Ovarian Cancer: The Silent Killer

Ovarian cancer is a disease that all women need to know about. It is known as the silent disease. Why? Because many women do not experience any signs, thus delaying the diagnosis. This disease often doesn’t produce symptoms until it is too late. So, to move the phrase ‘late’ out from our health dictionary, that would be much better if we take an awareness to the warning signs that may indicate ovarian cancer, so that we can detect it earlier.

There are a few symptoms women may notice and pass off as PMS, aging, or as generally not feeling well :

• frequent urgency to urinate
• feeling full quickly after eating or difficulty eating
• bloating, pelvic and/or abdominal pain

Because these symptoms “whisper”, many women do not seek immediate treatment until the disease has unknowingly progressed. So, if you experience these warning signs daily, for three weeks or longer, see your doctor. It’s a must.

New Ovarian Cancer Treatment Working

New Ovarian Cancer Treatment Working

Nov. 15, 2006 -- Aggressive combination therapy for ovarian cancer is worth the cost and toxicity, a new study shows.

The new treatment more than doubles survival time from two and a half years to five and a half years.

Ovarian cancer is a killer. It's often well advanced by the time it's diagnosed. Without treatment, most patients die in two and a half years.

In patients who can tolerate it, doctors today use a combination of platinum-based chemotherapy plus drugs called taxanes. Most recently, they've begun injecting the drugs directly into the abdominal cavity.

It seems to work better than older treatments. But might less aggressive therapy work just as well? A team of researchers from Britain, Greece, and the U.S. decided to find out.

Maria Kyrgiou, MD, of Queen Charlotte's and Chelsea Hospital in London, and colleagues analyzed 198 clinical studies. The studies, conducted between 1971 and 2006, tested 120 different chemotherapy regimens on 38,440 women with ovarian cancer.

The bottom line: Compared with single-agent chemotherapy without platinum-based drugs or taxanes, the new combination -- given by abdominal injection -- cuts the risk of death by more than half (55%). When given in other ways, the combination cuts death risk by 42%.

Platinum-based drug combinations without taxanes cut deaths by 40% when given by abdominal injection and by 30% when given in other ways. Taxanes alone don't do much good.

"Compared with the early days, when neither platinum nor taxanes were available and chemotherapy was clearly no better than supportive care [in terms of death] ... survival can now be more than doubled using currently available regimens," Kyrgiou and colleagues conclude.

The researchers note that not all patients will be able to tolerate aggressive combination therapy.

"These benefits should be tailored to the individual patient and balanced against tolerability," they warn.

Kyrgiou and colleagues report their findings in the Nov. 15 issue of the Journal of the National Cancer Institute.

A User-Friendly Vaccination Schedule

A User-Friendly Vaccination Schedule

Gene thought to assist chemo may help cancer thrive

A gene thought to be essential in helping chemotherapy kill cancer cells, may actually help them thrive. In a new study of chemo patients, scientists at the Georgia Institute of Technology and the Ovarian Cancer Institute found that 70 percent of subjects whose tumors had mutations in the gene p53 were still alive after five years. Patients with normal p53 displayed only a 30 percent survival rate. The findings raise the possibility of a new strategy for fighting cancer - namely, developing drugs to disable the functioning of this gene in the tumors of patients undergoing chemotherapy. The results appear in the May 16 edition of the open access journal PLoS ONE.

“P53 has long been recognized as a key player in directing chemotherapy-damaged cancer cells to self annihilate, but less attention has been paid to p53’s role in repairing damaged cells,”said John McDonald, chair of Georgia Tech’s School of Biology and chief research scientist at the Ovarian Cancer Institute.

When a cell is malfunctioning or injured, the gene p53 is called into action and tries to repair the cell. If the cell can't be repaired, p53 starts a process known as apoptosis that kills the cell. It's p53's role as one of the genes involved in initiating cell death that has led cancer researchers to long believe that the gene is essential to successful chemotherapy. The idea is that p53 assists in killing the cancerous cells that the chemo treatment injures.

But in this latest trial, Georgia Tech researchers found that p53 may be a “double-edged sword.” Chemotherapy patients whose tumors had a mutated p53 gene that didn't work had a much better survival rate than those who had normal p53.

In the study, researchers took malignant and benign ovarian tumors straight from the operating room and compared their gene expression profiles. Some of the cancer patients had been treated with chemotherapy prior to surgery, and some had not. At this point researchers didn't consider whether the patients actually had malignant tumors or had been treated with chemotherapy. However, they found that the gene expression profiles of the tumors clustered the chemotherapy-treated patients into two groups: those whose profiles were similar to cancer patients who had not been treated with chemo and those whose profiles were similar to patients with benign tumors.

As they continued their analysis, they found that the main difference between the groups' genetic profiles was the gene p53. While both groups had roughly the same amount of the protein encoded by p53, the cancer group had mutations in their p53 that caused the gene’s corresponding protein not to function.The benign group's p53 was normal.

Five years later, only 30 percent of the chemotherapy cancer patients clustering in the benign group were alive, while 70 percent of those clustering in the cancer group were still alive. The stage of cancer at the time of surgery had no correlation to who survived and who didn't. What did seem to have an effect was whether p53 was working or not in the chemotherapy-treated tumors.

A standard belief in cancer research is that a working p53 is essential in helping chemo patients because it turns on the killing mechanism for the cells that were damaged by chemo. But McDonald points out that p53 can also help repair damaged cells. If p53 is repairing cancer cells, that may lead to cancer recurrence.

"We think p53 may actually help some cancer cells make a comeback,” he said. "Based on our results, we propose that p53 may help repair some of the cancer cells damaged by chemotherapy leading to tumor recurrence and explaining the higher mortality rate of patients whose tumors had a functioning p53. If we are correct, inhibiting p53 in tumors being treated with chemotherapy may substantially improve patients' long-term survival."

McDonald and colleagues are continuing to test their theory by conducting studies in cell cultures and mice. If it bears out, then disabling the gene in tumors, through medications or new genetic techniques during chemotherapy may help patients survive. Source : Georgia Institute of Technology

Student shows that breast cancer drug could work for ovarian cancer

An inspiring teacher who died from ovarian cancer prompted Victoria Bentley to see if she could use her scientific knowledge to find a new treatment for the disease which is the fifth-highest cause of cancer deaths in Canada.

Knowing that ovarian cancer grows in response to the hormone estrogen just like breast cancer she wondered if Tamoxifen — the breast cancer treatment drug– would also suppress ovarian cancer cells. The sixteen-year old Halifax student applied Tamoxifen to human ovarian cancer cells which made them “supersensitive” to levels of estrogen. Instead of the hormone causing the cancer cells to proliferate, it inhibited their growth she said.

Tamoxifen is not approved for use for ovarian cancer and there is a lack of concrete evidence that it could work until now says Bentley.

“It’s surprising that something that I showed to be a viable treatment option was not recognized as such by such important institutions as the US FDA.”

Equally surprising perhaps is that busy with piano lessons and practice, national debating contests and school that the Grade 11 student had time to do medical research.

Her experiment also uncovered a potential new tool for assessing the effectiveness of ovarian cancer treatments. Bentley explains: “I demonstrated that the expression levels of progesterone receptors are linked to cancer cell inhibition.” In other words, if the cancer treatment is working then progesterone receptor expression changes.

“The practical applications of biotechnology are astounding, and I think that this is an amazing field of work” she says.

“This project also exposed be to the thriving biotechnology sector within Nova Scotia, which I really wasn’t aware of up until now.”

Her mentor was Dr. Michelle Mujoomdar, post-doctoral fellow, Department of Biology, Dalhousie University.

Posted: May 17th, 2007 under Nova Scotia.

Source: http://biotechchallenge.ca/?p=102

Who do you know that has had ovarian cancer?
My mother Sharon Setser had ovarian cancer. She battled it on and off for eight years. It eventually grew outside of her ovaries and into her stomach. She got to were she couldn't eat or have a bowel movement. The tumors were so big that they couldn't even put in a feeding tube. She went from Thanksgiving 2005 until December 16, 2005 without holding anything down. This was the day that she passed away. Ovarian Cancer is a horrible disease and we need to do more to help others. That's why I started this website in memory of my mom and to spread awareness of this horrible disease. Please take part in this and help others. May God Bless You!