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

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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

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June 3, 2013, 12:05 a.m.

Bachelor of bioscience (major in genetics) at La Trobe University

What's genetics?

It's the study of origin, of inherited traits and variation, explains associate lecturer Jodie Young, a course adviser for the biosciences. Students at La Trobe can study genetics as part of the bachelor of bioscience, the bachelor of science or the bachelor of biological sciences (advanced science) degrees. For those in the bachelor of bioscience stream, there's a general foundation in the first year in which you'll take subjects including animal evolution and diversity, organisation and function of cells, plant science, genetics and chemistry. You'll then choose a biological major or two in the second year, with students often pairing genetics with zoology, microbiology or biochemistry. Second and third-year genetics subjects include molecular and human genetics, and ecological and evolutionary genetics.

Sounds busy.

Indeed. Along with studying the biosciences, you'll take additional electives which can come from science or from anywhere in the university. This means you can pair biosciences with psychology, sociology or even archaeology.

Cool. So who signs up?

According to Ms Young, a real mix of students enrol in genetics, including those who have never studied biology before. She says that some students take genetics as a first-year elective and become hooked. To get into the bachelor of biosciences at La Trobe's Melbourne campus in Bundoora, you needed an ATAR of 75.9 in 2013. You can also start on the bachelor of bioscience at La Trobe's Albury-Wodonga campus but, for those majoring in genetics, you'll need to transfer to Bundoora in year two. An ATAR of 62.1 was needed in 2013 for entry to Albury-Wodonga. In total, Ms Young estimates that 30 or 40 students major in genetics each year.

And after three years . . .

Some students choose to go on to honours and research. Others do a graduate diploma in teaching, while others choose genetics counselling, forensic work with the police or become reps for science companies.

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Gene genies

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Posted: Sunday, June 2, 2013, 3:01 AM

The two lesions can be a sign of a genetic syndrome, Muir-Torre, which predisposes patients to internal malignancies.

These patients often have the two growths, sebaceous neoplasms and keratoacanthomas, and are at higher risk for tumors of the colon, the reproductive and urinary systems, and the breast.

These malignancies occur together because these patients have a defect in genes involved in copying DNA. They have abnormal "mismatch repair" genes, meaning their cells don't proofread DNA for errors when duplicating cells. This lack of error-checking leads to accumulated mutations, and even cancer. Moreover, this syndrome is very easy to inherit across generations, and often affects multiple patients in a family.

Recognizing the warning signs, I counseled the patient about the need for more aggressive screening and a genetic workup.

She was nervous. She asked all the right questions. Was this necessary? What would it mean for the rest of her family, or her own prospects of getting or keeping health (or life) insurance?

These questions are tough to answer, but we know that our best chance at treating cancer is early diagnosis. And that, of course, was her main question: "Does this mean I have cancer?"

The scary answer was "we don't know."

Over the last decade, we have seen explosive advances in our knowledge of human DNA. Sometimes, it is hard for people - patients and doctors - to see or use those advances. But the work is paying off. There are now cost-effective tests to look for genetic mutations.

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2 skin cancers point to genetic risk

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SFWC Lifestyle and Cancer Awareness Workshop - Breast Cancer Genetics
Supporting Families with Cancer Lifestyle and Cancer Awareness Workshop, University of Leicester, 23 February 2013 - Breast Cancer Genetics by Dr Joyce Solomons.

By: ClinicalGenetics

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2013 05 24 10 49 Bob Williamson Genetics and Cystic Fibrosis
Bob Williamson has been a world renown Cystic Fibrosis Researcher and speaks here on many topics related to CF and Genetics and also responds to audience questions on this webinar.

By: Cystic Fibrosis Queensland

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2013 05 24 10 49 Bob Williamson Genetics and Cystic Fibrosis - Video

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Informative Speech on ADD/ADHD and Genetics
This is an informative speech on ADD/ADHD and Genetics as a risk factor.

By: Natasha Wigginton

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Informative Speech on ADD/ADHD and Genetics - Video

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Genetics 8
School.

By: Devan Olsem

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Genetics 8 - Video

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CHICAGO--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) today highlighted ongoing clinical development programs for ADCETRIS (brentuximab vedotin) in frontline Hodgkin lymphoma (HL) and mature T-cell lymphoma (MTCL) and progress with collaborator antibody-drug conjugate (ADC) programs that were presented at the 49th Annual Meeting of the American Society of Clinical Oncology being held May 31 June 4, 2013, in Chicago, IL. The phase 3 clinical trials, called ECHELON-1 and ECHELON-2, are evaluating ADCETRIS for the frontline treatment of HL and MTCL, including patients with systemic anaplastic large cell lymphoma (sALCL) and other types of peripheral T-cell lymphoma. ADCETRIS is an ADC directed to CD30, a defining marker of HL and sALCL, which was granted accelerated approval by the FDA in August 2011 for relapsed HL and relapsed sALCL. In addition, encouraging phase 1 data were presented from two ADC clinical programs being developed by Genentech, a member of the Roche Group (RO.SW) (SWX:ROG)(RHHBY), using Seattle Genetics technology.

ADCs represent an innovative and growing field in the fight against cancer, which is evident by the interest in this therapeutic approach at the ASCO annual meeting, said Clay B. Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. As the first ADC to be approved by the FDA in this new class, we are focused on broadening the evaluation of ADCETRIS in earlier lines of therapy with our ongoing ECHELON-1 and ECHELON-2 global phase 3 trials, which are designed to redefine the standard of care for frontline treatment of HL and MTCL. While we advance our internal programs, our collaborators are making important progress utilizing our ADC technology. Notably, Genentech is presenting encouraging phase 1 data for two ADC candidates in solid tumor settings.

Seattle Genetics is the leader in developing ADCs, a technology designed to harness the targeting ability of antibodies to deliver cell-killing agents directly to cancer cells. Of the approximately 30 ADC candidates currently in development, more than half utilize Seattle Genetics proprietary ADC technology.

Phase III Trial of Brentuximab Vedotin Plus Doxorubicin, Vinblastine, and Dacarbazine (A+AVD) Versus Doxorubicin, Bleomycin, Vinblastine, and Dacarbazine (ABVD) as Front-line Treatment for Advanced Classical Hodgkin Lymphoma (HL) (Abstract #TPS8612)

Recent phase 1 data presented at the 2012 American Society of Hematology (ASH) Annual Meeting demonstrated that A+AVD, which removes bleomycin from the standard frontline ABVD regimen, was associated with a manageable safety profile and a complete remission (CR) rate of 96 percent in the treatment of newly diagnosed HL patients. A global phase 3 study, called ECHELON-1, is an ongoing open-label, randomized, multi-center trial designed to investigate A+AVD versus ABVD as frontline therapy in patients with advanced classical HL. The primary endpoint is modified progression free survival (mPFS) per independent review facility assessment using the Revised Response Criteria for malignant lymphoma (Cheson, 2007). Secondary endpoints include overall survival (OS), CR rate and safety. The trial is being conducted in North America, Europe, Latin America and Asia. The study will enroll approximately 1,040 eligible patients (approximately 520 patients per treatment arm) who have histologically-confirmed diagnosis of Stage III or IV classical HL and who have not been previously treated with systemic chemotherapy or radiotherapy.

Phase III Trial of Brentuximab Vedotin and CHP Versus CHOP in the Frontline Treatment of Patients with CD30+ Mature T-Cell Lymphomas (MTCL) (Abstract #TPS8611)

Recent phase 1 data presented at the 2012 ASH Annual Meeting demonstrated that ADCETRIS in combination with cyclophosphamide, doxorubicin and prednisone (A+CHP) in the frontline treatment of MTCL was associated with a manageable safety profile and 100 percent objective response rate, including 88 percent CRs. A global phase 3 study, called ECHELON-2, is an ongoing randomized, double-blind, placebo-controlled, multi-center trial designed to investigate A+CHP versus cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) as frontline therapy in patients with CD30-expressing MTCL. Approximately 300 patients (approximately 150 patients per treatment arm) will be randomized to receive A+CHP or CHOP for six to eight cycles every three weeks. The primary endpoint is progression-free survival (PFS) per independent review facility assessment using the Revised Response Criteria for malignant lymphoma. Secondary endpoints include OS, CR rate and safety. The trial is being conducted in North America, Europe and Asia.

ADCETRIS is currently not approved for frontline treatment of HL and MTCL. For more information about ECHELON-1 and ECHELON-2, visit http://www.clinicaltrials.gov.

A Phase I Study of the Safety and Pharmacokinetics of DNIB0600A, an Anti-Napi2b-vc-MMAE Drug Conjugate, in Patients with Non-Small Cell Lung Cancer (NSCLC) and Platinum-Resistant Ovarian Cancer (OC) (Abstract #2507)

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Seattle Genetics Highlights ADCETRIS® (Brentuximab Vedotin) Frontline HL and MTCL Clinical Development Programs and ...

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Spotlight on Genomics: Understanding Our Genes - A Step to Personalized Medicine
Visit: http://www.uctv.tv/) Learn about the essential role of genomics in the development of stem cell based therapies. Craig Venter, president and founder ...

By: UCtelevision

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Spotlight on Genomics: Understanding Our Genes - A Step to Personalized Medicine - Video

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Instay Rehabilitation after Traumatic Spinal Cord Injury by Rochester Wellness in Dubai
One of our patients,TSB had a RTA and Traumatic Spinal Cord Injury.He was admitted to Rochester Wellness, Dubai for the instay rehabilitation care. He slowly...

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Instay Rehabilitation after Traumatic Spinal Cord Injury by Rochester Wellness in Dubai - Video

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World #39;s First Human Embryonic Stem Cell Trial for Spinal Cord Injury: Kate Sharify #39;s Story
Visit: http://www.uctv.tv/) Katie Sharify was one of five people with spinal cord injuries to participate in the world #39;s first clinical trial testing human embryonic stem cells. The Geron...

By: UCtelevision

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World's First Human Embryonic Stem Cell Trial for Spinal Cord Injury: Kate Sharify's Story - Video

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Our Patient #39;s progress after Traumatic Spinal Cord Injury by Rochester Wellness Rehabilitation
TSB, one of our patients for instay rehabilitation was admitted in Dubai after a severe spinal cord injury and now his progress report update as he is able t...

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Walking Progress of Our Patient after Traumatic Spinal Cord Injury by Rochester Wellness, Dubai
Check out the walking progress of TSB, who was admitted to instay rehabilitation, Dubai after a severe spinal cord injury and a RTA.

By: Rochester Well

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Walking Efforts after Severe Spinal Cord Injury by our Patient in Rochester Wellness, Dubai
Check out the walking efforts of TSB, one of our patients who was admitted for instay rehabilitation in dubai after a traumatic spinal cord injury.

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Walking Efforts after Severe Spinal Cord Injury by our Patient in Rochester Wellness, Dubai - Video

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Heroin OD leads to spinal cord injury : see my journey on FB "Jazzmin #39;s Journey : Directed by God
Due to lack of oxygen, because of a drug od, jazzmin is a quad, and is very hopeful she walks again,but this lil mama knows the odds, just cant accept them.

By: Jazzmins Journey

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Heroin OD leads to spinal cord injury : see my journey on FB "Jazzmin's Journey : Directed by God - Video

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The Rhyme Along - Hip Hop Karaoke LA - 05.25.13 - Cell Therapy by Ryan and Shaye
From our event at Blu Monkey Bar Lounge, May 25, 2013. The Rhyme Along is a monthly event in Los Angeles featuring Hip Hop Karaoke Videos from the Golden E...

By: TheRhymeAlong

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The Rhyme Along - Hip Hop Karaoke LA - 05.25.13 - Cell Therapy by Ryan and Shaye - Video

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NCGAS - IU Supercomputing Center for Genomics Research
In this video Bill Barnett and Craig Stewart discuss the IU Supercomputing Center for Genomics Research and its role in aiding biologists in gene research.

By: IUPTI

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NCGAS - IU Supercomputing Center for Genomics Research - Video

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An international team of researchers led by principal investigator Paul S. Mischel, MD, a member of the Ludwig Institute for Cancer Research and professor in the Department of Pathology at the University of California, San Diego School of Medicine has found that a singular gene mutation helps brain cancer cells to not just survive, but grow tumors rapidly by altering the splicing of genes that control cellular metabolism.

The findings are published online in the journal Cell Metabolism.

Mischel, who heads the Ludwig Institute's molecular pathology laboratory based at UC San Diego, and colleagues focused upon a process called alternative splicing, in which a single gene encodes for multiple proteins by including or excluding different, specific regions of DNA.

Alternative splicing is a tightly regulated and normal activity in healthy cells. For Mischel and colleagues in Los Angeles, Ohio and Japan, the question was whether mutations of a gene called EGFRvIII caused differential alternative splicing in glioblastoma multiformes (GBMs), the most common and aggressive type of malignant brain tumor. Median survival after GBM diagnosis is just 15 months with standard-of care radiation and chemotherapy. Without treatment, it is less than five months.

The scientists were particularly interested in whether the EGFRvIII mutation induced alternative splicing events that resulted in deregulation of normal cellular metabolism. "We focused on the Warburg Effect,' a common metabolic derangement in cancer that enables tumor cells to metabolize glucose in a way that provides both a sufficient supply of energy and a source of building blocks that can be used for growth," Mischel said.

They discovered a complex but compelling series of consequential events: The EGFRvIII mutation controls expression of a splicing factor called HNRNPA1, which initiates an alternatively spliced form of a regulatory protein called Max. The alternative form is called Delta Max.

Max is associated with MYC, a gene that drives tumor growth and the Warburg Effect in cancer. "Unlike the regular form of Max," said Mischel, "Delta Max actually enhances c-MYC activity, specifically by promoting the glycolytic phenotype of the tumor cells." In other words, the EGFRvIII mutation and subsequent alternative splicing commandeer the cell's metabolic machinery in a way that lets it take up and use glucose to promote rapid tumor growth.

Mischel noted that the findings are specific to the EGFRvIII mutation and GBMs. It's not known whether other oncogenes are able to exploit alternative splicing in similar fashion.

The findings, according to Mischel, provide two clear insights. First, they highlight the central role of EGFRvIII in GBM pathogenesis and its critical role in altering cellular metabolism in tumors. Second, they show that oncogenes can regulate cell metabolism through alternative splicing, which may provide a new set of targets for oncogene-specific drug development.

Co-authors are Ivan Babic, Kenta Masui and Beatrice Gini, Ludwig Institute for Cancer Research, UCSD; Erik S. Anderson, Department of Microbiology, Immunology and Molecular Genetics, UCLA; Kazuhiro Tanaka, Department of Neurosurgery, Kobe University, Japan; Deliang Guo, Department of Radiation Oncology, Ohio State University Medical Center; Bing Li and Siavash K. Kurdistani, Department of Biological Chemistry, UCLA; Shaojun Zhu, David Nathanson and Rui Li, Carolina Espindola Camacho and Heather R. Christofk, Department of Molecular and Medical Pharmacology, UCLA; Yuchao Gu, Ludwig Institute for Cancer Research, UCSD and Department of Molecular and Medical Pharmacology, UCLA; Genaro R. Villa, Ludwig Institute for Cancer Research, UCSD and Department of Molecular and Medical Pharmacology, UCLA; David Akhavan, Department of Molecular and Medical Pharmacology, UCLA; Sergey Mareninov, Department of Pathology and Laboratory Medicine, UCLA; Ascia Eskin and Stanley F. Nelson, Department of Human genetics, David Geffen School of Medicine, UCLA; William H. Yong, Department of Pathology and Laboratory Medicine, UCLA; Webster K. Cavenee, Ludwig Institute for Cancer Research, UCSD and UCSD Moores Cancer Center; Timothy F. Cloughesy, Department of Neurology, David Geffen School of Medicine, UCLA; and Douglas L. Black, Howard Hughes Medical Institute and Department of Microbiology, Immunology and Molecular Genetics, UCLA.

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Gene mutation gives boost to brain cancer cells

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Human Genetic Engineering Con
New Project 4.

By: Drew Connolly

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Human Genetic Engineering Con - Video

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The world's last passenger pigeons perished a century ago.

But a Santa Cruz-based research project could send them flocking into the skies again, using genetic engineering to restore the once-abundant species and chart a revival for other long-gone creatures.

The promise and peril of "resurrection biology" -- which could bring back other long-gone species such as the woolly mammoth and Tasmanian tiger but runs the risk of undermining conservation efforts -- was the topic for experts who gathered Friday at Stanford's Center for Law and the Biosciences.

"The grand goal is to bring the passenger pigeon back to life," said researcher Ben Novak of Revive and Restore, supported by entrepreneur Stewart Brand's Long Now Foundation of San Francisco and conducted at the University of California, Santa Cruz. "We're at the baby step of stage one."

After studying old and damaged gene fragments of 70 dead passenger pigeons in the lab of UCSC Professor Beth Shapiro, the team will assemble -- in computers -- the genetic code of the bird once hunted to extinction. They hope to complete that within a year.

Within two years, they plan to synthesize the actual DNA code, using commercially available nucleotides. This material will be inserted into the embryo of the passenger pigeon's closest living relative, a band tail pigeon.

Then there will be new challenges, she said.

"We need to turn it into a creature. We have to raise a captive breeding herd. Then there is

Passenger pigeons once numbered in the billions, blackening the skies and inspiring naturalists like John James Audubon, John Muir and Aldo Leopold. However, they had vanished by the first World War, victims of hunting and habitat loss.

But resurrected flocks reintroduced into a modern environment could be an invasive species, noted Andrew Torrance of the University of Kansas Law School. They also would be genetically modified organisms, subject to federal regulation.

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Researchers' plan to revive extinct species raises hopes

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This undated handout provided by ExhibitEase LLC shows a 3D computer generated Image of woolly mammoth emerging from ice block. (AP Photo/Mammoth Genome Project, Steven W. Marcus)

The world's last passenger pigeons perished a century ago. But a Santa Cruz-based research project could send them flocking into the skies again, using genetic engineering to restore the once-abundant species and chart a revival for other long-gone creatures.

The promise and peril of "resurrection biology" which could bring back other long-gone species such as the woolly mammoth and Tasmanian tiger but runs the risk of undermining conservation efforts was the topic for experts who gathered

This preserved passenger pigeon, held by the Great Smoky Mountains National Park, is shown Thursday, Sept. 4, 2003, in Knoxville, Tenn., during the unveiling of a painting of the bird to benefit the Smokies' Tremont Institute. (AP Photo/Wade Payne)

"The grand goal is to bring the passenger pigeon back to life," said researcher Ben Novak of Revive and Restore, supported by entrepreneur Stewart Brand's Long Now Foundation of San Francisco and conducted at UC Santa Cruz. "We're at the baby step of stage one."

After studying old and damaged gene fragments of 70 dead passenger pigeons in the lab of UCSC professor Beth Shapiro, the team will assemble in computers the genetic code of the bird once hunted to extinction. They hope to complete that within a year.

Within two years, they plan to synthesize the actual DNA code, using commercially available nucleotides. This material will be inserted into the embryo of the passenger pigeon's closest living relative, a band-tailed pigeon.

Then there will be new challenges, Shapiro said.

"We need to turn it into a creature. We have to raise a captive breeding herd.Then there is the tricky part of

A replica of a saber-tooth tiger is seen during the "Giganten Der Eizeit" exhibition opening on May 31, 2011 in St Peter-Ording, Germany. (Photo by Krafft Angerer/Getty Images)

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Scientists examine the ethics of reviving extinct animal species

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Public release date: 30-May-2013 [ | E-mail | Share ]

Contact: Diana Quattrone diana.quattrone@fccc.edu 215-815-7828 Fox Chase Cancer Center

CHICAGO, IL (May 28, 2013)Nearly two-thirds of solid tumors carry at least one mutation that may be targeted, or medicated, by an existing compound, according to new findings from researchers Fox Chase Cancer Center that will be presented at the 49th Annual Meeting of the American Society of Clinical Oncology on June 3. The results suggest that it may one day become commonplace for doctors to sequence tumors before deciding on a treatment regimen.

"Extended sequencing of a patient's tumor is not something that's routinely done now," says study author Patrick Boland, MD, a hematology/oncology fellow at Fox Chase. "Our ultimate hope is that, if we determine testing is worthwhile, it becomes routine for a doctor to send off a tumor sample to look for mutations before deciding on a course of treatment."

In some forms of cancer, such as lung cancer, doctors do check for a limited number of mutations. Mutations found with this focused testing only affect the treatment of a small proportion of patients. However, most tumors likely have many mutations, some of which may be targeted specifically by drugs already on the market, or under development.

To investigate, 77 patients with solid tumorsprimarily inflammatory breast cancer and colon cancer underwent genetic profiling looking for nearly 200 mutations associated with cancer. Boland and his co-author Alan Skarbnik reviewed the DNA sequencing to analyze the net results of testing and consider the potential impact on patient care.

Most of the patients96%carried one mutation or more. Nearly two-thirds had at least one mutation the researchers termed "actionable," meaning it is targeted by a drug that is on the market or in development. Many of the mutations were amplifications, in which multiple copies of a single gene were present, which ramps up its effect on the body.

Boland stresses that even though these genetic alterations are present, in many cases it's not clear which ones if any are driving the cancers. "Even if we find a [change], we don't know if it's something that's driving the tumor to grow, or something that just happened along the way." The results from this study highlight the need for more research to understand the basic biology of tumors, he notes. "We need our colleagues in the basic sciences to continue investigating the genetic underpinnings of cancer, so we can determine which mutations are most important to target."

The sequenced data was reviewed by the patients' doctors, and in some cases, they prescribed new medications that targeted the identified mutations. Even though patients had all triedand failedtreatments in the past, some responded well to the new medicine, including one patient who has been on the treatment for at least 6 months.

A major limiting factor in sequencing all tumors, says Boland, is costthe list price of the sequencing test used in the study, from the company Foundation Medicine, is nearly $6,000. "We hope that, once sequencing tumors becomes the standard of care, it will be routinely covered by insurance."

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Many solid tumors carry genetic changes targeted by existing compounds

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Human Genetics - Scavenger Hunt Introduction

By: Nomad1217 #39;s channel

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Human Genetics - Scavenger Hunt

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Hendrix Genetics corporate video, english version

By: HendrixGenetics

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Hendrix Genetics corporate video, english version - Video

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