Licochalcone A inhibits growth of gastric cancer cells by arresting cell cycle progression and inducing apoptosis


The aim of this study was to determine the anticancer effects of seven licorice compounds in MKN-28, AGS, and MKN-45 gastric cancer cells and human gastric epithelium immortalized cells. We also explored the mechanism of action of licochalcone A (LCA), the most cytotoxic licorice compound, by analyzing its influence on cell cycle progression and apoptosis. The results indicated that LCA was the most cytotoxic licorice compound of those tested, and it inhibited gastric cancer cells growth in a dose-dependent manner, with an IC50 value of approximately 40μM. LCA affected gastric cancer cell viability by blocking cell cycle progression at the G2/M transition and inducing apoptosis. LCA treatment increased the expression of Rb and decreased the expression of cyclin A, cyclin B and MDM2 in MKN-28, AGS and MKN-45 cell lines. In addition, LCA-induced apoptosis by its effects on the expression of PARP, caspase-3, Bcl-2 and Bax. These data provide evidence that LCA has the potential to be used in the treatment of gastric cancer.

source: cancer letter

Nephrolithiasis-associated bone disease: pathogenesis and treatment options


Nephrolithiasis remains a formidable health problem in the United States and worldwide. A very important but underaddressed area in nephrolithiasis is the accompanying bone disease. Epidemiologic studies have shown that osteoporotic fractures occur more frequently in patients with nephrolithiasis than in the general population. Decreased bone mineral density and defects in bone remodeling are commonly encountered in patients with calcium nephrolithiasis. The pathophysiologic connection of bone defects to kidney stones is unknown. Hypercalciuria and hypocitraturia are two important risk factors for stone disease, and treatments with thiazide diuretics and alkali, respectively, have been shown to be useful in preventing stone recurrence in small prospective trials. However, no studies have examined the efficacy of these agents or other therapies in preventing continued bone loss in calcium stone formers. This manuscript reviews the epidemiology, pathophysiology, and potential treatments of bone disease in patients with nephrolithiasis.

source: nature kidney

 

Nanocrystals seed calcification in more ways than one


Although much progress has been made in the past five years in understanding the mechanisms leading to accelerated vascular calcification in patients with chronic kidney disease, it remains unclear how an environment high in phosphate can impinge so significantly on the calcification process. The study by Sage et al. highlights an important and novel role for calcium phosphate nanocrystals, produced in a high-phosphate environment, in rapidly driving calcification of vascular smooth muscle cells via enhanced production of bone morphogenetic protein-2.

source: nature kidney

Abnormal circadian blood pressure pattern 1%-year after kidney transplantation is associated with subsequent lower glomerular filtration rate in recipients without rejection


Abnormal circadian blood pressure (BP) pattern is common after kidney transplantation but its relationship to long term allograft function is unclear. Of 119 kidney recipients who had ambulatory BP monitoring 1 year from transplantation, 36 patients without history of rejection were selected. Twenty-nine recipients were followed for 4 years and seven for 3 years. Iothalamate glomerular filtration rate (GFR) was obtained at 3 weeks then annually. Dippers (n = 10) had day-night systolic BP (SBP) drop (ΔSBP) of ≥10%, nondippers (n = 15) had ΔSBP 0–9%, whereas reverse dippers (n = 11) had nocturnal rise in SBP. Compared with dippers, reverse and nondippers had a higher Banff cv score at 1 year (P = .03), lower GFR at last follow-up (73.7 ± 18.1, 55.7 ± 16.3, and 56.6 ± 21 mL/min/1.73 m2 for dippers, non-, and reverse dippers, respectively, P = .05) and higher kidney function loss (8.0 ± 20, −9 ± 17, and 1 ± 14 mL/min/1.73 m2 for dippers, non-, and reverse dippers, respectively, P = .02). GFR at 4 years and at last follow-up independently correlated with ΔSBP at 1 year (r = 0.46, P = .01; r = 0.34, P = .03). The current study indicates that abnormal circadian BP pattern at 1 year identifies a group of kidney recipients at risk for increased kidney function loss and lower GFR 3–4 years from transplantation.

source: science direct

Menveo®


Novartis announced today that it received approval from the US Food and Drug Administration (FDA) for the use of

Novartis announced today that it received approval from the US Food and Drug Administration (FDA) for the use of Menveo® (Meningococcal [Groups A, C, Y and W-135] Oligosaccharide Diphtheria CRM197 Conjugate Vaccine) for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis serogroups A, C, Y and W-135 in individuals 2 to 10 years of age[1]. Menveo received initial FDA approval in 2010 for use in adolescents and adults from 11 to 55 years of age[1].         

The FDA approval of Menveo for use in children 2 to 10 years of age is based on Phase III trial data involving 5,297 participants in that age group. In the pivotal trial, the safety and immunogenicity of Menveo against each of the four serogroups were compared with those of the other currently US-licensed ACW-135Y meningococcal conjugate vaccine[1]. Novartis also agreed to conduct three post marketing studies.

Separately, Novartis received a Refuse To File (RTF) letter from the FDA regarding the Company’s supplemental Biologics License Application (sBLA) for the use of Menveo in infants from 2 to 12 months. The sBLA had been submitted to the FDA in November 2010. Novartis plans to resubmit a sBLA in 2011 for the expanded use of Menveo in infants and toddlers from 2 months to 2 years old.

“The approval of Menveo for the use in children 2-10 years of age is another important step towards our goal to protect people of all ages against this devastating disease,” said Andrin Oswald, Division Head of Novartis Vaccines and Diagnostics. “The response from the FDA on our Menveo infant file is disappointing. We believe that concerns raised are of procedural nature and plan to resubmit the sBLA within the next few months. This will also provide us with an opportunity to supplement the file with additional clinical data that support expanded use of Menveo in infants and toddlers from 2 months to 2 years old.”

About Menveo
As of January 2011, Menveo is registered in more than 40 countries for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis serogroups A, C, W-135 and Y in people from 11 years of age. Menveo has been administered to more than 18,500 participants in clinical trials across all age groups worldwide, and studies are ongoing in infants, toddlers, adolescents and adults[2]. Menveo received initial FDA licensure in May 2010 for use in adolescents and adults (11 to 55 years of age)[1]. Pivotal phase III data presented in October 2010 at the 48th Annual Meeting of the Infectious Diseases Society of America (IDSA) showed that Menveo induced immune responses in a high percentage of infants against four important meningococcal disease-causing serogroups (A, C, Y and W-135)[2].

In the EU, Menveo is known as Meningococcal Group A, C, W135 and Y Conjugate Vaccine. Novartis Vaccines plans to submit additional data to the European Medicines Agency to support the use of Menveo in infants and children 0 to 10 years of age in the first half of 2011. The label extension for use in children 2 to 10 years of age has already been submitted in Canada[2].

Important Safety Information
Menveo should not be administered to individuals with known hypersensitivity to any component of Menveo or other meningococcal vaccines, or other vaccines containing derivatives of Corynebacterium diphtheriae. Because of the risk of hematoma, Menveo should not be administered to individuals with any bleeding disorder, such as hemophilia or thrombocytopenia, nor to persons receiving anticoagulant therapy, unless the potential benefit outweighs the risk of administration. Menveo should not be administered to people who have an acute severe febrile illness, although a mild fever of short duration is not a contraindication. Due to the absence of supporting data, the decision to administer Menveo to pregnant women should be evaluated according to the risk of meningococcal infection.

The most common local adverse reactions to Menveo include injection site pain, erythema, and induration. The most common systemic adverse reactions include headache, myalgia, malaise, nausea, arthralgia, chills, rash and fever. Some reactions may be severe.

Vaccination with Menveo may not protect all individuals. Patients who are immunocompromised or receiving immunosuppressive therapy may have an inadequate response to vaccination.

® (Meningococcal [Groups A, C, Y and W-135] Oligosaccharide Diphtheria CRM197 Conjugate Vaccine) for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis serogroups A, C, Y and W-135 in individuals 2 to 10 years of age[1]. Menveo received initial FDA approval in 2010 for use in adolescents and adults from 11 to 55 years of age[1].         

The FDA approval of Menveo for use in children 2 to 10 years of age is based on Phase III trial data involving 5,297 participants in that age group. In the pivotal trial, the safety and immunogenicity of Menveo against each of the four serogroups were compared with those of the other currently US-licensed ACW-135Y meningococcal conjugate vaccine[1]. Novartis also agreed to conduct three post marketing studies.

Separately, Novartis received a Refuse To File (RTF) letter from the FDA regarding the Company’s supplemental Biologics License Application (sBLA) for the use of Menveo in infants from 2 to 12 months. The sBLA had been submitted to the FDA in November 2010. Novartis plans to resubmit a sBLA in 2011 for the expanded use of Menveo in infants and toddlers from 2 months to 2 years old.

“The approval of Menveo for the use in children 2-10 years of age is another important step towards our goal to protect people of all ages against this devastating disease,” said Andrin Oswald, Division Head of Novartis Vaccines and Diagnostics. “The response from the FDA on our Menveo infant file is disappointing. We believe that concerns raised are of procedural nature and plan to resubmit the sBLA within the next few months. This will also provide us with an opportunity to supplement the file with additional clinical data that support expanded use of Menveo in infants and toddlers from 2 months to 2 years old.”

About Menveo
As of January 2011, Menveo is registered in more than 40 countries for active immunization to prevent invasive meningococcal disease caused by Neisseria meningitidis serogroups A, C, W-135 and Y in people from 11 years of age. Menveo has been administered to more than 18,500 participants in clinical trials across all age groups worldwide, and studies are ongoing in infants, toddlers, adolescents and adults[2]. Menveo received initial FDA licensure in May 2010 for use in adolescents and adults (11 to 55 years of age)[1]. Pivotal phase III data presented in October 2010 at the 48th Annual Meeting of the Infectious Diseases Society of America (IDSA) showed that Menveo induced immune responses in a high percentage of infants against four important meningococcal disease-causing serogroups (A, C, Y and W-135)[2].

In the EU, Menveo is known as Meningococcal Group A, C, W135 and Y Conjugate Vaccine. Novartis Vaccines plans to submit additional data to the European Medicines Agency to support the use of Menveo in infants and children 0 to 10 years of age in the first half of 2011. The label extension for use in children 2 to 10 years of age has already been submitted in Canada[2].

Important Safety Information
Menveo should not be administered to individuals with known hypersensitivity to any component of Menveo or other meningococcal vaccines, or other vaccines containing derivatives of Corynebacterium diphtheriae. Because of the risk of hematoma, Menveo should not be administered to individuals with any bleeding disorder, such as hemophilia or thrombocytopenia, nor to persons receiving anticoagulant therapy, unless the potential benefit outweighs the risk of administration. Menveo should not be administered to people who have an acute severe febrile illness, although a mild fever of short duration is not a contraindication. Due to the absence of supporting data, the decision to administer Menveo to pregnant women should be evaluated according to the risk of meningococcal infection.

The most common local adverse reactions to Menveo include injection site pain, erythema, and induration. The most common systemic adverse reactions include headache, myalgia, malaise, nausea, arthralgia, chills, rash and fever. Some reactions may be severe.

Vaccination with Menveo may not protect all individuals. Patients who are immunocompromised or receiving immunosuppressive therapy may have an inadequate response to vaccination.

source: novartis release

Toxic Ash Clouds Might Be Culprit in Biggest Mass Extinction


Tiny particles embedded in ancient Canadian rocks have provided new clues about what might have triggered Earth’s deadliest mass extinction. The ultimate cause, researchers say, might be globe-smothering clouds of toxic ash similar to that spewed by modern-day coal-fired power plants.

The die-off, which occurred worldwide about 250 million years ago at the end of the Permian period, was even more extensive than the one that wiped out the dinosaurs. More than 90% of marine species went extinct, and land-based ecosystems suffered almost as much. Scientists have long debated the reasons. Favorite hypotheses include an asteroid impact, massive volcanic eruptions in Siberia, and toxic oceans. Geochemist Stephen Grasby of the Geological Survey of Canada in Calgary and colleagues report online today in Nature Geoscience a new twist on the volcano notion.

Rocks that now make up the northernmost islands of the Canadian Arctic formed millions of years ago as seafloor sediments off the northwestern coast of a supercontinent called Pangaea. When Grasby and his team analyzed rocks from just before the Permian mass extinction, they noticed unusual microscopic particles. Besides the usual miniscule clumps of organic matter, they also found tiny bubble-filled particles called cenospheres. These frothy little blobs form only when molten coal spews into the atmosphere, the researchers say. Today, the fly ash produced by coal-fired power plants brims with cenospheres, but they are largely trapped by pollution-control equipment before they escape the smokestack. Millions of years ago, they must have been created when massive amounts of molten rock—more than 1 trillion metric tons—erupted through overlying coal deposits in Siberia to form lava deposits known as the Siberian Traps.

Because the late Permian cenospheres are approximately the same size and likely about the same weight as the smallest particles of volcanic ash, they could have easily risen to an altitude of about 20 kilometers in the atmosphere and then been swept around the world by jet stream winds. And like coal ash produced today, the particles would have been loaded with toxic metals such as chromium and arsenic. When the ancient cenospheres eventually dropped into the seas, they would have converted surface waters into a toxic soup, the researchers speculate. Then, they say, after most life died, decomposition would have robbed the water of its dissolved oxygen, smothering many of the survivors.

“The evidence is pretty compelling,” says Gregory Retallack, a geologist at the University of Oregon, Eugene. Geophysicist Norman Sleep of Stanford University in Palo Alto, California, agrees. The team’s findings “are an extremely major discovery,” he says. As the ecological consequences piled up, he notes, the chain of events set in motion by the massive Siberian eruptions “went from something bad for life to a complete disaster.” Finding cenospheres in late Permian rocks worldwide would bolster the notion that the tiny particles played a major role in causing the extinction, says Grasby.

source: science now

Growth Hormone Also a Memory Booster


Your ginkgo biloba, rosemary, and other purported brain boosters may soon face competition—from an unexpected source. Researchers have found that insulin-like growth factor 2 (IGF-2), a naturally occurring hormone, can boost memory retention in animals. The discovery offers a rare glimpse into a mysterious stage of the learning process, and it may one day provide scientists with a new way to treat memory impairments, such as those caused by dementia.

For neuroscientists chasing down the molecules that make up memories, IGF-2 isn’t the most likely of targets. It’s better known for roles in cell growth and repair. But IGF-2 has been spotted in the hippocampus, a region of the brain associated with learning and memory. That made researchers wonder whether it was actually playing a part in cognition.

So neuroscientist Cristina Alberini and her team at the Mount Sinai School of Medicine in New York City devised a memory test for rats that would help pinpoint IGF-2’s modus operandi. The team came up with a box that was lit on one side and unlit on the other. Rats that entered the dark side got a mild foot shock. The rats’ subsequent hesitation to return to the dark after getting shocked gave the scientists a measure of how well they remembered the traumatic event.

Naturally occurring IGF-2 levels in the rats’ hippocampuses peaked after receiving the foot shock, and all of the rodents were fairly good at retaining the unpleasant memory. In fact, for weeks after their shock, some rats hesitated to enter the dark side of the box.

The researchers then ran the experiment again, this time injecting some of the rats’ brains with extra IGF-2 at different times after their training, such as immediately after a shock or more than a day later. The IGF-2 boost enhanced their recall dramatically. “Their hesitation, or latency, more than doubled,” says Alberini. “It’s a very potent effect.”

IGF-2 improved a rodent’s memory only when administered in a precise window of time—roughly within 24 hours after the foot shock—which coincides with a stage in the learning process called “memory consolidation.” That’s a poorly understood transition period when a memory is still malleable but becoming more established and robust.

The team’s results, published today in Nature, offer a new piece of the consolidation puzzle, says neurobiologist Alcino Silva of the University of California, Los Angeles, who was not involved in the study. “We know a lot about the first few seconds of learning but not so much about the hours and days later,” he says. “Looking at this period is a big contribution. I’m envious, actually.”

The results may also contribute to developing memory-boosting drugs. The fact that IGF-2 is naturally occurring and can cross the blood-brain barrier makes it a promising candidate for treating memory-impairing diseases or even forgetfulness, Alberini notes. But any clinical applications are a long way off, as one key question remains unanswered—namely, how exactly IGF-2 boosts memory. Preliminary results suggest the growth factor strengthens the connections between nerve cell synapses during consolidation, says Alberini. Her team’s next steps will explore the mechanism, in hopes of one day putting IGF-2 to work in humans.

source: science now

Orangutan Genome Full of Surprises


The orangutan, the most sedentary of the great apes, has unusually stable DNA, too. Researchers have just completed the sequencing of the entire genome of our orange-haired relative, and they have found to their surprise that its DNA has changed much less dramatically over time than has that of humans or chimpanzees. “The orangutan is the odd man out,” says Devin Locke, a structural geneticist at Washington University School of Medicine in St. Louis, Missouri, who headed the orangutan sequencing project.

The orangutan genome had one other big surprise. Locke and colleagues sequenced six Sumatran and five Bornean orangutans, which are classified as different species. The apes have been physically separated for at least 21,000 years—the last time land bridges between the two islands existed—and earlier studies estimated that they became distinct species more than 1 million years ago. But the new analysis, reported online today in Nature, rewrites history: it appears they parted ways just 400,000 years ago. “Most previous studies used small sets of markers and a limited amount of DNA sequence,” says Locke. “The statistical power is so much greater when you have the whole genome at your disposal.”

The orangutan now joins chimpanzees and humans as the third great ape to have its genome sequenced. “The orangutan genome is a wonderful resource,” says evolutionary geneticist Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. “It will help clarify how each part of human and African ape genomes are related to each other and evolved.”

Such insights are already coming in. Orangutans originated some 12 million to 16 million years ago, giving their genomes much more time to evolve than those of humans and chimpanzees, which split into their own lineages 5 million to 6 million years ago. But a comparison of the three genomes shows that humans and chimpanzees lose or gain new genes at twice the rate of orangutans.

The reason may have to do with stretches of DNA called retrotransposons. These key drivers of evolution jump around the genome, creating new genes, crippling existing ones, or altering gene regulation. The new data reveal that common retrotransposons known as Alu elements have moved around the orangutan genome much less than they have in the human and chimpanzee genomes. “I don’t want to say that [Alu retrotransposition events] are shut off in orangutans, but they’ve been suppressed,” says Locke.

The researchers also discovered that, over time, the structure of orangutan chromosomes has changed little, which may be linked to the Alu element finding. Other researchers have suggested that the robust structural variation in humans and chimps may have spurred increased intelligence. But Locke notes that orangutans are also highly intelligent. “If orangutans have had very little structural variation, maybe this decouples structural variation from intelligence,” he says.

A separate but related study published today in Genome Research reports yet another unexpected finding from a comparison of the three great ape genomes. A team led by Mikkel H. Schierup and Thomas Mailund of Aarhus University in Denmark (both co-authors of the Nature report) discovered that some regions of the human genome more closely resemble the orangutan than the chimpanzee. This reflects the fact that at the time humans split off from a common ancestor with chimps, both species had the same ancestral orangutan DNA. But humans and chimpanzees have evolved separately for millions of years. In the process, chimps for mysterious reasons lost some orangutan DNA that humans retained.

More surprises are sure to come as researchers compare the genomes of even more apes. Projects to sequence the other two great apes, gorillas and bonobos, are under way.

source: science now

Better Molecular Pens


Someday, nanotechnologists fancy, they’ll be able to build materials atom by atom from the bottom up, LEGO-style. Right now they’re still working on the two-dimensional equivalent: writing ultrafine lines and dots of selected molecules on ultrasmooth surfaces. Unfortunately, all the molecular “pens” developed so far have been either too blunt-tipped or too costly for broad use. Now a new technique might enable nanotechnologists to quickly and cheaply write molecular features across a large area. Down the road, the approach could help scientists rapidly prototype novel nanostructures for use in everything from studying stem cells to the molecular triggers involved in cancer.

The tried-and-true way to put fine patterns on surfaces is optical lithography, used for decades to carve circuits onto computer chips. But lithography is very expensive and doesn’t work well with many materials, such as fragile biomolecules. To solve those problems, researchers have tried stamping molecular inks onto surfaces with rubber molds, or using arrays of tiny pyramids with ultrasharp tips as quills. The stamps are cheap, but they have trouble printing features less than 50 nanometers wide. The arrays have much better resolution. But because they depend on springlike cantilevers to keep the moving tips in contact with the surface, they are complicated to operate—and, again, expensive.

Three years ago, researchers led by Chad Mirkin of Northwestern University in Evanston, Illinois, reported a possible fix. In an article in Science, they unveiled a new design that did away with cantilevers by making the tips out of a springy plastic that flexed to maintain contact with the surface. The downside was that the softer plastic couldn’t take as sharp a point as the hard silicon pyramids could.

Now, Mirkin and colleagues are back with a hybrid design: hard tips mounted on a springy polymer layer instead of cantilevers. It’s the best of both worlds, Mirkin says: The new tips can write molecular patterns with a resolution less than 50 nanometers, but an array of thousands of them costs less than $1. In a paper published online this week in Nature, the researchers describe using an array of 4750 tips to write 19,000 copies of the pyramid portrayed on the United States $1 bill, each consisting of 6982 42-nanometer-wide dots.

“This is excellent work,” says Stephen Chou, a nanopatterning expert at Princeton University. Joseph DeSimone, a nanopatterning and nanomedicine expert at the University of North Carolina, Chapel Hill, agrees. “Placing the spring in the polymer is pretty clever,” he says. “It gets rid of the cantilevers and reduces the complexity and cost of the system.” Mirkin says the new arrays could create cheap arrays of DNA and other biomolecules for diagnosing diseases or studying how different combinations of biomolecules affect things such as the development of stem cells or the progression of cancer cells. That may not be molecular LEGO, but it ain’t hay.

source: science now

Obesity May Up Death Risk in Older Women With Colon Cancer


Here’s yet another reason to avoid obesity throughout your life: Doing so may improve your chances of survival if you’re diagnosed with colon cancer.

Women past menopause who are obese and diagnosed with colon cancer appear to face a greater risk of dying from all causes than those who are at a healthy weight or merely overweight, a new study shows.

And trying to lose weight after the diagnosis may be too late, researchers cautioned. Abdominal obesity even prior to the diagnosis of colon cancer was associated with an increased risk of dying after contracting the disease, according to study author Anna Prizment, a postdoctoral fellow at the University of Minnesota Masonic Cancer Center, in Minneapolis.

Body shape may play a role as well.

Women with the disease who have an unhealthy waist-to-hip ratio and a large waist are at increased risk of death, Prizment added.

The study is published in the September issue of Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.

Colon cancer is the second leading cause of cancer-related death among women and men combined. It is expected to kill more than 51,000 people — including nearly 25,000 women — in the United States in 2010, according to the American Cancer Society.

Many studies have found a link between excess body weight and a higher risk of colon cancer. “But not so many studies have examined how obesity affects survival of the colon cancer patient,” Prizment said.

So, with her colleagues, she evaluated women who had participated in the Iowa Women’s Health Study, focusing on 1,096 women participants who were diagnosed with colon cancer between 1986 and 2005. Body and weight measurements were obtained before the colon cancer diagnosis.

The study was retrospective, meaning that the data used had been recorded for reasons other than research.

During the follow-up period of up to 20 years, 493 women died. Among this group, colon cancer was the underlying cause in 289 deaths.

Obese women — those with a body-mass index (BMI) of 30 or higher — had a 45% increase in all causes of death compared to women with a healthy weight, according to Prizment. Their risk of dying from colon cancer also climbed by 32% compared to healthy weight women, but that finding was not significant from a statistical point of view. However, the 45% increase in all causes of death was clinically significant.

The researcher also found that the risk of dying was higher among underweight women, those with a BMI below 18.5. “But we don’t want to talk much about them because we had too few of them,” Prizment said.

Prizment expanded on the unhealthy waist-to-hip ratio and large waist associations that she found were associated with a higher risk of dying from colon cancer.

A waist-to-hip ratio of 0.80 or below for women is considered low-risk. For instance, a woman with a waist of 27 inches and hips of 36 inches has a waist-to-hip ratio of .75.

Women with waists of 37.5 inches or higher had a higher death risk than those with a healthier waist size, she found.

Exactly why the obese women with unhealthy waist-to-hip ratios and big waists are at increased risk of death from colon cancer compared to slimmer women isn’t known. “They may be diagnosed at an advanced stage,” Prizment said. “They may have less access to health care. There could be a direct biological mechanism.”

Her advice for women? “Maintain a healthy body weight is the only recommendation we can give for all postmenopausal women,” she said.

Until the new study, findings about excess body size in colon cancer patients and risk of death have been mixed and conflicting, said Dr. Peter Campbell, director of the tumorrepository for the American Cancer Society.

One strength of the new study, he said, is that “body size was measured before they had the diagnosis.” Measuring after diagnosis may not give a true picture, he said, as weight loss can occur after the diagnosis.

“It’s lifelong body size that’s important [to know in gauging risk],” he said. “This study adds important new information to our understanding of body size and health.”

He agreed with Prizment that the finding underscores the importance of maintaining a healthy body weight with age.

source: medicinenet.com