Smoking, Fuel Use in China Projected to Cause Millions of Deaths

If current levels of smoking and biomass and coal fuel use in homes continues, between 2003 and 2033 there will be an estimated 65 million deaths from chronic obstructive pulmonary disease (COPD) and 18 million deaths from lung cancer in China, accounting for 19 percent and 5 percent of all deaths in that country during this period.

Researchers at the Harvard School of Public Health (HSPH) predict that the combined effects of these two major factors alone will be responsible for more than 80% of COPD deaths and 75 percent of lung cancer deaths in China over a 30-year period. But interventions to reduce smoking and household use of biomass fuels and coal for cooking and heating could significantly reduce the number of deaths.

The findings are from a study that will appear online on October 4 and in the October 25 print issue of The Lancet. It is the first quantitative analysis to look at the combined effects of smoking and household fuel use on COPD, lung cancer and tuberculosis (TB).

Respiratory diseases are among the 10 leading causes of deaths in China. About half of Chinese men smoke and in more than 70 percent of homes in China residents cook and heat their homes with wood, coal and crop residues. Smoking and pollution from indoor burning of these fuels are major risk factors for COPD and lung cancer and have been linked with tuberculosis (TB). Globally, more than 900 million of the world's 1.1 billion smokers currently live in low-income and middle-income countries and about one half of the world's population uses biomass fuels and coal for household energy.

Using data on smoking, fuel use and current as well as projected levels of COPD, lung cancer and TB, the authors set out to estimate the effects of modifying smoking and fuel use on future COPD and lung cancer deaths and TB incidence. They grouped the results into scenarios based on whether interventions involved moderate control of smoking and fuel use, aggressive control or a complete cessation of exposures to the pollutants.

They found that reducing those two risk factors would significantly decrease deaths from COPD and lung cancer. If smoking and biomass and coal use were to be eliminated gradually over the next 30 years, an estimated 26 million COPD deaths (40 percent of projected COPD deaths) and 6 million lung cancer deaths (34 percent of projected lung cancer deaths) would be avoided. For moderate and aggressive control scenarios, deaths from these diseases could be reduced by an estimated 17 percent to 34 percent among men and 18 percent to 29 percent among women. There will also be major benefits for TB, above and beyond those that can be achieved through treatment.

Hsien-Ho Lin, a graduate student in the department of epidemiology at HSPH and the lead author of the study, says "this analysis shows that smoking and fuel use, which affects hundreds of millions of people in China, will be a defining feature of future health in that country."

Policy responses and specific interventions could help reduce the enormous disease burden from smoking and household fuel use. In the article, the authors suggest that at the national level, for example, authorities could create regulatory and economic policies that reduce smoking and promote clean household fuels. At the individual level, TB patients could be offered tobacco cessation programs.

"There are proven ways to reduce tobacco smoking and to provide homes with clean-burning energy alternatives. China can save millions of premature deaths from respiratory diseases in the next few decades if it leverages its effective policy system to implement these interventions," says Majid Ezzati, associate professor of international health at HSPH and senior author of the study.

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Lung Cancer Cells' Survival Gene Seen as Drug Target

One of the deadliest forms of cancer appears to carry a specific weakness.

When a key gene called 14-3-3zeta is silenced, lung cancer cells can't survive on their own, researchers have found.

The gene is a potential target for selective anti-cancer drugs, says Haian Fu, professor of pharmacology, hematology & oncology at Emory University School of Medicine and Emory Winship Cancer Institute.

The research results will be published the week of Dec. 24 in the Proceedings of the National Academy of Sciences (PNAS). The paper's first author is Zenggang Li, PhD, a postdoctoral fellow in Dr. Fu's laboratory.

Lung cancer kills more Americans annually than any other type of malignancy, according to the National Cancer Institute. Yet treatment options are very limited, Dr. Fu says.

"The recent trend towards targeted therapies requires us to understand the altered signaling pathways in the cell that allow cancer to develop," he says. "If you think about genes that are dysregulated in cancer as drivers or passengers, we want to find the drivers and then, aim for these drivers during drug discovery."

Fu and his collaborator, Fadlo Khuri, MD, deputy director of clinical and translational research at Emory Winship Cancer Institute, chose to focus on the gene 14-3-3zeta because it is activated in many lung tumors. In addition, recent research elsewhere shows that survival of lung cancer patients is worse if the gene is on overdrive in their tumors, Dr. Fu says.

14-3-3 genes are found in mammals, plants and fungi. In the human body, they come in seven flavors, each given a Greek letter. Scientists describe the proteins they encode as adaptors that clamp onto other proteins. The clamping function depends on whether the target protein is phosphorylated, a chemical switch that regulates processes such as cell division, growth, or death.

"We knew that 14-3-3 is important in controlling EGFR (epidermal growth factor receptor) signaling, which is a main pathway driving lung cancer," Fu says. A couple of recently introduced drugs that were shown to be effective against lung cancer target EGFR, he adds.

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Study Identifies Gene Alterations in Lung Cancer

An international team of scientists, supported in part by the National Human Genome Research Institute (NHGRI), one of the National Institutes of Health (NIH), has announced that its systematic effort to map the genomic changes underlying lung cancer has uncovered a critical gene alteration not previously linked to any form of cancer. The research, published in the advance online issue of the journal Nature, also revealed more than 50 genomic regions that are frequently gained or lost in lung adenocarcinoma, the most common type of lung cancer in the United States.

“This view of the lung cancer genome is unprecedented, both in its breadth and depth,” says senior author Matthew Meyerson, a senior associate member of the Broad Institute of MIT and Harvard in Cambridge, Mass., and an associate professor at Dana-Farber Cancer Institute and Harvard Medical School in Boston. “It lays an essential foundation, and has already pinpointed an important gene that controls the growth of lung cells. This information offers crucial inroads to the biology of lung cancer and will help shape new strategies for cancer diagnosis and therapy.”

Each year more than 1 million people worldwide die of lung cancer, including more than 150,000 in the United States. The new study focused on lung adenocarcinoma, which, according to the National Cancer Institute (NCI), is the most frequently diagnosed form of lung cancer in the United States, accounting for approximately 30 percent of cases.

New approaches to cancer treatment rely on a deeper understanding of what goes wrong in tumor cells to spur uncontrolled growth. Through decades of research, it has become clear that lung cancer -- like most human cancers -- stems mainly from DNA changes that accrue in cells throughout a person’s life. But the nature of these changes and their biological consequences remain largely unknown, which has inspired the recent formation of multi-disciplinary teams that are using new genomic tools and technologies to study cancer in a more systematic, comprehensive manner.

The latest study was conducted as part of the Tumor Sequencing Project (TSP), an ongoing effort to apply large-scale approaches to the identification of genomic changes in lung adenocarcinoma. NHGRI is a major funder of TSP, which unites scientists and clinicians throughout the cancer research community.

“This outstanding work clearly demonstrates the value of comprehensive approaches for exploring the genomic underpinnings of cancer. The impacts of these findings extend far beyond lung cancer and indicate that many more important cancer-related genes still await our discovery,” NHGRI Director Francis Collins says. “Now, we must forge ahead and apply this strategy as quickly as possible to other common types of cancer.”

Specifically, the TSP researchers uncovered a total of 57 genomic changes that occur frequently in lung cancer patients. Of these changes, more than 40 appear to be associated with genes not previously known to be involved in lung adenocarcinoma. More research is needed to precisely identify and characterize these genes, but researchers are excited by the possibility that their findings may suggest new ways of attacking this deadly cancer.

The most common abnormality identified by the TSP team involves a region on chromosome 14 that encompasses two known genes, neither of which had been previously associated with cancer. Through additional studies in cancer cells, the researchers discovered that one of the genes, NKX2.1, influences cancer cell growth. NKX2.1 normally acts as a master regulator that controls the activity of other key genes in cells lining the lungs’ tiny air sacs, called alveoli. The discovery that a gene functioning in a select group of cells - rather than in all cells - can promote cancer growth may have broad implications for the design of drugs for a wide range of cancers.

“The genomic landscape of lung cancer gives us a systematic picture of this terrible disease, confirming things we know, but also pointing us to many missing pieces of the puzzle. More broadly, the study represents a general approach that can and should be used to analyze all types of cancer,” says Eric Lander, one of the study’s co-authors and founding director of the Broad Institute of MIT and Harvard.

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