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  • richardmitnick 9:23 am on March 8, 2017 Permalink | Reply
    Tags: , , Cancer, cure cancer, , , Push button,   

    From Paulson: Women in STEM – “Push button, cure cancer” Ph.D. candidates Nabiha Saklayen and Marinna Madrid 

    Harvard School of Engineering and Applied Sciences
    John A Paulson School of Engineering and Applied Sciences

    March 7, 2017
    Adam Zewe

    Two Harvard graduate students want to make curing blood cancer or HIV as easy as pressing a button.

    2
    Saklayen and Madrid are excited to move forward with their startup, Cellino. (Photo by Adam Zewe/SEAS Communications)

    1
    Cellino is a spinoff of the nanotechnology research being conducted in the Mazur lab. (Photo by Adam Zewe/SEAS Communications)

    Ph.D. candidates Nabiha Saklayen and Marinna Madrid have launched a startup to develop a simple, push-button device clinicians could use for gene therapy treatments. Their enterprise, Cellino, hopes to commercialize technology being developed in the lab of Eric Mazur, Balkanski Professor of Physics and Applied Physics at the John A. Paulson School of Engineering and Applied Sciences.

    The early-stage laboratory spinoff, which the pair launched in November, claimed first prize in the International Society for Optics and Photonics (SPIE) Startup Challenge, a pitch-off contest between more than 40 startups from around the world. In addition to winning $10,000 cash and $5,000 in optics products, Saklayen and Madrid were lauded for the impressive business potential of their startup.

    Their technique uses laser-activated nanostructures to deliver gene therapies directly into cells. When a laser is shined onto the nanostructures, the intense hot spots can open transient pores in nearby cells, Saklayen explained.

    “These pores are open long enough for any cargo that is around in the surrounding liquid to diffuse into the cell, and then the pores seal,” she said. “It is sort of like a magical opening where we can deliver molecules into the cell without damaging it, in a very targeted, quick way.”

    Developing effective intracellular delivery methods is a problem that has plagued biologists for decades, partly because the plasma membrane that surrounds a cell is selectively permeable and bars most molecules from entering.

    “Biologists have tried a number of different methods to do this, including viruses and chemical and physical processes, but none of them have been consistent enough and safe enough to be used reliably in treatments for blood disease,” said Madrid.

    The reliability of the nanostructure method developed at SEAS would give it a leg up over current practices. The biggest hurdle Madrid and Saklayen face now is translating the Mazur lab’s technology into a scalable, turnkey device.

    Their goal is to package the technology into a shoebox-sized device that contains everything a user needs—the laser, substrates, optical components, and computer interface. A user would put a patient’s cells and the nanofabricated chips into the device and use a touch screen to treat the cells, which could then be implanted into the patient.

    According to the Cellino team, those cells could be used to treat a number of different blood diseases, including HIV and blood cancers. By delivering gene-editing molecules into a patient’s hematopoietic stem cells, for instance, a clinician could repopulate a patient’s bone marrow with HIV-resistant cells. To treat cancers that affect the blood, the technology could be used to weaponize a patient’s T-cells, and then return them to the blood stream to attack the cancer.

    “What I find really exciting about this project is it is really pushing the barriers of what is the norm,” Saklayen said. “People talk about curing blood cancer all the time, but we have this unique opportunity to really enable that. That is the most inspiring part—we have an opportunity to make a difference in people’s lives. That is what drives me everyday to keep working hard.”

    As they move forward with Cellino, Saklayen and Madrid are working closely with Harvard’s Office of Technology Development (OTD), which has filed patent applications to secure the lab’s intellectual property and develop a viable commercialization strategy for the technology. Alan Gordon, a Director of Business Development in OTD, has been advising the team on how to develop a business plan and launch the company.

    After graduating from the Ph.D. program this spring, Saklayen will pursue Cellino full time. Madrid plans to graduate early so she can soon focus solely on the company, too. The co-founders have applied to a number of startup incubators and plan to enter additional pitch competitions to gain more validation for both their technology and their business plan.

    “There is definitely a production challenge when you talk about making things at a larger scale, but we are making good progress,” Madrid said. “The technology is very powerful because it is so streamlined. Now it is all about packaging.”

    Mazur is proud of his students’ accomplishments and excited for the potential of their startup. “This work is really transformative and opens the door to new therapies for currently incurable diseases,” he said.

    See the full article here .

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    Stem Education Coalition

    Through research and scholarship, the Harvard School of Engineering and Applied Sciences (SEAS) will create collaborative bridges across Harvard and educate the next generation of global leaders. By harnessing the power of engineering and applied sciences we will address the greatest challenges facing our society.

    Specifically, that means that SEAS will provide to all Harvard College students an introduction to and familiarity with engineering and technology as this is essential knowledge in the 21st century.

    Moreover, our concentrators will be immersed in the liberal arts environment and be able to understand the societal context for their problem solving, capable of working seamlessly withothers, including those in the arts, the sciences, and the professional schools. They will focus on the fundamental engineering and applied science disciplines for the 21st century; as we will not teach legacy 20th century engineering disciplines.

    Instead, our curriculum will be rigorous but inviting to students, and be infused with active learning, interdisciplinary research, entrepreneurship and engineering design experiences. For our concentrators and graduate students, we will educate “T-shaped” individuals – with depth in one discipline but capable of working seamlessly with others, including arts, humanities, natural science and social science.

    To address current and future societal challenges, knowledge from fundamental science, art, and the humanities must all be linked through the application of engineering principles with the professions of law, medicine, public policy, design and business practice.

    In other words, solving important issues requires a multidisciplinary approach.

    With the combined strengths of SEAS, the Faculty of Arts and Sciences, and the professional schools, Harvard is ideally positioned to both broadly educate the next generation of leaders who understand the complexities of technology and society and to use its intellectual resources and innovative thinking to meet the challenges of the 21st century.

    Ultimately, we will provide to our graduates a rigorous quantitative liberal arts education that is an excellent launching point for any career and profession.

     
  • richardmitnick 4:29 pm on February 6, 2017 Permalink | Reply
    Tags: , Cancer, , , UW joins elite effort for better cancer tests in primary care   

    From U Washington: “UW joins elite effort for better cancer tests in primary care” 

    U Washington

    University of Washington

    01.31.2017
    Brian Donohue

    1
    Dr. Eunice Chen examines a patient at the UW Neighborhood Olympia Clinic. Clare McLean

    Primary-care doctors make first-line decisions about which patients – say, with an abnormal mole or a gastric complaint – should be referred out for cancer tests that are often expensive, invasive or difficult to schedule quickly.

    “That uncertainty is part of our everyday work as family doctors,” said Dr. Matthew Thompson, director of family medicine at the University of Washington School of Medicine and a practitioner at the UW Neighborhood Northgate Clinic in Seattle.

    3
    Dr. Matthew Thompson directs the family medicine program in the UW School of Medicine.

    So he’s jazzed about his department’s inclusion in an international effort that aspires to get better cancer diagnostics into primary-care doctors’ hands – to recognize cancers faster and reduce unwarranted referrals that wring patients’ emotions and wallets.

    “These technologies will take investment and development and testing, and I think primary care doctors will welcome that, as will our patients,” Thompson said.

    “CanTest,” a $6 million project funded by Cancer Research UK, makes UW Medicine a partner of the University of Cambridge and a handful of other elite research schools around the world; UW Family Medicine will direct its small share into the Primary Care Innovation Lab.

    “When the right test and technology comes up, we want to see which clinics in our WWAMI-based Practice & Research Network would be good sites for further studies,” Thompson said, referring to a group of 60 clinics across Washington, Wyoming, Alaska, Montana and Idaho.

    “Some of this is sharing; maybe there’s something that works in Australia or Denmark that we could be using here. How can we learn from each other across countries with the same kind of cancer issues?”

    4
    Technology aiming to screen for lung cancer with an exhalation is an example of a diagnostic pursued by this research grant. Owlstone Inc

    Over a five-year span of the grant, Cancer Research UK will train and support scientists to develop and share new screenings.

    “We want to nurture a new generation of researchers from a variety of backgrounds to work in primary-care cancer diagnostics, creating an educational melting pot to rapidly expand the field internationally,” said Dr. Fiona Walter, co- lead investigator at Cambridge.

    Dr. Willie Hamilton, co-lead researcher from the University of Exeter, said: “As a GP (general practitioner) myself, I know it can be frustrating to wait weeks for results before making any decisions for my patients. We’re trying to reduce this time by assessing ways that GPs could carry out these tests by themselves, as long as it’s safe and sensible to do so.”

    “We’re open to assessing many different tests, and we’re excited to hear from potential collaborators.”

    In addition to Hamilton, Walter and Thompson, the project’s senior faculty include Richard Neal, Yoryos Lyratzopoulos, Jon Emery, Hardeep Singh and Peter Vedsted. The Baylor College of Medicine in Houston is the only other U.S. site.

    See the full article here .

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    u-washington-campus
    The University of Washington is one of the world’s preeminent public universities. Our impact on individuals, on our region, and on the world is profound — whether we are launching young people into a boundless future or confronting the grand challenges of our time through undaunted research and scholarship. Ranked number 10 in the world in Shanghai Jiao Tong University rankings and educating more than 54,000 students annually, our students and faculty work together to turn ideas into impact and in the process transform lives and our world. For more about our impact on the world, every day.

    So what defines us — the students, faculty and community members at the University of Washington? Above all, it’s our belief in possibility and our unshakable optimism. It’s a connection to others, both near and far. It’s a hunger that pushes us to tackle challenges and pursue progress. It’s the conviction that together we can create a world of good. Join us on the journey.

     
  • richardmitnick 11:25 am on February 6, 2017 Permalink | Reply
    Tags: , Cancer, , , Mullerian Inhibiting Substance (MIS), Ovarian Chemo Shield?   

    From HMS: “Ovarian Chemo Shield?” 

    Harvard University

    Harvard University

    Harvard Medical School

    Harvard Medical School

    January 30, 2017
    SUE MCGREEVEY

    A hormone that plays a role in fetal development may help protect the ovaries from chemo damage.

    1
    Scientists report that a naturally occurring hormone that plays a role in fetal development may help protect the ovaries from chemo damage. Photo credit: Magicmine/Getty Images.

    A naturally occurring hormone that plays an important role in fetal development may be the basis for a new type of reversible contraceptive that can protect ovaries from the damage caused by chemotherapy drugs.

    In their report receiving online publication in PNAS, a team from the Pediatric Surgical Research Laboratories in the Harvard-affiliated Massachusetts General Hospital (MGH) Department of Surgery describes using Mullerian Inhibiting Substance (MIS) to halt, in a mouse model, the early development of the ovarian follicles in which oocytes mature, an accomplishment that protects these primordial follicles from chemotherapy-induced damage.

    “MIS has long been suspected as an inhibitor of the initial stages of follicular development, but the complete blockade of the process was unexpected and opened up a number of new applications for the hormone,” said corresponding author David Pepin, an assistant professor of Surgery at Harvard Medical School (HMS).

    “Because most of what we know about female reproduction is focused on the late stages of follicle maturation, our current therapies – including contraceptive drugs – are all targeted at those processes.

    The ability to target earlier stages and potentially maintain the larger pool of quiescent oocytes called the ovarian reserve not only could maintain fertility during chemotherapy but also could be applied to modern fertility treatments,” he said.

    During embryonic development, MIS is secreted by the testes of male embryos to prevent the maturation of structures that would give rise to female reproductive organs.

    Patricia Donahoe, director of the Pediatric Surgical Research Laboratories and a co-author of the PNAS paper, has been investigating the potential use of MIS to treat ovarian cancer and other reproductive tumors for several years.

    As part of that continuing work, Pepin made the surprising observation that overexpression of MIS in female animals completely blocked the maturation of follicles, keeping them at the inactive, primordial stage and rendering the animals infertile.

    Chemotherapy’s anti-cancer effects depend on its ability to damage rapidly growing cells, including cells in maturing ovarian follicles. But chemotherapy is also believed to accelerate the activation of primordial follicles, essentially using up the ovarian reserve over a matter of months instead of years.

    The idea that ovarian suppression could preserve fertility in women undergoing chemotherapy is not new, but the ability to halt activation of primordial follicles during chemotherapy was not previously possible.

    Current hormonal contraceptives act at later stages, after the follicle has been committed to either grow or perish, so the unique action of MIS in maintaining follicles at the primordial stage offered intriguing new possibilities.

    In a series of experiments with female mice, the research team first showed that increasing MIS levels either by twice-daily injection of the purified protein or by gene therapy led to a gradual but significant decrease in the number of growing follicles, leading after several weeks to an almost complete lack of growing follicles but maintaining a consistent level of primordial follicles.

    Halting MIS treatment, either by discontinuing the injections or by transplanting follicle-depleted ovarian tissues from gene-therapy treated mice into untreated control animals, led to resumption of follicle development in as little as 12 days, indicating that the effect is reversible.

    Mice in which MIS levels were elevated by gene therapy gradually lost their fertility, and those with higher MIS levels were completely infertile after six weeks.

    Both methods of MIS administration were able to protect the ovarian reserve from the effects of common chemotherapy drugs, resulting in primordial follicle counts from 1.4 to nearly 3 times higher than in mice not receiving MIS during chemotherapy, with counts depending on the particular chemotherapy drug used and the route of MIS administration.

    “We have just begun to scratch the surface of the implications of MIS for reproductive and overall health,” Pepin said.

    “Its unique mechanism of action means it could be useful in treating many conditions that cause primary ovarian insufficiency or premature menopause. Long-term contraceptive use would probably require replacement of hormones such as estrogen to prevent the side effects of ovarian shutdown, which would be less of a concern for short-term treatment during chemotherapy. Gene therapy with MIS could also offer a nonsurgical alternative to veterinary sterilization procedures,” Pepin said.

    Pepin’s team is now investigating the quality of the oocytes preserved by MIS treatment after chemotherapy, along with elucidating the molecular mechanisms by which MIS inhibits follicle activation, which may lead to the development of small-molecule oral alternatives.

    The researchers have also formed a company, Provulis LLC, to develop clinical applications of MIS treatment and are planning clinical trials.

    See the full article here .

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    Established in 1782, Harvard Medical School began with a handful of students and a faculty of three. The first classes were held in Harvard Hall in Cambridge, long before the school’s iconic quadrangle was built in Boston. With each passing decade, the school’s faculty and trainees amassed knowledge and influence, shaping medicine in the United States and beyond. Some community members—and their accomplishments—have assumed the status of legend. We invite you to access the following resources to explore Harvard Medical School’s rich history.

    Harvard University campus

    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 4:47 pm on February 2, 2017 Permalink | Reply
    Tags: , Cancer, , , Yale scientists identify key defect in brain tumor cells   

    From Yale: “Yale scientists identify key defect in brain tumor cells” 

    Yale University bloc

    Yale University

    February 1, 2017

    Ziba Kashef
    ziba.kashef@yale.edu
    203-436-9317

    1
    © stock.adobe.com

    In a new study, Yale researchers identified a novel genetic defect that prevents brain tumor cells from repairing damaged DNA. They found that the defect is highly sensitive to an existing FDA-approved drug used to treat ovarian cancer — a discovery that challenges current practice for treatment of brain tumors and other cancers with the same genetic defect, said the scientists.

    The study was published on Feb. 1 by Science Translational Medicine.

    Certain malignant brain tumors and leukemias have mutations in genes known as IDH1 and IDH2. The mutations render the cancers sensitive to treatment with radiation therapy or chemotherapy, significantly increasing the survival time for patients with the mutations. To better understand this sensitivity, a cross-disciplinary team of researchers led by Yale created models of the mutation in cell cultures.

    The researchers tested several existing cancer drugs on the mutated cell lines. They found that tumor cells with the mutant genes were particularly sensitive to a drug, olaparib, recently approved for the treatment of hereditary ovarian cancer. The drug caused a 50-fold increase in brain tumor cell death.

    Known as a PARP inhibitor, the drug acts on a defect in the DNA repair mechanism in the brain tumor cells, they said.

    These findings run counter to current practices in oncology. “Our work at Yale has practice-changing implications, as our data suggest an entirely new group of tumors can be targeted effectively with DNA repair inhibitors, and that possibly these patients currently are not being treated with the most optimal approaches,” said senior author Dr. Ranjit Bindra, assistant professor of therapeutic radiology and of experimental pathology.

    Co-senior author Dr. Peter Glazer, professor of therapeutic radiology and of genetics, noted, “Our work raises serious caution regarding current therapeutic strategies that are aimed at blocking mutant IDH1 and IDH2 protein function, as we believe the DNA repair defect should be exploited rather than blocked.”

    Based on these studies, the authors are designing a clinical trial to test whether DNA repair inhibitors, such as olaparib, are active against IDH1- and IDH2-mutant tumors. They anticipate that this trial will be open for enrollment later in 2017.

    “The opportunity to translate Yale science directly into the clinic is just so exciting, as it shows our ability to pivot seamlessly between the bench and the bedside, which is a key mission of our cancer center,” says Bindra.

    Co-first authors are Parker Sulkowski and Chris Corso. Additional authors are Nathaniel Robinson, Susan Scanlon, Karin Purshouse, Hanwen Bai, Yanfeng Liu, Ranjini Sundaram, Denise Hegan, Nathan Fons, Gregory Breuer, Yuanbin Song, Ketu Mishra-Gorur, Henk de Feyter, Robin de Graaf, Yulia Surovtseva, and Maureen Kachman. Bindra and Glazer are inventors on a related patent application.

    This research was supported by the National Institutes of Health (NIH), the American Cancer Society, the Cure Search for Children’s Cancer Research Foundation, and the Connecticut Department of Public Health.

    See the full article here .

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    Yale University comprises three major academic components: Yale College (the undergraduate program), the Graduate School of Arts and Sciences, and the professional schools. In addition, Yale encompasses a wide array of centers and programs, libraries, museums, and administrative support offices. Approximately 11,250 students attend Yale.

     
  • richardmitnick 1:21 pm on January 30, 2017 Permalink | Reply
    Tags: , Cancer, ,   

    From Wash U: “Study unveils new way to starve tumors to death” 

    Wash U Bloc

    Washington University in St.Louis

    January 24, 2017
    Julia Evangelou Strait

    1
    Unlike a healthy cell, a sarcoma cell (above) relies on environmental sources of arginine, an important protein building block. Remove environmental arginine and the cell must begin a process called autophagy, or “self-eating,” to survive. A second hit to its survival pathways then kills the cell, according to a new study at Washington University School of Medicine in St. Louis. Areas of autophagy are shown in green and the cell nucleus in blue. (Image: Jeff Kremer)

    For decades, scientists have tried to halt cancer by blocking nutrients from reaching tumor cells, in essence starving tumor cells of the fuel needed to grow and proliferate. Such attempts often have disappointed because cancer cells are nimble, relying on numerous backup routes to continue growing.

    Now, scientists at Washington University School of Medicine in St. Louis have exploited a common weak point in cancer cell metabolism, forcing tumor cells to reveal the backup fuel supply routes they rely on when this weak point is compromised. Mapping these secondary routes, the researchers also identified drugs that block them. They now are planning a small clinical trial in cancer patients to evaluate this treatment strategy.

    The research is published Jan. 24 in Cell Reports [link is below].

    Studying human cancer cells and mice implanted with patients’ tumor samples, the researchers demonstrate that a double hit — knocking out the weak point and one of the tumor cells’ backup routes — shows promise against many hard-to-treat cancers. Though present in multiple cancer types, the weak point is particularly common in sarcomas — rare cancers of fat, muscle, bone, cartilage and connective tissues. Doctors treat sarcomas primarily with traditional surgery, radiation and chemotherapy, but such treatments often are not effective.

    “We have determined that this metabolic defect is present in 90 percent of sarcomas,” said senior author Brian A. Van Tine, MD, PhD, an associate professor of medicine. “Healthy cells don’t have this weakness. We have been trying to create a therapy that takes advantage of the metabolic defect because, in theory, it should target only the tumor. Basically, the defect allows us to force the tumor cells to starve.”

    To grow and proliferate, tumor cells must have basic building materials. The researchers’ strategy relies on the fact that the vast majority of sarcomas have lost the ability to manufacture their own arginine, a protein building block that cells need to make more of themselves. Lacking this ability, the cells must harvest arginine from the surrounding environment. The supply of arginine in the blood is abundant, and cancer cells have no trouble scavenging it. But remove this environmental supply of arginine and the cells have a problem.

    “When we use a drug to deplete arginine in the blood, the cancer cells panic because they’ve lost their fuel supply,” Van Tine said. “So they rewire themselves to try to survive. In this study, we used that rewiring to identify drugs that block the secondary routes.”

    Unlike most cancer therapies, depleting arginine in the blood does not affect healthy cells. Normal cells don’t rely on external sources of arginine because they don’t have the cancer’s metabolic defect. They continue to make their own arginine, so there is no induced starvation in normal cells even when there is no arginine in the blood. Van Tine said this strategy is based on the properties of a tumor — it shuts down tumor metabolism specifically and nothing else.

    Unable to make or obtain external arginine, the tumor cells’ fuel supply routes are forced inward. The cells must begin to metabolize their internal supply of arginine in a process called autophagy, or “self-eating.” In the case of sarcomas, this state slows or pauses cancer growth but does not kill the cell. During this period, tumor cells appear to be buying time to find yet another internal work-around.

    “Cancer doesn’t die when you halt its primary fuel supply,” Van Tine said. “Instead, it turns on all these salvage pathways. In this paper, we identified the salvage pathways. Then we showed that when you drug them, too, you kill cells. Our study showed that tumors actually shrink under these conditions. This is the first time tumors have been shown to shrink using just metabolism drugs and no other anti-cancer strategies.”

    The arginine-depleting drug is currently in clinical trials investigating its safety and effectiveness against liver, lung, pancreatic, breast and other cancers. But so far, it has been ineffective likely because it has activated the salvage pathways allowing cancer growth to continue. The researchers said the drug may yet become a vital metabolic therapy for cancer as long as it is used in combination with other drugs targeting the backup pathways.

    Van Tine and the study’s first author, Jeff C. Kremer, a PhD student in Van Tine’s lab, explained that when cancer cells with this metabolic defect are deprived of environmental arginine, they are forced to shift from a system that burns glucose to a system that burns a different fuel called glutamine. They showed that adding a glutamine inhibitor to the arginine-depleting drug is lethal to the cells. Eliminating arginine from the blood also rewires serine biology, another backup fuel, so adding serine inhibitors also causes cell death.

    This strategy could be applied beyond rare sarcoma tumors because the metabolic defect is often present in other cancers, including certain types of breast, colon, lung, brain and bone tumors, the researchers said. The new study includes data showing similar anti-tumor responses in cell lines from these cancer types. Van Tine also pointed out that all of the drugs used in the study are either already approved by the U.S. Food and Drug Administration for other conditions or in ongoing clinical trials investigating cancer drugs.

    Based on this study and related research, Van Tine and his colleagues at Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine are planning a clinical trial of the arginine-depleting drug in patients with sarcomas.

    “We will start with a baseline trial testing the arginine-depleting drug against sarcomas with this defect, and then we can begin layering additional drugs on top of that therapy,” Van Tine said. “Unlike breast cancer, for example, sarcomas currently have no targeted therapies. If this strategy is effective, it could transform the treatment of 90 percent of sarcoma tumors.”
    This work was supported by grants from CJ’s Journey; The Sarcoma Foundation of America; a Sarcoma Alliance for Research and Collaboration Career Development Award; and Polaris Pharmaceuticals. Polaris Pharmaceuticals provided funding and the arginine-depleting drug, ADI-PEG20 (pegylated arginine deiminase).

    Kremer JC, Prudner BC, Lange SES, Bean GR, Schultze MB, Brashears CB, Radyk MD, Redlich N, Tzeng S, Kami K, Shelton L, Li A, Morgan Z, Bomalaski JS, Tsukamoto T, McConathy J, Michel LS, Held JM, Van Tine BA. Arginine deprivation inhibits the Warburg effect and upregulates glutamine anaplerosis and serine biosynthesis in ASS1-deficient cancers. Cell Reports. Jan. 24, 2017.

    See the full article here .

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    Washington University’s mission is to discover and disseminate knowledge, and protect the freedom of inquiry through research, teaching, and learning.

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  • richardmitnick 12:50 pm on January 24, 2017 Permalink | Reply
    Tags: , Blood-brain barrier, Cancer, Glioblastoma — an aggressively cancerous brain tumor, , Neural stem cells sense the growing tumor, Shawn Hingtgen, Survival rates shrink to just one year, Tumor-homing stem cells, , You are your own best source for stem cells   

    From UNC: “A Living Scalpel to Fight Brain Cancer” 

    U NC bloc

    University of North Carolina

    January 10th, 2017
    Nicole Baker

    1
    UNC pharmacy professor Shawn Hingtgen engineers a new technique to treat glioblastoma, a deadly brain tumor.

    In February 1937, the famous American composer George Gershwin proudly stood before the Los Angeles Symphony Orchestra. During his performance of Concerto in F, the smell of burning rubber hit his nostrils hard and he fumbled on stage, ultimately blacking out. After seeing a doctor who found no sign of serious illness, he went on to complete the musical comedy “A Damsel in Distress” and resumed his normal activities. By June, though, he regularly suffered from headaches and dizzy spells. Then, in July, he slipped into a coma and died.

    Today, a diagnosis of glioblastoma — an aggressively cancerous brain tumor — is often equated with a death sentence. It marks what can become a long descent into cognitive impairment, excruciating headaches, personality changes, failing motor skills, and an inability to speak. For the patient who arrives at their primary care physician reporting recurrent headaches and then eventually learns they have a glioblastoma, they may be told that they have a 5 percent chance of survival for the next five years. For patients with especially aggressive tumors, survival rates shrink to just one year.

    Few treatments exist for glioblastoma and the need for better patient care is dire. Typically, surgery is performed to extract a tumor several centimeters in size from the brain, and then patients are administered chemotherapy or radiation. Even so, most patients with the disease have little hope of long-term remission. Shawn Hingtgen, an assistant professor in the UNC Department of Phamacoengineering and Molecular Pharmaceuticals, is dedicated to reversing the grim prognosis faced by these patients.

    Rallying healthy cells to fight cancer

    “We’re making tumor-homing stem cells that act as drug carriers to target brain cancer,” Hingtgen explains with enthusiasm. “These stem cells can seek out the tumor and deliver drugs to destroy cancer cells in a way that other drugs cannot.”

    While surgical removal of the tumor followed by chemotherapy or radiation can be moderately successful for some patients with glioblastoma, the trouble is often that surgeons can neither locate nor remove all of the elusive patches of cancer woven throughout the brain tissue. Glioblastomas typically do not metastasize to other organs of the body like breast, lung, or pancreatic cancers, but the tumor cells can penetrate deep into inaccessible regions of the brain, far from their origin.

    “The patient is going to come in and have surgery if they can, then they’ll receive oral chemo and radiation,” Hingtgen says. “But due to the nature of this disease, and many other cancers, the surgeons can never get the entire tumor out. They can’t see every piece of it, so they never know what they’ve missed.”

    While the site of the primary tumor is cleared during surgery, there is no safe or effective way to seek out and destroy the spidery tendrils of cancer tissue that wind away from the initial tumor without damaging a patient’s brain. But hope is on the horizon. Where even a surgeon’s most meticulous scalpel is unable to remove a sliver of tumor, a type of stem cell designed by Hingtgen and his colleagues are able to clean up the rest.

    Hingtgen’s stem cells are derived from skin cells that are transformed through manipulation of gene expression into neural, or brain, stem cells. In effect, the cells lose some of the characteristics that make them specific to skin tissue and gain a more rudimentary and flexible nature, reverting back to a state where they have the potential to become any type of neuronal cell.

    Stem cells lend surgeons a hand

    Stem cells are especially adept at sensing the chemical signature given off by cancer cells. “Neural stem cells sense the growing tumor and are attracted to it,” Hingtgen says. “Our neural stem cells will migrate toward and bump into the tumor tissue, but won’t be able to kill the tumor by themselves, so that’s why we have them carry and deliver anti-cancer drugs.”

    These cancer-fighting molecules consist of both current clinical candidates used in other types of cancer treatment as well as experimental agents. They can severely curtail the growth of cancer and lead to tumor cell death. It’s often difficult to treat brain tumors with drugs because of the blood-brain barrier — a difficult-to-penetrate membrane that keeps harmful toxins away from the brain. This prevents successful delivery of anti-cancer agents. Neural stem cells loaded with drugs and inserted directly into the brain act as ground forces that deliver these cancer-toxic agents directly to the tumor.

    A bumpy journey

    The road to a scientific breakthrough is often paved with difficultly. So far, experiments with mice have proven successful, but using both skin and glioblastoma tissue from actual humans has been fraught with minor difficulties. “Every person and every case of glioblastoma is different, so the tissue we’ve received to work with comes with its own set of challenges,” Hingtgen says. “The good news is that we are figuring out how to overcome these tissue-specific differences.”

    Early in development, the stem cells also had trouble growing inside the brain tissue of mice following surgical removal of the main glioblastoma tumor, according to Hingtgen. In some cases, surgical removal of the primary tumor allowed its hidden margins to fill in the empty space and grow better. Like a malignant rosebush that blossoms more robustly after pruning, these diffuse wisps of tumor can grow with a vengeance after surgery. The neural stem cells in the surgical cavity need to stay there long enough for them to deliver drugs to remaining tumor cells.

    “The stem cells were being washed away or destroyed by the immune system, so we turned to the expertise of the joint UNC and NCSU Biomedical Engineering department. They fashioned a flexible scaffold on which to embed the stem cells before inserting them into the mouse brain,” Hingtgen says.

    This scaffold is essentially a tiny, disc-shaped platform made of fibrous protein on which the stem cells can attach and grow. Following surgical removal of a glioblastoma, the cup-like structure is positioned in the place where the tumor was previously growing. The scaffold has so far proven successful at retaining the neural stem cells long enough for them to seek out and destroy glioblastoma in mice. In fact, the survival rate nearly tripled for mice that received the treatment.

    It takes a village to treat a disease

    Hingtgen credits the hard work of his team for the success of this potential therapy. From the folks in his lab, to the bioengineers, his FDA contacts, collaborators at other universities, and perhaps most importantly, the surgeons and clinicians from whom he’s sought advice, it’s proof that conquering one of the most foreboding human maladies requires a team of dedicated experts.

    As a relatively new assistant professor, Hingtgen acknowledged early on that he would need some help to see his vision through. Before he moved to UNC, he recalls nervously calling Matt Ewend of the UNC Department of Neurosurgery to ask for some advice. Ewend was on a ski lift with his family when he received the call, but Hingtgen’s vision excited him enough to schedule a meeting.

    “From the beginning, Matt has been a massively helpful member of the team,” Hingtgen says. “In our first meeting, he said to me, ‘We’ve got to make these stem cells from the patients themselves, and you’ve got to get these cells to me so I can put them into the patient.’”

    Personalized patient care

    Taking Ewend’s advice to heart, Hingtgen is trying to bring stem cell therapy to the personalized medicine front. “You are your own best source for stem cells, and using your cells will limit the trouble of tissue rejection following implantation. We can’t just go in and lop cells out from a person’s brain, though, so the skin gives us a more readily available source of cells to transform into neural stem cells,” he says.

    Hingtgen originally started using mouse skin in his experiments, but has since been able to extend his work to human skin and clinical samples from the brains of patients with cancer. Published work from his lab demonstrates that his neural stem cells loaded with the anti-cancer molecule, TRAIL, can drastically halt the growth of a tumor and can almost triple the survival of mice implanted with glioblastoma tissue.

    The stem cells and scaffold would both be classified as “first-in-human” trials by the FDA, and deciding which drugs the stem cells should carry adds yet another layer of complication to getting this treatment approved for human trials. Hingtgen works closely with experienced individuals to help his research navigate the careful rules established by the FDA to determine whether a treatment is both safe and effective for human patients.

    He remains hopeful that FDA approval for clinical trials will be swift: “We are working on making our final product, and we’re lucky to have a good team, so we can move quickly.”

    From the breast to the brain

    In the future, Hingtgen sees potential to use stem cells for other types of cancer treatment. He’s already got plans in motion to try his system with tumors that start in the breast and spread to the brain. Additionally, he’s working with pediatric neurosurgeons to evaluate the potential of neural stem cell therapy for medulloblastoma, a type of brain cancer that primarily affects children.

    The ominous portent of these life-taking tumors does not dim the hope or the resolve of Hingtgen. It’s comforting to know that patients suffering from the nefarious ordeal of brain cancer have such an energetic and dedicated ally. “The main thing I’ve always wanted to do — and still want to do — is put this technology to use in patients and make a difference in their lives.”

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  • richardmitnick 10:58 am on January 22, 2017 Permalink | Reply
    Tags: An open-science effort to replicate dozens of cancer-biology studies is off to a confusing start., Cancer, Cancer reproducibility project releases first results, , Muddy waters,   

    From Nature: “Cancer reproducibility project releases first results” 

    Nature Mag
    Nature

    18 January 2017

    Monya Baker
    Elie Dolgin

    An open-science effort to replicate dozens of cancer-biology studies is off to a confusing start.

    1
    Dozens of papers reporting efforts to attack cancer cells are being checked in an open-source project. Stanley Flegler/Visuals Unlimited, Inc./Science Photo Library

    Erkki Ruoslahti was on track to launch a drug trial in people with cancer this year, but his plan may now be in ­jeopardy. A high-profile project designed to gauge the reproducibility of findings from dozens of influential papers on cancer biology publishes results for its first five papers this week, including one by Ruoslahti. And scientists who tried to replicate his findings say that they can’t get his drug to work. For the other four papers, the replication results are less clear.

    Ruoslahti, a cancer biologist at the Sanford Burnham Prebys Medical Discovery Institute in La Jolla, California, disputes the verdict on his research. After all, at least ten laboratories in the United States, Europe, China, South Korea and Japan have validated the 2010 paper [1] in which he first reported the value of the drug, a peptide designed to penetrate tumours and enhance the cancer-killing power of other chemotherapy agents. “Have three generations of postdocs in my lab fooled themselves, and all these other people done the same? I have a hard time believing that,” he says.

    A single failure to replicate results does not prove that initial findings were wrong — and shouldn’t put a stain on individual papers, says Tim Errington, the manager of the reproducibility project, who works at the Center for Open Science in Charlottesville, Virginia. Investigators should take results as information, not condemnation, says Errington. “If we just see someone else’s evidence as ­making it hard for the person who did the original research, there is something wrong with our culture.”

    But Ruoslahti worries that the failure to reproduce his results will weaken his ability to raise money for DrugCendR, a company in La Jolla that he founded to develop his therapy. “I’m sure it will,” he says. “I just don’t know how badly.”

    Repeated attempts

    The Reproducibility Project: Cancer Biology launched in 2013 as an ambitious effort to scrutinize key findings in 50 cancer papers published in Nature, Science, Cell and other high-impact journals. It aims to determine what fraction of influential cancer biology studies are probably sound — a pressing question for the field. In 2012, researchers at the biotechnology firm Amgen in Thousand Oaks, California, announced that they had failed to replicate 47 of 53 landmark cancer papers [2]. That was widely reported, but Amgen has not identified the studies involved.

    The reproducibility project, by contrast, makes all its findings open — hence Ruoslahti’s discomfort. Two years in, the project downsized to 29 papers, citing budget constraints among other factors: the Laura and John Arnold Foundation in Houston, Texas, which funds the ­project, has committed close to US$2 million for it. Full results should appear by the end of the year. But seven of the replication studies are now complete, and eLife is publishing five fully analysed efforts on 19 January.

    These five paint a muddy picture (see ‘Muddy waters). Although the attempt to replicate Ruoslahti’s results failed [3], two of the other attempts [4], [5] “substantially reproduced” research findings — although not all experiments met thresholds of statistical significance, says Sean Morrison, a senior editor at eLife. The remaining two [6], [7] yielded “uninterpretable results”, he says: because of problems with these efforts, no clear comparison can be made with the original work.

    Muddy waters

    http://dx.doi.org/10.1126/scitranslmed.3001318
    http://dx.doi.org/10.1126/science.1183057
    http://dx.doi.org/10.1073/pnas.1121623109
    http://dx.doi.org/10.1016/j.cell.2011.08.017
    http://dx.doi.org/10.1038/nature11071

    “For people keeping score at home, right now it’s kind of two out of three that appear to have been reproduced,” says Morrison, who studies cancer and stem cells at the University of Texas Southwestern Medical Center in Dallas.

    Nature spoke to corresponding authors for all of the original reports. Some praised the reproducibility project, but others worried that the project might unfairly discredit their work. “Careers are on the line here if this comes out the wrong way,” says Atul Butte, a computational biologist at the University of California, San Francisco, whose own paper was mostly substantiated by the replication team.

    1
    Erkki Ruoslahti says he’s worried that the reproducibility project’s inability to validate his findings will affect his ability to launch a cancer drug trial.

    The reason for the two “uninterpretable” results, Morrison says, is that things went wrong with tests to measure the growth of tumours in the replication attempts. When this happened, the replication researchers — who were either at contract research labs or at core facilities in academic institutions — were not allowed to deviate from the peer-reviewed protocols that they had agreed at the start of their experiments (in consultation with the original authors). So they simply reported the problem. Doing anything else — such as changing the experimental conditions or restarting the work — would have introduced bias, says Errington.

    Such conflicts mean that the replication efforts are not very informative, says Levi Garraway, a cancer biologist at the Dana-Farber Cancer Institute in Boston, Massachusetts. “You can’t distinguish between a trivial reason for a result versus a profound result,” he says. In his study, which identified mutations that accelerate cancer formation, cells that did not carry the mutations grew much faster in the replication effort7 — perhaps because of changes in cell culture. This meant that the replication couldn’t be compared to the original.

    Devil’s in the details

    Perhaps the clearest finding from the project is that many papers include too few details about their methods, says Errington. Replication teams spent many hours working with the original authors to chase down protocols and reagents, in many cases because they had been developed by students and postdocs who were no longer with the lab. Even so, the final reports include long lists of reasons why the replication studies might have turned out differently — from laboratory temperatures to tiny variations in how a drug was delivered. If the project helps to bring such confusing details to the surface, it will have performed a great service, Errington says.

    Others think that the main value of the project is to encourage scepticism. “Commonly, investigators take published results at face value and move on without reproducing the critical experiments themselves,” says Glenn Begley, an author of the 2012 Amgen report.

    That’s not the case for Albrecht Piiper, a liver-cancer researcher at the University Hospital Frankfurt in Germany. Piiper has replicated Ruoslahti’s work in his own lab [8]. Despite the latest result, he says, he has “no doubt” about the validity of Ruoslahti’s paper.

    eferences

    1. Sugahara, K. N. et al. Science 328, 1031–1035 (2010).
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    2. Begley, C. G. & Ellis, L. M. Nature 483, 531–533 (2012).
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    3. Mantis, C. et al. eLife 6, e17584 (2017).
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    4. Aird, F. et al. eLife 6, e21253 (2017).
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    5. Kandela, I. et al. eLife 6, e17044 (2017).
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    6. Horrigan, S. K. et al. eLife 6, e18173 (2017).
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    7. Horrigan, S. K. et al. eLife 6, e21634 (2017).
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    8. Schmithals, C. et al. Cancer Res. 75, 3147–3154 (2015).
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  • richardmitnick 8:46 am on January 21, 2017 Permalink | Reply
    Tags: , Cancer, , Pancreatic tumors rely on signals from surrounding cells,   

    From SALK: “Pancreatic tumors rely on signals from surrounding cells” 

    Salk Institute bloc

    Salk Institute for Biological Studies

    January 19, 2017

    Salk scientists find that targeting the interaction between a pancreatic tumor and its microenvironment could weaken cancer.

    1
    Tumor cells stained with a marker for cancer (green) appear near stromal cells (red). Credit: Salk Institute.

    Just as an invasive weed might need nutrient-rich soil and water to grow, many cancers rely on the right surroundings in the body to thrive. A tumor’s microenvironment—the nearby tissues, immune cells, blood vessels and extracellular matrix—has long been known to play a role in the tumor’s growth.

    Now, Salk scientists have pinned down how signals from this microenvironment encourage pancreatic tumors to grow by altering their metabolism. Blocking the pathways involved, they reported in Proceedings of the National Academy of Sciences the week of January 16, 2017, can slow the growth of a pancreatic cancer.

    “Pancreatic cancer is a deadly disease and is very understudied when it comes to how it communicates with the microenvironment,” says senior author Ronald Evans, director of Salk’s Gene Expression Laboratory, a Howard Hughes Medical Institute investigator and holder of the March of Dimes Chair in Molecular and Developmental Biology. “Our findings open up a lot of avenues for future study.”

    Pancreatic cancer has the worst five-year survival rate of any major cancer and is expected to be the second leading cause of cancer deaths by the year 2030. It’s notoriously resistant to both chemotherapies and emerging immunotherapies, Evans says, emphasizing the importance of new treatment paradigms.

    2
    A marker for cancer (green) appears near stomal cells (red) in tumor cells. Credit: Salk Institute.

    Previous research has shown that the signals coming from surrounding stromal cells include both supportive signals—which help pancreatic tumors grow—and suppressive signals—which try to fight the cancer. To understand specifically how pancreatic cancer cells take advantage of any supportive signals, Evans’s team first had to come up with a method to mimic how pancreatic cancer cells grow so closely integrated with the stroma.

    “We worked out a culture system so that we could grow human pancreatic cells in a three-dimensional system in both the presence and absense of stromal signals,” says first author Mara Sherman, a former Salk postdoctoral research fellow now at Oregon Health & Science University.

    When stromal signaling molecules—isolated from patients or generated in the lab—were present, the metabolism of pancreatic cancer cells changed, the researchers found. Not only were levels of metabolic compounds different, but the expression of certain genes involved in metabolism was turned up, and the epigenome of the cells—molecular markers on DNA that change gene expression on a broader scale—was altered.

    “The tumor is essentially hacking into that stromal microenvironment and grabbing what it needs to up its metabolism,” says Michael Downes, a Salk senior scientist involved in the research.

    3
    From left: Ronald Evans, Mara Sherman, Ruth Yu, Ann Atkins, Tiffany Tseng and Michael Downes. Credit: Salk Institute.

    To try to block this “hacking” of the microenvironment by the cancer cells, the team turned to a drug called JQ1, which is known to block the epigenome changes that they’d observed. Indeed, when JQ1 was added to the 3D culture system, it reversed the genetic changes to the pancreatic cancer cells that the stromal signals had caused. Moreover, when mice with pancreatic tumors were treated with JQ1, tumor growth was slowed.

    More work is needed to reveal whether JQ1, or similar compounds, can shrink or slow the growth of pancreatic tumors in humans and what other pathways in the cancer cells may be responding to the tumor microenvironment, but the findings pave the way for that research.

    Other researchers on the study were Ruth T. Yu, Tiffany W. Tseng, Sihao Liu, Morgan Truitt, Nanhai He, Ning Ding, Annette Atkins, and Mathias Leblanc of the Salk Institute; Cristovao Sousa of Harvard Medical School; Christopher Liddle of the University of Sydney; Eric Collisson of the University of California, San Francisco; John Asara of Beth Israel Deaconess Medical Center; and Alec Kimmelman of the Dana-Farmer Cancer Institute.

    The work and the researchers involved were supported by grants from the National Institutes of Health, the Glenn Foundation for Medical Research, the Leona M. and Harry B. Helmsley Charitable Trust, and Ipsen/Biomeasure.

    See the full article here .

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    Every cure has a starting point. Like Dr. Jonas Salk when he conquered polio, Salk scientists are dedicated to innovative biological research. Exploring the molecular basis of diseases makes curing them more likely. In an outstanding and unique environment we gather the foremost scientific minds in the world and give them the freedom to work collaboratively and think creatively. For over 50 years this wide-ranging scientific inquiry has yielded life-changing discoveries impacting human health. We are home to Nobel Laureates and members of the National Academy of Sciences who train and mentor the next generation of international scientists. We lead biological research. We prize discovery. Salk is where cures begin.

     
  • richardmitnick 3:28 pm on January 18, 2017 Permalink | Reply
    Tags: , C. Vivian Stringer, Cancer, Gianna DeVeitro, , Rutgers Women's Basketball   

    From Rutgers: “Rutgers Alumna Gains Strength in Battle Against Cancer from Supporters” 

    Rutgers University
    Rutgers University

    January 17, 2017
    Sherrie Negrea

    1
    Gianna DeVeitro, right, with C. Vivian Stringer, head coach of the Scarlet Knights. Gianna is a former student manager of the women’s basketball team. Photo: Courtesy of Larry Perfetti

    Gianna DeVeitro ‘16 had just graduated from Rutgers and celebrated the end of college by visiting a friend in Florida. She was back home in New Jersey looking for a job at a TV station or magazine when she suddenly began having severe abdominal pain and a fever.

    Her family physician suspected acid reflux, but when her pain intensified, DeVeitro was sent to Inspira Medical Center Woodbury, near her home in Deptford. She was released but readmitted two days later when her fever reached 102, and this time, her doctor ordered a blood analysis. “When the pathologist was looking at the blood smear, they then noticed I had abnormal cells, and they knew I had leukemia,” DeVeitro says.

    Her diagnosis of acute myeloid leukemia last July began a roller-coaster of treatment that has consumed DeVeitro’s life, from her first round of chemotherapy (which failed) to the second, followed by a bone marrow transplant at the Hospital of the University of Pennsylvania. A week after her potentially life-saving transplant, a drug she was allergic to caused her temperature to spike to nearly 107.

    Through it all, however, DeVeitro has been comforted in her battle against cancer by the support of a close-knit group of Rutgers alumni, athletes and coaches who have one thing in common: Rutgers women’s basketball. Since her diagnosis, Scarlet Knights team members, coaches and fans have all rallied round DeVeitro, who was a student manager of the team and a member of the Rutgers Women’s Club Basketball.

    As a student manager for the team for two years, DeVeitro spent up to five hours a day scheduling and tracking the players’ practice, timing their drills and buying groceries and drinks for the girls. “Everyone wants to give back to Gianna because she gave so much to us,” says C. Vivian Stringer, head coach of the Scarlet Knights. “She’s so young and beautiful, and the world’s ahead of her – and then for this to happen.”

    Just five days before her bone-marrow transplant in November, Stringer and the entire team visited DeVeitro at the Hospital of the University of Pennsylvania after their game at Drexel University in Philadelphia. Stringer recalls how impressed she was with DeVeitro’s positive attitude toward her treatment.

    “It did us well to feel the energy and see what it means to have a spirit of fight inside,” says Stringer, adding that DeVeitro reminded her of her father, who had both his legs amputated but then went back to work as a coal miner. “Gianna is a living spirit for all of us.”

    DeVeitro’s fight to overcome leukemia also attracted the attention of Larry Perfetti, a three-time Rutgers graduate and retired psychologist whose daughter Kiersten died of cancer when she was 22. Like her parents, Kiersten, who had attended Goucher College for one year before her diagnosis, was a loyal Scarlet Knights fan.

    “She was the most fanatic of the Rutgers women’s basketball fans,” says Perfetti, a Highland Park resident who once brought his family to France to accompany the basketball team on tour. “She considered Coach Stringer her basketball mother. Coach Stringer taught her how to play basketball, and she was very encouraging. And Coach Stringer flew back from Iowa to attend our daughter’s wake.”

    2
    Coach Stringer and the Scarlet Knights team visit DeVeitro, center, at the Hospital of the University of Pennsylvania. Photo: Courtesy of Larry Perfetti

    A year before she died in 2008, Kiersten founded a nonprofit called Kier’s Kidz to raise money to help children and young adults with cancer by funding organizations such as the Ronald McDonald House and Alex’s Lemonade Stand. Since Kier’s Kidz received tax-exempt status in 2012, it has provided direct financial and emotional support to children and young adults with cancer and their families.

    In October, Perfetti, the CEO of Kier’s Kidz, created a crowd-funding site on the platform youcaring.com to help DeVeitro’s family with their financial hardships. DeVeitro mother, Tina, who is single, was forced to quit her job as a medical assistant last August so she could provide round-the-clock care for Gianna. The crowd-funding campaign has so far raised $3,725 of its targeted $35,000 needed to help the family survive financially until Tina can return to work, Perfetti says.

    Since her release from the hospital the day after Thanksgiving, DeVeitro has been recovering at home while recording her daily progress on her Facebook page, One Cell At A Time. She still plans to use her journalism and media studies degree from Rutgers’ School of Communication and Information to find a job but also hopes to write a book about her experience battling leukemia.

    Her goal is to educate people about the disease and the need for bone marrow donors to help patients overcome it. “I just want to bring as much awareness about leukemia as possible,” she says. “And I just want more people to become donors, because it really does save lives.”

    For media inquiries, contact Carla Cantor at ccantor@ucm.rutgers.edu or 848-932-0555.

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  • richardmitnick 12:45 pm on January 17, 2017 Permalink | Reply
    Tags: , Cancer, ,   

    From Vanderbilt: “Softening tumor tissue could aid cancer treatments” 

    Vanderbilt U Bloc

    Vanderbilt University

    Jan. 16, 2017
    Liz Entman

    Softening tumors’ blood vessels may help more chemo reach the cancer

    Normally, the glue that holds cells together in the human body – what scientists call the extracellular matrix – is soft and pliable. But when a metastatic tumor forms it causes the matrix surrounding it to stiffen.

    According to a new study, this mechanical effect produces changes in the blood vessels that feed the tumor in a way that can reduce the effectiveness of chemotherapeutics and radiation treatments. The finding suggests that softening this protective layer could make existing cancer treatments more effective.

    2
    Cynthia Reinhart-King (Steve Green/Vanderbilt)

    The study was published Dec. 22 in the Proceedings of the National Academy of Sciences, by a team of researchers led by Vanderbilt Professor of Biomedical Engineering Cynthia Reinhart-King, which includes postdoctoral researcher François Bordeleau in the Reinhart-King group along with collaborators from Cornell University. The report is titled Matrix Stiffening Promotes a Tumor Vasculature Phenotype.

    For years, the idea has been that the way to treat tumors was to starve them by killing off their blood vessels. While that works in some cases, in others it only serves to make the tumor more aggressive, Reinhart-King said, adding: “There are ways tumors can grow in the absence of those nutrients, and they get more aggressive. At the same time, they may also stop responding to some chemotherapeutics and radiation treatments.”

    A metastatic tumor’s blood vessels tend to be malformed and more permeable than blood vessels in healthy tissue. For this reason, fluid tends to leak from the vessels, building up pressure inside the tumor that prevents drugs from getting to their target.

    “Basically, as fluid leaks out of the blood vessels, it causes high pressures to build up in the tumor. These high pressures can cause blood flow to stall or even reverse and vessels tocollapse,” Reinhart-King said. “So fluid, including the drugs, cannot reach the tumor tissue.”

    3
    Image of a mammary tumor stained for cell nuclei (in blue), blood vessels (in green) and the protein beta-catenin that causes cells to stick together (in red) (Reinhart-King Lab / Vanderbilt)

    Unlike in previous work in this area, Reinhart-King and Bordeleau see the vascular breakdown as a product of the stiffening of the tumor and its matrix, which triggers proteins in cells to alter vascular growth and integrity. Previous work has targeted chemical factors, in particular vascular endothelial growth factor.

    “The idea that you would want to restore barrier integrity and help blood vessels is not a new one,” Reinhart-King said. “The idea that we discovered is that it’s controlled through matrix stiffness.” This, in turn, suggests that promoting healthy vasculature through a softening of the extracellular matrix would use the tumor itself as a conduit for delivering cancer-killing drugs.

    “What we show,” Reinhart-King said, “is that we can drive a lot of the same behaviors that are typically thought to occur due to chemical changes, by changing the mechanical properties of the tumor.”

    This work was supported by National Institutes of Health grants R01-HL127499 and R01-CA163255 and National Science Foundation awards 1055502 and 435755.

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