A substantial number of lung and colorectal cancer patients continue to smoke after being diagnosed, a new study has revealed. When a patient receives a cancer diagnosis, the main focus is to treat the disease. But stopping smoking after a cancer diagnosis is also important because
continuing to smoke can negatively affect patients responses to treatments, their subsequent cancer risk, and, potentially, their survival.

A team led by Elyse R. Park, PhD, MPH, of the Massachusetts General Hospital/Harvard Medical School in Boston, studied how many patients quit smoking around the time of a cancer diagnosis, and which smokers were most likely to quit.

The investigators determined smoking rates around the time of diagnosis and five months after diagnosis in 5,338 lung and colorectal cancer patients.

At diagnosis, 39 percent of lung cancer patients and 14 percent of colorectal cancer patients were smoking, five months later, 14 percent of lung cancer patients and 9 percent of colorectal cancer patients were still smoking.

These results indicate that a substantial minority of cancer patients continue to smoke after being diagnosed. Also, although lung cancer patients have higher rates of smoking at diagnosis and following diagnosis, colorectal cancer patients are less likely to quit smoking following diagnosis.

Factors and characteristics that predicted continued smoking differed by cancer type. Lung cancer patients who continued smoking tended to have Medicare or other public health insurance, have a lower body mass index, have low emotional support, not have received chemotherapy, not have had surgery, have had prior heart disease, and have smoked a high number of cigarettes per day at some point during their lives.

Colorectal cancer patients who continued to smoke tended to be male, have completed less education, be uninsured, not have had surgery, and have once smoked a high number of cigarettes per day.

"These findings can help cancer clinicians identify patients who are at risk for smoking and guide tobacco counseling treatment development for cancer patients," said Dr. Park.

An Emory University neuro-imaging study shows that personal values that people refuse to disavow, even when offered cash to do so, are processed differently in the brain than those values that are willingly sold.

"Our experiment found that the realm of the sacred - whether it's a strong religious belief, a national identity or a code of ethics - is a distinct cognitive process," says Gregory Berns, director of the Center for Neuropolicy at Emory University and lead author of the study. The results were published in Philosophical Transactions of the Royal Society.

Sacred values prompt greater activation of an area of the brain associated with rules-based, right-or-wrong thought processes, the study showed, as opposed to the regions linked to processing of costs-versus-benefits.

Berns headed a team that included economists and information scientists from Emory University, a psychologist from the New School for Social Research and anthropologists from the Institute Jean Nicod in Paris, France. The research was funded by the U.S. Office of Naval Research, the Air Force Office of Scientific Research and the National Science Foundation.

"We've come up with a method to start answering scientific questions about how people make decisions involving sacred values, and that has major implications if you want to better understand what influences human behavior across countries and cultures," Berns says. "We are seeing how fundamental cultural values are represented in the brain."

The researchers used functional magnetic resonance imaging (FMRI) to record the brain responses of 32 U.S. adults during key phases of an experiment. In the first phase, participants were shown statements ranging from the mundane, such as "You are a tea drinker," to hot-button issues such "You support gay marriage" and "You are Pro-Life." Each of the 62 statements had a contradictory pair, such as "You are Pro-Choice," and the participants had to choose one of each pair.

At the end of the experiment, participants were given the option of auctioning their personal statements: Disavowing their previous choices for actual money. The participants could earn as much as $100 per statement by simply agreeing to sign a document stating the opposite of what they believed. They could choose to opt out of the auction for statements they valued highly.

"We used the auction as a measure of integrity for specific statements," Berns explains. "If a person refused to take money to change a statement, then we considered that value to be personally sacred to them. But if they took money, then we considered that they had low integrity for that statement and that it wasn't sacred."

The brain imaging data showed a strong correlation between sacred values and activation of the neural systems associated with evaluating rights and wrongs (the left temporoparietal junction) and semantic rule retrieval (the left ventrolateral prefrontal cortex), but not with systems associated with reward.

"Most public policy is based on offering people incentives and disincentives," Berns says. "Our findings indicate that it's unreasonable to think that a policy based on costs-and-benefits analysis will influence people's behavior when it comes to their sacred personal values, because they are processed in an entirely different brain system than incentives."

Research participants who reported more active affiliations with organizations, such as churches, sports teams, musical groups and environmental clubs, had stronger brain activity in the same brain regions that correlated to sacred values. "Organized groups may instill values more strongly through the use of rules and social norms," Berns says.

The experiment also found activation in the amygdala region, a brain region associated with emotional reactions, but only in cases where participants refused to take cash to state the opposite of what they believe. "Those statements represent the most repugnant items to the individual," Berns says, "and would be expected to provoke the most arousal, which is consistent with the idea that when sacred values are violated, that induces moral outrage."

The study is part of a special issue of the Philosophical Transactions of the Royal Society, titled "The Biology of Cultural Conflict." Berns edited the special issue, which brings together a dozen articles on the culture of neuroscience, including differences in the neural processing of people on the opposing sides of conflict, from U.S. Democrats and Republicans to Arabs and Israelis.

"As culture changes, it affects our brains, and as our brains change, that affects our culture. You can't separate the two," Berns says. "We now have the means to start understanding this relationship, and that's putting the relatively new field of cultural neuroscience onto the global stage."

Future conflicts over politics and religion will likely play out biologically, Berns says. Some cultures will choose to change their biology, and in the process, change their culture, he notes. He cites the battles over women's reproductive rights and gay marriage as ongoing examples.

We inherit 40 percent of our lifetime intelligence while the environment we grow up in impacts the rest 60 percent, researchers say.

Scientists at University of Queensland, Australia studied a unique group of nearly 2000 unrelated people in Scotland who were tested for their intelligence, using the same test, at age 11 and again at age 65, 70 or 79 years.

Most people who began life with above average intelligence were above average when they were older, while others who had below average intelligence tended to stay below average, a website reported.

However, the researchers did notice that there were some whose intelligence improved and some whose got worse compared to others.

They also took genetic samples and quantified the role genes play in determining how much transformation there is in intelligence as we age.

"We estimate roughly a quarter to a third of that change is genetic," Professor Peter Visscher, lead author of the study said in a statement.

"Measuring detailed environmental factors over a person's entire life course is very difficult."

The study revealed that overall, environment contributes more than genes to determining intelligence, although, both play an important role.

We just read a study regarding a fluorescent dye to be used for the diagnosis of esophageal cancer. Now, this report by scientists from the Columbia University has unfolded the origins of throat cancer.

The team accessed a new genetically programmed mouse prototype of chronic esophageal inflammation, also called esophagitis, in this research. They stumbled upon varied molecular changes occurring during the development of Barrett's esophagus and esophageal adenocarcinoma (EAC) in the mouse model.

"All told, the findings present a new model for the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma," specified research leader Timothy C. Wang.

The researchers found that higher proportions of a molecule called interleukin 1 apparently led to esophagitis and growth of progenitor cells, which were maintained by the Notch signaling pathway. So far, scientists believed that physiological alterations seen in Barrett's esophagus begin in the lower esophagus. However, the findings showed that the aforesaid condition supposedly took place in a region called gastric cardia.

The latter is a region lying between the lower portion of the esophagus and the upper part of the stomach secreting acids. Another belief that these changes usually happen in goblet cells appeared to be untrue. These alterations occurred principally in columnar-like epithelial cells.

The scientists concluded that inhibition of the notch signaling pathway is likely to impede the survival and growth of pre-malignant cells. This could be used as a new strategy in patients suffering from Barrett's esophagus and who are at high risk for cancer.

In a new study, scientists have tried to solve the mystery surrounding how the anti diabetic drug metformin could reduce the risk of developing cancer and what were the mechanisms involved.

In 2005, news first broke that researchers in Scotland found unexpectedly low rates of cancer among diabetics taking the drug, which is commonly prescribed to patients with Type II diabetes.

Many follow up studies reported similar findings, some suggesting as much as a 50 percent reduction in risk.

Fr the current study, researchers from McGill University and the University of Montreal reported an unexpected finding " they learned that exposure to metformin reduces the cellular mutation rate and the accumulation of DNA damage.

It is well known that such mutations are directly involved in carcinogenesis, but lowering cancer risk by inhibiting the mutation rate has never been shown to be feasible.

"It is remarkable that metformin, an inexpensive, off patent, safe and widely used drug, has several biological actions that may result in reduced cancer risk " these latest findings suggest that it reduces mutation rate in somatic cells, providing an additional mechanism by which it could prevent cancer," Newswise quoted Michael Pollak, professor in McGill's Departments of Medicine and Oncology, researcher at the Lady Davis Institute for Medical Research at the Jewish General Hospital and the study's director.

The study, carried out in collaboration with the laboratory of Dr. Gerardo Ferbeyre at Universite de Montreal's Department of Biochemistry, suggests that metformin reduces DNA damage by reducing levels of reactive oxygen species ROS.

ROS are known to be DNA damaging agents produced as by products when cells generate energy from nutrients. This action appears to take place in mitochondria, the cellular organelles that produce energy in cells by "burning" nutrients.

Past studies have identified the mitochondria as a site of action for metformin related to its anti diabetic function, but those studies had not considered that the drug also acted here to reduce ROS production, thereby reducing the rate at which DNA damage accumulates.

"We found that metformin did not act as a classic antioxidant," Ferbeyre said.