Here's an interesting story: Women in the Canadian province of Quebec are less likely than women elsewhere to take preventative action after learning that they have a certain gene linked to breast and ovarian cancers. Women who carry the BRCA1 or BRCA2 gene mutations have a higher risk of developing cancer, prompting many women to either have their breast or ovaries removed. Two thirds of women in Quebec took no preventative actions after learning of their risk, while only one third failed to take preventative steps in the rest of the country.

So, my thought for the day is: What would prevent someone from taking action against a disease that could kill them? Religious beliefs? Lack of knowledge about the disease? Lack of money? And if you found out you were at a high-than-normal risk for breast cancer, would you act right before it had the chance to get to you, or would you take your chances?

Roger Ebert, one of America's best known film critics, has not been able to speak since he had emergency cancer surgery on July 1 to repair a burst blood vessel near the site of his June 16 surgery to remove a cancerous growth on his salivary gland. But he can still give a thumbs up or thumbs down as he reviews movies on his Web site.

Starting today, clips from Ebert & Roeper and Ebert's prior episodes of his movie review TV show will be posted here. It just may be the largest collection ever of video-based online movie reviews -- 5,000 movie reviews spanning the past 20 years will be featured.

Ebert is not quite sure when he might return to television as he awaits another surgery to restore his voice. In the meantime, he screens as many as three films a day. He watches DVDs at night to catch up on those he missed, and he's writing more than ever, he says.

According to a New England Journal of Medicine article, the answer is no. Women with the breast cancer mutations BRCA1 and BRCA2 seem to have similar survival rates as women without these gene mutations.

A clinical trial was conducted including 1,500 patients. The researchers wanted to see if the patients with gene mutations had worse outcomes then those that did not have the gene mutations.

The researchers found:

• Overall, deaths rates from breast cancer were not significantly different among patients with BRCA1 and BRCA2 mutations from those without the mutations.
• Among patients who underwent treatment with chemotherapy, death rates from breast cancer were not significantly different between patients with BRCA1 and BRCA2 mutations from those without the mutations.

New research may one one day help in the diagnosis and prognosis of the nation's number four cancer killer of men and number five cancer killer of women. The killer: pancreatic cancer.

Findings from an Ohio State University study show pancreatic cancer cells may leave signs in gene-related molecules called microRNAs.

Published in The Journal of the American Medical Association, this study examined pancreatic tissue from 65 people with the disease and 42 people with chronic inflammation of the pancreas, called chronic pancreatitis.

It might not be possible at this time to eradicate cancer altogether. But we may be able to stop cancer cells in their tracks through a process called senescence.

In senescence, cells don't divide. And when cells don't divide, they don't grow. In such a scenario then, cancer cells wouldn't divide and therefore couldn't grow.

Think about this:

According to lab tests on mice, triggering senescence in certain cells hampers the growth of some tumors.

Researchers at the University of Texas M.D. Anderson Cancer Center in Houston are the ones behind the scenes on this project -- the study appears online in EMBO Reports, a publication of the European Molecular Biology Organization -- and all eyes are on the p53 gene.

The p53 gene lives within cells and works to nip cancer in the bud by springing to action in damaged cells that may be spinning themselves into a cancer frenzy.

Researchers say senescence ordered by the p53 gene is extremely important in suppressing tumor formation and is as important as apoptosis -- a type of programmed cell death. But in some cancers, senescence might not be enough to halt cancer, they found.

OK, so senescence is not a perfect approach to halting all cancers. But it seems to work for some -- so I say for now, let's take what we can get.

Researchers have found that when cells become cancerous, they become 100 times more likely to genetically mutate than non-cancerous cells. This explains why tumor cells have so many mutations. Good news on the research front. But bad news on the treatment front -- because therapies that target a certain gene may be largely ineffective in controlling cancer.

"This is very bad news, because it means that cancer cells in a tumor will have mutations that protect them from therapeutics," says lead researcher Dr. Lawrence Loeb, professor of pathology and biochemistry at the University of Washington School of Medicine in Seattle, who presented his findings February 18 at the meeting of the American Association for the Advancement of Science in San Francisco.

Loeb says chemotherapy drugs target specific oncogenes -- genes that affect the malignancy of a cell -- but if cancer cells are mutator cells, then a single tumor may have cells with all sorts of oncogenes. And while chemotherapy may kill some cancerous cells, millions of others will live on.

It's not all bad news, though, says Loeb who believes this research may help doctors determine the stage and malignancy of tumors by testing the number of mutations. It may also help researchers understand what makes a cancer cell a mutator and how to slow the rate of mutation.

"The idea is that if you might normally get exposed to something in the environment at 20 years old that would give you cancer by age 55, then if we cut the mutation rate in half, you might not get cancer until age 90, and you may even die of something else before that," Loeb explained.

Scientists have uncovered a gene they say may be cancer's master switch.

Like a circuit breast of sorts, the newly identified gene, CHD5, has an important job -- it's a tumor suppressor that prevents cancer from developing. But when it slacks on its job, cells begin to misbehave and tumors can form.

One professor of genetics says the gene, located on chromosome 1, governs the activity of a wide array of other genes involved in tumor-suppression. Its reach is large. And the implications of improper functioning are significant.

Cancers associated with the malfunctioning gene include brain tumors such as gliomas and breast, ovarian, prostate, and colorectal cancers.

A lot of people have been looking for this gene for decades. And now that it's been located, it will influence cancer research for years to come. The discovery will provide valuable new insight into targeted drugs and diagnostics and will turn up patients who need more aggressive treatment.

"We are really excited about our discovery," says the lead investigator of the research, which is published in the journal Nature.

In a radical new approach to attacking cancer, researchers will soon attempt to kill tumors by infecting them with viruses that cause ailments like the common cold.

This virus therapy treatment -- considered the third pillar alongside chemotherapy and radiation -- could one day become standard battle against cancer.

One Belfast doctor says anything that could improve the lives of cancer patients is worth a try. And try is exactly what Leonard Seymour, Professor of Gene Therapy at Oxford University, plans to do when he begins leading trials later this year.

Seymour, who has been working with viruses that kill cancer cells while sparing healthy tissue, will use a stealth virus masked from the body's immune system with a polymer coat that could travel through the bloodstream and reach tumors.

Two viruses are likely candidates for study in the first clinical trials -- adenovirus, cause of a cold-like virus, and vaccinia, cause of cowpox and a component in the smallpox vaccine.

Preliminary research on mice shows that virus therapy works well on tumors resistant to standard cancer drugs. But several years of trials will be necessary before the therapy can be considered for use on all cancers.

A decade of research specific to the inherited form of pancreatic cancer has turned up a gene that could lead to earlier diagnosis and treatment for one of the deadliest forms of cancer.

The magical gene -- called palladin -- was discovered at the University of Washington after the extensive study of one family that has lost nine members over four generations to pancreatic cancer and has nine additional members with early signs of the disease.

Washington resident Ryan Chappell, a member of this family who had his pancreas removed just before cancer could strike, is very excited about this breakthrough.

"I feel really good that my family has not suffered (in vain)," the 21-year-old says. "Something has been accomplished from their contribution."

What the Chappell family has contributed to research is an understanding of a breakdown in a gene that makes a protein for the skeleton of pancreas cells. In this one family, the gene was mutated and produced large amounts of a misshapen protein that rolls like tumbleweed through the body, migrating 50 percent faster than other cells.

Scientists hope to translate their research findings into a diagnostic test to find excess amounts of the protein and to prevent the cancer cells from moving.

For now, early detection of pancreatic cancer rare because the pancreas is deep in the body, making it difficult to feel or see tumors through imaging tests. Symptoms -- like jaundice, abdominal and back pain, and digestive problems -- usually surface only after the cancer has spread.

Cancer of the pancreas is rare but is the third-leading cause of cancer death among people age 40 to 60.

Aspirin, and other nonsteroidal anti-inflammatory drugs (NSAIDs), are known to halt the growth of some cancers, such as colorectal cancer, breast cancer and ovarian cancer, but no one could really explain why. Obviously, as a result it was believed that chronic inflammation might be leading to increased cancer risks. Still, no one could explain how any of this was happening enough to harness the ability to replicate it.

Beth Israel Deaconess Medical Center and Columbia University Medical Center researchers have announced the discovery of a novel tumor suppressor gene that works with NSAIDS to stop the growth of cancer cells.

"Current clinical trials are evaluating a range of NSAIDs for a variety of cancers without any clear vision of the best way to use them," states Towia Libermann, PhD, Director of the BIDMC Genomics Center and Associate Professor of Medicine at Harvard Medical School. "The fact that upregulation of this single gene MDA-7/IL-24 -- correlated not only with cell death induction of numerous types of cancer but also among various diverse classes of NSAIDs, makes this discovery particularly exciting."

As a result of this discovery, researchers believe newer targeted cancer therapies can be developed. To read more about the discovery, visit Beth Israel Deaconess Medical Center and Columbia University Medical Center's Study Explains How NSAIDs Halt Cancer Growth.

Some of the previous posts we have on inflammation, cancer and aspirin are:

• Aspirin: amazing wonder drug in fighting cancer
• Inflammation link between rheumatoid arthritis and cancer
• What aspirin reveals about cancer

A study that appears in the December issue of Science reports that a chemical compound called mifepristone present in the abortion pill may prevent breast tumors from developing. The compound has been found to prevent the growth of breast tumors caused by the mutant gene responsible for breast and ovarian cancers.

Mifepristone showed to prohibit progesterone, a hormone involved with the female reproductive cycle. Women who are diagnosed with BRCA 1 mutation often have their breasts or ovaries removed to reduce the risk of developing cancer.

Eva Lee, lead author of the study and professor of developmental cell biology and biological chemistry, says "We found that progesterone plays a role in the development of breast cancer by encouraging the proliferation of mammary cells that carry a breast cancer gene. Mifepristone can block that response. We're excited about this discovery and hope it leads to new options for women with a high risk for developing breast cancer".

BRCA 1 is widely studied by cancer geneticists because a mutated version of this gene significantly raises the possibility of breast or ovarian cancers. By age 70, more than 50 percent of women with the mutated gene with develop breast or ovarian cancer. The researchers studied mice with the BRCA 1 mutation. The mice that were treated with mifepristone, an anti-progesterone compound did not develop breast cancer by the time they reached one year of age. All of the untreated mice developed tumors by eight months of age.

The researchers found that progesterone encourages the development of cancer when the mutated BRCA 1 gene is present because it speeds up the division of cancer cells. Mifepristone was found to block a binding process that is necessary for progesterone to cause the cell division. The researchers feel that anti-progesterone therapy could provide women with an increased risk for breast cancer with more treatment options in the future.

No one is suggesting women use the abortion pill RU-486 to keep a well-known breast cancer gene from doing its dirty work, but scientists have successfully used this pill to keep tumors at bay in mice bred with the BRCA1 gene. And while this breakthrough may not benefit the human population just yet, it does indicate there may be something on the horizon to help women who carry the gene and are destined to develop breast cancer.

The BRCA1 gene spurs the sex hormone progesterone that RU-486 happens to block. If researchers could create a safer hormone blocker, it may offer an alternative for women with the bad gene. Today, there are just a few options for these women -- and all of them are anxiety-producing.

Currently, women can receive more frequent cancer screenings to catch cancer in its earliest form, remove both breasts while they are still healthy, take the hormone-blocking drug Tamoxifen, and remove the ovaries to cut the risk of both breast and ovarian cancers. A better option is necessary for women faced with an almost certainty of developing cancer.

The deputy chief medical officer for the American Cancer Society calls this study elegant research. But he stresses that "it would not be appropriate in any way, shape or form that women start taking RU-486 for this purpose." Long-term use of this abortion drug can cause other side effects, including immune system suppression.

Cancer specialists applaud this development. Yet they caution women to not get their hopes up yet. They say this is an avenue worth pursuing on a research level. But it's clearly too soon to start recommending use of an agent like RU-486 for breast cancer prevention.

There are various risk factors that can contribute to the development of breast cancer. Being female is the single biggest risk factor that on its own puts all women in jeopardy. But there are other risks -- many beyond our control and some more significant than others -- that can help explain why some women are diagnosed with the most common cancer in women in the United States. And why others are not.

Researchers have identified a damaged gene -- BRIP1 -- that doubles the risk of familial breast cancer in a small percentage of women. BRIP1 is a DNA repair gene that can lead to uncontrollable cell growth if not functioning properly. Researchers have concluded that the damaged gene increases risk for breast cancer from eight to 16 percent by age 70.

These findings won't change patient care but they may offer comfort to women who develop breast cancer and cannot pinpoint the occurrence to the commonly mutated BRCA1 and BRCA2 genes -- mutations that are responsible for the disease 80 percent of the time. And while the study of BRIP1 does add to the pool of research on breast cancer, it does not warrant screening at this time. It's just a small piece of the puzzle that one day may prove significant. For now, the risk of breast cancer resulting from a damaged BRIP1 gene is modest.