Women with breast cancer who receive chemotherapy appear more likely than those treated with radiation therapy to experience a major change in work status, according to a com/cgi-bin/fulltext/122322555/HTMLSTART” target=_new>study published in the journal Cancer, Reuters reports. For the study, Dana-Farber Cancer Institute researcher Michael Hassett and colleagues used a large health insurance claims database to identify 3,233 women who were first diagnosed with breast cancer between 1998 and 2002. All of the women were younger than age 64, insured, and working full time or part time as of diagnosis. About 54% of the women received chemotherapy, and 58% received radiation therapy.

Hassett said that most of the women did “not experience a significant change in their employment after cancer diagnosis and treatment.” However, of the 6.6% who experienced such a change, those who received chemotherapy had a 1.8-fold greater risk of leaving work, retiring or going on long-term disability leave in the subsequent year. Sixty-seven percent of women who experienced a change went from full-time employment to early retirement, while the rest went from full-time employment to long-term disability or retirement, or their status was unknown. Although the study looked at many factors, only chemotherapy and older age were associated with an increased likelihood of a change in employment. Hassett said that most of the participants in the study worked for large employers that offered health insurance. He added that further research is needed to evaluate the effect of cancer diagnosis and treatment on work status for women who are self-employed or work for smaller companies (Hendry, Reuters, 6/30).

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Researchers at Ben-Gurion University of the Negev (BGU) have discovered that gene mutations that once helped humans survive may increase the possibility for diseases, including cancer.

The findings were recently the cover story in the journal Genome Research.

The team of researchers from BGU’s National Institute for Biotechnology in the Negev (NIBN) set out to look for mutations in the genome of the mitochondria, a part of every cell responsible for energy production that is passed exclusively from mothers to their children. The mitochondria are essential to every cell’s survival and our ability to perform the functions of living.

“Our ancestors responded to environmental changes, such as climate shift, with mutations that increased their chances of survival. But today, these same mutations predispose us toward complex diseases such as cancer,” according to researcher Dr. Dan Mishmar, a molecular biologist from the Department of Life Sciences at BGU. “Although mitochondria’s role in the emergence of new species has been investigated recently, the idea that they are responsible for our susceptibility to illness startles many.”

To test this hypothesis, the researchers analyzed the genome mitochondria mutations from 98 unrelated individuals. Combinations of mutations tended to occur in tumors in precisely the same DNA building blocks that changed during evolution. The team also found that the mitochondrial genome of humans who migrated out of Africa to Europe 100,000 years ago carried seven mutations found in almost all of today’s Europeans.

“The concept that the same principles that drive evolution toward the emergence of new species govern the emergence of diseases is new,” Mishmar explains. “A clinician looks at the genome of a tumor, or other disease, and compares it to the normal population, looking for new mutations that do not occur there. I assume the mutations are already part of the population and have had a survival function. When these same mutations reoccur in the correct environment, they can cause disease.”

As reported in the leading journal Genome Research, “We show, strikingly, that evolution repeated itself in cancer. If we better understand how evolution moved, we can understand the genetic basis of many complex disorders. Since mitochondria play a central role in disease, if we understand how they work and the way they changed our ability to survive in different conditions in ancient times, we can understand the mechanics of the disease. And we’ll understand a lot about the way certain people develop diseases and others have a lower tendency toward those same diseases. This may lead to new methods of disease prevention or cures.”

Along with Dr. Mishmar whose background as an archaeologist is evident in his current medical research, the research team consisted of Dr. Eitan Rubin, from the Department of Microbiology and Immunology, and graduate students Ilia Zhidkov and Erez A. Livneh.

Source:
Andrew Lavin

American Associates, Ben-Gurion University of the Negev

UCSF researchers have identified a new “feed-forward” pathway linking estrogen receptors in the membrane of the uterus to a process that increases local estrogen levels and promotes cell growth.

The research is significant in helping determine why tamoxifen and other synthetic estrogens are linked to increased rates of endometriosis and uterine cancer, and identifies a pathway that could be targeted in drug therapies for those diseases, researchers say.

Findings are published in the July 1, 2009 issue of Cancer Research, the journal of the American Association for Cancer Research.

The research found that when activated by estrogens, endometrial cells obtained from patients suffering from endometriosis or human uterine cancer cells initiate a previously unknown cascade of signals that leads to cellular replication and further estrogen production, the paper says.

The ensuing cycle leads to abnormal growth of the cells lining the uterus, or endometrium, which occurs in endometriosis and uterine cancer, according to senior author Holly A. Ingraham, PhD, a professor in the UCSF School of Medicine’s Department of Cellular and Molecular Pharmacology.

“It turns out that displaced endometrial cells, such as those used in this study, are estrogen factories,” said Ingraham, who also is affiliated with the UCSF Helen Diller Family Comprehensive Cancer Center and the UCSF Center for Reproductive Sciences. “They pump out estrogen in a feed-forward pathway, so the more estrogen they produce, the more estrogen they’re capable of producing.”

While this pathway was previously unknown, Ingraham said a June 2009 paper led by researchers at the University of New Mexico and published in the journal Nature Chemical Biology showed that blocking the GPR30 receptor in this pathway decreases uterine proliferation in a mouse. The two together, she said, validate what researchers now think may be a key area in addressing both uterine cancer and endometriosis.

Uterine cancer is the fourth most common cancer in women, with more than 37,000 women being diagnosed each year in the United States alone, according to data from the Centers for Disease Control.

Endometriosis, in which endometrial cells grow in areas other than the uterus, is the most common gynecological disease and affects more than 5.5 million women in North America, according to the National Institutes of Health. The disease often causes severe pain and can lead to infertility.

Working in collaboration with clinicians at Northwestern University in Chicago, the UCSF team analyzed cells from women with ectopic endometriosis. By studying those patients’ endometrial cells, the team was able to identify an unusual, circular pathway involving these cells, the transmembrane estrogen receptor GPR30 and the nuclear receptor SF-1.

The researchers propose that this pathway increases local concentrations of estrogen and, together with classic estrogen-receptor signaling, control the proliferative effects of these estrogens in promoting endometriosis and endometrial cancers.

The UCSF team used a unique chemical biology approach, making use of a tamoxifen-like compound developed in the laboratory of co-author Thomas Scanlan, PhD, who is affiliated with both the UCSF Department of Pharmaceutical Chemistry and the Department of Chemical Biology at the Oregon Health Sciences University in Portland.

“Tamoxifen and other synthetic estrogens have been known to increase the risk of uterine cancer, but until now, we didn’t know why that was on a cellular level,” Ingraham said. “We think this pathway is going to be an important one in solving that mystery.”

The lead investigator on the paper was Benjamin C. Lin. Lin and co-author Sandra C. Tobias are affiliated with the Department of Pharmaceutical Chemistry at UCSF. Other co-authors are Miyuki Suzawa, in the UCSF Department of Cellular and Molecular Pharmacology; Raymond D. Blind in the UCSF Department of Pharmaceutical Chemistry and Department of Cellular and Molecular Pharmacology; and Serdar E. Bulun, in the Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University. The authors report no potential conflicts of interest in this research.

Source:
Kristen Bole

University of California - San Francisco