
Chemotherapy is poison that happens to kill cancer cells faster than it kills healthy cells; that it wreaks havoc on the bodies of patients is unsurprising. But chemo may also affect their unborn children. According to a new study in PNAS, the offspring of mice treated with chemotherapy have higher rates of mutation, even though the offspring themselves were never exposed to the drugs.
The results suggest that these mutations arise from genome destabilization caused by exposure to chemo, rather than just mutated sperm from the treated father. Male mice in the study were exposed to one of three common anticancer drugs—cyclophosphamide, mitomycin C, or procarbazine—and then allowed to mate with untreated females. After sequencing a small piece of DNA from the offspring, the researchers found that mice with treated fathers had mutation rates up to twice that of mice with untreated fathers. Notably, these mutations were present in DNA inherited from both the treated father and untreated mother.
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Hugo Chavez, president of Venezuela, has speculated that the fact that he and four other South American leaders have all recently come down with various cancers could be a sign that the US has developed methods to give people cancer. Uh, is that even possible? Slate‘s Explainer does a thorough, interesting walk-through of all the reasons why the answer is, “Not reliably.”
You could…contaminate the victim’s diet with high levels of aflatoxin, which is associated with liver cancer. Or you could infect him with any of a number of cancer-causing biological agents. Helicobacter pylori contributes to the development of gastric cancer, and human papillomaviruses can cause cervical, anal, and a few other forms of cancer. But these tactics probably wouldn’t produce cancer in the short term and aren’t guaranteed to have any effect at all. In countries with high aflatoxin exposure, like China and parts of Africa, fewer than 1 in 1,000 people develop liver cancer.
If we knew how to give people cancer reliably, we might be better at preventing it. As it stands, cancer prevention, except for a few stand outs like quitting smoking, is can be just as hit-or-miss as cancer contraction.
Read more at Slate.
Image courtesy of nicogenin / flickr

Under a laser light, tumor cells light up.
What’s the News: Getting out every last bit of a tumor can be difficult–when you’ve got a patient open on the operating table, cancer cells don’t look any different from normal ones. But tag tumor cells with a glowing protein and turn the lights off, as scientists did in a recent study, and those things stand out like glo-sticks on the Fourth of July.
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The blood oxygen-monitoring chip, which is about 2 cm long and encased in plastic, is still in the
early stages of testing.
What’s the News: Scientists in Germany are developing a chip that keeps track of blood oxygen levels for implanting near tumors, reports Kate Baggot at Technology Review. When blood oxygen levels drop, signalling a burst of tumor growth, doctors would be alerted immediately, jump-starting the treatment process.
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Specially trained sniffer dogs can smell something on the breath of lung cancer patients.
Dogs will sniff anything and everything, and can even tell identical twins apart by scent. And tumors, you may be surprised to learn, have their own very faint smells. To figure out how to diagnose internal cancers that are frequently overlooked until too late from just a breath sample, scientists have been working with dogs to see if these smells can be reliably differentiated from, say, the smell of breakfast, that last cigarette, or emphysema.
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Modified immune cells decimated chronic lymphocytic leukemia, scientists found.
What’s the News: Striking results in a very small study have got the web a-buzz about a new cancer treatment: With three leukemia patients at the ends of their ropes, scientists modified some of their immune cells with a gene that enabled them to hunt down cancer cells. Remarkably, the treatment wiped out more than two pounds of tumor tissue in each patient, and the three have now been in remission for a year.
But what weight does such a small study carry, what about the side effects, and what do these results mean for people with other cancers?
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What’s the News: Due to a vicious disease, the population of the endangered Tasmanian devil has decreased by at least 70 percent since 1996. The cancer, devil facial tumor disease, spreads when an infected devil bites another, typically during feeding or mating. Because Tasmanian devils are so genetically similar, their bodies don’t recognize the intruding cancer cells as foreign.
But now, researchers have sequenced the genome of two devils and created a genetic test that could help breeders select genetically diverse mates. The test will help conservationists breed future generations of Tasmanian devils that are prepared for the cancer, as well as other types of diseases.
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What’s the News: Three new drugs have been shown to improve survival and slow disease progress in patients with metastatic melanoma. This advanced form of the disease is the deadliest type of skin cancer, with patients surviving for an average of only 6 to 9 months. Phase III clinical trials of the treatments—a new chemotherapy drug, an immune-system treatment combined with traditional chemotherapy, and a vaccine combined with another immune treatment—were recently published in the New England Journal of Medicine.
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Metastatic melanoma cells
What’s the News: Souped-up cells from a patient’s own immune system could one day be used to treat advanced melanoma, according to a preliminary study published in Science Translational Medicine investigating the safety of the technique. The researchers manipulated a patient’s immune system cells to better recognize cancer cells in the lab and then re-introduced those cells into the body—an approach called “adoptive T-cell therapy.”
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What’s the News: Scientists have developed a new carbon nanotube device (pictured above) that’s capable of detecting single cancer cells. Once implemented in hospitals, this microfluidic device could let doctors more efficiently detect the spread of cancer, especially in developing countries that don’t have the money for more sophisticated diagnostic equipment. Any improvement in detecting cancer’s spread is important, says MIT associate professor of aeronautics and astronautics Brian Wardle, because “of all deaths from cancer, 90 percent are … from tumors that spread from the original site.”
What’s the Context:
- The researchers’ original microfluidic device from four years ago featured tens of thousands of microscopic silicon posts coated with tumor-sticking antibodies: when cancer cells bumped into the posts, they’d stick. But if cancer cells didn’t bump into a silicon post, they’d go undetected. The group says their new version is eight times better.
- When cancer cells migrate, there are “usually only several [cancer] cells per 1-milliliter sample of blood” containing billions of other cells, making cancer exceedingly difficult to detect.
- This new dime-sized microfluidic machine works in the same way, but the solid silicon tubes were switched out for highly porous carbon nanotubes. This allows the blood to actually flow through the tubes instead of just around them, increasing the likelihood of catching a cancer cell.
- In other cancer detection news, some are using dogs to sniff out cancer and others use genetic tests to figure out cancer risks.
- Combating cancer ranges from new cancer-fighting drugs to just ignoring cancer (sometimes).
Not So Fast: The process of commercializing a technology like this takes quite a while; the previous version from four years ago is being tested in hospitals now and is may be commercially available “within the next few years.”
Next Up: The scientists are currently tweaking the device to try to catch HIV.
Reference: Grace D. Chen et al. “Nanoporous Elements in Microfluidics for Multiscale Manipulation of Bioparticles.” Small. DOI: 10.1002/smll.201002076
Image: Brian Wardle/MIT
What’s the News: Scientists have identified three gene mutations that lead to acute myeloid leukemia, a cancer that afflicts white blood cells, which may lead to better cancer drugs in the future. As Wellcome Trust Sanger Institute hematologist George Vassiliou told the BBC, his team’s study “found critical steps that take place when the cancer develops. Identifying the biological steps … means we can look for new drugs to reverse the process.”
How the Heck:
- The researchers discovered the major mutation by switching on the Npm1 gene in mice: They observed that about one third of the mice went on to develop leukemia.
- They knew some other genes were involved because not all the mice contracted cancer. So next, they randomly mutated mouse genes, and then analyzed the mutations in the ones that developed cancer, identifying two other mutations in the process. The second mutation affected cell growth and division and the third affected the cell’s environment.
What’s the Context:
Not So Fast: Researchers caution that it could take decades before new cancer-fighting drugs based on this study come on the market. This present study only used mice as subjects.
Reference: George S Vassiliou et al. “Mutant nucleophosmin and cooperating pathways drive leukemia initiation and progression in mice.” Nature Genetics. doi:10.1038/ng.796
Image: Wikimedia Commons / Bruce Wetzel

They’re about three and a half feet tall and their origins are mysterious, but an isolated group of Ecuadorians with a genetic mutation causing dwarfism are making news for another reason: They hardly ever get cancer or diabetes. Medical researchers say the villagers’ genetic protection from these diseases could lead to preventative treatments for the general population–and could therefore increase human longevity.
The villagers’ condition is called Laron syndrome, which is caused by an insensitivity to growth hormone.
Laron syndrome results from a mutation in the gene that codes for growth hormone receptor (GHR), a protein that binds with the human growth hormone and ultimately results in the production of the insulin-like growth factor 1 (IGF1), causing cells to grow and divide. When a person has two of these mutated and non-working genes, they can develop the disease. [LiveScience]
Jaime Guevara-Aguirre, the leader of the study about the Ecuadorians appearing in Science Translational Medicine, has been looking into their condition and extraordinary resistance to age-related diseases for more than two decades, since his serendipitous discovery of the people while riding horseback in Ecuador.
“I discovered the population in 1987,” Dr. Guevara-Aguirre said in an interview from Ecuador. “In 1994, I noticed these patients were not having cancer, compared with their relatives. People told me they are too few people to make any assumption. People said, ‘You have to wait 10 years,’ so I waited. No one believed me until I got to Valter Longo in 2005.” [The New York Times]
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