Cancer

Scott Baio Regrets Erin Moran Drug Comments, Didn’t Know She Died from Cancer

If I Knew About the Cancer

Scott Baio feels terrible for ripping his co-star, Erin Moran, for her drug use and says he never would have done it if he’d known she was battling cancer.

Scott tells TMZ he was wrong to insinuate Erin — his “Happy Days” and “Joanie Loves Chachi” co-star — had died from drug-related problems. He went pretty hard on her during a radio interview Monday morning.

He…

New Therapy Shrinks Five Types of Pediatric Cancers in Mice

Cancerous pediatric brain tumors are some of the most aggressive cancers to affect children, and are frequently fatal. They’re difficult to treat due to their proximity to sensitive brain tissue in tiny brains, and children’s bodies can rarely tolerate the side effects of the levels of chemotherapy and radiation necessary to shrink tumors.

But recently, researchers at Stanford Medicine, the Lucile Packard Children’s Hospital, and several other institutions successfully tested a promising immunotherapy treatment that shrank multiple tumor types in mouse models. Immunotherapy treatments harness the body’s own immune system to fight the cancer, and usually come with few to no side effects compared to chemotherapy drugs and radiation.

The collaborative study, published in Science Translational Medicine, showed results on the five most common types of pediatric tumors: Group 3 medulloblastomas (MB), atypical teratoid rhabdoid tumors (ATRT), primitive neuroectodermal tumors (PNET), pediatric glioblastoma (PG), and diffuse intrinsic pontine glioma (DIPG).

The Stanford researchers designed their study after the recent discovery of a molecule known as CD47, a protein expressed on the surface of all cells. CD47 sends a “don’t eat me” signal to the immune system’s macrophages—white blood cells whose job it is to destroy abnormal cells. “Think of the macrophages as the Pac-Man of the immune system,” Samuel Cheshier, lead study author and assistant professor of neurosurgery at Stanford Medicine, tells mental_floss.

Cancer cells have adapted to express high amounts of CD47, essentially fooling the immune system into not destroying their cells, which allows tumors to flourish. Cheshier and his team theorized that if they could block the CD47 signals on cancer cells, the macrophages would identify the cells on the cancerous tumors and eat them—without any toxicity to healthy cells. To do so, they used an antibody known as anti-CD47, which, as its name implies, blocks CD47 on the cancer from binding to a receptor on the macrophage called SIRP-alpha.

“It is this binding that tells the macrophage, ‘Don’t eat the tumor,’” he says. The anti-CD47 fits perfectly into the binding pocket where CD47 and SIRP-alpha interact, “like a jigsaw puzzle,” helping the macrophage correctly identify the tumor as something to be removed. “Anti-CD47 is the big power pill in Pac-Man that makes him able to eat the ghosts,” says Cheshier.

Even better, not only does…

Genetic risk of getting second cancer tallied for pediatric survivors

childhood cancer
RISK ROUNDUP Some pediatric cancer survivors carry genetic mutations that increase the risk of a later, second cancer.

WASHINGTON — A second cancer later in life is common for childhood cancer survivors, and scientists now have a sense of the role genes play when this happens. A project that mined the genetic data of a group of survivors finds that 11.5 percent carry mutations that increase the risk of a subsequent cancer.

“We’ve always known that among survivors, a certain population will experience adverse outcomes directly related to therapy,” says epidemiologist and team member Leslie Robison of St. Jude Children’s Research Hospital in Memphis. The project sought “to find out what contribution genetics may play.” The team presented their work at the American Association of Cancer Research meeting April 3.

“This is a nice first step,” says David Malkin, a pediatric oncologist at the University of Toronto. “The results validate the thoughts of those of us who believe there is a genetic risk that increases the risk of second malignancies.”

Five-year survival rates for kids with cancer have grown to more than 80 percent. But “there are long-term consequences for having been diagnosed and treated for cancer as a child,” notes Robison. Some survivors develop a later, second cancer due to the radiation or chemotherapy that treated the first cancer (SN: 3/10/07, p. 157).

The researchers examined 3,007 survivors of pediatric cancer who routinely undergo medical evaluation at St. Jude. About a third had leukemia as children. By age 45, 29 percent of this group had developed new tumors, often in the skin, breast or thyroid.

The team cataloged…

Random mutations play large role in cancer, study finds

GROWING PAINS As cells divide and grow to replenish and repair organs, accidental mutations may crop up in cancer-associated genes. A new study suggests such random mistakes are the source of 66 percent of mutations in cancer cells (illustrated here) across the board.

Researchers have identified new enemies in the war on cancer: ones that are already inside cells and that no one can avoid.

Random mistakes made as stem cells divide are responsible for about two-thirds of the mutations in cancer cells, researchers from Johns Hopkins University report in the March 24 Science. Across all cancer types, environment and lifestyle factors, such as smoking and obesity, contribute 29 percent of cancer mutations, and 5 percent are inherited.

That finding challenges the common wisdom that cancer is the product of heredity and the environment. “There’s a third cause and this cause of mutations is a major cause,” says cancer geneticist Bert Vogelstein.

Such random mutations build up over time and help explain why cancer strikes older people more often. Knowing that the enemy will strike from within even when people protect themselves against external threats indicates that early cancer detection and treatment deserve greater attention than they have previously gotten, Vogelstein says.

Vogelstein and biomathematician Cristian Tomasetti proposed in 2015 that random mutations are the reason some organs are more prone to cancer than others. For instance, stem cells are constantly renewing the intestinal lining of the colon, which develops tumors more often than the brain, where cell division is uncommon. That report was controversial because it was interpreted as saying that most cancers are the result of “bad luck.” The analysis didn’t include breast and prostate cancers. Factoring in those common cancers might change the results, some scientists said. And because the researchers looked at only cancer within the United States, critics charged that the finding might not hold up when considering places around the world where different environmental factors, such as infections, affect cancer development.

In the new study, Vogelstein, Tomasetti and Hopkins colleague Lu Li examined data from 69 countries about 17 types of cancer, this time including breast and prostate. Again, the researchers found a strong link between cancer and tissues with lots of dividing stem cells. The team also used DNA data and epidemiological studies to calculate the proportions of mutations in cancer cells caused by heredity or environmental and lifestyle factors. Remaining mutations were attributed to random errors — including typos, insertions or deletions of genes, epigenetic changes (alterations of chemical tags on DNA or proteins that affect gene activity) and gene rearrangements. Such errors unavoidably happen when cells divide.

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Chance cancer

For many organs, more of the mutations that lead to cancer come from random mistakes in DNA…