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By comparing three genomes — the genome of a 44-year-old black woman who had “triple negative” breast cancer and the genomes of her breast tumor and a metastatic tumor that developed in her brain — the scientists identified 20 genetic changes in a subset of breast tumor cells that probably played a role in the spread of the cancer that led to her death within a few months.

The findings suggest that sequencing entire genomes of cancer patients, along with the genomes of their primary and metastatic tumors, could improve understanding of how tumors spread and possibly lead to the development of new drugs that target important cancer-causing genetic errors, according to the researchers, from the Washington University School of Medicine in St. Louis.

“We are getting an intimate look at the lethal spread of a breast cancer, which is now possible because we can sequence entire genomes quickly at reasonable cost,” Elaine Mardis, co-director of the university’s Genome Center and the study’s senior author, said in a university news release.

“This work lays the foundation for understanding the genetic basis of tumor progression and metastasis and for identifying new drug targets that can improve the outlook for women with this disease,” she added.

The study is published in the issue of Nature.

German researchers used an internationally recognized and validated nicotine dependence test to assess the smoking habits of 197 employed participants in the Cologne Smoking Study.

The study found that workers who experience job-related stress are likely to smoke less than they normally would, and so have a lower dependence on nicotine. Long working hours and strict company smoking rules may explain the unexpected findings.

“Heavy workload may drive employees to smoke only in their spare time,” study leader Anna Schmidt, of the University of Cologne, said in a news release.

The researchers also found that nicotine dependence was less likely among people who were married, religious and had a higher level of education.

The study was published in the journal Tobacco Induced Diseases.

A U.S. research team examined gene variations across the human genome, or full DNA sequence, of 2,269 people with late-onset Alzheimer’s and 3,107 people without the disease. This research — known as a genome-wide association study — looks throughout the entire genome for small differences, or variants, in long stretches of DNA that are more prevalent in those with a particular disease or condition.

About 9 percent of those with late-onset Alzheimer’s had a specific variation in the gene MTHFD1L on chromosome 6, according to the study. Only about 5 percent of those who did not have Alzheimer’s had the variant.

Late-onset Alzheimer’s, which affects those 60 and up, is the most common form of the brain disorder.

With the number of people with Alzheimer’s expected to nearly double from 18 million worldwide to 34 million by 2025, according to the World Health Organization, researchers have been hunting for genes that play a role in Alzheimer’s disease. The hope is that understanding the function of the genes could help in developing better treatments, which are sorely lacking.

So far, the primary known genetic contributor to late-onset Alzheimer’s is a variant of the gene APOE on chromosome 19. The Alzheimer’s-linked APOE variant occurs in about 40 percent of people who develop late-onset Alzheimer’s, while about 25 to 30 percent of the general population has it, according to the National Institute on Aging.

The influence of the MTHFD1L variation is not as strong as APOE, and the variation itself is not as common in the population, said principal investigator Margaret Pericak-Vance, director of the University of Miami Miller School of Medicine’s John P. Hussman Institute for Human Genomics.

But what makes the current finding so interesting is how it might connect to previous research about MTHFD1L. The gene is involved with the metabolism of folate, which in turn can influence levels of homocysteine.

Elevated homocysteine, which is often tied to folic acid deficiencies in the diet, have been shown to be a risk factor for coronary artery disease and late-onset Alzheimer’s.

Previous genome-wide studies have also implicated another variation in MTHFD1L in coronary artery disease.

Taken together, the research hints at ways in which the gene variant might be associated with changes in blood vessel function in the brain that impact Alzheimer’s, Pericak-Vance said.

“The key reason people are excited about this is that it melds the genetics and the biology,” Pericak-Vance said. “Maybe we can put the biology together with genetics and come up with some way to either treat it or approach it.”

While lots of genetic variants have been singled out as possible contributors to Alzheimer’s, the findings often can’t be replicated or repeated, leaving researchers unsure if the results are a coincidence or actually important, said Dr. Ron Peterson, director of the Mayo Alzheimer’s Disease Research Center in Rochester, Minn.

“The strength of his study is it includes a large number of subjects, they looked at a large number of [DNA sequence variations], and they replicated previously reported findings, which gives you confidence that they are correct,” Peterson said.

The study is slated to be presented at the American Academy of Neurology’s meeting in Toronto.

The finding won’t immediately lead to a better treatment or cure, said Angela M. Christiano, co-author of the study, published April 15 in the journal Nature. And though it’s “just a tiny little piece of the puzzle,” it could provide perspective about a component of male-pattern baldness known as shrinkage, said Christiano, director of the Center for Human Genetics at Columbia University.

Contrary to popular belief, male-pattern baldness doesn’t cause hair to stop growing. Instead, hair still grows but it’s short and fine, like peach fuzz, Christiano said.

“If you look at a very bald scalp, they are still making tiny little peach-fuzz hairs,” she said. “A follicle is still there. The hardware is still there to grow a hair of some kind.”

People with a rare condition called hereditary hypotrichosis simplex have the same problem, although it begins at birth.

In the new study, Christiano and her colleagues examined the genetic makeup of members of two Pakistani families and one Italian family whose members have inherited the condition. The researchers discovered a gene in which a mutation appears to cause the problem.

The gene, called APCDD1, is located in a region of chromosome 18 that has been shown in previous studies to be linked to other forms of hair loss. The researchers also found that APCDD1 inhibits a signaling pathway that has long been shown to control hair growth in mice, but has not been extensively linked to human hair growth.

In addition to providing more insight into hereditary hypotrichosis simplex, the gene research “gives us an inroad into understanding male-pattern baldness” because the conditions are similar, Christiano said. It may be a matter of reprogramming the hair software because the hardware is still there, she said.

Part of the challenge of studying baldness is that mice don’t suffer from the equivalent of male-pattern baldness, making animal research less effective in understanding how hair growth works, she said.

Dr. Doris Day, a dermatologist in New York City, said that about half of people older than 50 have hair loss. “It can be debilitating, especially to women, who have fewer options for treatment,” Day said.

Drugs such as Rogaine and Propecia treat baldness, but they do so by preventing future hair loss rather than growing new hair, Christiano said.

Also, Day said, the medications have side effects. “Most of the drugs block hormones or enzymes,” she said. “However, they are not specific to the scalp so side effects can include decreased libido as well as potential damage to the liver.”

“The medications need to be taken indefinitely in order to remain effective,” she said, “and for some people, the medications do not adequately control the hair loss.”

A gene-based treatment, by contrast, might allow hair to grow normally. And understanding the genetic basis of baldness could help researchers find better treatments for other conditions, such as alopecia, which causes hair loss, Christiano said, adding that she has alopecia.

SOURCES: Angela M. Christiano, Ph.D., director, Center for Human Genetics, Columbia University Medical Center, New York City; Doris Day, M.D., dermatologist, New York City;

Cancer cells spread and grow because they can divide indefinitely.

But a study in mice showed that blocking a cancer-causing gene called Skp2 forced cancer cells to go through an aging process known as senescence — the same process involved in ridding the body of cells damaged by sunlight.

If you block Skp2 in cancer cells, this process is triggered, Pier Paolo Pandolfi of Harvard Medical School in Boston and colleagues reported in the journal Nature.

And Takeda Pharmaceutical Co’s experimental cancer drug MLN4924 — already in early-stage clinical trials in people — appears to have the power to do just that, Pandolfi said in a telephone interview.

The finding may offer a new strategy for fighting cancer.

“What we discovered is if you damage cells, the cells have a built-in mechanism to put themselves out of business,” Pandolfi said. “They are stopped irreversibly from growing.”

For the study, the team used genetically altered mice that developed a form of prostate cancer.

In some of these, they inactivated the Skp2 gene. When the mice reached six months of age, they found those with an inactive Skp2 gene did not develop tumors, while the other mice did.

When they analyzed the tissues from lymph nodes and the prostate, they found many cells had started to age, and they also found a slow rate of cell division.

This was not the case in mice with normal Skp2 function.

They got a similar effect when they used the Skp2-blocking drug MLN4924 in lab cultures of human prostate cancer cells.

To see if this would work in mice, they transplanted the cells and treated the mice with the drug.

“We put human cancer cells into mice. We fed them with a drug and these cells do senesce (age),” Pandolfi said.

“The same mechanism of damage caused by the sun can be evoked pharmacologically in cancer cells.”

He said this Skp2-related aging pathway appears to be active in cancer, and not other cells. “We have no intention of aging the patient. But only the cancer,” he said.

(Editing by Todd Eastham)

“Look around you. We are surrounded by [diabetes] risk,” Christine T. Tobin, president of health care and education at the American Diabetes Association, said in a news release. She said that Americans “need to change the future of diabetes now. One of the first steps is to find out if you or a loved one is at risk for developing type 2 diabetes by taking the Diabetes Risk Test. Knowing your risk can be the first step towards stopping this dreadful disease.”

The group is urging people to take the Diabetes Risk Test on March 23, the annual American Diabetes Association Alert Day. The test (available at stopdiabetes.com or 1-800-DIABETES) asks participants questions about weight, age, family history and other potential risk factors for type 2 diabetes. Based on their answers, participants are told whether they’re at low, moderate or high risk for diabetes. Those at high risk are encouraged to talk with their doctor.

Major risk factors for type 2 diabetes include being overweight, sedentary, over the age of 45 and having a family history of diabetes. Blacks, Hispanics, Native Americans, Asian-Americans and Pacific Islanders are at increased risk, as are women who’ve had gestational diabetes or have had a baby weighing more than 9 pounds at birth.

Left untreated, type 2 diabetes can lead to heart disease, stroke, kidney disease, eye damage or nerve damage that can lead to amputations.

If current trends continue, about one in three American children born today will develop diabetes. Of the approximately 24 million Americans with diabetes, nearly 6 million have type 2 diabetes and don’t know it.

“Studies have shown that type 2 diabetes can be prevented or delayed by losing just 5 to 7 percent of body weight through 30 minutes of regular physical activity, five days a week and healthy eating,” Tobin said. “We encourage everyone to gather their friends, family, loved ones and co-workers, and find ways to live healthier lifestyles today.”

SOURCE: American Diabetes Association, news release.

Insurance plans that use financial incentives and other methods to encourage patients to receive care from doctors who keep medical costs lower are becoming increasingly common. But these efforts may not be based on reliable estimates of doctor performance and may not achieve the intended savings, according to the RAND Corp., a non-profit research organization.

In the study, researchers looked at 13,788 physicians and found that about one-quarter of them would be misclassified under the system of cost-profiling commonly used by insurance plans.

“Our findings raise questions about the utility of cost-profiling tools for high-stakes activities such as tiered health plans and the likelihood that wide use of these strategies will reduce health-care spending,” study lead author John L. Adams, a senior statistician at RAND, said in a news release. “Consumers, physicians and those who pay for health care are all at risk of being misled by the results from these tools.”

Adams said these ranking systems may be useful for some purposes, such as warning physicians that their treatment methods appear to cost more than those used by their peers and suggesting they re-examine their practice styles.

However, the ranking systems “are not reliable enough at this point to make decisions about encouraging patients to see certain providers or excluding some doctors from insurance networks. Much work remains to be done to improve these systems before they are used for high-stakes activities,” Adams stated.

The findings are published in the issue of the New England Journal of Medicine.

Researchers in the Netherlands and Canada studied 134 patients with chronic low back pain who hadn’t been able to go to work for about six months, on average. The patients, aged 18 to 65, were randomly assigned to receive usual care or to take part in a program called “integrated care.”

The integrated care program included adjustments made to the workplace environment and an exercise program that taught patients how to move safely and become more active.

Over a year, the patients who took part in the integrated care program returned to work after an average of 88 days instead of an average of 208 days for those who received usual care, according to the report published online March 17 in BMJ.

Although there were no statistically significant differences between the groups in reported levels of pain improvement, the study authors noted that the integrated care program significantly improved patients’ functional status and reduced their disability both at home and at work.

SOURCE: BMJ, news release.

But now new research finds that the survival benefit from that preventive surgery is small and not equal among all women.

“The survival benefit was limited to a small subset of all breast cancer patients [studied],” said study author Dr. Isabelle Bedrosian, an assistant professor of surgical oncology at the University of Texas M.D. Anderson Cancer Center, in Houston.

Those most likely to derive a survival benefit, she said, were those younger than 50 who had been diagnosed with early-stage cancers that were estrogen receptor (ER)-negative.

ER-negative tumors don’t require estrogen to grow, as do ER-positive tumors, and the prognosis is poorer for the ER-negative cancers, according to the American Cancer Society.

The study is published online Feb. 25 in the Journal of the National Cancer Institute.

According to Bedrosian and others, experts have long known that women diagnosed with breast cancer have an elevated risk of developing cancer in the opposite breast. Removing that breast as a preventive measure reduces, but does not eliminate, the risk of cancer in that breast.

“But we have never really established the difference it makes in the survival of breast cancer patients,” she said. So, Bedrosian and her colleagues used data from the Surveillance, Epidemiology and End Results (SEER) database, evaluating 107,106 women with breast cancer who had undergone mastectomy for that cancer between 1998 and 2003, along with a subset of 8,902 who had the opposite breast removed as a preventive measure.

After a five-year follow-up, 88.5 percent of those who had the opposite breast surgery were alive, versus 83.7 percent of those who did not, a difference of less than 5 percent. The improved survival was clear for a select group, mostly the women aged 18 to 49 with early-stage, ER-negative tumors, the researchers found.

There was no information from the database on whether the women had genetic mutations to boost breast cancer risk, Bedrosian noted.

After five years, what might happen? “We actually would expect that number [the nearly 5 percent benefit] would increase over time,” Bedrosian said.

The findings makes sense to Dr. Allison W. Kurian, an assistant professor of medicine at Stanford University School of Medicine in Stanford, Calif., who has published research on the topic.

“These results are consistent with other studies,” she said, including her own research published in 2009 in the same journal, which found that the risk for a breast cancer in the opposite breast is affected by a variety of factors, with those having ER-negative tumors in the original breast cancer having a higher risk of getting second tumors in the opposite breast.

Bedrosian said her research suggests most women diagnosed with breast cancer shouldn’t be concerned about the opposite breast: “We cannot demonstrate for most of them a survival benefit [with preventive mastectomy on the opposite breast].”

However, she said, psychological factors should also be taken into account. “There are some patients who may feel they still want to do this,” she said.

Kurian agreed: “This paper does give more information [about the outlook for various women], but it remains a personal decision for women to discuss with their doctor.”

SOURCES: Isabelle Bedrosian, M.D., assistant professor, surgical oncology, University of Texas M.D. Anderson Cancer Center, Houston; Allison W. Kurian, M.D., assistant professor, medicine, Stanford University School of Medicine, Stanford, Calif.; Journal of the National Cancer Institute, online