On Tuesday, researchers announced that a three-drug cocktail may help women with HER2-positive breast cancer better than any other drug used on its own. About one quarter of women with breast cancer make up this HER2 category.

Tests on mice revealed using the three drugs along with breast cancer drug tamoxifen helped wipe out tumors altogether. And the tumors did not come back. This is the first time mice were cured of a very aggressive human breast tumor. Incidentally, when a single drug was used, tumors returned within several weeks.

The three wonder drugs used in this study -- all are monoclonal antibodies that precisely target certain aspects of tumors -- are the experimental drug pertuzumab; trastuzumab, also known as Herceptin; and gefitinib, or Iressa.

Published in the Journal of the National Cancer Institute, this study supports the notion that HER2-positive tumors eventually become resistant to one drug and attacking them on several fronts seems to work better.

Twenty to thirty percent of breast cancers over express a protein referred to as the human epidermal growth factor receptor, better known as HER2 over expression.

Herceptin is an agent that is targeted against the HER2 receptor and helps to slow or stop the spread of cancer cells that over express this protein. Unfortunately, some women that do have the over expression of HER2 on their breast cancer cells do not respond to treatment with Herceptin.

The Journal of the National Cancer Institute has published a report that says among breast cancer patients with HER2 over expressing cancer cells, those whose cells also express a receptor called p95HER2 have a poor anti-cancer response rate with Herceptin.

The study included forty seven women with metastatic breast cancer. All were treated with Herceptin. Nine of these patients also expressed the receptor p95HER2.

The results showed that only 11 percent of the women with the p95HER2 expression showed an anti-cancer response to Herceptin. Of the patients who did not express p95HER2 demonstrated a response of 51 percent. The report also showed that laboratory testing of cancer cells that do express p95HER2 demonstrated anti-cancer activity with a drug called Tykerb.

The researchers concluded that patients with HER2-over expressing breast cancer who also express p95HER2 appear to be more resistant to treatment with Herceptin and "may require alternative or additional anti-HER2–targeting strategies." Patients with HER2-over expressing breast cancer may wish to speak with their physician regarding their individual risks and benefits of participating in a clinical trial further evaluating biologic markers that may help predict responses to certain therapies.

Katherine Schaefer was investigating methods for treating the inflammation seen in Crohn's disease and ulcerative colitis when something terrible happened -- she noticed her carefully cultured cells were dead. And then something wonderful happened -- she realized she had stumbled upon a potential new method of attacking cancerous tumors that have become resistant to existing drugs.

Schaefer and her colleagues at the University of Rochester Medical Center in New York were testing a compound called a PPAR-gamma modulator -- a compound never considered a cancer drug, or a drug of any kind really -- when Schaefer made a calculation error and used a lot more of the compound than she should have. And her cells died.

Upon further study, Schaefer found the compound killed just about every possible epithelial tumor cell. These cells line organs such as the colon and also the skin. The compound, that works like taxane drugs but without eventual tumor resistance, also killed colon tumors in mice without making them sick.

The research team, whose findings are published in the journal International Cancer Research, plans more safety tests in mice. And eventually, if their outcomes are promising, they plan to design something they can patent as a new drug -- because they would love to see this disastrous lab experiment one day lead to treatment for cancers of the colon, esophagus, liver, and skin.

Sprycel is an oral agent that has recently been approved by the FDA. It works by stopping the production of proteins involved in cancer growth.

The American Society of Hematology presented results that stated that treatment with Sprycel (dasatinib) provides better outcomes compared to giving higher doses of Gleevec (imatinib), in patients with chronic myeloid leukemia (CML), who have stopped responding to standard doses of Gleevec.

In the clinical trial the patients were either treated with Sprycel or increased doses of Gleevec to see who had the better response.

Study results indicated:

• Patients who had achieved a major anticancer response with the standard dose of Gleevec initially, achieved a 35 percent complete response to Sprycel, compared with only 7 percent of those treated with the increased doses of Gleevec.
• Patients who did not receive a major anticancer response with the standard dose of Gleevec initially, achieved a 44 percent major anticancer response to Sprycel, compared to only 7 percent of those treated with the increased doses of Gleevec.
• The main side effect of Sprycel was low levels of blood cells, which may be partly corrected with the use of Neulasta.

The research has concluded that Sprycel provides superior responses to increased-doses of Gleevec among patients with chronic-phase CML who have stopped responding to prior Gleevec therapy.

Tamoxifen has been used successfully for over 20 years. The researchers know that over time Tamoxifen can lose its effectiveness. Many women diagnosed with Stage IV breast cancer that have tumors that are estrogen-receptor positive can be put on Tamoxifen to control the disease. After some time the patient becomes resistant to Tamoxifen and has to be switched to another drug.

A molecule, called disulfide benzamide or DIBA, could provide a way to overcome that resistance and restore the effectiveness of Tamoxifen. Findings are published in the December issue of Cancer Cell that show how mice engineered to develop Tamoxifen resistant tumors and human breast cancer cells in the lab were given the molecule. In both cases the tumor growth slowed.

William Farrar, head of the Cancer Stem Cell Section of the National Cancer Institute's Center for Cancer Research and the studies lead author, says "DIBA is what is known as a lead compound, which means it merely opens the door to suitable drugs." He also says that "DIBA itself is probably not appropriate for humans, because of solubility problems". The team plans to try and develop another compound fashioned after the properties of DIBA and hopeful have this be able to be administered orally.

One important aspect of the research was that it focused only on an acquired resistance to Tamoxifen over time. It did not study why some estrogen positive tumors initially are resistant to the drug.

Glioblastoma is the deadliest form of brain cancer, most often striking patients in their 50s and 60s who after diagnosis typically have only 10 to 12 months to live.

Glioblastoma is a shocking diagnosis -- and while the tumors don't tend to spread outside the brain, they resist surgery and return even when half the brain is removed. They also are resistant to most treatment. Clearly, insight into this deadly cancer is a must. Thankfully, a little slice of insight has just emerged.

Armed with findings from experiments in mice, researchers report they've discovered a clue that might help unravel the mystery of glioblastomas.

Studies show that some mice recovered from a human form of brain cancer when given bone morphogenetic proteins that appeared to interfere with the cancer growth process in stem-like cells. This leads researchers to believe the proteins could be used to stop cancer growth and prevent it from recurring.

The research is not ready for prime time, says one of the researchers who maintains there is still a long way to go. Yet the findings are promising -- and they suggest stem cells may play a critical role in tumor formation.

About 17,000 to 18,000 Americans develop brain cancer each year. Half of these patients will be diagnosed with glioblastoma.

It's not surprising marathon runners face an increased risk of skin cancer due to long-term sun exposure. What's surprising is that so many are not taking measures to protect themselves from the sun's damaging rays.

A team of Austrian researchers, all of them dermatologists, became interested in studying long-distance runners when they realized they had collectively treated eight ultra-marathon runners with malignant skin cancer over a period of 10 years. All researchers are themselves enthusiastic runners, and two of them participate in marathons. The topic was near and dear to their hearts.

Research was conducted on white runners, so it is unclear if the findings -- listed below -- apply to black runners.

• Only 56 percent of runners in the study reported wearing sunscreen. Most were unaware of the increased risk to their skin -- and even the running researchers report it is good to be reminded to wear the right gear and regularly use sunscreen

• Many runners race with a lot of skin exposed. And sometimes training clothing covers different areas than racing clothing. Shoulders that are covered during training may be exposed during the long hours of a marathon. During triathlons, most wear a bathing suit for the duration of the event, leaving most skin susceptible to burning. Runners can lower their risk by training during morning and evening hours and wearing water-resistant sunscreen. They can wear clothing made of new fabrics that screen harmful ultraviolet rays.

• It's possible that endurance athletes may have suppressed immune systems caused by repeated tissue damage, leaving them more vulnerable to skin cancer.

While some marathon runners take pride in a bronzed skin -- proof they are running in the elements -- researchers hope runners will consider the risk they face. In some races, volunteers offer to quickly apple sunscreen on athletes who don't want to lose precious seconds as they race for the finish line. It's a start.

"The normal response of prostate cells when male hormones are blocked is cell death," said George Kulik, assistant professor of cancer biology and senior researcher at Wake Forest University School of Medicine. "The cancer cells find a way to resist the treatment and we wanted to discover the mechanism."

Researchers have discovered the canny and shrewd way prostate cancer cells manage to defy death and become resistant to hormone treatment. The prostate cancer cells are using three separate pathways to send signals to cancer cells by inactivating a protein, BAD, meant to cause cell death.

If animal and human studies further prove what the researchers have discovered, new drug therapies could be developed to keep BAD active and doing its job in helping to destroy prostate cancer cells.

One of the best systematic therapies for prostate cancer is to lower the hormone levels in the patient. Lowering the hormones that stimulate the growth of prostate cancer cells usually result in the cancer shrinking or growing more slowly.

The problem with the hormonal treatments is that they usually stop working because the cancer cells become resistant over time. The researchers at the Wake Forest University School of Medicine have found a protein that is involved in the survival strategy of the cancer cell.

Researchers understanding the mechanisms that are at work in the cell that leads to the resistance of hormonal treatments is promising. This could lead to understanding why other treatments like chemotherapy also stop working over time.

Manchester doctors at the Christie Hospital in Didsbury are importing manuka honey from New Zealand to treat mouth and throat cancer patients after surgery in the hope honey can reduce inflammation and prevent methicillin-resistant Staphylococcus aureus, MRSA. Most people have this common type of bacterium in their nose and on their skin, but if healthy, the bacterium won't cause problems.

For hospitalized patients, there is a risk MRSA will spread through cuts, wounds, surgical incisions or catheters. The main problem with MRSA is that it has become resistant to some, but not all, antibiotics.

For the last several months, Manchester Royal Infirmary doctors have been using special honey-coated dressings to treat wounds. Now -- privately funded by community members and cancer patients themselves -- cancer patients at Christie Hospital in Didsbury will participate in this new study to test the effectiveness of the imported honey in preventing infection.

To read more about manuka honey, the company has a website here. The National Honey Board has published information on the antibacterial properties of honey here. The Sydney University's School of Molecular and Microbial Biosciences has published From nature's pantry: The healing properties of honey regarding research done on the antibacterial activity of certain types of honey.

At the end of March, we told you about nine lawsuits filed in a California court against the makers of five of the most popular sunscreen brands in the U.S. -- Coppertone, Hawaiian Tropic, Banana Boat, Neutrogena and BullFrog -- accusing sunscreen makers of misleading consumers on how well their lotions block the sun's harmful rays, putting millions of people at risk of skin cancer.

Over the weekend, over 166 separate news stories have been filed about these lawsuits. At first I wondered why now, over two months after the news first came out about the lawsuits, suddenly the peaked interest. Are we short on new health news? Maybe.

However, with all the additional coverage, I was able to learn that the accusations might not be a matter of exaggerated claims alone, but a scurrilous attempt to skirt the laws in deliberately misrepresenting the value of sunscreen products for the purpose of profit at the expense of human lives in increased skin cancer risks. Have we just come to a time when we might as well assume that all companies deceive and that our government seems incompetent to protect its citizens? Maybe so.

Here's how this whole situation happened, and why there are now nine lawsuits filed against some of the biggest names in sunblock lotion products. Sunscreen makers claim their sunscreen lotion is waterproof and acts as a sunblock. Years ago, the FDA wanted the claims changed to read water resistant instead of waterproof and sunscreen instead of sunblock. Because the FDA has never imposed the changes, the big name sun lotion makers chose to go with the more descriptive wording that made the lotions sound more effective than they were in actual fact. To some, it might seem a matter of semantics but words have power. The change from sunblock to sunscreen and waterproof to the more accurate water resistant could mean a potential difference in profits. What's at stake? Years of consumer health.

When researchers transplanted white blood cells from a strain of  cancer-resistant mice into ordinary laboratory mice with advanced cancers, the transplant cured the cancers. According to Wake Forest University School of Medicine researchers, even highly aggressive forms of cancer with extremely large tumors were destroyed. This is breaking news. It gets better. After the white cell transplant from the super cancer-resistant mice wiped out the cancer, the white cells also protected the ordinary mice from any new deadly cancers. And it keeps getting better.

Previous studies showed that cancer-resistance in mice can be inherited. The current cancer-resistant mice all come from a single mouse discovered seven years ago. The researchers said that the cancer resistance trait has been passed to more than 2,000 descendants in 14 generations. The white cell transplant that killed the cancer came from these mice. When they can figure out how to translate all of this to the benefit of humans, the possibility for cancer cure is amazing. Truly amazing.

The Canadian Cancer Society is calling for a ban on the use of pesticides in private gardens, lawns, parks, recreational facilities and on golf courses because of the potential cancer risks associated with the chemicals used in maintaining ornamental gardens and lawns. In a statement published at the cancer society website, "We base this concern on the conclusions of the International Agency for Research on Cancer, IARC, that state that some substances used in pesticides are classified as known, probable or possible carcinogens. Since ornamental use of pesticides has no countervailing health benefit and has the potential to cause harm, we call for a ban on the use of pesticides on lawns and gardens." I think that is a substantially clear statement that does not leave much margin for misinterpretation of what they mean in the call for a ban on chemical pesticide use.

According to Pesticide Free Lawns Coalition, over 100 million pounds of pesticides are used by homeowners in homes and gardens each year. While much attention is directed at the agricultural use of cancer-causing pesticide use, it might surprise the homeowner to know that suburban lawns and gardens receive more pesticide applications per acre than most other land areas, including agricultural areas. Chemicals used on lawns and gardens do not stay on the lawn or in the garden, but drift inside to pollute indoor air and surfaces. The Pesticide Free Lawns Coalition estimates of the 30 commonly used lawn pesticides, 19 are linked to cancer.

Toronto Master Gardeners offer a set of Go Natural in the Garden fact sheets that help the homeowner find alternative methods for maintaining a healthy garden and lawn.