National Sun Safety Week – June 1st through June 7th

The sun’s ultraviolet (UV) rays can damage your skin in as little as 15 minutes. Follow these recommendations to help protect yourself and family. 

Shade. Seek the shade especially between the hours of 10am and 4pm when rays are at their strongest. Your best bet to protect your skin is to use sunscreen and wear protective clothing when you’re outside.

Clothing. A T-shirt has an SPF rating lower than 15 so make sure to use other types of protection when you know you will be outside in the sun.  Plan to wear long-sleeved shirts and long pants when possible and remember that clothes made from tightly woven materials typically offer the best protection. A dry T-shirt also offers much more protection against UV than a wet T-shirt. 

Hat. For the best protection, wear a hat with a brim that will shade your face, ears, and back of your neck. Tightly woven fabrics, such as canvas, works best to protect your skin from UV rays and void straw hats with holes that let sunlight through.

Sunglasses. Sunglasses protect your eyes from UV rays and reduce the risk of cataracts. Sunglasses that block both UVA and UVB rays offer the best protection. Most sunglasses sold in the United States, regardless of cost, meet this standard.

Sunscreen. Sunscreens works by absorbing, reflecting, or scattering sunlight. They contain chemicals that interact with the skin to protect it from UV rays. Higher numbers indicate more protection so make sure to put on broad spectrum sunscreen with at least SPF 15 before you go outside, even on slightly cloudy or cool days.

Application. Apply 1 ounce (2 tablespoons) of sunscreen to your entire body 30 minutes before going outside. Sunscreen does wear off so make sure to put it on again if you continue to stay out in the sun for more than two hours, after swimming, sweating, or toweling off.

Examine.  Examine your skin once a month to look for any suspicious lesions. Follow the ABCDE’s of Melanoma to identify if you should follow up with your primary care physician at


Provided by Kendall Taylor of the Valley Schools Employee Benefits Trust (VSEBT) in the June 2015 Wellstyles Monthly Newsletter.


Kendall Taylor, VSEBT

Kendall Taylor, VSEBT


Exercise boosts tumor-fighting ability of chemotherapy in cancer patients, researchers say



While exercise has been found to benefit cancer patients both physically and psychologically, researchers say a new study proves it can also boost the effect chemotherapy has on a patient.

In a study by a team at the University of Pennsylvania, researchers using a mouse model of melanoma found that combining exercise with chemotherapy shrunk tumors more than chemotherapy alone.

The researchers sought to find whether exercise would protect against negative cardiac-related side effects of the cancer drug doxorubicin, which is known to damage heart cells.

The team first injected melanoma cells into four teams of mice. They then injected two groups with doxorubicin and the other two with a placebo. Over a two-week period mice in one of the groups injected with the drug and one of the untreated groups walked 45 minutes, five days a week, on treadmills, while the other two groups did not.

While data showed that exercise did not help protect against cardiovascular damage, it did show that in mice that had received the drug and exercised, tumors significantly shrunk.

“We looked, and the exercise didn’t do anything to the heart – it didn’t worsen it, it didn’t help it,” Joseph Libonati, senior author of the study and associate professor at Penn School of Nursing, said in a news release. “But the tumor data – I find them actually amazing.”

The team plans to examine further how exercise enhances the effect doxorubicin has on tumors, but are encouraged that results may help find ways to cut down on cardiovascular damage caused by the drug.

“If exercise helps in this way, you could potentially use a smaller dose of the drug and get fewer side effects,” Libonati said.

Newly discovered biomarker can better guide treatment for melanoma patients

Newly discovered biomarker can better guide treatment for melanoma patients

By Loren Grush

Published October 22, 2013
  • Melanoma CDC.jpg

    This image depicts the gross appearance of a cutaneous pigmented lesion, which had been diagnosed as superficial spreading malignant melanoma (SSMM). (CDC.GOV)

Researchers have discovered a new biomarker that can predict whether melanoma patients with mutations in the BRAF gene will respond to certain kinds of cancer medications.

The discovery could help better guide treatment for patients with the disease, as they are often subjected to ineffective therapies to which their bodies are resistant.

The BRAF gene has been found to be an effective drug target for treating melanoma cancers, and the Food and Drug Administration (FDA) has approved two drugs inhibiting this gene.  However, patients with melanomas harboring mutations in the BRAF gene are sometimes resistant to these medications, and most people who initially respond to BRAF-targeting therapies eventually relapse, as their tumors become resistant to the drugs.

While BRAF mutations are present in only 7 percent of all human cancers, they are seen in approximately 50 percent of melanomas.  And there’s no concrete way of knowing which patients with BRAF mutations will respond to BRAF-targeting treatments and which ones will not.

“For virtually untreatable cancers, we’re seeing response rates of 60 to 80 percent with BRAF-targeting drugs.” Dr. Ryan Corcoran, a clinical investigator and assistant professor at the Massachusetts General Hospital Cancer Center and Harvard Medical School in Boston, Mass., told   “…But 60 to 80 percent response rate means there are still 20 to 40 percent of patients who don’t respond.  Determining which patients are most likely to respond (to these drugs) and perhaps should be diverted to an alternative therapy could be really beneficial.”

Corcoran said that previous research has identified numerous mechanisms behind the resistance to BRAF inhibitors, but it can be a daunting task screening patients for these mechanisms. So he and his team decided to analyze them further.

“We thought, ‘Perhaps all these resistance mechanisms converge into a key downstream pathway,’” Corcoran said.  “Then maybe we could get a more universal yes-or-no predictor to see if patients respond to the drugs.”

After analyzing genetic models in the lab, Corcoran and his team found that the signaling pathway TORC1 was a key converging point for these mechanisms and that the presence of a protein called S6 could serve as a good predictor of sensitivity to BRAF-inhibiting medication.

“There’s a protein substraight called S6, which is involved in protein translation in the cell,” Corcoran said. “It’s basically used as an indicator of TORC1 activity.  When the pathway is active, the presence of S6 is elevated, and vice versa.”

In their models, the researchers found that melanoma cancers that were sensitive to BRAF inhibitors saw a suppression of S6 after treatment.  In contrast, almost all melanoma cancers that were resistant to the drugs maintained higher levels of S6 post treatment.

To further verify this finding, the researchers collected tumor biopsies from nine melanoma patients, which had been taken before and after treatment with BRAF-targeting drugs.  The found that one subset of patients had an effective shutdown of S6 after treatment, compared to the other patients who had maintained levels of S6 after treatment.  Ultimately, the group of patients with effective suppression of S6 had a more than fivefold increase in repression-free survival compared to the those who had maintained S6.

“That suggests that if we can identify early on these patients who down regulate or fail to down regulate S6, we can predict who is most likely to respond,” Corcoran.

Applying this new knowledge, Corcoran and his team developed a new technique that can rapidly monitor, in real time, the levels of S6 in tumor cells.  Using fine-needle aspiration biopsies from melanoma patients before and during the first couple weeks of their treatment with BRAF-targeting drugs, they could assess the activity of the S6 signaling pathway and quickly determine a patient’s resistance.

“It’s still in concept phase, but …if you have a way of determining (resistance), you can spare (a patient) unnecessary treatment,” Corcoran said. “By identifying this subgroup, you can do that at a much earlier point, rather than waiting two months, as is done, for a repeat CT scan.  So this is really a way to guide treatment more rapidly and divert more patients to more effective therapy.”

The research was presented at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics.