Femara (letrozole) is an aromatase inhibitor that works by suppressing the production of estrogen. In postmenopausal women estrogen is still produced in the body by the adrenal gland. Decreasing this production is a way of decreasing the risk of recurrence.

Tamoxifen on the other hand works by blocking the estrogen receptors on the cancer cell itself resulting in slower growth of the cell or cell death. Tamoxifen can be given to post or premenopausal women but Femara would only be prescribed to women that are postmenopausal. The reason being, is that a premenopausal women will still have estrogen produced by the ovaries. Femara would not be effective in this instance.

A Phase III clinical trial that is ongoing shows preliminary results that Femara is superior than Tamoxifen in women with early stage disease that are postmenopausal. The results of the study were published in the Annals of Oncology.

Lung cancer tumors in mice are shrinking -- with the help of a hormone important in the control of blood pressure.

This new discovery, led by scientists at Wake University School of Medicine, suggests some drugs used to manage blood pressure might also prevent or treat lung cancer.

This all came about when it was noticed that lung cancer rates were lower among those treated for high blood pressure with angiotensin-converting enzyme, or ACE, inhibitors. These drugs, including Capoten and Lotensin, increase levels of angiotensin-(1-7) in the bloodstream.

In studies, the angiotensin-(1-7) hormone caused a 30 percent decrease in tumor volume in mice. Tumors in mice not treated with the hormone more than doubled.

This study, published in the journal Cancer Research, is the first demonstration of the effect in animals.

My good friend Deb, a young breast cancer survivor, emailed me this morning. She told me that she just filled her last prescription for Tamoxifen today. In the email she said it was a 'weird feeling'. I myself, will be going off Tamoxifen this October and will have fulfilled my five years on the drug as well.

I asked Deb to tell me more about how she felt and what it means in her life now that she will be discontinuing Tamoxifen for her breast cancer treatment.

"I have truly mixed feelings! It is bittersweet. It can be a scary, anxiety-provoking thought just thinking about ending it. It was my protection and security after chemotherapy for so long. I know that Tamoxifen still has effects in my body for years after stopping. I have three months left and I will stop Tamoxifen in June. Part of me is glad to stop it, to not have to remember to take a pill daily and my breast cancer treatment is now complete."

"Yet there is the other part of having to trust my body again. It failed me once. It means I'll have to modify some things in my life, substitute for taking a pill to fight off cancer. It means taking exercise more seriously, exercise can cut your risk for recurrence up to fifty percent. It means I'll stick to my diet a little better. I may also decide to take a Cox 2 inhibitor, like celebrex, as an anti-inflammatory. When Vioxx was pulled from the market, these similar Cox 2 inhibitors were pulled from clinical trials, now those trials are back open and are showing benefit. I have injuries in my knees, so will be taking it for that as well."

"In a sense I'll be flying on my own again. I remember them saying five years thinking how long that would be, it actually slipped right by. I will get tested to see if I'm in menopause, but seriously doubt that I am. It would be nice to go on an AI, but I really don't want to be in menopause quite yet. So, my prescription is diet and exercise and perhaps a Cox 2 inhibitor as preventative. I will still continue to see my oncologist every six months. I will continue to celebrate life and live it to its fullest and appreciate those things and people that truly make a difference in my life"

Deb Kirkland -- Young Breast Cancer Survivor

According to the results of an international study, postmenopausal women who have taken tamoxifen for early stage estrogen-receptor positive breast cancer for two to three years might increase their chances of survival by switching to newer breast cancer drugs called aromatase inhibitors.

Study researchers found this drug switch-up reduced the number of events linked to poor survival by 32 percent -- although no difference has been found in overall survival at this early point in the trial.

"These findings provide some limited evidence to advise all women being administered tamoxifen to switch, even though this approach is not devoid of potentially serious side effects," say experts at the National Cancer Institute.

Side effects appear to be minimal, however, and the up side of treatment with aromatase inhibitors is the fact that they don't seem to carry the risk of death from other causes like with tamoxifen, which can cause stroke or endometrial cancer.

This study is expected to be published in the March 15 issue of the journal Cancer.

A report has been released by Breast Cancer Action (BCA), a grassroots education and advocacy organization, on the side effects of aromatase inhibitors (AIs). The report is called "Side Effects Revealed: Women's Experiences with Aromatase Inhibitors". The study analyzed 612 women's responses to an online survey of AIs and their side effects. You can find the report online at http://www.bcaction.org/AIreport.

The results showed that 92 percent reported at least one side effect. Nearly 30 percent reporting stopping the use of AIs--84 percent of those that stopped taking the drug reported that it was because of the intolerable side effects. Almost fifty percent of those that stopped taking the drug because of side effects complained of joint-related problems. Other side effects included stroke, cough, swelling of extremities, flu-like symptoms, and anxiety. Many women said they had joint related issues, vaginal atrophy and dryness and general pain.

Many of the women said they did not receive information about short or long term side effects from their physicians. Executive Director of BCA, Barbara Brenner, said "Patients know about the side effects before their doctors do--they experience them firsthand. Now that hundreds of women taking aromatase inhibitors have spoken, it's time for the medical research community to respond with additional research on the side effects of these drugs."

A previous post related to this topic:

Breast cancer survivors reject chemoprevention drugs

I'm coming up on my last year on tamoxifen. I often wonder if it would be beneficial to me to begin taking an aromatase inhibitor following my five years of tamoxifen. According to an article published in the journal Cancer, premenopausal women with breast cancer that has spread to at least four lymph nodes received the most benefit from aromatase inhibitors following treatment with tamoxifen. Postmenopausal women with cancer that has spread to three or less nodes only seem to get a 1-2 percent benefit from the addition of an aromatase inhibitor following tamoxifen.

I don't seem to fit in either category since I had premenopausal breast cancer with less than four lymph nodes positive. I also thought that if you are premenopausal that aromatase inhibitors were not beneficial at all and only postmenopausal women were able to take these drugs.

Aromatase inhibitors work by reducing the amount of estrogen your body makes. Your adrenal glands produce a substance called androstenedione, which gets converted into estrogen in tissues such as fat and muscle. The conversion requires the enzyme called aromatase. Aromatase inhibitors stop the conversion of androstenedione to estrogen. However, if your ovaries are still functioning then the body still will have estrogen that can help cancer to grow and the aromatase inhibitors will not stop the estrogen production of the ovaries.

The study that was done concluded - it appears that women who are premenopausal and those whose cancer has spread to four or more lymph nodes would derive greater benefit from the addition of aromatase agents following tamoxifen.

I am assuming that they mean if these premenopausal women are then put into a postmenopausal state, either happening by chemotherapy or shutting down the ovaries by injection or oophorectomy.

This is a confusing article that doesn't seem to make sense. Any insights?

A type of Non-Hodgkin's lymphoma (NHL) called mantle cell lymphoma accounts for about five to ten percent of all lymphomas. According to an article recently published in the Journal of Clinical Oncology, Velcade (bortezobib) is an effective treatment option for patients with mantle cell lymphoma that has stopped responding to prior treatments.

Velcade is an agent known as a proteasome inhibitor. Proteasome inhibitors are drugs that block the action of proteasomes, proteins found in virtually all cells that regulate several aspects of cellular activity. By blocking the activity of proteasomes it can lead to the death of cancer cells. Bortezobib is the first therapeutic proteasome inhibitor to be approved for use in the United States.

Researchers conducted a clinical trial to evaluate Velcade in the treatment of fifteen patients with mantle cell lymphoma that has recurred or progressed following prior therapies. Anticancer responses occurred in 33 percent of patients and after over 13 months follow up, over half the patients were still surviving.

One of the keys to finding a cure for cancer is to understand how cancer grows and spreads within the body. Angiogenesis is our body's ability to form new blood vessels. This is important and needed for the body to help heal wounds and is also a part of a woman's menstruation each month. Its function in our bodies is a positive thing most of the time.

Angiogenesis also has a role in how cancer cells grow to become tumors. Cancer cells need a blood supply to live and grow. The cancerous tumor actually develops its own blood supply by sending messages to nearby blood vessels. These vessels then have the ability to grow toward the tumor. The tumor then has its own blood vessels to thrive, survive and grow.

This was not taken seriously back in 1961 when Dr. Judith Folkman came up with the theory of angiogenesis. He felt strongly that tumors could not grow bigger than a head of a pin without blood supply. He thought that an entirely new way to treat cancer would be to block this blood vessel growth to the tumor. Decades of work has proven this theory to be correct. What changed a lot of people's minds was an experiment that was done at the end of the 1970's at Dr. Folkman's lab. Tumor cells were put into a rabbit's eye, a place in the eye where there are no blood vessels. Blood vessels did grow toward and into the eye where the cancerous cells lived.