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NEW YORK (Reuters Health) - Lower-income women appear less likely to survive breast cancer than their more-affluent counterparts, and later diagnosis may largely explain why, a new study suggests.

Using data on more than 100,000 U.S. women diagnosed with breast cancer between 1998 and 2002, the study found that those living in economically depressed areas had poorer survival rates through the end of 2005.

When socioeconomics were considered alone, women in the poorest areas were almost one-third more likely to die during that period than those living in the highest-income areas.

When other factors were weighed, the timing of a woman's diagnosis seemed to explain much of the income gap, according to findings published in the online journal BMC Cancer.

Lower-income women were more likely to be diagnosed at a later stage: 13 percent of those in the two lowest-income areas were diagnosed after the cancer had spread beyond the breast, compared with just under 10 percent of women in the two highest-income areas.

Past studies have shown that women with lower incomes and less education have, on average, poorer breast cancer survival rates.

These latest findings suggest that later diagnosis may largely explain why, according to study author Dr. Xue Qin Yu, a researcher at Cancer Council New South Wales, in Kings Cross, Australia.

However, lower rates of recommended treatments were also a factor, Yu told Reuters Health in an email.

The study found that women in lower-income areas were less likely to receive radiation as part of their first course of treatment: 55 percent to 58 percent of women in the two higher-income groups received radiation, versus 48 percent in each of the two lower-income groups.

Radiation is typically recommended to destroy any remaining cancer cells after a breast tumor, or the breast itself, has been surgically removed.

Exactly why there were income-related treatment differences is unclear. But lack of insurance or poorer overall health among lower- income women could be at work, Yu writes -- as could bias on the part of doctors, or higher rates of treatment refusal among poorer women.

Race also seemed to make a "modest" contribution to the connection between socioeconomics and breast cancer survival, Yu found.

Just under 80 percent of black women were alive one year after diagnosis, versus roughly 90 percent of women of other races. Much of the racial gap seemed to be explained by differences in diagnosis and treatment, but not all of it; biological factors might play a role, Yu notes, but it is not possible to tell from this study.

According to Yu, the findings point to a need for "targeted interventions" to increase breast cancer screening and early treatment of lower-income women.

That, the researcher said, could include education for women and more government funding of screening programs for low-income or uninsured women.

SOURCE: BMC Cancer, online October 13, 2009.

Copyright © 2009 Reuters Limited.

LONDON (Reuters) - Scientists who watched tumor cells spread in living mice said on Sunday they had found a gene signal controlling how cancer cells move, which could help companies design new drugs to fight the disease.

Scientists working for Cancer Research UK used hi-tech imaging techniques to watch how breast cancer cells spread in mice. They found that a genetic signal, known as TGF-beta, was crucial to whether cells moved as single entities or in clumps.

TGF-beta signaling is only active in singly moving cells, not in collectively moving cells. And in singly moving cells, the signal is on when they move and off when they stop in a new place to grow, they reported in the journal Nature Cell Biology.

"The results helped us to find the set of genes that are behind the spread of breast cancer -- and that the genes need to be first turned on and then off in order for single cancer cells to be able to relocate," said Erik Sahai, head of the tumor cell biology lab at Cancer Research UK's London institute.

He said several pharmaceutical firms were investigating how to stop TGF-beta from functioning, but stressed they were "very much in the development phase."

"As yet there is no new drug in the pipeline," said Sahai, "But because we now know what these cancer cells are actually doing, it gives us lots of new ideas about how to stop them."

CANCER SPREAD

A study published in May 2007 in the Journal of Clinical Investigation found that treating cancer with surgery, chemotherapy or radiation raised levels of TGF-beta and could actually cause tumors to spread.

But as yet, relatively little has been known about how cancer cells spread through the body because it is very difficult to track them when they are moving.

"In a medium-sized tumor there could be a billion cells -- and only a small proportion might break away and spread. So it is like trying to find, and understand, a moving needle in a very big haystack," said Sahai.

Sahai and his team used two groups of fluorescently labeled breast cancer cells inside live mice and tracked them with a technique called multiphoton confocal microscopy.

When the TGF-beta signal was blocked, the tumor spread via clumps of cells in the lymphatic system -- limiting how far it could go, the researchers said.

But cells that could receive the TGF-beta signal moved as single entities, and the TGF-beta signal was first turned on -- allowing the cells to spread through the blood, and then turned off -- allowing them to grow again in a new location.

"It seems they can't multitask," said Sahai. "They can't move and grow at the same time, they can only do one or the other."

SOURCE: Nature Cell Biology, online October 18, 2009.

Copyright © 2009 Reuters Limited.

LONDON (Reuters) - Some treatments for inflammatory bowel disease increase the risk of infection-related cancers, French scientists said on Monday, but the benefits of the drugs still outweigh the risks.

Thiopurine drugs -- immunosuppressive medicines that inhibit the body's immune system -- are regularly used to treat inflammatory bowel disease, the researchers said, but can increase the risk of cancers linked to viral infections.

Laurent Beaugerie and colleagues at the Saint-Antoine hospital in Paris looked at more than 19,000 patients with inflammatory bowel disease. Around 30 percent of the patients were taking thiopurines, 14 percent had stopped taking them and 56 percent had never taken them.

Following up after almost 3 years, the researchers found 23 new cases of cancers -- one of Hodgkin's lymphoma and 22 of non-Hodgkin lymphoma.

Statistical analysis showed that patients receiving thiopurines -- like azathioprine produced by several generic drugmakers and by GlaxoSmithKline as Imuran -- had a more than five-fold increased risk of lymphoma compared with those who had never received the drugs, the researchers said in a study published in The Lancet journal.

Older male patients with a longer history of inflammatory bowel disease also had increased lymphoma cancer risk.

"The absolute cumulative risk...in young patients receiving a 10-year course of thiopurines remains low -- (less than 1 percent) -- and does not undermine the positive risk-benefit ratio of these drugs," the researchers wrote.

But for elderly patients and for unlimited treatment periods, more studies were needed to assess the risk, they said.

Commenting on the study, Geert D'Haens of the Imelda GI Clinical Research Center and Paul Rutgeerts University Hospital Gasthuisberg, both in Belgium, said doctors should be cautious in prescribing thiopurines for prolonged periods.

But they said that despite the slightly increased risk of lymphoma, the drugs would "probably remain one of the cornerstones of treatment."

SOURCE: The Lancet, published online October 19, 2009.

Copyright © 2009 Reuters Limited.

CHICAGO (Reuters) - A common antidepressant combined with an intensive treadmill training program helped people with partial spinal cord injuries walk better and faster, U.S. researchers said on Sunday.

They said Forest Laboratories' antidepressant Lexapro or escitalopram, which affects a message-carrying brain chemical called serotonin, helps strengthen remaining nerve connections along the spine, giving patients with spinal cord injuries more ability to control their muscles during training.

"The drug is enhancing the effects of the therapy," said George Hornby, a research scientist at the Rehabilitation Institute of Chicago, who is presenting his findings at the Society for Neuroscience's meeting in Chicago.

"The drug on its own isn't a miracle drug. What you need is the drug plus the training," Hornby said in a telephone interview.

The findings are the first in humans and builds on studies in animals that found giving serotonin-like drugs after spinal cord injuries can promote recovery of walking when paired with an intensive training program.

For their study, Hornby and colleagues tested the effects of antidepressants in 50 people who had partial ability to move a year after they had suffered a spinal cord injury.

Of these, 34 patients could walk on their own, but slowly.

All 50 underwent an eight-week walking program on a motorized treadmill, assisted by a robot or physical therapist. Up to 40 percent of their body weight was supported in a harness.

Five hours before training, they were given either 10 mg of Lexapro or a placebo.

While both groups improved, those who took Lexapro were able to walk much faster, Hornby said.

He said the drugs appeared to work by increasing muscle spasms experienced by people with spinal cord injuries, something most doctors consider to be a negative side effect of these types of injuries.

Hornby said the muscle spasms represent reflexes, which can be trained. Patients who have a spinal cord injury "rely on those reflexes to walk," he said.

The volunteers only got an antidepressant only on the day of training, but the benefits lasted after the drug was out of their systems, Hornby said.

He thinks the drug is strengthening the residual connections between the brain and the spinal cord.

"It helps you drive that muscle harder, and it's easier for the brain to activate the muscle," he said.

The researchers plan to do more studies using different antidepressants to see which works best. And they may also try electrical stimulation of muscles to see if that enhances the effect.

Copyright © 2009 Reuters Limited.

CHICAGO (Reuters) - An experimental drug appears to cross a protective barrier in the brain that screens out most chemicals, offering potentially better ways to treat brain tumors, U.S. researchers said on Sunday.

The drug, made by privately held Angiochem Inc of Montreal was safe and showed evidence it could shrink tumors in two separate early phase studies totaling more than 100 people with a brain cancer called glioblastoma.

Made up of a network of blood vessels, the blood-brain barrier prevents 95 percent of all chemicals from leaving the bloodstream and entering the brain.

It protects the brain from harmful chemicals, bacteria and other substances. But it also presents major challenges for treating disease in the brain, such as Alzheimer's or cancers -- which must typically be treated by surgery and radiation.

The drug, called ANG1005, also worked among people whose cancers had spread or metastasized to the brain, the researchers reported at the annual meeting of the Society for Neuroscience in Chicago.

In both studies, tumors shrank in patients who got a higher dose of ANG1005 also showed signs of working in patients whose cancers resisted the chemotherapy drug taxane.

"It is highly encouraging to see that ANG1005 has shown the potential to be effective in metastatic brain cancers and against drug-resistant tumors," Dr. Jan Drappatz of Dana-Farber Cancer Institute and Brigham and Women's Hospital in Boston, who is studying the drug, said in a statement.

Drappatz said tumors shrank significantly in some patients and some neurological problems were reversed in several.

Studies of brain tumor samples showed concentrations of the drug in the tumors, proving it successfully crossed the blood-brain barrier and accumulated.

To cross this barrier, the Angiochem drug hijacks a protein called low-density lipoprotein receptor-related protein that is commonly found on the surface of the blood-brain barrier.

"The development of novel ways to cross the blood-brain barrier has considerable potential for treating a host of debilitating and prevalent diseases and disorders," Dr. John Kessler of Northwestern University said in a statement.

Copyright © 2009 Reuters Limited.