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MDD’s Oncology Extra WEDNESDAY, MARCH 6, 2013 PAGE 1 OF 2

A D D I T I O N A L D E V E L O P M E N T S I N O N E O F M E D - T E C H ’ S K E Y S E C T O R S

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Keeping you up to date on recent developments in oncology

Toward ‘gamifying’ cancer diagnosis . . . Making sense of diagnostic images is not always easy, but according to a March 1 statement by Cancer Research UK (London), there may soon be a time when a single image can be examined by thousands of pairs of eyes in an effort to pinpoint whether the lesion is indeed a cancerous one. Cancer Research UK indicates it is “bringing together the charity’s world-leading scientists alongside technology gurus, such as Amazon Web Services, Facebook and Google, to design and develop a mobile game to accelerate cures for cancer,” games that can be loaded onto smart- phones. The statement explains that “anyone with a smart phone and five minutes to spare on a bus journey will be able to play an enjoyable game that will simultaneously investigate vital scientific data.” The first phase in this effort will be to assemble forty computer programmers, gamers, graphic designers and others to participate in a weekend “hackathon,” to turn Cancer Research UK’s raw gene data into a game format, which will bear the working title of GeneRun, a diagnostic game “for citizen scientists to play,” the state- ment notes. Cancer Science UK remarks that its research into the causes of cancer has yielded enormous amounts of data, but remarked that those data “need to be analyzed by people rather than machines.” At present, diagnostic software is not able to “detect subtle changes” in tissues, at least not to the degree of precision the human eye can offer, and Cancer Science UK says that the hope is that “with the collective power of hundreds of thousands of people across the globe helping our scientists to analyze this data we could drastically speed up research – hopefully saving lives faster.” The statement notes that GeneRun is not the first program of its type, noting that a previous game, Cell Slider, “launched as a beta test in October 2012 to analyze archived cancer tissue samples.”

Growth factor block could aid medulloblastoma treatments . . . Elimi- nating cancer entirely is the overall objective, but in the meantime scientists are often focused on suppress- ing tumor growth, and researchers at a number of institutions including Massachusetts General Hospi- tal (MGH; Boston) believe they have arrived at a means of blocking the growth of medulloblastomas. The March 3 MGH statement reminds that medulloblastomas, which originate in the cerebellum, make up roughly “20% of all pediatric brain tumors and is 10 times more common in children than in adults.” Aggres- sive use of surgery, chemotherapy and radiation can boost patient survival, but those treatments can exert long-term effects on development, behavior, and neurology, “particularly in the youngest patients,” the statement points out. However, researchers believe they have arrived at a molecular pathway that may be vital in the proliferation of medulloblastoma, and hence possibly a mechanism by which to block these brain tumors. One of the drivers for this effort was a series of studies by Peter Carmeliet, MD, of the Vesa- lius Research Center (Leuven, Belgium), who established that an antibody against placental growth fac- tor (PlGF) “could block angiogenesis in a number of adult tumors.” Perhaps the most interesting thing about P1GF is that it is not required for typical post-natal development, and hence could serve as a vehicle for tumor anti-angiogenesis. Other research suggested that high expression of the P1GF receptor neuropilin 1 (Nrp1) was “associated with poor survival in patients,” the statement explains. Another finding of interest was that most PlGF was “produced by surrounding supportive tissue called stroma and not by the tumor cells,” and hence any therapy that blocks interactions between P1GF and Nrp1 could not only block tumor growth, but would also be “less likely to lead to treatment resistance than are therapies directly targeting mutations that drive tumor growth.” Rakesh Jain, PhD, director of the Steele Laboratory for Tumor Biology at MGH and corresponding author of the study, explained that “the importance of tumor-stromal interac- tions has been recognized for decades, especially the formation of new blood vessels to supply tumors,” but he added that these developments support “the exciting possibility that targeting that pathway in medulloblastoma could be more broadly effective with fewer side effects for patients.” However, Jain cau- tioned that antibodies against both PlGF and Nrp1 “have been developed and tested in adult patients,” but that any expectation that they could be safely used for pediatric patients “needs to be established in clinical trials.” The results of this study appear in Cell.

WEDNESDAY, MARCH 6, 2013 MDD’S ONCOLOGY EXTRA PAGE 2 OF 2

U Saskatchewan ready to go with MIP . . . The medical isotope crunch has driven a lot of efforts to boost supplies of technetium-99, and a Feb. 28 statement by the University of Saskatch- ewan (Saskatoon) indicates that one such effort is ready to roll. The statement notes that scientists in charge of the Canadian Light Source synchrotron are ready to test a facility dubbed the Medical Isotope Project (MIP) after hearing from the Canadian Nuclear Safety Commission that the facility is licensed. The MIP still has to undergo “rigorous testing to ensure the facility is ready to produce medical isotopes in the very near future,” the statement notes, but if all goes well, Canada will have at least enough from this one facility to handle the needs of the nation’s population of 30 million. The statement explains that the MIP operation will use a particle accelerator to bombard a target of molybdenum-100 with high-energy X-rays, which will free a neutron from the nuclei of some of the molybdenum-100 atoms. This process produces molybdenum-99, which of course decays into technetium-99. After a cycle of X-ray blasting, workers at the facility will recapture the remaining molybdenum-100 for recycling into fresh targets. Mark de Jong, PhD, director of accelerators at CLS, said “we have made tremendous progress so that we can begin the produc- tion of isotopes very soon,” adding that the objective is “to produce medical isotopes safely, reliably and affordably, and we have almost reached that goal.”

Large volume of data built a ‘snip’ at a time . . . Single-nucleotide polymor- phisms, or SNPs, have been of intense recent interest where cancer treatment is concerned, and a recent memo posted at the website of the National Cancer Institute suggests that a large database of “snips,” as SNPs are sometimes called, might lead to a better model for predicting an inherited predisposition to can- cer. NCI scientists are said to have come up with “a new paradigm” to assess hereditary risk based on poly- genic analysis, and the memo remarks that each SNP “contributes a very small amount to overall disease risk, but [have] a strong effect when grouped together.” NCI’s Nilanjan Chatterjee, PhD, and colleagues have worked to develop what is described as a “very large” genome-wide association study (GWAS) to craft the kinds of polygenic models that can compute an individual’s risk scores for hereditary diseases. NCI notes that there are “likely to be thousands of SNPs responsible for common health outcomes,” adding that a polygenic model for prostate cancer based on the current data at NCI “would categorize 7% of the popula- tion as a high-risk group,” a tally said to be “at least twice the risk for prostate cancer compared to men at average risk.” The NCI researchers are said to be of the mind that a tripling of GWAS sample sizes could improve the risk-stratification of the prostate cancer model and render 12% of the population high-risk men, although NCI did not specify precisely what would qualify as high risk in that approach. The authors are said to have cautioned that any strategy for early diagnosis and prevention that focuses strictly on geneti- cally high-risk individuals “would be incomplete,” and that information “about other risk factors, including family medical history, would be needed to enhance the broader utility of these models.” The results of this work appeared in the March 3, 2013, edition of Nature Genetics.

— Compiled by Mark McCarty, MDD Washington Editor [email protected]

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