It would set drug development speed records and defy all odds for a drug to enter clinical use within a decade after this sort of tentative laboratory experiment. Yet the story presents this single study that involved not even a single human subject as one that promises to “stop many types of the disease in their tracks” and to allow doctors to use chemotherapy and radiotherapy “with no risk of the disease taking hold elsewhere.” This is exactly the kind of story that leaves readers feeling whipsawed when clinical trials in actual patients may prove disappointing down the road.
Scientists have every right to get excited when they find a new gene or make some advance that they believe holds promise for combating a particular disease. It is up to journalists to rein them in with careful analysis of the evidence and hard questions. This story offers neither. To the families who lose half a billion people every year to cancer in the United States alone, this is the kind of false hope that may cause more harm than good.
This is such an early stage finding it would be premature to throw out cost figures, and there are no comparable treatments that come to mind to serve as cost comparators.
The story does not attempt to quantify the benefits. It says that “levels of the natural inhibitor protein were boosted and the cancer cells remained dormant.” Did this happen every time the scientists blocked the gene? How many times did they repeat this exercise? Did their actions ever make the cancer worse?
There are no mentions of possible harms that might come from blocking a gene. The story calls the gene a “rogue” and a “culprit” but does little to explain what it does. It says it is both inside cancer cells and outside them, destroying “a naturally-occurring protein in the body which normally prevents cancer cells from spreading.” As anyone who has been through cancer treatment knows, knocking out cancer cells through radiation and chemotherapy can take a heavy toll on a person. People can die from infections and other complications. One question might have helped answer the harms question: “When you blocked this rogue gene, what happened to all of the normal cells around the cancer cells?” Anything that alters cell function in tumors could have powerful effects on normal tissue, too. The researchers noted in their article that they have yet to “establish normal and disease expression patterns of all three WWP2 isoforms”. If they don’t yet fully understand the normal form and function of WWP2, the potential for unanticipated effects is a serious concern that the story should have addressed.
The story makes no attempt to evaluate the quality of the evidence. This story badly misrepresents the tentative and uncertain nature of the findings. Only in exceptional cases has a laboratory finding such as this progressed in a straight line to a clinically useful treatment. Indeed, while this report may well spur excitement among researchers, there is nothing that suggests this finding is any more likely to be useful to actual cancer patients than the many other laboratory findings about cancer metastases that have been announced over the past few decades.
The story does not engage in disease-mongering.
The story uses no independent sources. It quotes just two people: Surinder Soond and Andrew Chantry, the two authors of the paper published in Oncogene. (You need a subscription to view it.) The claims made in this story needed independent analysis.
The story makes no comparisons with alternatives. It mentions chemotherapy and radiotherapy in passing. Reading the story carefully, one might believe that any treatment developed from this finding would work only in conjunction with these other treatments. But we can’t be sure. The story should have mentioned other proposed interventions intended to disrupt the spread of cancer cells, including some drugs that are already in clinical trials.
The story says that “the findings mean drugs could be developed in the next 10 years that could be used to halt the aggressive spread of many forms of cancer, including breast cancer, brain, colon and skin cancer.” The story says nothing about all the hoops that remain for a finding to go from the lab to the drug store. Nor does it mention anything about the many cancer “breakthroughs” that have failed to fundamentally alter the rates of cancer incidence or mortality over many decades.
The story says, “Surinder Soond, who worked on the study, said it was a “novel and exciting approach to treating cancer and the spread of tumors which holds great potential.”” Quoting the author, though, does not prove that the approach is novel. The study itself also says that the findings are novel: “Significantly, this is the first report of an interdependent biological role for distinct HECT E3 ubiquitin ligase isoforms, and highlights an entirely novel regulatory paradigm that selectively limits the level of inhibitory and activating Smads.” Of course, that would not make much sense to most readers. So the story should have found a way to explain to readers why the approach to cancer treatment identified was a true advance that opened a new world of possibilities or whether it was a small improvement. And having an independent source evaluate the novelty would have helped as well.
The story does not appear to rely solely on a news release.
Systematic, Criteria-Driven
Monday at #ADA2021, an infectious disease epidemiologist, a journalist, and a researcher shared perspectives on communication of risk in the era of COVID-19: http://ow.ly/ROfR30rMeE7 @AstleyCM @garyschwitzer @berthahidalgo @ADA_DiabetesPro
Shoutouts to @susan_bewley @drkevinknopf @MichaelBaum11 in this call for more than fawning coverage from press releases for these kinds of stories.
Also, linked history inside goes back 5 years just on Grail apparently trying to become Holy Grail. https://twitter.com/garyschwitzer/status/1408849696416841731
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