceDaily (May 7, 2012) The cells that slough off from a cancerous tumor into the bloodstream are a genetically diverse bunch, Stanford University School of Medicine researchers have found. Some have genes turned on that give them the potential to lodge themselves in new places, helping a cancer spread between organs. Others have completely different patterns of gene expression and might be more benign, or less likely to survive in a new tissue. Some cells may even express genes that could predict their response to a specific therapy. Even within one patient, the tumor cells that make it into circulating blood vary drastically.

The finding underscores how multiple types of treatment may be required to cure what appears outwardly as a single type of cancer, the researchers say. And it hints that the current cell-line models of human cancers, which showed patterns that differed from the tumor cells shed from human patients, need to be improved upon.

The new study, published May 7 in PLoS ONE, is the first to look at so-called circulating tumor cells one by one, rather than taking the average of many of the cells. And it's the first to show the extent of the genetic differences between such cells.

"Within a single blood draw from a single patient, we're seeing heterogeneous populations of circulating tumor cells," said senior study author Stefanie Jeffrey, MD, professor of surgery and chief of surgical oncology research.

For over a century, scientists have known that circulating tumor cells, or CTCs, are shed from tumors and move through the bloodstreams of cancer patients. And over the past five years, there's been a growing sense among many cancer researchers that these cells -- accessible by a quick blood draw -- could be the key to tracking tumors non-invasively. But separating CTCs from blood cells is hard; there can be as few as one or two CTCs in every milliliter of a person's blood, mixed among billions of other blood cells.

To make their latest discovery, Jeffrey, along with an interdisciplinary team of engineers, quantitative biologists, genome scientists and clinicians, relied on a technology they developed in 2008. Called the MagSweeper, it's a device that lets them isolate live CTCs with very high purity from patient blood samples, based on the presence of a particular protein -- EpCAM -- that's on the surface of cancer cells but not healthy blood cells.

With the goal of studying CTCs from breast cancer patients, the team first tested whether they could accurately detect the expression levels of 95 different genes in single cells from seven different cell-line models of breast cancer -- a proof of principle since they already knew the genetics of these tumors. These included four cell lines generally used by breast cancer researchers and pharmaceutical scientists worldwide and three cell lines specially generated from patients' primary tumors.

"Most researchers look at just a few genes or proteins at a time in CTCs, usually by adding fluorescent antibodies to their samples consisting of many cells," said Jeffrey. "We wanted to measure the expression of 95 genes at once and didn't want to pool our cells together, so that we could detect differences between individual tumor cells."

So once Jeffrey and her collaborators isolated CTCs using the MagSweeper, they turned to a different kind of technology: real-time PCR microfluidic chips, invented by a Stanford collaborator, Stephen Quake, PhD, professor of bioengineering. They purified genetic material from each CTC and used the high-throughput technology to measure the levels of all 95 genes at once. The results on the cell-line-derived cells were a success; the genes in the CTCs reflected the known properties of the cell-line models. So the team moved on to testing the 95 genes in CTCs from 50 human breast cancer patients -- 30 with cancer that had spread to other organs, 20 with only primary breast tumors.

"In the patients, we ended up with a subset of 31 genes that were most dominantly expressed," said Jeffrey. "And by looking at levels of those genes, we could see at least two distinct groups of circulating tumors cells." Depending on which genes they used to divide the CTCs into groups, there were as many as five groups, she said, each with different combinations of genes turned on and off. And if they'd chosen genes other than the 95 they'd picked, they likely would have seen different patterns of grouping. However, because the same individual CTCs tended to group together in multiple different analyses, these cells likely represent different types of spreading cancer cells.

Originally posted here:
Not all tumor cells are equal: Huge genetic diversity found in cells shed by tumors

Michael Pacanowski, PharmD, MPH; Shashi Amur, PhD; Issam Zineh, PharmD, MPH Author Affiliations: Genomics Group, Office of Clinical Pharmacology, Office of Translational Sciences, Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland.

Treatment of chronic hepatitis C (CHC) is a prototype for personalized medicine. Combination therapy with peginterferon alfa plus ribavirin was the standard of care for more than a decade. Greater understanding of the disease and determinants of treatment response have improved sustained virologic response (SVR) rates from less than 10% with interferon alfa in the 1990s to more than 80% with contemporary triple therapy regimens that include direct acting antivirals (DAAs) (Figure). Patient-specific factors such as viral genotype and early on-treatment responses are considered in therapeutic individualization. New approaches to search the human genome for predictors of drug response led to the discovery that single-nucleotide polymorphisms (SNPs) near the host IL28B gene are among the strongest predictors of response to peginterferon alfa and ribavirin. This Viewpoint discusses the evolution of CHC pharmacogenetics, its real-time incorporation into recent regulatory science evaluations, and its application in future drug development.

cDNA indicates complementary

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New Genetic Discoveries and Treatment for Hepatitis C [Viewpoint]

Dell:

WHAT The team of parents, genetic and translational medicine scientists and pediatric oncologists trailblazing personalized medicine in the treatment of deadly pediatric cancers is convening in Austin to discuss the status of the worlds first personalized medicine clinical trial for pediatric cancer and plan next steps at the NMTRC Symposium 2012. Neuroblastoma affects 1 in 100,000 children and is responsible for 1 in 7 pediatric cancer deaths.

WHO Parents, advocates, oncologists from the Neuroblastoma and Medulloblastoma Translational Research Consortium (NMTRC) and biomedical researchers from the Translational Genomics Research Institute (TGen), who are using high performance computing and cloud technology from Dell to identify targeted treatments based on the specific genetic vulnerabilities of each childs tumoran approach that could be used to treat all pediatric and adult cancers in the future.

WHY Personalized medicinetreatment based on the specific vulnerabilities of each tumor is overcoming longstanding barriers to treatment of pediatric cancer. There has been only one new treatment for pediatric cancer approved by the FDA since the 1980s, compared to 50 treatments approved for adult cancer in this same timeframe. As a result, pediatric oncologists use treatments designed for adults to treat children, with toxic side effects that are frequently as physically detrimental to the child as the cancer itself.

WHEN The following events will be available via live-stream: May 16 1-2 pm CT: Keynote: Molecular-Profiling for Optimized Precision Therapy, Dr. Timothy Triche, University of Southern California/ Childrens Hospital Los Angeles

2-4 pm CT: Panel Discussion: Kids Cloud: Access to Data Boundaries Dr. Melinda Merchant - National Cancer Institute Dr. Gary Marchant - Arizona State University Nancy Goodman - Kids V. Cancer Foundation Patrick Lacey - Friends of Will Foundation Andy Mikulak - Maxs Ring of Fire Foundation Dr. Giselle Sholler - Van Andel Institute Dr. Spyro Mousses - Translational Genomics Research Institute Dr. James Coffin - Dell

WHERE Participate and join the conversation via the #HealthCloud hashtag on Twitter. Tune in via Live-Stream here: http://www.fittotweet.com/live/nmtrc/.

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Innovators in Pediatric Cancer to Share Progress on Ground-Breaking Personalized Medicine Clinical Trial

Public release date: 7-May-2012 [ | E-mail | Share ]

Contact: David Sampson ajpmedia@elsevier.com 215-239-3171 Elsevier Health Sciences

Philadelphia, PA, May 7, 2012 While active monitoring of serum prostate specific antigen (PSA) levels in men over 50 has greatly improved early detection of prostate cancer, prediction of clinical outcomes after diagnosis remains a major challenge. Researchers from the University of Pittsburgh School of Medicine have found that a genetic abnormality known as copy number variation (CNV) in prostate cancer tumors, as well as in the benign prostate tissues adjacent to the tumor and in the blood of patients with prostate cancer, can predict whether a patient will experience a relapse, and the nature of the relapse aggressive or indolent. Their report is published in the June issue of The American Journal of Pathology.

Copy number variations are large areas of the genome with either duplicated or missing sections of DNA. "Our analysis indicates that CNV occurred in both cancer and non-cancer tissues, and CNV of these tissues predicts prostate cancer progression," says lead investigator Jian-Hua Luo, MD, PhD, associate professor in the Divisions of Molecular and Cellular Pathology, and Anatomic Molecular Pathology, Department of Pathology, University of Pittsburgh School of Medicine. "Prediction models of prostate cancer relapse, or of the rate of PSA level increase after surgery, were generated from specific CNV patterns in tumor or benign prostate tissues adjacent to cancer samples."

To detect the abnormalities, scientists conducted a comprehensive genome analysis on 238 samples obtained from men undergoing radical prostatectomy: 104 prostate tumor samples, 85 blood samples from patients with prostate cancer, and 49 samples of benign prostate tissues adjacent to a tumor. A third of the samples were from patients exhibiting recurrence with a PSA level increasing at a rapid rate, doubling in less than four months (rapid increases are associated with lethal prostate cancer); a third from patients exhibiting recurrence with a PSA level increasing at a slow rate, doubling time greater than 15 months; and a third with no relapse more than five years after surgery. Three commercially available prostate cancer cell lines were also tested to validate the results.

Deletions of large segments of specific chromosomes occurred with high frequency, whereas amplification of other chromosomes occurred in only a subset of prostate cancer samples. Similar amplification and deletion of the same regions also occurred in benign prostate tissue samples adjacent to the cancer. Prostate cancer patients' blood was found to contain significant CNVs. Most were not unique and overlapped with those of prostate cancer samples.

Using gene-specific CNV from tumor, the model correctly predicted 73% of cases for relapse and 75% of cases for short PSA doubling time. The CNV model from tissue adjacent to the prostate tumor correctly predicted 67% of cases for relapse and 77% of cases for short PSA doubling time. Using median-size CNV from blood, the genome model correctly predicted 81% of the cases for relapse and 69% of the cases for short PSA doubling time.

Dr. Luo notes that there are several potential clinical applications using CNV tests. "For a patient diagnosed with prostate cancer, CNV analysis done on blood or normal tissues would eliminate the need for additional invasive procedures to decide a treatment mode. For a patient already having a radical prostatectomy, CNV analysis on the tumor or blood sample may help to decide whether additional treatment is warranted to prevent relapse. Despite some limitations, including the need for high quality genome DNA, CNV analysis on the genome of blood, normal prostate, or tumor tissues holds promise to become a more efficient and accurate way to predict the behavior of prostate cancer."

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Genetic abnormalities in benign or malignant tissues predict relapse of prostate cancer

07-05-2012 15:43 Jonathan Kahn, Professor at Hamline University School of Law, frames how the relationship between genetics and society should be understood in an opening plenary at the 2010 Tarrytown Meeting. The Tarrytown Meetings bring together people working to ensure that human biotechnologies and related emerging technologies support rather than undermine social justice, equality, human rights, ecological integrity and the common good. Find out more about the Tarrytown Meetings here: To find more videos, check out the Tarrytown Youtube channel:

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Jonathan Kahn: Setting the Stage for Understanding Genetic Technologies- Tarrytown 2010 - Video

CAMBRIDGE, Mass. & BOTHELL, Wash.--(BUSINESS WIRE)--

Millennium: The Takeda Oncology Company, a wholly owned subsidiary of Takeda Pharmaceutical Company Limited (TSE:4502) and Seattle Genetics, Inc. (Nasdaq: SGEN - News), today announced the initiation of an international pivotal phase 3 clinical trial evaluating ADCETRIS (brentuximab vedotin) in patients with CD30-expressing cutaneous T-cell lymphoma (CTCL) who received at least one prior systemic therapy. The global multi-center study with ADCETRIS, an antibody-drug conjugate (ADC) directed to CD30, will be conducted in the United States, Europe, Australia and Brazil. The trial is being conducted under a Special Protocol Assessment (SPA) agreement from the U.S. Food and Drug Administration (FDA) regarding the trial design. The study also received European Medicines Agency (EMA) scientific advice.

Millennium is pleased to announce the initiation of the pivotal trial of ADCETRIS in patients with relapsed CD30-expressing CTCL. We recognize this as a significant milestone in our efforts to explore the potential of this targeted therapy in other indications, said Karen Ferrante, MD, Chief Medical Officer, Millennium. Looking forward, this study may support the potential to supplement therapeutic options for patients, from traditional systemic chemotherapy to ADCETRIS, a targeted therapy.

Data from patients with cutaneous lesions observed in our pivotal trial in systemic anaplastic large cell lymphoma (sALCL) and interim data from investigator-sponsored trials in CTCL with ADCETRIS provide a strong rationale for initiating this phase 3 trial, said Thomas C. Reynolds, M.D., Ph.D., Chief Medical Officer, Seattle Genetics. CTCL is an important part of our development plan to broadly evaluate ADCETRIS in CD30-expressing malignancies. This trial complements many other ongoing and planned trials for patients in need, including two additional phase 3 trials for front-line Hodgkin lymphoma (HL) and front-line mature T-cell lymphomas expected to start by late 2012 or early 2013.

CD30 is a member of the tumor necrosis factor receptor (TNFR) family and is a characteristic cell surface receptor for activated T-cells and B-cells, including the malignant cells of HL and sALCL. According to published literature, up to 50 percent of CTCL patients lesions express CD30(1-3). Under a previously announced collaboration agreement with Ventana Medical Systems, Inc. (Ventana), Millennium and Seattle Genetics, Ventana is developing a molecular companion diagnostic test for use in this CTCL patient population.

Study design

The study is a randomized, open-label, phase 3 trial of ADCETRIS versus investigators choice of methotrexate or bexarotene in patients with CD30-positive CTCL, including those with primary cutaneous anaplastic large cell lymphoma (pcALCL) or mycosis fungoides (MF). The primary endpoint of the study is overall response rate (ORR), lasting at least 4 months, with ADCETRIS in patients with CD30-positive MF or pcALCL compared to that achieved with therapy in the control arm. The key secondary endpoints are complete response (CR), progression-free survival (PFS), and burden of symptoms. Approximately 124 patients will be enrolled in the pivotal trial.

For more information about the trial, please visit http://www.clinicaltrials.gov.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

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Millennium and Seattle Genetics Initiate Global Phase 3 Trial of ADCETRIS™ in Patients with CD30-Expressing Relapsed ...

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (Nasdaq:SGEN - News) today reported financial results for the first quarter ended March 31, 2012. The company also highlighted the ADCETRIS (brentuximab vedotin) product launch, ongoing and planned clinical development activities and upcoming milestones.

First quarter 2012 ADCETRIS net product sales were $34.5 million, an increase of 4 percent from $33.2 million in the fourth quarter of 2011. ADCETRIS gross product sales increased by 12 percent in the first quarter of 2012 compared to the fourth quarter of 2011, but this increase was offset by an expected increase in gross-to-net discount in the first quarter of 2012 driven by Public Health Services program discounts that became effective during January.

The commercialization of ADCETRIS continues to be strong, and we are pleased by the acceptance and utilization of ADCETRIS among oncologists and patients with relapsed Hodgkin lymphoma (HL) and systemic anaplastic large cell lymphoma (sALCL), said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. Our long-term vision for ADCETRIS is to expand its use into earlier lines of HL and sALCL therapy and into other CD30-positive malignancies. To that end, we are conducting a robust clinical development program with ADCETRIS, including clinical studies to broadly assess CD30 expression in both hematologic malignancies and solid tumors, as well as to evaluate activity and tolerability of ADCETRIS in these patient populations. Initial data from these clinical studies will be presented at the upcoming American Society of Clinical Oncology (ASCO) annual meeting and we have multiple late-stage trials that are already underway or are about to begin to further evaluate the broad potential of ADCETRIS. In addition, we and our collaborators are advancing a robust pipeline of clinical and preclinical ADC programs for a variety of cancers.

Recent ADCETRIS Highlights

Other Recent Highlights

Upcoming Milestones

The company is on track to achieve multiple near-term milestones for ADCETRIS and other pipeline programs, including:

First Quarter 2012 Financial Results

Revenues in the first quarter of 2012 were $48.2 million, compared to $12.2 million in the first quarter of 2011. First quarter 2012 revenues include ADCETRIS net product sales of $34.5 million. In addition, first quarter 2012 revenues reflect amounts earned under the companys ADCETRIS and ADC collaborations.

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Seattle Genetics Reports First Quarter 2012 Financial Results

07-05-2012 14:33 Project

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Nethania Gene therapy - Video

Todays post is a repost from October 2010. Ive got some major stuff cooking in the lab right now and I need all of my brain power for it. Enjoy the repost and I shall return!

Reader David sent me this paper the other day, and asked if I could blog about it. I said ok, maybe, and then I read

Gene therapy

oooooh

Sounds very cool, doesnt it? Sounds like the FUTURE! Wheres my JETPACK!!!?!?!

But of course gene therapy is kind of a buzzword. A lot of people throw it around, but it seems like a lot of people dont know what it really MEANS, and what it can be used for.

But it turns out, it can be used for quite a lot! And it may not be quite so far in the future. After all, theyre marketing jetpacks.

Alexander et al. Reversal of Depressed Behaviors in Mice by p11 Gene Therapy in the Nucleus Accumbens Science Translational Medicine, 2010.

So lets start with gene therapy and what it is, and then well go into why they used it in this particular paper. Gene therapy is based on the idea of inserting a gene into someones genome, either in the whole body or in specific parts, to change the gene expression of that cell or group of cells, and to use this technology to treat disease. In this case, what were talking about is viral-mediated gene expression. This is where we use a virus (for our own nefarious purposes mwah-ha-ha-ha!!), take out the nasty bits of the viral DNA, and load the virus with the gene you want to express. You then inject the virus into your area of interest (normally this is really site specific), and the virus, using its own virusy ways, will insert your gene of interest into your area of interest. The gene will get incorporated into the genome, and get expressed by your cells!

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Repost: Depressed mice, gene therapy, and p11

OLDSMAR, Fla., May 3, 2012 (GLOBE NEWSWIRE) -- via PRWEB - Cryo-Cell International, Inc. announced the appointment of Linda Kelley, Ph.D., as chief scientific officer. Dr. Kelley is responsible for overseeing Cryo-Cells state-of-the art laboratory, translational medicine initiatives and quality assurance program at its stem cell and cord blood banking facility in Oldsmar, Florida. She joins the company from the Dana Farber Cancer Institute at Harvard, where she was the director of the Connell OReilly Cell Manipulation Core Facility.

Dr. Kelley is an internationally recognized, cord blood stem cell scientist whose accomplishments have helped expand the scope of stem cell therapies from bone marrow transplantation to the treatment of heart, kidney, brain and other degenerative diseases. She was a member of the board of trustees of the Foundation for Accreditation of Cellular Therapy and chaired its Standards Committee. Dr. Kelley was one of 12 scientists selected by the Institute of Medicine of the National Academies of Science to serve on the panel that advised Congress on how to allocate $80 million in funding to optimally structure a national cord blood stem cell program.

While director of the Cell Therapy Facility at the University of Utah, she established that states first umbilical cord blood collection program that enabled families to donate their childrens cord blood to the national inventory. Dr. Kelley earned graduate and post-doctoral degrees in hematology and immunology at Vanderbilt University in Nashville, Tenn., where she also served as assistant professor in the Department of Medicine.

As a leader in our field, Cryo-Cell is delighted to have someone of Dr. Kelleys caliber directing our laboratory and translational medicine initiatives. Her expertise will ensure that we continue to exceed the industrys quality standards and maintain our tradition of offering clients the absolute best in cord blood, cord tissue, and menstrual stem cell cryopreservation services, said David Portnoy, chairman and co-CEO at Cryo-Cell. Under her guidance, Cryo-Cell will be propelled to the forefront of regenerative medicine.

Kelley replaces Julie Allickson, Ph.D., who is joining the Wake Forest Institute for Regenerative Medicine (WFIRM), where she will manage translational research. WFIRM is led by Anthony Atala, M.D., a Cryo-Cell board member and preeminent stem cell scientist.

The opportunity to work in a cutting-edge facility with a staff that is exceptionally well trained was very attractive to me, said Dr. Kelley. But equally important in my decision to join Cryo-Cell, was the commitment that co-CEOs David and Mark Portnoy have made to support the advancement of regenerative medicine through partnerships with Stanford University and private research facilities. Cryo-Cell is unique among stem cell cryopreservation firms in that regard.

About Cryo-Cell International, Inc. Cryo-Cell International, Inc. was founded in 1989. In 1992, it became the first private cord blood bank in the world to separate and store stem cells. Today, Cryo-Cell has over 240,000 clients worldwide from 87 countries. Cryo-Cell's mission is to provide clients with state-of-the-art stem cell cryopreservation services and support the advancement of regenerative medicine. Cryo-Cell operates in a facility that is compliant with Good Manufacturing Practice and Good Tissue Practice (cGMP/cGTP). It is ISO 9001:2008 certified and accredited by the American Association of Blood Banks. Cryo-Cell is a publicly traded company, OTC:QB Markets Group Symbol: CCEL. Expectant parents or healthcare professionals who wish to learn more about cord blood banking and cord blood banking prices may call 1-800-STOR-CELL (1-800-786-7235) or visit http://www.cryo-cell.com/.

Forward-Looking Statement Statements wherein the terms "believes", "intends", "projects", "anticipates", "expects", and similar expressions as used are intended to reflect "forward-looking statements" of the Company. The information contained herein is subject to various risks, uncertainties and other factors that could cause actual results to differ materially from the results anticipated in such forward-looking statements or paragraphs, many of which are outside the control of the Company. These uncertainties and other factors include the success of the Company's global expansion initiatives and product diversification, the Company's actual future ownership stake in future therapies emerging from its collaborative research partnerships, the success related to its IP portfolio, the Company's future competitive position in stem cell innovation, future success of its core business and the competitive impact of public cord blood banking on the Company's business, the Company's ability to minimize future costs to the Company related to R&D initiatives and collaborations and the success of such initiatives and collaborations, the success and enforceability of the Company's menstrual stem cell technology license agreements and umbilical cord blood license agreements and their ability to provide the Company with royalty fees, the ability of the reproductive tissue storage to generate new revenues for the Company and those risks and uncertainties contained in risk factors described in documents the Company files from time to time with the Securities and Exchange Commission, including the most recent Annual Report on Form 10-K, Quarterly Reports on Form 10-Q and any Current Reports on Form 8-K filed by the Company. The Company disclaims any obligations to subsequently revise any forward-looking statements to reflect events or circumstances after the date of such statements.

Contact: David Portnoy Cryo-Cell International, Inc. 813-749-2100 dportnoy(at)cryo-cell(dot)com

This article was originally distributed on PRWeb. For the original version including any supplementary images or video, visit http://www.prweb.com/releases/2012/5/prweb9469228.htm

Excerpt from:
Cryo-Cell International Taps Leader in Stem Cell Therapy to Serve as Chief Scientific Officer

03-05-2012 13:31 A study from Professor Franck Polleux's lab at The Scripps Research Institute has shown that an extra copy of a brain-development gene allowed neurons to migrate farther and develop more connections as human evolution progressed. The findings, published in the journal Cell, may offer a clue to autism and schizophrenia.

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Scripps Research Scientists Show How a Gene Duplication Helped our Brains Become 'Human' - Video

May 4, 2012

Brett Smith for Redorbit.com

Scientists may have just found a missing link in the form of a partial, duplicate gene that appears to be responsible for human brain development the most distinguishing characteristic of our species.

The genetic variation occurred in mans ape-like ancestor about two or three million years ago, according to a pair of studies published online in the journal Cell. A team led by researchers at the Scripps Research Institute found that a partial SRGAP2 gene duplicates interfere with the function of the original gene and allows maturing neurons to migrate farther and develop more connections.

This appears to be a major example of a genomic innovation that contributed to human evolution, said Franck Polleux, a professor at The Scripps Research Institute.

The SRGAP2 gene was first singled out for study by researchers because it helps drive development of the neocortex, which controls higher-order brain functions. Mutations in this gene have been found to cause certain brain disorders.

Another group of researchers led by Evan Eichler of the University of Washington discovered that SRGAP2 duplicated itself 3.5 million years ago, after humans and chimps diverged. One million years later, this partial copy, or daughter, of the original gene underwent its own duplication and created a granddaughter copy. Like a game of Telephone, each version of the gene underwent certain changes so that they resembled the original less and less with each successive copy.

These evolutionarily recent gene duplications are so nearly identical to the original genes that they arent detectable by traditional genome sequencing methods, said Polleux. Only in the last five years have scientists developed methods to reliably map these hominid-specific duplications.

To test their theory, Polleux and his colleagues put human copies of the daughter and granddaughter SRGAP2 genes into mice. The proteins made by these human genes bound to the original SRGAP2 and hindered the genes ability to do its job.

Although the mouse didnt develop a human brain, the neurons in the neocortex grew to look like human brain cells. The neurons also formed 50 to 60 percent more of these spines than normal mouse neurons, a sign of higher brain power.

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Human Brain Evolution Triggered By Duplicate Gene

ScienceDaily (May 3, 2012) Researchers at Weill Cornell Medical College and Rockefeller University have identified the first gene to be linked to a rare condition in which babies are born without a spleen, putting those children at risk of dying from infections they cannot defend themselves against. The gene, Nkx2.5, was shown to regulate genesis of the spleen during early development in mice.

The study, published online May 3 in Developmental Cell, raises the hope that a simple genetic screening test for Nkx2.5 mutations can be developed that will alert parents that their developing child may be missing the organ, which could then be confirmed with a diagnostic scan.

"The great news is that with the appropriate preventive antibiotic treatment these children will not succumb to fatal infections. This test could potentially save lives," says the study's lead investigator, Dr. Licia Selleri, an associate professor in the Department of Cell and Developmental Biology at Weill Cornell Medical College.

Because defense against infections depends, in part, on the spleen, children known to be born without the organ require treatment with a regimen of antibiotic therapy throughout their lives. But most diagnoses of this condition, congenital asplenia, are made during an autopsy after a child dies, suddenly and unexpectedly, from a rapidly lethal infection, usually from bacteria that causes pneumonia or meningitis, Dr. Selleri says. "For those reasons, we believe this condition is not quite as rare as believed. Not every child who dies from an infection is given an autopsy."

Long search for genetic culprits

Patients with congenital asplenia usually lack a spleen as the sole abnormality, but sometimes have abnormalities of the heart and blood vessels. The majority of those cases arise sporadically, so are not believed to be inherited. One form of this disorder is known as Isolated Congenital Asplenia (ICA), characterized by a spleen that is missing but with no other developmental abnormalities. The cause is believed to be genetic, but no candidate genes in humans had been found before this study.

This research project was a collaboration between Dr. Selleri and her colleagues, and Rockefeller University's Dr. Jean-Laurent Casanova, professor in the St. Giles Laboratory of Human Genetics of Infectious Diseases. Dr. Casanova had led a previous study describing 20 ICA patients, of which most children suffered their first serious infection by age one, and nine died of an invasive pneumonia.

Dr. Selleri has long been studying congenital asplenia in the laboratory using the mouse as a model system and had previously discovered that a transcription factor known as Pbx is the prime regulator of spleen development in mouse models. Dr. Matthew Koss, a recent Ph.D. graduate who had studied in Dr. Selleri's lab, led the effort to create a strain of mice that lacked Pbx in the spleen, and were born without a spleen. He identified a regulatory module that is controlled by Pbx and targets Nkx2.5, a gene downstream of Pbx, in the developing spleen of the mouse embryo. He also discovered that Pbx controls the growth of the spleen by directly regulating the expression of Nkx2.5, which in turn controls cell proliferation within the primitive spleen organ.

Then, in Dr. Casanova's lab, Alexandre Bolze, a graduate student, sequenced genetic samples from ICA patients and analyzed them using whole exome sequencing technology, which allows sequencing of the entire coding genome of multiple patients -- a technique routinely employed by Dr. Casanova. Bolze found that Nkx2.5 was mutated in a family of asplenic patients, some of which died from lethal infections -- confirming the importance of Nkx2.5 in human congenital asplenia as in the mouse model of the disorder.

"This study illustrates the unique strength in using mouse models and human genetics hand-in-hand," says Dr. Selleri. "It demonstrates how genetic pathways identified in mouse models can be exploited to further understand the pathogenesis of human disease towards a better prenatal diagnosis."

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First gene linked to missing spleen in newborns

Devangshu Datta: Towards an HIV cure Advances in genetic engineering techniques may finally help us win the battle against this global scourge Devangshu Datta / New Delhi May 04, 2012, 00:53 IST

Since AIDS, or acquired immune deficiency syndrome, was identified in 1981, there has been only one medically-certified cure. That occurred under unusual circumstances and it gave researchers an important clue about new ways to attack the disease. Recent advances in genetic engineering techniques have aided in this process. Some studies offer new hope of a cure for the 35 million estimated to be infected worldwide.

No disease inspires as much superstitious dread. So far, AIDS is estimated to have killed over 30 million people and it infects millions every year. It is especially prevalent in Sub-Saharan Africa.

HIV is transmitted through the exchange of body fluids. Common causes of infection (not necessarily in order) include unprotected sex, blood transfusions, sharing needles and so on. The associations with promiscuity and drug addiction make it hard to implement policies to stop HIV-spread. What works best is a combination of sex education and drug awareness programmes, coupled with easy availability of condoms and disposable needles. But in conservative societies like India, people object to sex education. Some religions also discourage the use of condoms.

Someone infected with HIV (HIV-positive) may survive years, without symptoms. The virus attacks a class of white blood cells called CD4 T-cells. It inserts itself into the cell and replicates. T-cells are part of the natural immune system. Once AIDS develops owing to HIV taking over T-cells, the immune system shuts down. Most AIDS patients die of cancer, pneumonia, or some other infection.

The new approaches involve inserting immune genes into HIV-positive patients, through genetic engineering of stem cells. Every researcher is cautious about claims of cures. The characteristic long symptom-less periods and HIVs ability to hide can be cruelly deceptive. HIV-positive people are also vulnerable to quacks. Many charlatans, including a cross-dresser who teaches yoga on Indian television, have claimed at various times to have found AIDS cures.

Some people have natural genetic immunity for various reasons. Advances in understanding of genomes have helped identify some of the causes of immunity. Researchers have known for a while that a mutated gene called CCR5 Delta 32 offers natural immunity to HIV.

The mutation is rare and found only in a few northern Europeans. The normal CCR5 gene, which most people possess, is the receptor HIV uses to enter T-cells. HIV cannot use the Delta-32 mutated gene and, hence, cannot replicate in a host who has two copies of the CCR5 Delta 32 gene (one inherited from each parent). Even one copy of Delta 32 seems to offer some protection. Only about one per cent of northern Europeans possess both copies.

In 2007, Timothy Ray Brown, an American resident in Berlin, was HIV-positive and also under treatment for leukaemia. Leukaemia causes an abnormal increase in white blood cells and a drop in red cells. Blood cells are produced by bone marrow. One drastic treatment is a bone marrow stem cell transplant from a healthy person. This helps regenerate healthy blood with a good haemoglobin ratio, and a new immune system. Its dangerous since the patients entire immune system must be destroyed prior to the transplant.

Browns doctors at the Charite University Medicine Berlin, Kristina Allers and Gero Hutter, found a compatible donor who belonged to that rare one per cent with the Delta-32 mutation. Five years later, after the transplant procedures, the Berlin Patient, as Brown is called in medical journals, is still HIV-free and doctors concur that this is a functional cure.

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Devangshu Datta: Towards an HIV cure

Public release date: 3-May-2012 [ | E-mail | Share ]

Contact: Rosanne Spector manishma@stanford.edu 650-725-5374 Stanford University Medical Center

STANFORD, Calif. The common occurrence of blond hair among the dark-skinned indigenous people of the Solomon Islands is due to a homegrown genetic variant distinct from the gene that leads to blond hair in Europeans, according to a new study from the Stanford University School of Medicine.

"This is one of the most beautiful examples to date of the mapping of a simple genetic trait in humans," said David Reich, PhD, a professor of genetics at Harvard University, who was not involved in the study.

The study identifying the gene responsible for blond hair in the Solomon Islands, a nation in the South Pacific, represents a rare case of simple genetics determining human appearance, and shows the importance of including understudied populations in gene mapping studies, said co-senior author Carlos D. Bustamante, PhD, professor of genetics at Stanford. The findings will be published May 4 in Science.

"Since most studies in human genetics only include participants of European descent, we may be getting a very biased view of which genes and mutations influence the traits we investigate. Here, we sought to test whether one of the most striking human traits, blond hair, had the same or different genetic underpinning in different human populations," Bustamante said.

Globally, blond hair is rare, occurring with substantial frequency only in northern Europe and in Oceania, which includes the Solomon Islands and its neighbors. "Its frequency is between 5 and 10 percent across the Solomon Islands, which is about the same as where I'm from," said co-first author Eimear Kenny, PhD, who was born in Ireland.

Many assumed the blond hair of Melanesia was the result of gene flow a trait passed on by European explorers, traders and others who visited in the preceding centuries. The islanders themselves give several possible explanations for its presence, said co-senior author Sean Myles, PhD, a former Stanford postdoctoral scholar who is now an assistant professor at the Nova Scotia Agricultural College. They generally chalked it up to sun exposure, or a diet rich in fish, he said.

After researchers at UCSF generated genetic data from the samples, Kenny, a postdoctoral scholar in Bustamante's lab, began the analysis in September 2010, the week she started at Stanford. "Within a week we had our initial result. It was such a striking signal pointing to a single gene a result you could hang your hat on. That rarely happens in science," she said. "It was one of the best experiences of my career."

In terms of genetic studies, the analysis was straightforward, said Kenny. But gathering the data, accomplished in 2009 by Myles and co-first author Nicholas Timpson, PhD, was more difficult. Much of the Solomon Islands is undeveloped, without roads, electricity or telephones. It's also one of the most linguistically diverse nations in the world, with dozens of languages spoken.

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Naturally blond hair in Solomon Islanders rooted in native gene, Stanford study finds

SAN DIEGO, May 3, 2012 /PRNewswire/ --Sequenom, Inc. (SQNM), a life sciences company providing innovative genetic analysis solutions, today reported revenue of $14.9 million for the first quarter of 2012, an increase of 10% compared to revenue of $13.5 million for the first quarter of 2011. First quarter 2012 revenues from the Sequenom Center for Molecular Medicine (Sequenom CMM) diagnostics services operating segment grew more than 187%, while revenues from the genetic analysis operating segment decreased 14% in the first quarter of 2012 as compared to the prior year period. Net loss for the first quarter of 2012 was $24.5 million, or $0.22 per share, as compared to net loss of $12.7 million, or $0.13 per share for the same period in 2011, reflecting an increase in costs associated primarily with the early commercialization of the Sequenom CMM MaterniT21 PLUS laboratory developed test (LDT).

As to be expected in the first year following the launch of a new LDT, gross margin was reduced in the first quarter of 2012 as compared to the same period one year ago, falling to 36% of revenue as compared to gross margin of 63% for the first quarter of 2011. Diagnostic services revenue is primarily recognized when cash is received and costs are recognized at the time services are performed. The delay in revenue recognition results in a decrease in gross margin, which is significantly magnified by increasing test volumes. Therefore, diagnostic revenue recognized in the current period does not relate directly to the costs incurred in the same period. This will continue until such time as the company converts to accrual accounting for diagnostic services revenue which is expected when sufficient reimbursement history has been established.

Gross margin is expected to continue to fluctuate on a quarterly basis due primarily to changes in sales volumes and the timing of cash receipts. During the first quarter of 2012, gross margin on diagnostic services revenue was negative, while gross margin on genetic analysis revenues increased by 3% to 74%, primarily due to a change in product mix, with higher margin consumables comprising a larger percentage of overall segment revenues.

Total operating expenses for the first quarter of 2012 were $29.8 million, as compared to total expenses of $21.6 million for the first quarter of 2011. This change reflects increased selling and marketing expenses resulting primarily from higher labor costs associated with increased headcount and an expanded diagnostic sales force, as well as increased research and development expenses associated with facilities allocation and overhead, higher operational supply expenses and labor related costs.

General and administrative expenses also increased for the first quarter, primarily due to increased facilities and legal expenses as compared to the same period one year ago. Total stock-based compensation expense was $2.9 million for the first quarter of 2012, as compared to $2.6 million as recorded during the first quarter in 2011.

"Our performance during the quarter reflects the successful achievement of our operational goals throughout the organization, specifically those associated with the expansion of Sequenom CMM's testing services and the launch and rapid adoption of the MaterniT21 PLUS laboratory developed test," said Paul V. Maier, Sequenom's CFO. "We ended the quarter with a favorable cash position as we continued to strengthen our balance sheet, raising $58.2 million during the period through an underwritten public offering, the proceeds of which will primarily be used to fund the expansion of our operations in support of the growing demand for our testing services."

As of March 31, 2012, total cash, cash equivalents, and marketable securities were $119.7 million. Net cash used in operating activities was $23.3 million for the first quarter, while purchases of capital equipment for the same period totaled $1.8 million, funded primarily through utilization of the Company's credit facility. As of March 31, 2012, the Company had borrowed $17.0 million under the credit facility.

Operational Updates

The Company recently reported that more than 12,700 total tests, including in excess of 4,900 MaterniT21 PLUS laboratory-developed tests (LDT) offered by Sequenom CMM, were accessioned during the first quarter of 2012, a 140% increase over the same period in 2011.At the close of the first quarter of 2012, the number of MaterniT21 PLUS samples accessioned on an annualized basis equated to approximately 30,000 tests. As of the last week in April, the52-week runrate had increased to more than 45,000 tests.

"The first quarter of 2012 has been an active and productive one for Sequenom and Sequenom CMM, as we have received and responded to the strong interest in Sequenom CMM's testing services, particularly with regard to Sequenom CMM's MaterniT21 PLUS LDT," said Harry Hixson, Jr., Ph.D., Chairman and CEO of Sequenom. "It is our goal to build on this positive momentum as the year progresses. We will continue to expand our reach to meet growing demand and deliver on our objective of providing high quality testing services offered by Sequenom CMM to physician customers nationwide."

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Sequenom, Inc. Reports Financial Results For The First Quarter Of 2012

MICHAEL FIELD/Fairfax NZ

BLOND BEAUTY: A Solomon Island boy displays his locks.

A new genetic line in blond hair has been discovered in an unlikely place - among the people of Melanesia in the Solomon Islands and Fiji.

The magazine Science reports today that scientists now realise that blond hair evolved independently at least twice in human history.

Around 10 per cent of Solomon Islanders had the blond gene, said study author Sean Myles, a geneticist at Nova Scotia Agricultural College in Truro, Canada.

Strikingly there was almost no variation in shades of blond hair.

"It looked pretty obvious to me that it was a real binary trait. You either had blond hair or you didn't," Myles told Science.

After testing 1209 Solomon Islanders scientists compared the entire genetic makeup of 43 blond and 42 dark-haired islanders.

The two groups, they found, had different versions of a crucial gene, TYRP1, one that coded for a protein involved in pigmentation. Switching one "letter" of genetic code - replacing a "C" with a "T" - meant the difference between dark hair and blond hair. A similar mutation creates blond mice by reducing the melanin content in their fur.

The gene was recessive, which meant that blonds inherited it from both parents.

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New genetic line of blond hair discovered

Excess sun exposure, a diet rich in fish, and gene inheritance from ancient explorers and traders, are all possible theories why some dark-skinned indigenous Solomon Islanders are naturally blonde, according to new research published today in the journal Science.

The study, led by Stanford University researchers, found that 5 to 10 percent of the indigenous Solomon population have a gene that is responsible for blondeness. The trait, however, is distinctly different from the gene that causes blond hair in Europeans. Their findings reveal a genetic variant which has led the islanders to have simultaneously the darkest skin pigmentation outside of Africa and the highest prevalence of blonde hair outside of Europe.

Previous studies have proven that pigmentation is largely genetic but also has evolved to adapt to the Suns ultraviolet rays with populations near the equator having the darkest skin and hair color. However, the native Solomon Islanders differ from this trend.

This is one of the most beautiful examples to date of the mapping of a simple genetic trait in humans, David Reich, PhD, a professor of genetics at Harvard University, who was not involved in the study, said in a Stanford press release.

The research, co-led by researchers at Stanford University and Dr. Nic Timpson from the University of Bristol, sought out to find why these islanders possess such strikingly dissimilar hair and skin patterning in the world.

For the study, the team took samples from a pool of more than 1,000 Melanesian participants, 43 of which had blonde hair and 42 of which had dark hair. They carried out genetic analyses on the samples to compare their genomes. The results showed that across the whole genome, one key gene area contained the gene variation TYRP1 responsible for cell differences that produce dark pigmentation.

TYRP1 is known to influence pigmentation in humans. But the researchers found the variant of TYRP1 that causes the blonde hair in Solomon Islanders is entirely absent from the genomes in Europeans.

Here you go into an unstudied population with a small sample size and you can really find some cool things, said study coauthor Carlos Bustamante, a geneticist at Stanford Universitys School of Medicine. So what about other places, like what about light pigmentation in parts of Africa? How do we not know the genetic basis of skin and hair pigmentations across the globe?

Naturally blonde hair is a surprisingly unusual trait in humans which is typically associated with people from Scandinavian and Northern European countries, said Timpson. Our findings help explain the fascinating differences in these physical characteristics, but also underline the importance of genetic mapping using isolated populations to help shed new light on the epidemiology of disease.

Many experts believed the blonde hair of Melanesia was the result of a trait passed on by Europeans who visited the islands centuries ago.

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Blondeness In Solomon Islanders Due To Genetic Variations

ScienceDaily (May 3, 2012) Researchers at Seattle Children's Research Institute and their collaborators have discovered a pair of defective genes that cause a rare congenital malformation syndrome that can make it impossible for the child to breathe or eat properly without reparative surgery. In a study led by Michael L. Cunningham, MD, PhD, medical director of the Seattle Children's Hospital's Craniofacial Center, a research team pinpointed two genes known as PLCB4 and GNAI3 in a genetic pathway that affects children with auriculocondylar syndrome (ACS). ACS is a rare disorder in which a child's bottom jaw develops as an upper jaw and, in some cases, incorrectly fuses to the base of the skull.

As part of the study, the DNA of five children with similar facial features characteristic of ACS was sequenced. Cunningham and his colleague Mark J. Rieder, PhD (University of Washington) used exome sequencing, selectively sequencing those regions of the patients' DNA believed to constitute the majority of disease-causing mutations. The study, to be published in the May edition of American Journal of Human Genetics, is one of the first genomic studies to identify causative mutations in two genes for the same disorder in the same pathway in a single analysis, Dr. Cunningham said.

While children with ACS have normal cognitive development, severe cases may require an immediate tracheostomy, feeding tubes, and ultimately extensive facial reconstructive surgery to allow them to eat and breathe properly.

"Although ACS is rare, our findings suggest that these genes may also play a role in more common disorders of the jaw and ears," said Dr. Cunningham, who is also chief of the division of craniofacial medicine and professor of pediatrics in the Department of Pediatrics at the University of Washington School of Medicine. "It's possible that more common jaw problems, like the lower jaw abnormality known as Robin sequence and other skull and facial abnormalities such as craniofacial microsomia, are also caused by genes in this pathway."

ACS, a syndrome first described by scientists in 1978, is believed to affect less than one in 50,000 births, though the precise frequency is not known. It is not uncommon for the condition to be misdiagnosed or for diagnosis to be delayed. According to Dr. Cunningham it was the precision of case choice that allowed this discovery.

Of the five cases studied, two of the parents did not have this condition but were carriers for the mutation. "Now that we know the genetic pathway for ACS, we will be able to better identify and counsel people who have normal facial appearances but carry these genes, about the likelihood of passing on this mutation to their children,'' Dr. Cunningham said.

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The above story is reprinted from materials provided by Seattle Children's.

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Genetic pathway of rare facial malformation in children pinpointed

(CBS News) Love meat? Hate meat? The reason for your answer may come down to genes. In a new study, scientists investigated whether people with a stronger sensitivity to the smell of pork are more likely to be meat-eaters.

Flavor is a combination of factors including taste and smell. According to the study, some people have receptors that detect a steroid called androstenone, which is found in high concentrations in male pigs - and in turn pork. Most commercially raised animals in the U.S. are actually castrated to get rid of the smell, but previous research has found that people who have two copies of the gene that helps sense androstenone still smell the odor - and might have a mixed reaction to pork.

"For those who are very sensitive to it, it's really disgusting. It's a sweaty, urine-like odor," Dr. Hiroaki Matsunami, an associate professor of molecular genetics and microbiology at Duke University in Durham, N.C. , told WebMD. "For others, you can smell it, but it's not as bad. Those people say it smells fragrant, chemical, or sweet."

For the study, published in the journal PLoS ONE, researchers examined the difference between people with one copy of the gene that helps detect androstenone and those with two. The study had 23 participants - 13 regular eaters and 10 "professional sensory assessors" who have sensitive noses and are trained to pick up certain scents. Participants were exposed to androstenone daily for six weeks, and then asked to evaluate samples of cooked meat with different levels of androstenone.

The participants rated the taste and smell of the meat - and then the researchers tested their genes. What did they find? Participants who rated the flavor of pork as bad were more likely to have two copies of the gene that picks up the scent.

"I was surprised at how cleanly this experiment showed who smelled what," Matsunami said in a university news release. "The results showed that people with two copies of the functional variant of the gene for that odor receptor thought that the meat smelled worse with higher levels of androstenone added."

These findings suggest that vegetarians may have a genetic predisposition against meat, according to Matsunami.

What do you think of the smell of meat?

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Genetics may explain why some people hate meat, study says

DUBLIN--(BUSINESS WIRE)--

Dublin - Research and Markets (http://www.researchandmarkets.com/research/z2qzpp/genetics_6th_edit) has announced the addition of John Wiley and Sons Ltd's new book "Genetics, 6th Edition International Student Version" to their offering.

Genetics is one of the most popular texts in use for the introductory course. It opens a window on the rapidly advancing science of genetics by showing exactly how genetics is done. Throughout, the authors incorporate a human emphasis and highlight the role of geneticists to keep students interested and motivated. The sixth edition has been updated to reflect the latest developments in the field of genetics. Genetics continues to educate today's students for tomorrow's science by focusing on features that aid in content comprehension and application.

New to this Edition:

- A new one-column design better showcases important pieces of art and avoids the overwhelmed reaction readers have to the crowded layouts found in many other texts. Boxed sections will be reduced in size to help maintain the flow of the text.

- The Focus On boxes (one per chapter) have been revised to include the most current developments in genetics as well as the most relevant topics to students.

- A streamlined topical coverage, vetted by a panel of Genetics instructors, makes for a text that is manageable in size. Snustad 6e will provide instructors and students with in-depth explanations of only those topics frequently covered in a one-semester course.

- Animated solutions to the solve it problems in the text, utilize Camtasia software. These tutorials provide step-by-step solutions that appear as if they are written-out by hand as an instructor voice-over explains each step.

- Supported by the Wiley Resource kit. The Wiley Resource Kit provides an easy way to provide you with media & assessment. The Resource Kit can be delivered through any Learning Management System (LMS). The offer is free to students, requires no cartridge or CTB license fees from Wiley.

For more information visit http://www.researchandmarkets.com/research/z2qzpp/genetics_6th_edit

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Research and Markets: Genetics, 6th Edition International Student Version Continues To Educate Today's Students for ...

LOS ANGELES--(BUSINESS WIRE)--

Response Genetics, Inc. (Nasdaq:RGDX - News),a company focused on the development and commercialization of molecular diagnostic tests for cancer, will announce its first quarter financial results and an operational update in a press release to be issued before the market opens on Thursday, May 10, 2012. The company will host a conference call that same day at 10:00 a.m. EDT to discuss its financial results.

CONFERENCE CALL DETAILS

To access the conference call by phone on May 10 at 10:00 a.m. EDT, dial (800) 537-0745 or (253) 237-1142 for international participants. A telephone replay will be available beginning approximately two hours after the call through May 17, and may be accessed by dialing (855) 859-2056, (404) 537-3406, or (800) 585-8367. The replay passcode is 77936576.

To access the live and archived webcast of the conference call, go to the Investor Relations section of the Company's Web site at http://investor.responsegenetics.com. It is advised that participants connect at least 15 minutes prior to the call to allow for any software downloads that might be necessary.

About Response Genetics, Inc.

Response Genetics Inc. (RGI) is a CLIA-certified clinical laboratory focused on the development and sale of molecular diagnostic tests for cancer. RGIs principal customers include oncologist, pathologists and hospitals. In addition to diagnostic testing services, the Company generates revenue from the sales of its analytical testing services of clinical trial specimens to the pharmaceutical industry. RGI was founded in 1999 and its principal headquarters are located in Los Angeles, California. For additional information, please visit http://www.responsegenetics.com.

Forward-Looking Statement Notice

Except for the historical information contained herein, this press release and the statements of representatives of RGI related thereto contain or may contain, among other things, certain forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements involve significant risks and uncertainties. Such statements may include, without limitation, statements with respect to the Companys plans, objectives, projections, expectations and intentions, such as the ability of the Company to announce its financial results and provide a conference call, to continue to provide clinical testing services to the medical community, to continue to expand its sales force, to continue to build its digital pathology initiative, to attract and retain qualified management, to continue to provide clinical trial support to pharmaceutical clients, to enter into new collaborations with pharmaceutical clients, to enter into new areas such as companion diagnostics, and to continue to execute on its business strategy and operations, to continue to analyze cancer samples, the potential for using the results of this research to develop diagnostic tests for cancer, the usefulness of genetic information to tailor treatment to patients, and other statements identified by words such as projects, may, could, would, should, believes, expects, anticipates, estimates, intends, plans or similar expressions.

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Response Genetics, Inc. to Release First Quarter Financial Results and Host Conference Call on May 10, 2012

By Randy Dotinga HealthDay Reporter

WEDNESDAY, May 2 (HealthDay News) -- New research shows that gene therapy can have long-lasting effects on the immune cells of HIV patients -- a promising sign -- even though the specific treatment being studied did not eradicate the virus.

This approach is one of several gene therapy strategies that are being investigated by scientists as possible ways to keep the AIDS virus from spreading in the blood.

In this case, "people were treated by gene therapy and nothing bad happened. It was safe," said study co-author Frederic Bushman, a professor of microbiology at the University of Pennsylvania.

In addition, he said, the treated immune cells managed to remain around for about a decade. "The general picture that emerges about genetic alterations to human immune cells is that they can persist for a long time if you do it right."

The study appears in the May 2 issue of Science Translational Medicine.

Researchers have long been exploring gene therapy -- in which cells in the body are genetically modified -- as a possible treatment for infection with HIV, the virus that causes AIDS. The idea is that the therapy would offer a permanent alternative to costly medications that come with potentially disabling side effects.

"Just think about what an HIV patient has to do: take drugs every day for the rest of his life, and the minute he stops taking them, the virus starts coming back," said John Rossi, chair of the department of molecular and cellular biology at the Beckman Research Institute of the City of Hope, in Duarte, Calif. He was not associated with the new research.

The study looks at 43 HIV-positive patients. Between 1998 and 2002, researchers removed blood from the patients, genetically modified it, and injected it back into them.

The plan was to program immune cells known as T cells to kill HIV cells.

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Gene therapy for HIV safe, but effectiveness still unclear

28-04-2012 19:32 IPO was diagnosed with a partial tear of her cranial cruciate ligament through x-rays. I decided to try and treat her conservatively but ultimately decided to perform stem cell therapy on her since the procedure yields many positive results. This is the "Before" video... stay tuned in 3-4 weeks for updates on her results.

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Before the Procedure - Stem Cell Therapy (IPO) - Video

When Tyler was born, the umbilical cord was wrapped around his neck, causing a lack of oxygen to his brain that led to Tyler suffering a stroke during delivery. The stroke caused damage to the back of Tylers brain. Tyler was diagnosed with cerebral palsy and his mother, Lisa Biermann, was told to expect the worst: a child who would never walk, talk, or have any chance at a normal life.

Lisa refused to give up hope. She tried everything she could to help Tyler. Tyler could not walk because his feet would not sit flat on the floor. She tried botox injections every three months, braces, casts and even ankle cord surgery. Nothing worked.

Lisa said Tyler could not communicate with her at all. She never knew when he was in pain because he was unable to tell her.

Tyler was considered to be blind, with a prescription that was over nine units nearsighted, and his eyes jumped around. Even with glasses, he could not focus his vision, and doctors did not believe he could see, or ever would see.

Until he was 8 years old, Lisa would carry Tyler from his classes at Woodland Park Elementary.

When Tyler was 8, he had a seizure. Dr. David Steenblock, who is based in California, heard about Tyler and offered to help him with umbilical cord stem cell therapy. Lisa said she thought hard about it, and because she had tried everything else and nothing had worked, she decided to try the stem cell therapy, which Dr. Steenblock told her had no side effects.

In December 2007, Lisa, Dr. Steenblock and his team took Tyler for the treatment, which had to be done in Tijuana, Mexico, because stem cells injection is currently not legal in the United States. Three months later, they went for a second injection.

The stem cells were given to Tyler intravenously for a period of approximately 45 minutes.

Lisa said within weeks, she saw monumental changes in Tyler. All the milestones he never reached as a baby, he began reaching.

Within three months Tyler could put his feet flat on the floor and could walk independently. At six months post-treatment, he no longer needed the painful braces that gave him bunions.

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Stem cell therapy for WCMS student has remarkable results