We're still basking in the hot sun, bronzing our bodies in tanning beds, and playing outdoors without slathering on the sunscreen. What will it take, I wonder, for our society to catch on, to take real steps toward preventing skin cancer?

It seems education isn't enough. Most of us know by now all it takes is one bad sunburn to increase our risk of skin cancer, yet we continue to collect burn after burn after burn. Perhaps like all habit-forming behaviors -- think smoking -- it takes something tragic in our lives to inspire change. When someone we know gets lung cancer after a lifetime of smoking or someone we know develops melanoma after years of sunbathing, maybe we get the hint. Maybe

Now, I know you don't personally know this young woman -- she calls herself Miss Melanoma -- but I suggest you read her story. And I recommend you take what happened to her -- she lost part of her foot to melanoma and is currently battling a spread of the disease -- and allow it to really sink in, allow it to motivate you to take cover from the sun, before something like this happens to you. Because it can.

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.

United States Representative Charles Norwood, who left Washington last week to enter into the care of hospice, died yesterday at his home after battling cancer and lung disease. He was 65.

Norwood, whose passing prompted the House to observe a moment of silence Tuesday in his honor, suffered since 1998 from chronic lung disease and later metastatic cancer that spread from his lungs to his liver. Last week, he announced he would no longer accept treatment, that he would allow hospice to care for him for the remainder of his days.

A dentist from Augusta, Georgia, Norwood was the first Republican to represent northeastern Georgia since the Civil War. A conservative passionately opposed to government bureaucracy and adamantly supportive of patients' rights, he hoped to one day become Georgia's first Republican Governor.

Norwood's medical decline began when his lung condition -- idiopathic pulmonary fibrosis -- began restricting his ability to breathe and necessitated a lung transplant in 2004.

Known for zipping around the Capitol with a motorized cart and oxygen tank, Norwood developed cancer on his non-transplanted lung reportedly due to the immune suppression drugs he took after his transplant. And although his cancer was surgically removed and his health did improve, doctors learned this past November his cancer had spread.

The vacancy left by Norwood's death will not be filled immediately due to governmental process. In Georgia, within 10 days of the seat being vacated, the governor must request a special election to the secretary of state. And the election must be held no fewer than 30 days later.

Norwood is survived by his wife, Gloria; two sons, Charles and Carlton; and four grandchildren.

Some women opt to remove their ovaries to prevent breast cancer recurrence. I considered it -- and then decided I would not take such an extreme measure when I wasn't all that sure I was done having children.

Now, ovary removal may not be necessary -- because a new chemical equivalent of surgery allows women to temporarily shut down their ovaries while preserving their fertility.

The shutdown of the ovaries is called chemopause, and women who choose to go this route receive monthly injections -- considered a super-hormone treatment -- of a drug that blocks the male hormone testosterone and is often used to treat prostate cancer.

Chemopause has big advantages. It doesn't require surgery. And it's not permanent. Women who want to have children can stop the treatment in order to conceive. And women who have trouble with side effects can discontinue use of the surgery-sparing drugs.

The ovary-suppressing drugs -- triptorelin, goserelin, leuprolide, and buserelin -- can be used in place of or on top of standard chemotherapy and hormone therapy and are showing promise in their ability to decrease incidences of breast cancer recurrence.

Medical professionals agree there is value in ovarian suppression. Studies show women whose periods do not return after chemotherapy -- which often causes early menopause -- have lower relapse rates than women whose periods resume. So shutting down the ovaries and stopping menstruation may not be such a bad idea -- and not such an extreme measure either.