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Chronic lymphocytic leukemia is a type of cancer in which specific white blood cells - called B lymphocytes, or B cells - build up in the blood, bone marrow and lymph nodes. The lifespan of a normal B cell is limited by an internal self-destruct program, but in cancer cells, this mechanism breaks down. B cells that don't self-destruct live on to multiply and eventually accumulate in dangerous amounts.
Now a team of scientists headed by Prof. Idit Shachar of the Weizmann Institute's Immunology Department and Dr. Michal Haran of the Hematology Institute of the Kaplan Medical Center have discovered what makes these cells stay alive. The pair then launched a targeted attack on this survival mechanism and managed to raise cell mortality rates significantly.
Their findings, which appeared recently in Proceedings of the [US] National Academy of Sciences (PNAS), may lead to future treatments for this disease, as well as for other diseases in which B lymphocytes accumulate.
In previous research, Shachar had found that a specific receptor - a protein on the outer surface of healthy B cells - fulfills a crucial role in helping these cells survive. She wondered if the same protein might also be a factor in the abnormally high survival rates of cancerous B cells.
Members of Shachar's research team, including Inbal Binsky, Diana Starlets, Yael Gore and Frida Lantner, together with Kaplan Medical Center doctors Haran, Lev Shvidel, Prof. Alan Berrebi and Nurit Harpaz, scientists from Yale University and David Goldenberg of the Garden State Cancer Center in New Jersey, examined B cells taken from chronic lymphocytic leukemia patients. They discovered that, even in the earliest stages of the disease, these cells have an unusually high level of both the survival receptor and another protein that binds to the receptor. The scientists found that this protein, in binding to the receptor, initiates a series of events that leads to enhanced cell survival. For instance, in one of these events, a substance is produced that helps regulate the cells' lifespan. This substance causes another protein to be produced, which then keeps the self-destruct program from being activated.
The team treated the chronic lymphocytic leukemia cells with an antibody that attached to the survival receptor, blocking its activity and causing the cancer cell death rate to soar. The antibodies they used are produced by the New Jersey company Immunomedics, and are currently entering clinical trials for the treatment of several types of cancer. Following this research, the company is planning trials for chronic lymphocytic leukemia, as well.
Shachar noted: "The abnormally elevated levels of this receptor seem to be important factors in the development of this disease right from the beginning, and they are responsible for the longevity of these cancerous B cells. Blocking the receptor or other stages in the pathway they activate might be a winning tactic in the war against cancers involving B cells."
'Success' against TB
The Health Ministry's program for fighting tuberculosis, now marking its 10th anniversary, was cited on the World Health Organization's European Region Web site as a "success story." It was published before a meeting of health ministers of 53 member countries in the region, due to be held in Berlin on October 22.
Dr. Daniel Chemtob, the ministry's national TB program manager, described a decade of implementation of Israel's national TB program.
Israel had a low rate of TB in the 1970s and early 1980s, and therefore significantly reduced its TB infrastructure by integrating it into the general health system. But then mass immigration from TB-endemic countries in the middle 1980s and 1990s forced the country to face the problem again. The ministry bolstered its own facilities at the headquarter level and in the 15 district health offices.
Directly observed therapy (DOT) is regarded as the best way to treat TB, as it involves a "cocktail" of antibiotics that must be consumed for months. If patients are directly observed, they are unlikely to stop taking them when they feel better but the bacteria are not destroyed.
The district health office investigates contacts of each TB patient and treats latent cases. The district health office also supervises the work done by the nine dedicated TB centers around the country, allowing full collaboration of the four health funds, which subsidize the centers' costs. Health system workers who treat new immigrants and foreign workers with TB are taught cultural sensitivity, and patients who try to evade treatment are liable to legal sanctions. The program has raised compliance among TB patients from less than 27% 15 years ago to a cure rate of about 80% today.
COULD A SUNTAN PROTECT?
For years, the mantra of public health experts on tanning has been â€¦ don't. Cancer associations, have driven home the message that the exposure needed to get a tan increases your chances of getting skin cancer. But researchers at the Harvard-affiliated Dana Farber Cancer Institute in Boston recently conducted a series of experiments that put tanning in a different light. A suntan, they say, is the body's best effort to fend off the cancerous effects of ultraviolet (UV) light, the invisible portion of the spectrum that penetrates the skin and mutates DNA, the Harvard Health Letter reported recently.
So, should we toss our SPF 45 and become sun worshipers? No! The researchers are adamantly on the side of avoiding excessive sun or other UV exposure, and using sunscreen. But they're also looking for ways to harness the "tanning pathway" that might give fair-skinned people the protective benefits of a tan without the hazards of getting one.
A safe tan would be one produced by activating the skin's tanning process without running the risk of DNA damage. It's unclear if truly safe UV exposure can ever be achieved. The Harvard Health Letter suggests that for now, your best bet is to avoid excessive UV exposure - especially if you're blond or redheaded and don't tan well. And use sunscreen.