Patterns of cancer incidence and mortality across Europe are as varied as the continent’s geography. But a new report finds that, in general, obesity and tobacco use are driving cancer incidence, mortality, and survival across Europe: Overall cancer incidence has decreased since the mid-1990s in northern and western Europe except for obesity-related cancers, and incidence of and mortality from tobacco-related cancers is falling among men in northern, western, and southern Europe but increasing in central Europe.
The analysis, published in the June issue of the European Journal of Cancer, comes as two Europe-wide efforts related to cancer take shape: The European Code Against Cancer is about to be updated for the first time in 5 years, and the European Commission is gearing up to create a cancer plan for the entire European Union.
Cancer prevention and survivorship feature prominently in England’s latest update to its national cancer plan. The update—called the cancer reform strategy—comes with £370 million (US$740 million) in new funding, though critics say that’s not nearly enough to make effective changes.
“Cancer’s a fast-moving area, and we’ve made a lot of strides in a lot of different areas. [The cancer reform strategy] is moving the agenda on with a focus on areas that weren’t focused on as strongly in the cancer plan,” said Teresa Moss, director of the National Cancer Action Team, part of England’s National Health Service (NHS).
Although the original cancer plan in 2000 did cover some aspects of prevention, the update strengthens the focus. “It’s a slightly different emphasis,” said Catherine Foot, head of policy for Cancer Research UK. “For instance, in 2000, the evidence wasn’t as clear as it is now on the link between obesity and cancer. In 2000, the policy initiatives on diet and cancer were things like the 5-a-day fruit and vegetable initiative, whereas now, we’re looking at obesity and weight management. It’s a shift in priorities.”
The name Jon Sudbø is one that many in the cancer community will not soon forget. In early 2006, Sudbø admitted to fabricating patient data used in a study of nonsteroidal anti-inflammatory drugs and oral cancer risk published in The Lancet. Sudbø’s institution, the Norwegian Radium Hospital, promptly appointed a special commission to investigate all his research from the previous decade. The commission found evidence of falsified and fabricated data dating back to Sudbø’s Ph.D. project (J Natl Cancer Inst 2006;98:374–6).
The findings prompted the Norwegian government to formally put into place national research ethics committees tasked with proactive, preventive education on research integrity. The government also established a national office chaired by a judge to investigate cases of alleged scientific misconduct, and new legislation on ethics and integrity in research went into effect in July of this year.
The Sudbø case has parallels all over the world: Research misconduct made national headlines and led to a new national policy that defined the concept and set out a course of disciplinary action against future offenders. In September, the European Science Foundation and the U.S. Office of Research Integrity held the first world conference on research integrity to give researchers and policymakers from around the globe a chance to share their experiences in establishing such systems, as well as to discuss what a global framework for research integrity might look like.
The growing globalization of science is a major driving force behind a push to establish a world standard. “We are no longer dealing with single-investigator projects,” said Lida Anestidou, D.V.M., Ph.D., of the Institute for Laboratory Animal Research at the National Academies. “We have multicultural, multinational, multi-institutional, multi-investigator, very expensive investigations. Therefore, [the number of coauthors has] risen dramatically, and disputes over credit, over intellectual property, and over patents have all risen dramatically.”
It seems like cancer should be the least of the health worries in most of the countries on the African continent, where communicable diseases are the leading cause of death and the life expectancy in more than half of the countries is under 50 years.
Compared with those of Western countries, cancer rates in the region are relatively low. But the prognosis for cancer in Africa looks grim: In sub-Saharan Africa, there were 582,000 new cancers diagnosed in 2002, and 412,100 people died from the disease. If no interventions are put in place, it’s expected that the number of new cases diagnosed will rise to 804,000 and mortality will reach 626,400 by 2020.
The reasons why vary: Skyrocketing rates of human immunodeficiency virus (HIV)/AIDS have led to a rapid increase in the incidence of Kaposi sarcoma and other AIDS-related cancers; risk factors such as obesity and alcohol use are on the rise, affecting cancer and other noncommunicable diseases that share these risks; and there is a worrisome escalation in smoking rates among Africans, a trend that, if it continues, is sure to lead to a glut of tobacco-related cancers.
“I was taught in medical school that cancer is not a problem in Africa. But that is a myth,” said Twalib Ngoma, M.D., executive director of the Ocean Road Cancer Institute in Dar es Salaam, Tanzania. “If we don’t do something now, [cancer rates are] going to increase. We should not be complacent just because we find that infections are more of a problem now.”
Before Bali Pulendran started his first major protocol at the Emory Vaccine Center in Atlanta, he wanted to meet his subjects. So, in the fall of 2004 he and postdoc Marcin Kwissa drove the 25 miles to Lawrenceville, Georgia, and the Yerkes Primate Research Center’s field station. There, Pulendran and Kwissa stood face to face with their trial participants: 25 rhesus macaques. “I remember staring at them and thinking: ‘Wow, these are who we’re going to be vaccinating’,” says Pulendran.
Nearly two years have passed and those monkeys now reside in the next building over from Pulendran’s office, where they’ve entered the final phases of a clinical trial for an HIV DNA vaccine developed at the center. The vaccine has already successfully reduced viral load in nonhuman primates, and it’s being tested in humans. Pulendran is adding a new twist, however. Two groups of the immunized monkeys have also received an adjuvant that targets toll-like receptors (TLRs), key components of the innate immune system.
HIV vaccine strategies have been vexed by, among other things, the virus’s ability to disarm the immune system and the immune system’s inability to generate antibodies against the virus. But discoveries just in the past decade have uncovered a wellspring of innate immune targets that appear to converse with the adaptive response and may aid in shutting down HIV. “By giving a TLR ligand with the DNA vaccine, can you make the immune response stronger and get an even more profound effect on the viral load?” he asks. The strategy is young, and at 40 years old, so is Pulendran.
In August 2006, the 25 monkeys were brought to the Atlanta campus to be infected with SIV, and the excitement is palpable. The true test will be whether the subjects that received TLR adjuvants have significantly reduced viral loads. Pulendran has been awaiting the results from the virology lab for weeks. “I’m hopeful,” he says, pausing and then drawing in a deep breath. “But we’ll see.”
Jose M. Ordovas has been studying the role of lipoproteins in heart disease for decades. His laboratory and others have tried to tease out how these proteins factor into why some people
can eat an unhealthy diet – that is, lots of dietary fat – and still have high levels of what is often referred to as good high-density lipoprotein (HDL) cholesterol. The senior scientist and director of the Nutrition and Genomics Laboratory at Tufts University in Boston honed in on APOA1, which encodes the HDL component apolipoprotein (apo) A-I. A specific SNP in its promoter region (APOA1 – 75G/A) was first identified in the early 1980s, and studies in the decade followin scrutinized the association between the G and A alleles and HDL concentrations. The results varied widely. Some studies suggested that carriers of the A allele (about 25% of the population) had higher HDL levels than carriers of the more common G allele, but other studies came to the exact opposite conclusion.
In 2002, he and his colleagues tested whether dietary fat might modulate the effect of the allele. “We decided to consider whether APOA1 is regulated by nutrients, since people are eating different things,” Ordovas recalls. They looked at 755 men and 822 women who were participants in the Framingham Offspring Study, a population for which there are rigorous data on HDL levels, other cardiovascular risk factors, and dietary fat intake. They paired this information with genotype data for each patient and found that the polymorphism on its own didn’t have an effect on HDL level. Instead, in people heterozygous or homozygous for the A allele, “what we found is that polyunsaturated fatty acids, which are very good regulators of gene expression, happen to modulate the expression of this genotype,” Ordovas says.
It was the sort of finding that laid the foundation for the nascent field of nutrigenomics. At its core, the field is the study of how genes and nutrients interact to promote health or disease. It also includes understanding how gene and protein expression are affected by the presence or absence of specific nutrients, whether and how diet-regulated genes play a role in disease, the degree to which an individual’s diet affects the risk of disease given his or her genetics, and whether one’s diet may be altered to maintain that balance between health and disease.