Archive for the ‘Gene Therapy Research’ Category

CHICAGO (AP) New research suggests that bad genes may be responsible for more breast cancer cases in black women than has been previously known. About 1 in 5 African-American women with the disease have an inherited mutation that drastically raises their risk for breast and ovarian cancer, according to a study released Monday.

It may help explain why black women have higher rates of breast cancer at young ages, a more aggressive form of the disease, and worse survival. It doesn't mean that all black women are at risk or even that all blacks with cancer need genetic counseling or testing, said the study's leader, Dr. Jane Churpek of the University of Chicago.

Experts offer some advice about what to make of this information:

Q. What are the genes?

A. Mostly BRCA1 and BRCA2. Everyone has two copies of these genes, and a mutation in one can give a woman up to an 87 percent risk of developing breast cancer and up to a 54 percent risk for ovarian cancer. Sixteen other genes also can raise risk but are thought to be less common.

Q. Why might blacks have high risk?

A. African-Americans' genes are more diverse than those of many other racial and ethnic groups. Most of the mutations identified in this study were novel, or unique to each woman, Churpek said. It's possible that more detailed tests in whites and other groups might find a higher prevalence of mutations than previous studies have found in them, too.

Q. Should more black women be tested?

A. National guidelines do not specify any groups that should be tested except Eastern European (Ashkenazi) Jewish women with breast or ovarian cancer or a close relative who has had one of those diseases. Genetic counseling should be offered to black women who develop breast cancer before age 50, who have a close relative with the disease, or who have "triple-negative" breast cancer. Triple negative means tumors that are not fueled by estrogen, progesterone or the gene that the drug Herceptin targets.

Q. What can be done if a gene mutation is found?

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Advice for black women on breast cancer gene risk

CHICAGO, June 3, 2013 /PRNewswire/ -- Little is sacred for author Jaymie Simmon in her award-winning debut novel, The God Gene (2012, Twinbrook, Ltd., ISBN 978-1-937698-48-5, 408 pages, available at Amazon.com and Barnesandnoble.com) It reads at thriller pace, but takes a deep, darkly humorous dive into the American psyche at a point where information overload and political ambition collide. Simmon will introduce her book to the city in which it is set and sign copies at Chicago's iconic Printers Row Lit Fest on June 8 and 9 from 10 am until 6 pm.

(Photo: http://photos.prnewswire.com/prnh/20130603/AQ25020)

Multiple award-winnerThe God Gene won the 2013 National Indie Excellence Award for Literary Fiction. It was also a finalist in the 2013 Midwest Book Awards for Literary and Contemporary Fiction, and a finalist in the National Indie Excellence Award for Fiction. Simmon studied at the University of Chicago's Writer's Studio.

The storyThe story centers on Rosalind Evans, a beautiful, determined, 36-year-old cancer researcher at a Chicago university. She is completing work on a confidential pharma project when she discovers that the genetic code at the center of the second chromosome spells out The Ten Commandments. She fears her project has been hacked, but before she can investigate, a co-worker leaks the bizarre discovery to a popular blog. The story goes viral and the next morning the world wakes up to the news that there is a message from God in their DNA.

With the media fanning the flames, debate rages over the authenticity and meaning of the so-called God gene. Is it a hoax? A miracle? The end of times? Evans is the scapegoat for society's fear and uncertainty and becomes the victim of a conspiracy that reaches from the White House to the Vatican and from the ivory towers of academe to the boardrooms of big pharma. She must battle them all in order to regain her scientific integrity, her freedom, and ultimately, her life.

Author Jaymie Simmon says the idea for the book came from her insatiable appetite for political news. "I admit it: I'm a news junkie," Simmon says. "I've tried to quit, but American politics is like a Fellini movie; it's absurd, yet you can't take your eyes off it."

Praise for The God GeneJack Hatfield, Chairman of the Chicago Area Great Books Council, says, "I highly recommend The God Gene Fully developed characters. Interesting plot line. Very relevant to our times and its spiritual and moral ambiguity."

Phil Angelo of The Daily Journal says, "The humor here runs the gamut from laugh-out-loud to dark."

About the authorSimmon, a graduate of Northern Illinois University, chose to independently publish her book after researching both the indie and traditional publishing options. "Basically, I'm impatient. The God Gene took me seven years to write. I didn't want to wait another seven years for the traditional process to play out. When my work was finally published, I didn't want to be like Emily Dickenson. In other words, dead."

Simmon is an avid Lake Michigan sailor, cyclist, and community volunteer. She donates a portion of the proceeds from her book sales to charity. This year's recipient is BallouSkies, a charity that supports research for Duchenne Muscular Dystrophy.

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Satirical thriller The God Gene wins National Indie Excellence Award for Literary Fiction

M. Spencer Green / AP

Breast cancer survivor Alicia Cook holds photos of family members who have also been afflicted by breast cancer, outside her home in Chicago.

By Marilynn Marchione, The Associated Press

Gene flaws that raise the risk of breast cancer are surprisingly common in black women with the disease, according to the first comprehensive testing in this racial group. The study found that one-fifth of these women have BRCA mutations, a problem usually associated with women of Eastern European Jewish descent but recently highlighted by the plight of Angelina Jolie.

The study may help explain why black women have higher rates of breast cancer at young ages and a worse chance of survival.

Doctors say these patients should be offered genetic counseling and may want to consider more frequent screening and prevention options, which can range from hormone-blocking pills to breast removal, as Jolie chose to do.

"We were surprised at our results," said the study leader, Dr. Jane Churpek, a cancer specialist at the University of Chicago. Too few black women have been included in genetic studies in the past and most have not looked for mutations to the degree this one did, "so we just don't have a good sense" of how much risk there is, she said.

Churpek gave results of the study Monday at an American Society of Clinical Oncology conference in Chicago. The researchers include Mary-Claire King, the University of Washington scientist who discovered the first breast cancer predisposition gene, BRCA1.

Jolie revealed a few weeks ago that she carries a defective BRCA1 gene, giving her up to an 87 percent risk of developing breast cancer and up to a 54 percent risk for ovarian cancer. The actress's mother had breast cancer and died of ovarian cancer, and her maternal grandmother also had ovarian cancer. An aunt recently died of breast cancer.

Children of someone with a BRCA mutation have a 50 percent chance of inheriting it.

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Gene flaws linked to black women's greater breast cancer risk

Breast cancer survivor Alicia Cook holds photos of family members who have also been afflicted by breast cancer, outside her home in Chicago. New research shows genetic breast cancer is more common in black women than previously thought. (AP Photo/M. Spencer Green)

Gene flaws that raise the risk of breast cancer are surprisingly common in black women with the disease, according to the first comprehensive testing in this racial group. The study found that one-fifth of these women have BRCA mutations, a problem usually associated with women of Eastern European Jewish descent but recently highlighted by the plight of Angelina Jolie.

The study may help explain why black women have higher rates of breast cancer at young ages - and a worse chance of survival.

Doctors say these patients should be offered genetic counseling and may want to consider more frequent screening and prevention options, which can range from hormone-blocking pills to breast removal, as Jolie chose to do.

"We were surprised at our results," said the study leader, Dr. Jane Churpek, a cancer specialist at the University of Chicago. Too few black women have been included in genetic studies in the past and most have not looked for mutations to the degree this one did, "so we just don't have a good sense" of how much risk there is, she said.

Churpek gave results of the study Monday at an American Society of Clinical Oncology conference in Chicago. The researchers include Mary-Claire King, the University of Washington scientist who discovered the first breast cancer predisposition gene, BRCA1.

Jolie revealed a few weeks ago that she carries a defective BRCA1 gene, giving her up to an 87 percent risk of developing breast cancer and up to a 54 percent risk for ovarian cancer. The actress's mother had breast cancer and died of ovarian cancer, and her maternal grandmother also had ovarian cancer. An aunt recently died of breast cancer.

Children of someone with a BRCA mutation have a 50 percent chance of inheriting it.

In the U.S., about 5 to 10 percent of breast cancers are thought to be due to bad BRCA genes. Among breast cancer patients, BRCA mutations are carried by 5 percent of whites and 12 percent of Eastern European (Ashkenazi) Jews. The rates in other groups are not as well known.

The study involved 249 black breast cancer patients from Chicago area hospitals. Many had breast cancer at a young age, and half had a family history of the disease.

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Gene flaws surprisingly common in black women with breast cancer

Public release date: 3-Jun-2013 [ | E-mail | Share ]

Contact: Susi Hamilton susi.hamilton@unsw.edu.au 61-422-934-024 University of New South Wales

Even if Australians with newly diagnosed bowel cancer were routinely tested for a genetic predisposition to further cancers, one in three people would still not take the necessary steps to use that information to prevent further disease.

Researchers from UNSW Medicine took the extra step of screening for the hereditary Lynch syndrome in the 2,100 people with colorectal cancer who presented at a number of NSW hospitals* over a three-year period.

Researchers found that a significant number of these people (245) had a bowel cancer with features that suggested Lynch syndrome, which leaves people vulnerable to a range of other cancers including stomach, ovarian and uterine cancers. But as 30 per cent of people did not or could not act on the information found in the screening, by giving a blood sample and their consent, the diagnosis of Lynch syndrome was missed.

The study, which has just been published in the prestigious Journal of Clinical Oncology, is the first time the impact of routine screening for Lynch syndrome has been assessed on this scale.

"It's like what Angelina Jolie had with breast cancer," says the first author on the paper, Professor Robyn Ward, Head of the Adult Cancer Program at UNSW's Lowy Cancer Research Centre. "Every first degree relative parents, kids, siblings has a 50 per cent risk of the having the condition.

"Even though we have the technology and the tools, there are very human reasons why people don't, or can't, participate," she says. "Some of the reasons were unavoidable people had mental health issues or language problems, or they died before they could agree.

"Sometimes people agreed to genetic testing, but didn't want to know the outcome," says Professor Ward. "Like a young woman who tested positive for Lynch syndrome. Because we can't give her the results she can't give it to her family, either."

Every 18 months to two years, people with Lynch syndrome should have a colonoscopy. Often polyps or abnormalities can be removed then, without surgery.

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Despite good prognosis, some turn a blind eye to genetic screening

Public release date: 3-Jun-2013 [ | E-mail | Share ]

Contact: Mark Michaud mark_michaud@urmc.rochester.edu 585-273-4790 University of Rochester Medical Center

A multi-institutional team of researchers have pinpointed the genetic traits of the cells that give rise to gliomas the most common form of malignant brain cancer. The findings, which appear in the journal Cell Reports, provide scientists with rich new potential set of targets to treat the disease.

"This study identifies a core set of genes and pathways that are dysregulated during both the early and late stages of tumor progression," said University of Rochester Medical Center (URMC) neurologist Steven Goldman, M.D., Ph.D., the senior author of the study and co-director of the Center for Translational Neuromedicine. "By virtue of their marked difference from normal cells, these genes appear to comprise a promising set of targets for therapeutic intervention."

As its name implies, gliomas arise from a cell type found in the central nervous system called the glial cell. Gliomas progress in severity over time and ultimately become highly invasive tumors known as glioblastomas, which are difficult to treat and almost invariably fatal. Current treatments, which include surgery, radiation therapy, and chemotherapy, can delay disease progression, but ultimately prove ineffective.

Cancer research has been transformed over the past several years by new concepts arising from stem cell biology. Scientists now appreciate that many cancers are the result of rogue stem cells or their offspring, known as progenitor cells. Traditional cancer therapies often do not prevent a recurrence of the disease since they may not effectively target and destroy the cancer-causing stem cells that lie at the heart of the tumors.

Gliomas are one such example. The source of the cancer is a cell found in the brain called the glial progenitor cell. The cells, which arise from and maintain characteristics of stem cells, comprise about three percent of the cell population of the human brain. When these cells become cancerous they are transformed into glioma stem cells, essentially glial progenitor cells whose molecular machinery has gone awry, resulting in uncontrolled cell division.

Goldman and his team have long studied normal glial progenitor cells. These cells produce glia, a category that includes both astrocytes cells that support the function of neurons and oligodendrocytes cells that produces myelin, the fatty insulation that allows the long-distance conduction of neural impulses.

While Goldman's group's work has primarily focused on ways to use glial progenitor cells to treat neurological disorders such as multiple sclerosis, their understanding of the biology of these cells and mastery of the techniques required to sort, identify, and isolate these cells has also enabled them to explore the molecular and genetic changes that transform these cells into cancers.

Using human tissue samples representing the three principal stages of the cancer, the researchers were able to identify and isolate the cancer-inducing stem cells. Working with Goldman, lead authors Romane Auvergne, Ph.D. and Fraser Sim, Ph.D. then compared the gene expression profiles of these cancer stem cells to those of normal glial progenitor cells. The objective was to both pinpoint the earliest genetic changes associated with cancer formation and identify those genes that were unique to the cancer stem cells and were expressed at every stage of disease progression.

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Researchers identify genetic signature of deadly brain cancer

SYDNEY, June 4 (Bernama) -- One in three Australians with newly-diagnosed bowel cancer would not act on genetic screening that showed predisposition to other cancers, researchers at the University of New South Wales (UNSW) reported Tuesday.

Researchers from UNSW Medicine took the extra step of screening for hereditary Lynch syndrome in 2,100 people with bowel cancer being treated at NSW hospitals over a three year period, reports China's Xinhua news agency.

Lynch syndrome is an inherited disorder that increases the risk of many types of cancer. The researchers found that 245 of the patients in the study had a bowel cancer with features that suggested Lynch syndrome.

But 30 percent of the participants did not act on the results of their screening by giving a blood sample and their consent, and so the diagnosis of Lynch syndrome was missed.

"Even though we have the technology and the tools, there are very human reasons why people don't, or can't, participate," explained Robyn Ward, Head of the Adult Cancer Program at UNSW's Lowy Cancer Research Centre.

"Some of the reasons were unavoidable -- people had mental health issues or language problems, or they died before they could agree," she added.

Diagnosis of Lynch syndrome is important for the management of the disease, as sufferers are recommended to have a colonoscopy every 18 months to two years -- so polyps and abnormalities can be identified and removed without surgery.

The hereditary nature of Lynch syndrome, meaning that first-degree relations may also be at risk, wasn't always enough motivation for people to take part in testing.

"Sometimes people agreed to genetic testing, but didn't want to know the outcome," said Ward.

"Like a young woman who tested positive for Lynch syndrome. Because we can't give her the results she can't give it to her family, either."

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Australians Afraid Of Genetic Screening: Study

CARLSBAD, Calif. & IRVINE, Calif.--(BUSINESS WIRE)--

Applied Spectral Imaging Inc. (ASI) and BioDot Inc. have entered into an agreement in which both companies will engage in combined sales and marketing of an integration product that will directly link the GenASIs imaging and analysis instrument by ASI and the CellWriter automated dispensing system for FISH and Karyotyping by BioDot. The combined solution enables an end-to-end, automated workflow for FISH and Karyotyping, from slide production to sample analysis and result reporting.

Personalized medicine challenges laboratories to continuously expand their genetic analysis throughput rapidly and cost effectively. The ASI and BioDot platforms provide an end-to-end environment for managing samples from slide preparation to the generation of the analysis report. said Limor Shiposh, CEO of Applied Spectral Imaging Inc. Our combined offering for automated genetic analysis leverages the imaging and analysis accuracy, speed and quality results of ASIs GenASIs platform with the flexibility, efficiency and simplicity of BioDots CellWriter automated dispensing system for FISH and Karyotyping added Mrs. Shiposh.

We are excited to work with ASI on a combined automated workflow solution for FISH and Karyotyping. The cytogenetics workflow is highly complex and by integrating automated slide processing with automated microscopy, we can now deliver a data management product that greatly simplifies the scientists workday. BioDots CellWriter is able to automate cell dropping to deliver quality spread interphase and metaphase nuclei for analysis, bridging the automation gap between harvesting and automated microscopy, and bringing high throughput processing to this market. said Tom Tisone, CEO of BioDot Inc.

ASI and BioDot have confirmed the combined solutions effectiveness in performing automated FISH and karyotyping. As a part of the new product offering, the two companies will offer a set of software connectors enabling bidirectional and seamless data integration between the two solutions.

About Applied Spectral Imaging

Applied Spectral Imaging (ASI) makes patient care better through advanced biomedical imaging.

GenASIs by ASI is FDA cleared for FISH clinical applications such as ALK, UroVysion, HER2/neu, CEP XY and Karyotyping. ASI complies with major regulatory requirements and international quality standards.

ASI has been one of the industry's leading microscopy imaging solution providers since 1993, with over 30 registered patents in the US, Europe and Japan and over 2,500 systems deployed worldwide. With worldwide offices in the US, Europe and Asia, ASI has built a global network of over 50 distributors.

About BioDot

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BioDot and Applied Spectral Imaging Cooperate to Deliver Automated Genetic Analysis Solution

June 3, 2013 A multi-institutional team of researchers have pinpointed the genetic traits of the cells that give rise to gliomas -- the most common form of malignant brain cancer. The findings, which appear in the journal Cell Reports, provide scientists with rich new potential set of targets to treat the disease.

"This study identifies a core set of genes and pathways that are dysregulated during both the early and late stages of tumor progression," said University of Rochester Medical Center (URMC) neurologist Steven Goldman, M.D., Ph.D., the senior author of the study and co-director of the Center for Translational Neuromedicine. "By virtue of their marked difference from normal cells, these genes appear to comprise a promising set of targets for therapeutic intervention."

As its name implies, gliomas arise from a cell type found in the central nervous system called the glial cell. Gliomas progress in severity over time and ultimately become highly invasive tumors known as glioblastomas, which are difficult to treat and almost invariably fatal. Current treatments, which include surgery, radiation therapy, and chemotherapy, can delay disease progression, but ultimately prove ineffective.

Cancer research has been transformed over the past several years by new concepts arising from stem cell biology. Scientists now appreciate that many cancers are the result of rogue stem cells or their offspring, known as progenitor cells. Traditional cancer therapies often do not prevent a recurrence of the disease since they may not effectively target and destroy the cancer-causing stem cells that lie at the heart of the tumors.

Gliomas are one such example. The source of the cancer is a cell found in the brain called the glial progenitor cell. The cells, which arise from and maintain characteristics of stem cells, comprise about three percent of the cell population of the human brain. When these cells become cancerous they are transformed into glioma stem cells, essentially glial progenitor cells whose molecular machinery has gone awry, resulting in uncontrolled cell division.

Goldman and his team have long studied normal glial progenitor cells. These cells produce glia, a category that includes both astrocytes -- cells that support the function of neurons -- and oligodendrocytes -- cells that produces myelin, the fatty insulation that allows the long-distance conduction of neural impulses.

While Goldman's group's work has primarily focused on ways to use glial progenitor cells to treat neurological disorders such as multiple sclerosis, their understanding of the biology of these cells and mastery of the techniques required to sort, identify, and isolate these cells has also enabled them to explore the molecular and genetic changes that transform these cells into cancers.

Using human tissue samples representing the three principal stages of the cancer, the researchers were able to identify and isolate the cancer-inducing stem cells. Working with Goldman, lead authors Romane Auvergne, Ph.D. and Fraser Sim, Ph.D. then compared the gene expression profiles of these cancer stem cells to those of normal glial progenitor cells. The objective was to both pinpoint the earliest genetic changes associated with cancer formation and identify those genes that were unique to the cancer stem cells and were expressed at every stage of disease progression.

Out of a pool over 44,000 tested genes and sequences, the scientists identified a small set of genes in the cancerous glioma progenitor cells that were over-expressed at all stages of malignancy. These genes formed a unique "signature" that identified the tumor progenitor cells and enabled the scientists to define a corresponding set of potential therapeutic targets present throughout all stages of the cancer.

"One of the key things you are looking for in drug development in cancer is a protein or gene that is over-expressed, so that you can attempt to achieve therapeutic benefit by inhibiting it," said Goldman.

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Genetic signature of deadly brain cancer identified

CHICAGOBRCA gene mutations, flaws in a tumor-suppressing gene that raise the risk of breast cancer, are surprisingly common in black women with the disease, according to the first comprehensive testing in this racial group.

The study, presented Monday at the American Society of Clinical Oncology conference in Chicago, found that one-fifth of these women have BRCA mutations, a problem usually associated with women of Eastern European Jewish descent but recently highlighted by the plight of Angelina Jolie.

The study may help explain why black women have higher rates of breast cancer at young ages -- and a worse chance of survival: One recent study found black women were twice as likely to die within first three years of a breast cancer diagnosis compared to white women.

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Doctors say black female patients should be offered genetic counseling and may want to consider more frequent screening and prevention options, which can range from hormone-blocking pills to breast removal, as Jolie chose to do.

"We were surprised at our results," said the study leader, Dr. Jane Churpek, a cancer specialist and assistant professor of medicine at the University of Chicago. Too few black women have been included in genetic studies in the past and most have not looked for mutations to the degree this one did, "so we just don't have a good sense" of how much risk there is, she said.

The researchers include Mary-Claire King, the University of Washington scientist who discovered the first breast cancer predisposition gene, BRCA1.

Jolie revealed a few weeks ago that she carries a defective BRCA1 gene, giving her up to an 87 percent risk of developing breast cancer and up to a 54 percent risk for ovarian cancer. The actress's mother had breast cancer and died of ovarian cancer, and her maternal grandmother also had ovarian cancer. An aunt recently died of breast cancer following her op-ed.

More than 232,000 women are expected to be diagnosed with breast cancer in 2013, according to the National Cancer Institute.

Originally posted here:
Genetic flaws driving breast cancer in black women, study says

Savage Genetics - Camp Genetica(WIP)
just a clip of a tune i #39;m working on just want some feedback on it. Thanks. Savage.

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Savage Genetics - Camp Genetica(WIP) - Video

Rich Mcbuckets-No Church In The Wild [Video]
Rich Mcbuckets rips Jay-Z and Kanye West #39;s "No Church in the Wild". Follow on twitter @Richmcbuckets Directed and Edited by Asa B of Genetics Productions. Ch...

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Rich Mcbuckets-No Church In The Wild [Video] - Video

Genetics tutorial 4 solution part 1

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Genetics tutorial 4 solution part 1 - Video

31/05/2013: Pokémon Genetics: Early Beta

By: idliketobeahacker

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31/05/2013: Pokémon Genetics: Early Beta - Video

Genetics Softball_051713 Game Clips
Human Genetics vs Emergency Department.

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Genetics Softball_051713 Game Clips - Video

Genetics 7

By: Devan Olsem

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Genetics 7 - Video

How to Pronounce Segregate
Learn how to say Segregate correctly with EmmaSaying #39;s "how do you pronounce" free tutorials. Definition of segregate (oxford dictionary): verb Pronunciation...

By: Emma Saying

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AMES, Iowa, June 3, 2013 /PRNewswire/ -- NewLink Genetics Corporation (NLNK), an oncology-focused biopharmaceutical company specializing in immunotherapy, today announced results from a Phase 2 clinical study with its drug candidate algenpantucel-L.The open-label, two-armed, multi-center study evaluated algenpantucel-L plus standard-of-care adjuvant therapy (gemcitabine and 5-FU-modulated radiation therapy) in 69 patients with resected pancreatic cancer. The study defined disease-free survival at one year as its primary endpoint, and overall survival, safety and immunological correlative analysis as the secondary endpoints. The data from the study showed that one year disease-free survival was 62 percent, while overall survival was 86 percent. Data presented on elevated levels of three separate biomarkers (antibodies to mesothelin, CEA and/or alpha-gal) correlated with a statistically significant improvement in overall survival. Specifically, the data showed median overall survival was 42 months in patients with elevated levels of anti-mesothelin antibodies versus 20 months in patients without elevated levels. Moreover, the subset of patients that showed increases in two or more of the aforementioned biomarkers had median overall survival greater than 42 months (median overall survival not reached for this subset of patients).

All patients are beyond 3 years of follow-up with study data showing three-year long-term disease-free survival and overall survival are 26 percent and 39 percent, respectively. The safety and tolerability of algenpantucel-L was favorable with no serious drug-related (grade 4) adverse events reported; the most frequent drug-related adverse events reported in the study were skin reactions at the injection sites. A Phase 3 study with algenpantucel-L for patients with surgically resected pancreatic cancer, the IMPRESS (Immunotherapy for Pancreatic Resectable cancer Survival Study) study, is currently underway.

"The results of this study are very encouraging. The side effects of algenpantucel-L are minimal and quite tolerable. If the encouraging survival rates are confirmed in the randomized Phase 3 trial, it may very well change the standard of care and bring immunotherapy into the mainstream of pancreas cancer treatments," commented George A. Fisher, M.D., PhD., Professor of Medicine (Oncology) at Stanford University School of Medicine and leader of the Gastrointestinal Oncology Program at Stanford.

"Algenpantucel-L is the most advanced program to emerge from our HyperAcute platform, and we are highly encouraged by these study results, which provide evidence that algenpantucel-L is stimulating and educating the immune system to recognize and attack cancer," said Charles J. Link, Jr., M.D., Chairman and Chief Executive Officer of NewLink. "We are particularly interested in the data indicating that elevated levels of three separate biomarkers antibodies to mesothelin, CEA and/or alpha-gal in combination correlate with a statistically significant improvement in overall survival."

The data were discussed in an oral presentation entitled "Effect of algenpantucel-L immunotherapy for pancreatic cancer on anti-mesothelin antibody (Ab) titers and correlation with improved overall survival," by NewLink researchers and collaborators at the 2013 Annual Meeting of the American Society of Clinical Oncology (ASCO).

About HyperAcute Immunotherapy

NewLink's HyperAcute immunotherapy platform creates novel biologic products that are designed to stimulate the human immune system to recognize and attack cancer cells. HyperAcute product candidates are composed of human cancer cells that are tumor specific, but not patient specific. These cells have been modified to express alpha-gal, a carbohydrate for which humans have pre-existing immunity. These alpha-gal-modified cells stimulate a rapid and powerful human immune response that trains the body's natural defenses to seek out and destroy cancer cells. The objective of HyperAcute immunotherapies is to elicit an antitumor response by "educating" the immune system to attack a patient's own cancer cells. HyperAcute immunotherapies do not require any tissue from individual patients and use intact whole cells rather than cell fragments or purified proteins. We believe these unique properties of HyperAcute products result in the stimulation of a robust immune response.

NewLink's lead product candidate, algenpantucel-L (HyperAcute pancreas), is being studied in a Phase 3 trial (IMPRESS: "Immunotherapy for Pancreatic Resectable cancer Survival Study") under a Special Protocol Assessment with the U.S. Food and Drug Administration. This trial involves up to 722 patients with surgically resected pancreatic cancer. Algenpantucel-L is also being tested in a second Phase 3 study (PILLAR: "Pancreatic Immunotherapy with algenpantucel-L for Locally Advanced non-Resectable"), involving patients with locally advanced pancreatic cancer.

NewLink has several HyperAcute product candidates focused on other tumor types in various stages of development, including tergenpumatucel-L, which is in an adaptive design, randomized Phase 2B/3 clinical trial currently accruing up to 240 patients with non-small cell lung cancer.

About NewLink Genetics Corporation

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NewLink Genetics' Algenpantucel-L Shows Encouraging Disease-Free and Overall Survival in Phase 2 Study in Resected ...

AMES, Iowa, June 3, 2013 /PRNewswire/ --NewLink Genetics Corporation (NLNK), an oncology-focused biopharmaceutical company specializing in immunotherapy, today announced results from two clinical studies with indoximod, an orally administered small molecule drug candidate that inhibits the IDO pathway. Indoximod was tested in a Phase 1 study in combination with docetaxel and in a Phase 1B/2 study in combination with dendritic cell cancer vaccine (AD.p53DC). In both studies, data indicated that indoximod was well tolerated when combined with these anti-cancer agents. The data also indicated promising signs of anti-tumor activity. Based on these results, NewLink has recently advanced indoximod into two separate Phase 2 cancer trials in patients with metastatic breast cancer.

The Phase 1 trial of indoximod in combination with docetaxel was conducted in patients that failed prior treatments to determine the maximum tolerated dose and evaluate the safety and activity for the combination of indoximod and docetaxel. The data showed that in 22 evaluable patients, 18 percent (4/22) exhibited a partial response and 41 percent (9/22) had stable disease. Data indicated that the combination therapy was well tolerated with no increase in expected toxicities or unexpected drug-drug interactions. Further, the pharmacokinetic profile of the combination therapy was similar to the profile of each drug as a single agent. Based on these results, a randomized Phase 2 clinical study was initiated evaluating the potential of indoximod in combination with docetaxel in patients with metastatic breast cancer using 1200 mg twice per day (BID) of indoximod and 75 mg/m2 of docetaxel once every three weeks.

The Phase 1B/2 trial of indoximod in combination with a dendritic cell cancer vaccine (AD.p53DC) was conducted in 32 patients with metastatic solid tumors who failed prior treatments, 22 of whom had metastatic breast cancer. The primary objective of the study was to determine the maximum tolerated dose of the two agents when combined. Data indicated that the combination therapy was well tolerated and established the Phase 2 dose for the combination. Stable disease was observed in three patients during the initial treatment phase of the study. Of the 22 patients in the study with metastatic breast cancer, 11 patients that showed tumor progression after treatment with indoximod plus vaccine were subsequently treated with gemcitabine-based chemotherapy. Six of these 11 patients (54 percent) achieved an objective response, including a complete response in one patient who had received four prior chemotherapies. Based on these results, a Phase 2 clinical study was initiated evaluating the potential of indoximod in combination with the cancer vaccine in patients with metastatic breast cancer using 1600 mg BID of indoximod and the vaccine. This trial will also evaluate the impact of salvage therapy for patients using carboplatin and gemcitabine.

"Taken together, we believe the data from these trials demonstrate the significant potential of indoximod and its action as an IDO pathway inhibitor to disrupt the mechanisms by which cancer evades a patient's immune system and to boost the effect of other therapies, including cytotoxic agents and cancer vaccines for the treatment of solid tumors," commented Charles J. Link, Jr., MD, Chairman and Chief Executive Officer of NewLink Genetics.

Both studies were discussed in poster presentations at the 2013 Annual Meeting of the American Society of Clinical Oncology (ASCO) by NewLink researchers and collaborators. The first poster presentation was entitled "A phase 1 study of indoximod in combination with docetaxel in metastatic solid tumors." The second poster presentation was entitled "A phase I study of ad.p53 DC vaccine in combination with indoximod in metastatic solid tumors."

About IDO pathway inhibition

NewLink's IDO pathway platform is focused on developing small molecule drugs that disrupt mechanisms by which tumors evade a patient's immune system. IDO pathway inhibitors are another class of immune checkpoint inhibitors akin to the recently developed antibodies targeting CTLA-4 and PD-1 that are potential breakthroughs in cancer therapy. NewLink's IDO pathway inhibitors are orally administered small molecules that can be used in combination with other cancer therapeutics.

The IDO pathway regulates immune response by suppressing T-cell function and enabling local tumor immune escape. Recent studies have demonstrated that the IDO pathway is active in many cancers, both within tumor cells as a direct defense against T-cell attack, and also within antigen presenting cells in tumor draining lymph nodes resulting in peripheral tolerance to tumor associated antigens (TAAs). Cancers may use the IDO pathway to facilitate survival, growth, invasion and metastasis of malignant cells expressing TAAs that might otherwise be recognized and attacked by the immune system.

NewLink is actively developing two IDO pathway inhibitors. The most advanced is indoximod, which is being studied in various chemotherapy and immunotherapy combination clinical studies. The second IDO pathway inhibitor, NLG919, has shown promising preclinical results and is expected to enter clinical trials by the end of 2013.

About NewLink Genetics Corporation

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NewLink Genetics Presents Results from Two Phase 1 Studies with Immunotherapy Agent, Indoximod, at the ASCO 2013 ...

SALT LAKE CITY, June 3, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) announced today that Peter D. Meldrum, president and CEO, is scheduled to present at the Goldman Sachs 34th Annual Global Healthcare Conference, at 8:40 a.m. Pacific on June 11, 2013 at the Terranea Resort and Spa in Rancho Palos Verdes, California.

The presentation will be available to interested parties through a live audio webcast accessible through a link on the investor relations section of Myriad's Web site at http://www.myriad.com.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

MYGN-G

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Myriad Genetics to Present at the Goldman Sachs Global Healthcare Conference

One of New Zealands larger air shipments of sheep has dotted down in Australia to meet its growing demand for Kiwi sheep genetics.

The worlds largest red meat genetics company, Focus Genetics flew 100 Primera and Highlander rams across the Tasman, the third shipment in the last 12 months.

Focus Genetics Animal breeding specialist, Daniel Absolom says demand has been high.

"The demand for our rams in Australia exceeded all initial expectations. The programme is part of a long term plan to establish New Zealand sheep genetics in the Australian market.

"We have had a lot of inquiry from Australia over the last 15 years but we wanted to find the right partners before we sent any rams. The Primera and Highlander breeds are now well established both here in NZ and the UK and the time is now right for Australia."

Focus Genetics has partnered Paringa Livestock in Australia, providing them with Primera and Highlander sheep breeds.

Paringa Livestock Director, Tom Lawson says there is a growing demand in Australia for quality New Zealand sheep genetics because the lamb survival rates are better in extreme drought conditions.

"In the last two years the results from the Primera and Highlanders have been phenomenal. Although we are still in the early stages we are seeing proven results, so there has been a big rush from farmers to buy more."

"This year we have seen one of the worst droughts on record in Australia. During tough times farmers want top genetics. They dont want to take any risks."

The move into Australia has also attracted interest from Australian meat companies which are interested in higher yielding New Zealand lamb that has also been taste tested.

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Strong Aussie demand for NZ sheep genetics

FTB Minecraft Let #39;s Play- Episode 19: Gene Therapy
In this episode we finally set up the extra bees #39; machines and I show you how they work. Bee Breeding Guide: http://www.minecraftforum.net/topic/1262611-fore...

By: Badday117

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FTB Minecraft Let's Play- Episode 19: Gene Therapy - Video

Its not quite a Sherlock Holmes thriller, but the detective work undertaken by Dr Judith Blake in Edith Cowan Universitys School of Medical Science for her PhD could have far-reaching implications for the treatment of serious nerve damage.

Dr Blake has been on the hunt for cells in the peripheral nerve that express a gene known as Pax3, which is known to help maintain stem cells. In the process, she has discovered for the first time that adult peripheral nerve tissues contain stem cells that express the gene, meaning they can be targeted for future therapies.

Pax3 is what we call a developmental gene, that works in the embryo in particular, and it has been found to regulate the stem cells of many tissues, Dr Blake said. It used to be thought that Pax3 was only expressed in the embryo but recently it has been found that there are cells that express Pax3 in the adult.

The problem was that although some researchers reported Pax3 was being expressed in adult peripheral nerve tissues they couldnt find the cells of expression.

At the same time, other scientists had argued that there was no sign of Pax3 expression in adult peripheral nerve tissues.

Dr Blake and her supervisor, Associate Professor Mel Ziman, went looking, employing technologies able to search for the tiniest amount of gene and protein expression.

Knowing the role of Pax3 as well as our team did, it was either that the expression of Pax3 other people had reported was incorrect or that as it turned out there were stem cells there but they were difficult to find, she says.

There are so few stem cells in the adult peripheral nerve, they are very small, and they are quiescent, so that when they are not activated they do not have much gene expression, just a small amount at a baseline level to keep the cell maintained.

One of the key findings of our research was that we conclusively showed that there are cells expressing Pax3 in the adult peripheral nerve and that these cells were also found to express other key stem cell markers.

The implications of the work are significant and Dr Blake hopes that the work could provide new avenues for therapies to treat peripheral nerve disorders.

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Gene detective work offers therapy hope

Public release date: 2-Jun-2013 [ | E-mail | Share ]

Contact: Jeremy Moore jeremy.moore@aacr.org 215-446-7109 American Association for Cancer Research

PHILADELPHIA A subset of colorectal cancers responds to anti-epidermal growth factor receptor (anti-EGFR) therapies, but develops resistance within months. Among cancers that develop resistance to anti-EGFR therapy, some showed overexpression of a gene called MET, according to a study published in the June issue of Cancer Discovery, a journal of the American Association for Cancer Research. Preliminary data published in this study showed human tumors with MET amplification, grown in mice, responded to MET inhibitor drugs.

The MET gene is known to be amplified in about 10 percent of colorectal cancers, and is associated with worse prognosis.

The paper was also presented as part of an oral session at the 2013 American Society of Clinical Oncology Annual Meeting.

"Our studies provide evidence that colorectal cancer resistance to anti-EGFR therapies can be driven by MET gene amplification," said Alberto Bardelli, Ph.D., associate professor in the Department of Oncology at the University of Torino in Italy. "But what is more exciting is that we were able to detect these amplifications in the blood."

A subset of metastatic colorectal cancers responds to the anti-EGFR drugs cetuximab and panitumumab, but almost always develops resistance within several months of the initiation of therapy, according to Bardelli. Mutations in genes related to EGFR signaling, including KRAS, BRAF and NRAS, account for about 60 percent of the cases that develop resistance; the cause of resistance in tumors without these mutations is unknown.

"Unfortunately, patients whose tumors recur after anti-EGFR therapy are out of further options currently," said Bardelli. "The possibility that we can identify those who have MET amplification using a blood test is exciting because they might be treated with MET inhibitors."

Bardelli and his colleagues analyzed tumors from seven patients who developed resistance subsequent to anti-EGFR therapy, and identified three who did not have the previously known mutations. Using next-generation sequencing, they demonstrated amplification of the MET gene in these three tumor samples.

Blood samples collected at regular intervals during treatment with anti-EGFR therapy until relapse were available for two of the three patients. The researchers were able to detect MET amplification in the blood, and they demonstrated it occurred prior to relapse. The ability to detect MET amplification in blood provides a noninvasive, highly sensitive method for monitoring and predicting drug resistance and tumor recurrence, according to Bardelli.

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Some patients with treatment-resistant colorectal cancers may have a new option

Public release date: 2-Jun-2013 [ | E-mail | Share ]

Contact: Danielle Servetnick danielle.servetnick@jefferson.edu 215-955-2238 Thomas Jefferson University

(CHICAGO) The HER2 growth-factor gene is known to be over-active in breast and gastro-esophageal cancers. But now, irregularities in the genes 's expression among them mutations, amplifications, substitutions, and translocations have been found in 14 different advanced solid tumors.

The results of the study of more than 2,000 tumors, being presented at the annual meeting of the American Society of Clinical Oncology (ASCO), both surprised researchers and provided hope that some of these tumors might benefit from the three anti-HER2 therapies now in clinical use.

"No one ever thought that there would be such a variety of genomic alterations in HER2 in this many solid tumors," says Massimo Cristofanilli, MD, FACP, Professor of Medical Oncology and Director of the Jefferson Breast Center at the Kimmel Cancer Center and Thomas Jefferson University Hospital.

"But this may be good news, both clinically and scientifically," he says. "It tells us that these tumors might benefit from treatment that we already have on hand, and, from a research perspective, it builds on the idea that it is the genomic profile of a tumor that is relevant in providing biological information for planning of personalized treatments not where the cancer is located or where it develops.'

Dr. Cristofanilli is presenting the results of the study in an oral presentation at the ASCO meeting. He is one of a group of co-authors from many institutions who donated tumor samples to Foundation Medicine, a cancer diagnostics company in Cambridge, Massachusetts. Foundation Medicine led and paid for the study.

Dr. Cristofanilli contributed about 50 metastatic breast tumor samples for the analysis, and found out that one of his patients with advanced triple negative breast cancer had a HER2 mutation. "My patient was treated with Herceptin as well as chemotherapy, and derived clinical benefit," he says. "No one looks for HER2 mutations in this form of breast cancer. To me, this makes the case for the value of genome-driven therapy."

In the study, Foundation Medicine conducted a genetic screen of more than 182 genes and 14 genetic rearrangements known to be linked to cancer in 2,223 tumor specimens. Twenty different advanced solid cancers were represented.

Researchers found HER2 alterations in 14 types of solid tumors, including 29 percent of esophageal, 20 percent of uterine, 14 percent of breast, 12 percent of stomach carcinomas, and 6 percent of all lung cancer samples.

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Abnormalities in HER2 gene found in wide variety of advanced cancers