Stroke Drug Kills Cancer Cells and Leaves Normal Cells Intact

A never-approved drug developed to prevent the death of nerve cells after a stroke can efficiently kill cancer cells while keeping normal cells healthy and intact, an international team led by a Tel Aviv University researcher is reporting in the journal Breast Cancer Research.

Prof. Malka Cohen-Armon of TAU's Sackler School of Medicine found that the stroke drug -- a member of a family of phenanthridine derivatives developed by an American drug company -- worked to kill cancer in mice which had been implanted with human breast cancer cells.

"Not only did the drug kill the cancer, but when we investigated normal cells, we discovered that they'd reacted as though they hadn't come in contact with the drug," says Prof. Cohen-Armon. "This is the result we were hoping for. If human trials go well, we could have an entirely new class of drugs in our hands for the fight against cancer."

Stopping the deadly cycle of cancer cell growth

The immediate results of the study were only one of the promising findings in her research, she notes. The team also discovered a molecular mechanism in the cell cycle that can be arrested only in human cancer cells. This cell cycle arrest, they report, causes the cancer cells to die without affecting normal human cells.

"We've found a molecular triggering mechanism in cancer cells that, when set off, causes the cancer cells to die -- they just stop multiplying and die within 48 to 72 hours. Normal, healthy body cells are only temporarily arrested by the same mechanism -- they overcome this cell cycle arrest within 12 hours and continue to proliferate in the presence of the drug as normal un-treated cells," says Prof. Cohen-Armon. "All the human cancer cells we tested seemed to succumb to this compound."

She adds that, even if this particular drug doesn't reach the market to fight against cancer, an entirely new class of drugs might be built around mechanism the team has revealed.

Different strokes

The stroke drug was initially developed to prevent nerve cell death during inflammation and tissue damage in the brain after stroke. However, in pre-clinical studies, American researchers found that these compounds didn't work as well as they'd hoped. Today they are used only for research purposes in laboratory settings.

"The compound we used," says Prof. Cohen-Armon, "presented no traces of toxicity in mice. With this compound, we were able to show how one of the many molecular mechanisms regulating the cell cycle can be targeted, and the proliferation of cancer cells halted." The team is currently working to identify all the regulatory mechanisms involved in this specific process and hope that, in better understanding the science, they might point the way to a new class of anti-cancer drugs.

Her research team was joined by Asher Kastiel, a Ph.D. student from Prof. Shai Izraeli's team working at the Chaim Sheba Medical Center, and the veterinarian Dr. David Castel. All the experiments conform with the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health in the United States.

Electroscalpel Hunts Down Cancer Like a Cougar at a High School Kegger

When surgeons dig around inside of you trying to cut out a tumor, they're actually going off of pre-op info to find the tumor. An electroscalpel, combined with a mass spectrometer, will let them map cancerous cells in realtime.

The thing about electroscalpels is that they put off gaeous ions, which, besides being something you shouldn't breath in, it so happens are perfect for being analyzed via mass spectrometry—a method of identifying molecules based on their mass and change. A spectrometer pulls in the fumes from the electroscalpel, and analysis of the chemical sample happens almost instantly, allowing surgeons to, in near real time, "draw a map and say this part is healthy liver, that is connective tissue, this is adipose tissue, that is cancer" according Zoltán Takáts, a Justus-Liebig University professor who came up with the idea.

Like any other technology-driven medical advance when it comes to cancer, it's not cheap to implement: The electrosurgery setup alone is 8 grand, while the mass spectrometry setup is $120,000. We wonder how much the first medical tricorder is gonna cost.

Tanning Beds as Deadly as Mustard Gas, Arsenic

International cancer experts have moved tanning beds and other sources of ultraviolet radiation into the top cancer risk category, deeming them as deadly as arsenic and mustard gas.

For years, scientists have described tanning beds and ultraviolet radiation as "probable carcinogens."

A new analysis of about 20 studies concludes the risk of skin cancer jumps by 75 percent when people start using tanning beds before age 30. Experts also found that all types of ultraviolet radiation caused worrying mutations in mice, proof the radiation is carcinogenic. Previously, only one type of ultraviolet radiation was thought to be lethal.

The new classification means tanning beds and other sources of ultraviolet radiation are definite causes of cancer, alongside tobacco, the hepatitis B virus and chimney sweeping, among others.

The research was published online in the medical journal Lancet Oncology on Wednesday, by experts at the International Agency for Research on Cancer in Lyon, the cancer arm of the World Health Organization.

"People need to be reminded of the risks of sunbeds," said Vincent Cogliano, one of the cancer researchers. "We hope the prevailing culture will change so teens don't think they need to use sunbeds to get a tan."

Most lights used in tanning beds give off mainly ultraviolet radiation, which cause skin and eye cancer, according to the International Agency for Cancer Research.

The classification of tanning beds as carcinogenic was disputed by Kathy Banks, chief executive of The Sunbed Association, a European trade association of tanning bed makers and operators.

"The fact that is continuously ignored is that there is no proven link between the responsible use of sunbeds and skin cancer," Banks said in a statement. She said most users of tanning beds use them less than 20 times a year.

But as use of tanning beds has increased among people under 30, doctors have seen a parallel rise in the numbers of young people with skin cancer. In Britain, melanoma, the deadliest kind of skin cancer, is now the leading cancer diagnosed in women in their 20s. Normally, skin cancer rates are highest in people over 75.

Previous studies found younger people who regularly use tanning beds are eight times more likely to get melanoma than people who have never used them. In the past, WHO warned people younger than 18 to stay away from tanning beds.

Cogliano cautioned that ultravoilet radiation is not healthy, whether it comes from a tanning bed or from the sun. The American Cancer Society advises people to try bronzing or self-tanning creams instead of tanning beds.

New Anti-cancer Drug: 200 Times More Active In Killing Tumor Cells

A team of 24 researchers from the U.S., Europe, Taiwan and Japan and led by University of Illinois scientists has engineered a new anti-cancer agent that is about 200 times more active in killing tumor cells than similar drugs used in recent clinical trials.

The study appeared on march 2009 in the Journal of the American Chemical Society.

The new agent belongs to a class of drugs called bisphosphonates. These compounds were originally developed to treat osteoporosis and other bone diseases, but were recently found to also have potent anti-cancer and immune boosting properties.

Drug developers have tried for years to design drugs to inhibit cell survival pathways in tumor cells, focusing on a protein called Ras since nearly a third of all human cancers involve a mutation in the Ras gene that causes cell signaling to go awry. These efforts have met with limited success.

Bisphosphonates act on other enzymes, called FPPS and GGPPS, which are upstream of Ras in the cell survival pathway. Inhibiting these enzymes appears to be a more effective strategy for killing cancer cells.

When used in combination with hormone therapy in a recent clinical trial, the bisphosphonate drug zoledronate significantly reduced the recurrence of breast cancer in premenopausal women with estrogen-receptor-positive breast cancer. Similar results were reported previously for hormone-refractory prostate cancer.

But zoledronate quickly binds to bone, reducing its efficacy in other tissues.

"We're trying to develop bisphosphonates that will be very active but won't bind to the bone, because if they bind to the bone they're not going to go to breast, lung or other tissues," said University of Illinois chemistry professor Eric Oldfield, who led the new study.

Oldfield's team also wanted to design a compound that would inhibit multiple enzymes in the tumor cell survival pathway, rather than just one, an approach analogous to the use of multi-kinase inhibitors in cancer therapy.

Andrew Wang, of Academia Sinica, Taipei, and Illinois chemist Rong Cao began by producing crystallographic structures of the target enzymes and drug candidates, allowing the researchers to identify those features that would enhance the drugs' ability to bind to the enzymes. Using this and other chemical data, Illinois chemistry department research scientist Yonghui Zhang engineered new bisphosphonate compounds that bound tightly to multiple enzyme targets, but not to bone.

One of the new compounds, called BPH-715, proved to be especially potent in cell culture and effectively inhibited tumor cell growth and invasiveness.

Tadahiko Kubo, of Hiroshima University, then found that BPH-715 also killed tumor cells in mice. And Socrates Papapoulos, of Leiden University, the Netherlands, showed that the compound had a very low chemical affinity for bone.

In humans, compounds like BPH-715 and zoledronate have an added benefit in fighting cancer: They spur the proliferation of immune cells called gamma delta T-cells, which aid in killing tumor cells.

"The new drugs are about 200 times more effective than the drugs used in recent clinical trials at killing tumor cells and in activating gamma delta T-cells to kill tumor cells," Oldfield said. "They also prevent tumor progression in mice much better than do existing bisphosphonate molecules."