Dow Jones Reprints: This copy is for your personal, non-commercial use only. To order presentation-ready copies for distribution to your colleagues, clients or customers, use the Order Reprints tool at the bottom of any article or visit www.djreprints.com ||||| Two large research teams have produced exhaustive genomic studies that reveal the most detailed catalog yet of the mutations that drive two deadly cancers—endometrial cancer and acute myeloid leukemia. The two studies of samples taken from hundreds of patients suggest new possible drug targets and ways to divide cancers into subtypes that might respond differently to treatment. 
 
 The new data are the latest fruits of a major national effort to create an atlas of the DNA blueprints of at least 20 types of cancer. Genomic data have been churned out in the past few years for five other cancers, and more are expected over the next year. 
 
 While the results are being hailed as major technological and scientific feats that provide powerful insights into diseases in dire need of progress, they are just first steps toward the goals most patients and physicians care about: lengthening lives or curing cancer. 
 
 Dana-Farber Cancer Institute adult leukemia specialist Dr. David Steensma welcomed the new data, but also provided a bit of a reality check on how far the knowledge is from changing patient care, in an essay published in the New England Journal of Medicine called “The Beginning of the End of the Beginning in Cancer Genomics.” 
 
 Steensma argues that data-rich genome studies of cancer are a crucial step, providing information that will guide drug developers and the design of clinical trials. But he notes that as the era of generating these large reference datasets is coming to a close, a new phase of research will open up. The genome is a powerful starting position in the effort to transform patient care and treat cancers more effectively, not the end. 
 
 Mapping the genomic architecture of most major cancers is “already being done or almost done,” Steensma said. “That sort of huge survey, that sort of large landscape of what’s actually mutated in these tumors is going to be done within a year or two for all the common tumors, all the really big killers. ... So we’re getting to the end of that first era.” 
 
 Steensma draws an analogy to 1803, when explorers Meriwether Lewis and William Clark began preparing to map the west. The cancer genome atlas, Steensma argues, is like that first exploration of unknown territory. But that initial survey was just the beginning. Today, when property is sold, land surveyors still go out and denote boundaries; what were once the tools of discovery are now used in everyday transactions. Steensma foresees the same thing happening as knowing the genomic landscape of the tumors is integrated into the clinic. 
 
 Steensma views the new data as a boon that might help alter a depressing state of affairs in his field, in which treatment of acute myeloid leukemia hasn’t changed from a chemotherapy regimen that was developed when he was a kid playing Little League in the 1970s. 
 
 “There have been more than 30 trials trying to improve on that, and nothing has been shown to be better,” Steensma said. 
 
 Steensma says the new data point to new therapeutic strategies that could be tried and novelways to partition patients into groups. For example, a Cambridge biotechnology company, Agios Pharmaceuticals, has drugs in development that target a mutated gene found in a fraction of cases of AML. 
 
 The study of endometrial cancer, published in the journal Nature, similarly opens up new research avenues, said Raju Kucherlapati, a professor of genetics at Harvard Medical School and Brigham and Women’s Hospital and a co-author of the study. 
 
 Endometrial tumors are often classified based on the types of cells in the tumor and traditional pathological examination of the tissue. What the new study suggests, Kucherlapati said, is that genetic analysis could provide a more effective way of classifying the disease into subtypes, using criteria such as the number of extra copies of stretches of DNA. 
 
 “If you classify them [the tumors] based on these new criteria, you might be able to have better therapeutic approaches,” Kucherlapati said. For example, the new data indicate that a certain subset of patients might benefit from chemotherapy, rather than radiation. 
 
 That’s a hypothesis that will have to be tested in patients to see whether it turns out to be true. The paper also hints at the broader use of the cancer genome atlas, as a tool to navigate cancer. But identifying which features are important landmarks that could help guide treatment will require new studies, informed by the DNA databases now being compiled. ||||| “This is exploring the landscape of cancer genomics,” said Dr. David P. Steensma, a leukemia researcher at the Dana-Farber Cancer Institute who was not involved with the studies. “Many developments in medicine are about treatments or tests that are only useful for a certain period of time until something better comes by. But this is something that will be useful 200 years from now. This is a landmark that will stand the test of time.” 
 
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 Dr. Douglas Levine of Memorial Sloan Kettering Cancer Center, the principal investigator on the endometrial cancer study, said the group scoured the country for samples of this cancer. 
 
 The cancer has long been evaluated by pathologists who examine thin slices of endometrial tumors under a microscope and put them in one of two broad categories. But the method is not ideal. In general, one category predicts a good prognosis and tumors that could be treated with surgery and radiation, while the other holds a poorer prognosis and requires chemotherapy after surgery. But pathologists often disagree about how to classify the tumors and can find it difficult to distinguish between the two types, Dr. Levine said. 
 
 The new genetic analysis of hundreds of tumors found patterns of genetic aberrations that more precisely classify the tumors, dividing them into four distinct groups. About 10 percent of tumors that had seemed easily treated with the old type of exam now appear to be more deadly according to the genetic analysis and would require chemotherapy. 
 
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 Another finding was that many endometrial cancers had a mutation in a gene that had been seen before only in colon cancers. The mutation disables a system for repairing DNA damage, resulting in 100 times more mutations than typically occur in cancer cells. 
 
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 “That was a complete surprise,” Dr. Levine said. 
 
 It turned out to be good news. Endometrial cancers with the mutation had better outcomes, perhaps because the accumulating DNA damage is devastating to cancer cells. 
 
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 Another surprise was that the worst endometrial tumors were so similar to the most lethal ovarian and breast cancers, raising the tantalizing possibility that the three deadly cancers might respond to the same drugs. 
 
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 Jeff Boyd, executive director of the Cancer Genome Institute at Fox Chase Cancer Center, who was not involved with the new research, said the similarity among breast, ovarian and endometrial tumors was the best example yet of the idea that cancers are more usefully classified by their gene mutations than by where they originate. Though many scientists believe this view is correct, Dr. Boyd said, “It is very rewarding — I can’t overstate it” to see it validated with real data. 
 
 While the genetics of endometrial cancer had gone largely unstudied until now, acute myeloid leukemia has been investigated for decades, in part because leukemia cells are so accessible. They are in the blood and bone marrow. 
 
 Using microscopes and special staining methods, researchers had already discovered, for example, that chromosomes in these leukemia cells are often broken or hooked together in strange ways. They also knew that some chromosomal alterations were associated with a good prognosis, and others with a bad one. Patients with a good prognosis can usually be treated with chemotherapy alone while those with a worse prognosis need the expensive, difficult and risky treatment of last resort: a bone marrow transplant. It comes with a 10 percent death rate. 
 
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 The problem was that the traditional methods for categorizing the leukemia were imprecise, said Dr. Timothy Ley of Washington University in St. Louis, who led the study with Richard Wilson, also of Washington University. Nearly half the acute myeloid leukemias had normal chromosomes. There was no good way to decide which treatment these patients needed. Some did well with chemotherapy; some did poorly. 
 
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 “It was a huge conundrum,” Dr. Ley said. “For patients who cannot be cured with chemotherapy, we have a potentially curative therapy. But picking the right patients for a transplant was very difficult.” 
 
 The new study of 200 acute myeloid leukemias identified at least 260 genes that were mutated in at least 2 of the 200 leukemia samples, finding virtually all of the common genetic malfunctions that occur in it. Now researchers have a new foundation for assessing which cancers will be lethal unless the patient gets a risky bone marrow transplant and which can be treated with chemotherapy alone. 
 
 “We have the basic playbook,” Dr. Ley said. “We finally know what the major pathways are and what all the major mutations look like.” And knowing which genes are mutated also allows researchers to investigate drugs that target those genes. 
 
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 The next step will be for investigators to determine which mutations lead to good or bad outcomes. 
 
 “Within two or three years, risk assessment may be dramatically better,” Dr. Ley said. “It certainly sets the stage for the next era of therapy.”
– Two major studies of common cancers have zeroed in on the particular gene mutations associated with both, a breakthrough that could lead to better treatment for those with acute myeloid leukemia and endometrial cancer, reports the Boston Globe. But the studies also lend credence to a broader idea: that our traditional way of defining cancer by the organ in which it originates is outdated, reports the New York Times. Instead, it might be time to start thinking of cancer in terms of genetic mutations. In the latest studies, for example, researchers were surprised to discover that the worst endometrial tumors of the uterine were remarkably similar to the worst forms of breast and ovarian cancer. That raises "the tantalizing possibility that the three deadly cancers might respond to the same drugs," writes the Times' Gina Kolata. This emerging approach is called "precision medicine," notes the Wall Street Journal. The theory has been around for a while, but the new research under the sprawling Cancer Genome Atlas project seems to validate it. "It is very rewarding—I can't overstate it," says one expert not affiliated with the work.