Can Your Cat Cause Demonic Possession?

Cats are routinely associated with malevolent entities in horror stories. They are the favorite pet of witches and villains, a frequent denizen of haunted houses, and the object of several superstitions. Now doctors have linked felines to demonic possession!

Wait, what?

In a new case study published yesterday in the journal Medicine, scientists in China reported that acute infection with the common parasite Toxoplasma gondii triggered the onset of an unusual autoimmune disease called anti-N-methyl-D-aspartate (NMDA) receptor encephalitis. Anti-NMDA receptor encephalitis occurs when the body attacks one of its own brain proteins, leading to bizarre personality changes that mimic the stereotypical behaviors that come to mind when we think about demonic possession.

In this case report, a nine-year-old girl arrived at the hospital with seizures, headache, and vomiting. Then she developed unexplained personality and behavior changes. She tested positive for both anti-NMDA receptor antibodies and recent infection with the Toxoplasma parasite.

Anti-NMDA receptor encephalitis was the subject of the bestselling book, Brain on Fire: My Month of Madness, by Susannah Cahalan. In this memoir, which reads like an episode of Mystery Diagnosis, Cahalan describes her terrifying transformation from a vibrant young journalist to an unrecognizable and violent monster. As her condition progressed, she grew paranoid of others, thought family members were imposters, and lashed out at people. She lost control of her bodily movements, suffered seizures, and spoke in tongues. If you didn’t know better, you’d claim she needed an exorcist. Luckily, a neurologist properly diagnosed her disease and gave her immune suppressant drugs that drove it into remission.

Did Regan have a cat?

It is not clear why some people (mostly women) start making antibodies that attack the NMDA receptors in their brain. Some cases are linked to the development of tumors, especially teratomas in the ovaries. Certain viruses that infect the brain, including herpes simplex virus, have also been linked to anti-NMDA receptor encephalitis. Now it seems Toxoplasma, which also infects the brain, may be a trigger of this haunting disease, too.

Toxoplasma is a devious parasite with a complex life cycle. It is capable of infecting any warm-blooded animal, but can only complete its sexual cycle in the intestines of cats. After infecting a cat, the cat spews billions of infectious parasite oocysts into the litter box (or the environment) for up to two weeks. These oocysts are very sturdy and can last up to two years in the environment, giving them plenty of time to be inhaled or ingested by another animal (including humans). In addition to picking up oocysts from the litter box, garden, or sandbox, we can also acquire the infection by eating undercooked meat or unwashed fruits and vegetables.

Once a person becomes infected, the parasite disseminates throughout bodily tissues, including the brain and heart, and transitions into a latent stage called the tissue cyst. While current treatments can stop the parasite from replicating, no drug exists that can get rid of the tissue cysts. In other words, infection with Toxoplasma is permanent. The thought of having a brain filled with these parasites is disquieting, but most scientists believe the cysts are inert unless the individual becomes immune compromised, in which case the parasites can cause massive tissue damage from unchecked growth.

A growing number of scientists argue, however, that in certain individuals the Toxoplasma tissue cysts are not benign and may cause neurological disorders. One of the better-established correlations is the link between Toxoplasma infection and schizophrenia. Interestingly, up to 10% of schizophrenia patients test positive for anti-NMDA receptor antibodies.

The mechanism explaining how Toxoplasma infection may cause anti-NMDA receptor encephalitis remains to be elucidated. Toxoplasma infection is remarkably common (up to one-third of the global population is believed to carry this parasite), but anti-NMDA receptor encephalitis is rare. For now, the authors of the study advise that clinicians assess the possibility of Toxoplasma infection when evaluating a patient with anti-NMDA receptor encephalitis.

To prevent Toxoplasma infection and minimize your chances of becoming possessed by this parasite, be sure to thoroughly cook meat and wash produce and veggies. Wear gloves and a mask when gardening and keep sandboxes covered when not in use. You cannot catch Toxoplasma by petting your cat, but it is important to clean the litter box promptly and wash your hands with soap and water. Pregnant women, in particular, should heed these warnings as infection during pregnancy can lead to miscarriage or serious congenital birth defects. See the infographic below for more.

UPDATE (7/26/18): A new study was published today by Li et al. that used a mouse model of infection to show that anti-NMDA receptor autoantibodies are induced by the presence of latent Toxoplasma tissue cysts.

Brain on Fire has also been made into a movie that can be seen now on Netflix.

Contributed by: Bill Sullivan

Follow Bill on Twitter.

Could Parasites Be Causing Prostate Cancer?

Long ago in the mid-1600s, a fellow named Antonie van Leeuwenhoek started making lenses…as a hobby (remember, Facebook and Netflix were not invented yet). He was so adept at grinding glass that his lenses were able to magnify objects about 270 times their normal size. Leeuwenhoek soon discovered a whole new universe right here on earth, a universe of creatures so tiny that only his microscope could reveal them. He called them "animalcules."

With his powerful microscope, Leeuwenhoek became the first person to see amoebae, bacteria, and blood cells. For these revolutionary discoveries, he is considered “the father of microbiology.”

But after looking at endless water samples, the ever-curious Leeuwenhoek wondered what bodily fluids looked like under his microscope. While Leeuwenhoek examined blood, sweat, and tears (and a lot of dental plaque), a medical student in 1677 named Johan Ham told Leeuwenhoek that he spotted animalcules swimming in the semen he collected from a gonorrhea patient.

Believing these animalcules might be a result of disease, Leeuwenhoek procured a clean semen sample from his own stock - obtained fresh after proper lovemaking with his wife, he insisted. Leeuwenhoek confirmed Ham's finding and went on to discover the same tiny eel-like critters teeming in the semen from many other species. This is how we came to make the “seminal” discovery of sperm cells.

Other people in Leeuwenhoek’s day mistook these microscopic beasties squiggling around in the semen to be "merely" parasites, referring to them as “seminal Worms.” In fact, we didn’t realize that these “semen parasites” played a key role in fertilization until the 1870s when Oscar Hertwig spotted the fusing of nuclei from sperm and egg after contact…in sea urchins of all places.

We didn’t figure out where babies come from until fairly recently – 1870. White studying sea urchins, Oscar Hertwig noticed that the nucleus in the sperm fuses with the nucleus in the egg (the nucleus is the cellular organelle housing DNA).

While the mystery of sperm has been solved, we have indeed discovered a variety of pathogens that can inhabit our nether regions. Trichomoniasis, scrotal filariasis, and Chlamydia are just some of the unpleasant conditions caused by these most intimate of uninvited guests. An unsettling new study led by graduate student Darrelle Colinot at the Indiana University School of Medicine may have found yet another.

In experiments performed in mice, researchers found that the common single-celled parasite called Toxoplasma gondii disseminates to the prostate within two weeks after infection. And there it remains in the form of latent tissue cysts for at least sixty days, but probably for the rest of the host’s life. The presence of these parasitic cysts led to chronic inflammation in the prostate, which is a precursor to benign prostatic hyperplasia (BPH), the reason why older men have to get up multiple times to pee at night. Chronic inflammation in the prostate is also connected to prostate cancer, which afflicts more than 200,000 men in the US each year.

Parasites in prostates. The control panel shows cells from an uninfected mouse prostate (the nuclei are stained blue). The other panel shows the presence of a Toxoplasma tissue cyst (green) in the prostate 14 days post-infection (14 D.P.I.).

If Toxoplasma is also found to trigger chronic inflammation in human prostate, the finding takes on added significance given the prevalence of the parasite in the human population. According to the CDC, up to 22% of Americans are infected with the parasite, which is transmitted through oocysts that are excreted into the environment by infected cats or through tissue cysts present in game and livestock. 

Women are commonly advised to avoid gardening, changing the litterbox, and consuming undercooked meat while pregnant so the parasite doesn’t transmit to the fetus. Men may need to heed these warnings as well to avoid a prostate full of parasites, but a lot of critical work still needs to be done before we can ascertain whether this discovery has relevance to prostate issues in humans. Regardless, our study introduces Toxoplasma-infected mice as a powerful new model for the study of prostatic inflammation.

Prostate cancer is believed to arise from a constellation of events that can involve a person’s genes and environmental exposures. Infectious agents and carcinogens have previously been proposed as agents that can injure the prostate and lead to the development of chronic inflammation. Numerous types of bacteria and viruses have been shown to infect the prostate and cause an inflammatory response; this new study in mice suggests that the parasite Toxoplasma might be added to this list.

Contributed by:  Bill Sullivan

Note:  Bill Sullivan is a co-author on the study highlighted in this article.

Follow Bill on Twitter.

Reference:

Colinot, D., Garbuz, T., Bosland, M., Wang, L., Rice, S., Sullivan, W., Arrizabalaga, G., & Jerde, T. (2017). The common parasite induces prostatic inflammation and microglandular hyperplasia in a mouse model The Prostate DOI: 10.1002/pros.23362

Everybody’s Free To Wear Sunscreen…And Prevent Skin Cancer

Our last article discussed using sunscreen to help protect skin against damaging UV radiation. When used properly, sunscreen prevents sunburn and sun-induced skin aging, and protects from skin cancer. Studies have shown that sunscreen use reduces the incidence rate of squamous cell carcinoma (SCC) and melanoma, but currently no evidence supports a protective role against basal cell carcinoma (BCC).

While some people, including supermodel Gisele Bundchen, believe sunscreen is dangerous (she declared “I cannot put that poison on my body”) experts such as The Skin Cancer Foundation and the American Academy of Dermatology—and even Cosmopolitan magazine—disagree with her and other skeptics.

A large, randomized controlled trial examined the effect of daily sunscreen use on the development of skin cancers. Researchers followed 1621 Australians from 1992-2006. From 1992-1996, participants were randomly placed in a group and instructed to either use the study-provided broad spectrum SPF 16 sunscreen daily on face, arms, neck and hands, or to continue personal discretionary use of sunscreen. At the 2004 follow up, researchers noted that the daily sunscreen use group had a 35% rate reduction in the incidence of SCC (considering all SCCs that appeared throughout the entire study). However, the incidence of BCC was not statistically different between the two groups. More recent studies corroborate these results.

US Senator and 2008 Republican Presidential Candidate John McCain has had multiple melanomas removed. Other political figures have battled skin cancer, including former Presidents Jimmy Carter (metastatic melanoma) and Bill Clinton (BCC), and former First Lady Laura Bush (SCC).

In 2006, researchers followed up again, this time looking for melanoma. The overall incidence rate of melanoma was 50% less in the sunscreen intervention group than the discretionary use group (out of approximately 800 people in each group, 11 people in sunscreen group and 22 in the control group developed melanoma). It should be noted that these results had borderline statistical significance, with a P value of 0.051 (P = 0.05 is the accepted cutoff for significance). This essentially translates to a 5.1% probability of these findings being due to chance, rather than to the actual sunscreen intervention. Also, there was a 73% lower rate of invasive melanoma in the sunscreen group. Although there was no significant difference in number of melanomas diagnosed at the prescribed intervention sites, it is possible that sunscreen use reduced the risk, as participants in the sunscreen intervention group reported more frequent use of sunscreen over the whole body after the intervention terminated.

Although these results are not the most compelling, they nonetheless point to a protective role of sunscreen. Many factors may contribute to a less than straightforward outcome. First, the sunscreen intervention was in adults and lasted 4.5 years. Melanoma and BCC are thought to result from both long term sun exposure and intense, intermittent episodes (sunburns), whereas SCC is mainly caused by cumulative UV exposure (both natural and indoor tanning bed). Furthermore, blistering childhood sunburns are a risk factor for melanoma. One study that examined sunscreen use in children found a significant protective benefit. Regular use (applied any time sun exposure would exceed 30 min) of a broad-spectrum SPF 30 sunscreen over a 3-year period resulted in significantly fewer newly developed moles, the number of which is a risk factor for melanoma.

Second, participants in the non-sunscreen intervention group continued their discretionary use of sunscreen. No trial in humans could ever prohibit sunscreen use or provide a placebo for ethical reasons. Therefore, perfectly delineating the protective effect of sunscreen is difficult.

Many questionnaire-based studies that rely on participants’ memory of sunscreen use suffer from recall bias. Some of these studies showed no benefit of sunscreen for melanoma prevention but memory limits the reliability of these results. The bottom line is that sunscreen protects from UV radiation, a known human carcinogen.

The skin consists of two layers, the dermis and epidermis. The epidermis contains a variety of cell types, including squamous cells, basal cells and melanocytes. These are the sources for squamous cell carcinoma, basal cell carcinoma and melanoma, respectively.

UV radiation is implicated in up to 90% of nonmelanoma skin cancers, squamous cell carcinoma (SCC) and basal cell carcinoma (BCC). Mutations consistent with UV radiation were also found in the genomes of melanoma tumors; UV radiation is thought to be responsible for the majority of melanoma. Whereas SCC and BCC are more frequent, melanoma is more often fatal. While UV radiation is the single most important risk factor for skin cancer, it’s worth noting that it is not responsible for all skin cancers. Aside from environmental carcinogens, cancer can arise due to a person’s genetics (familial effect) or random mutations.

Acral melanoma is a type of skin cancer not caused by UV radiation and is genetically distinct from UV-induced cutaneous malignant melanoma. Bob Marley’s acral melanoma metastasized and ultimately claimed his life.

UVA radiation primarily damages the components of skin cells by generating reactive oxygen species, or ROS. These highly active molecules can cause single-strand breaks in the DNA or crosslink DNA to protein, resulting in mutations or improper functioning. Both UVA and UVB can cause a more significant type of DNA damage called pyrimidine dimers, where two adjacent pyrimidine nucleotides (the “C” and “T” of DNA; the “A” and “G” are purines) fuse together. Because the higher energy UVB is absorbed directly by DNA, UVB can cause other modifications that compromise the integrity of DNA, leading to instability of the genetic code.

Indeed, the cell has repair mechanisms to fix pyrimidine dimers and other errors, but sometimes the very genes encoding the repair mechanisms are mutated. UV-induced DNA damage can result in highly characteristic mutations in critical genes, for example in the tumor suppressor gene p53. As the “guardian of the genome”, the p53 protein is involved in directing the repair of mutations and guiding the cell through its controlled death pathway, called apoptosis. Mutations in p53 are thought to be among the first steps in development of non-melanoma skin cancer. Formation of malignant melanoma is more complicated and not fully understood.

Yes, p53 has its own superhero persona. That’s how cool (and significant) it is. Image by Susanne Harris.

Cells that carry mutations in p53 proliferate uncontrollably, a hallmark of cancer. In some cases, the immune system will recognize malignant cells as a threat and effectively eliminate them. However, UV radiation is also known to suppress the immune system by at least two mechanisms. One is by diminishing the production of antigen-presenting cells, which engulf foreign-looking cells and display an alert to activate the immune system). The other is by inducing the production of an immune suppressive cytokine, interleukin-10. Additionally, some skin cancer cells display proteins on their surface that prevent the immune cells from killing them. Thus, in addition to mutations in key genes, immune suppression and immune evasion contribute to the development of skin cancer.

Even the mutant Wolverine wears sunscreen! In this Instagram post, Hugh Jackman urged his fans to use sunscreen. He became a fervent sunscreen proponent after having a BCC removed from his nose.

Contributed by: Julia van Rensburg, Ph.D.
Follow Julia on Twitter.

van der Pols JC, Williams GM, Pandeya N, Logan V, & Green AC (2006). Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 15 (12), 2546-8 PMID: 17132769

Lee TK, Rivers JK, & Gallagher RP (2005). Site-specific protective effect of broad-spectrum sunscreen on nevus development among white schoolchildren in a randomized trial. Journal of the American Academy of Dermatology, 52 (5), 786-92 PMID: 15858467

Koh HK, Geller AC, Miller DR, Grossbart TA, & Lew RA (1996). Prevention and early detection strategies for melanoma and skin cancer. Current status. Archives of dermatology, 132 (4), 436-43 PMID: 8629848

Leiter U, & Garbe C (2008). Epidemiology of melanoma and nonmelanoma skin cancer--the role of sunlight. Advances in experimental medicine and biology, 624, 89-103 PMID: 18348450

Brenner M, & Hearing VJ (2008). The protective role of melanin against UV damage in human skin. Photochemistry and photobiology, 84 (3), 539-49 PMID: 18435612

Angelina Jolie’s Preemptive Strike Against Cancer

Angelina Jolie is back in the news, but not to promote a new film. Rather, she is promoting a personal decision to remove parts of her body before they turn cancerous. Two years ago, she underwent a double mastectomy to avoid the potential of developing breast cancer. This week, her sequel to this surgery was to have her ovaries and fallopian tubes removed. She wrote about this experience on March 24 in the New York Times.

On the surface, this may seem like an overly aggressive tactic to skirt cancer. However, Jolie’s family history is replete with tragic cancer deaths and she herself is a carrier of a mutant BRCA1 gene – more on that momentarily. Considered together, these attributes put Jolie in a high-risk category for cancer, so she elected to remove the time bomb from her system. Several doctors have applauded her decision given the circumstances. Jolie’s willingness to share her stories has created such an increase in awareness of genetic testing for disease that people call it the “Angelina Effect”.

Cancer…don’t mess with Angelina.

As discussed recently on THE ‘SCOPE, cancer is like a cellular rebellion and there is evidence that the cause of that rebellion is largely bad luck. In some cases, all it takes is one bad gene to incite the riot and in Jolie’s case it is BRCA1, which stands for BReast CAncer 1. BRCA1 is a key “biomarker” for cancer, meaning that the sequence of this gene can be an indicator for the likelihood that the cell housing it could go rogue and cause cancer one day. According to one study, women possessing a mutation in BRCA1 have a cumulative lifetime risk of 50%–85% of developing breast cancer and up to 60% of developing ovarian cancer. 

Looking at the diagram above, you don’t need to be a scientist to realize that BRCA1 is a cellular multitasker - best known for its tumor suppressive ability. A mutation in this important gene is likely to screw up a lot of things in the cell, potentially giving the green light for cancer to develop.

BRCA1 is a protein linked to many diverse cellular functions, some of which involve cell growth and the repair of damaged DNA. A mutation in the gene encoding BRCA1 can compromise the activities of the corresponding protein, wreaking havoc in the cell and potentially causing it to start replicating uncontrollably. So BRCA1 is a hero of sorts, a police officer that keeps cells in line. But if the officer is wounded, the cell has a ripe opportunity to rebel and take over the body in the form of cancer.

Angelina’s character Lara Croft can’t wait to get into tombs, but Angelina is doing all she can to delay entry into her own.

Removal of otherwise healthy organs that might go cancerous is not a trivial decision. First of all, biomarkers are informative but not a guarantee that disease is inevitable. Second, no surgery is without risk. Third, in Jolie’s case, her latest surgery will prompt early menopause and eliminate her ability to have more children. Fourth, while prophylactic surgery greatly reduces the risk of cancer, a small chance remains it could still develop. Finally, there are other less invasive treatment and monitoring options for individuals carrying a BRCA1 mutation or other risk factor associated with cancer. Consultation with a physician and oncologist is essential in order to weigh these risks against the results of genetic testing.

A preemptive strike against cancer by removing the suspect organ is not always a good strategy – consider brain tumors, for example!

 

Contributed by:  Bill Sullivan

Follow Bill on Twitter.


James, C., Quinn, J., Mullan, P., Johnston, P., & Harkin, D. (2007). BRCA1, a Potential Predictive Biomarker in the Treatment of Breast Cancer The Oncologist, 12 (2), 142-150 DOI: 10.1634/theoncologist.12-2-142

King, M. (2003). Breast and Ovarian Cancer Risks Due to Inherited Mutations in BRCA1 and BRCA2 Science, 302 (5645), 643-646 DOI: 10.1126/science.1088759

2-7 Offsuit: Is Cancer Just "Bad Luck"?

There are many forms of cancer that ravage the body, but the key feature they share is uncontrolled cell growth. Virtually any cell type can suddenly go rogue and start reproducing itself again and again – this is what we call a tumor. Some of these rogue cells venture to other parts of the body where they don’t belong and establish a new colony there – this is called metastasis. As cancerous tumors grow and spread around, they can do a number of things that endanger the life of the patient, such as interfere with organ function and steal nutrients from other cells or tissues.



This cartoon illustrates a general model for the development of cancer. A "benign" tumor is not considered cancerous because they do not invade other parts of the body. In contrast, "malignant" tumors, like that ugly looking thing above, are cancerous because they invade nearby tissues. If cells from a malignant tumor get into the bloodstream, they can establish life-threatening satellite tumors elsewhere in the body, making them all the more challenging to eliminate.

Cancer is caused by a change, or mutation, in one of our cell’s DNA. Our DNA contains tens of thousands of genes that encode proteins that make our cells tick. Some of these proteins regulate cell division, but they are normally shut off after the job is done. A mutation that turns one (or more) of these regulatory proteins back on can turn that cell into a Xerox machine stuck on "copy". Since there are so many different types of genes that can mutate in a wide variety of cell types, a “one size fits all” cure is very difficult to conceive.

Scientists (and many pseudoscientists) have long been trying to identify things in our environment that cause mutations that lead to cancer. Others have argued that cancer is just “bad luck” and that our genes play a larger role. This is important to sort out:  should we invest more money to identify potential carcinogens in the environment or to find ways to repair “bad” genes?

Every now and then, someone gets lung cancer who never took a single puff on a cigarette. Why? To understand the answer, consider poker. You can study dozens of books on how to play to win, practice for 10,000 hours, pay hundreds of dollars to learn all the secrets from the professional players. But none of this will help you if the dealer gives you junk cards. To look at this another way, there are some people who start chain smoking at twelve and live to be 90 with no trace of cancer (perhaps breathing through a tube in their throat, but no cancer). That’s like a rookie at the poker table being dealt a straight flush. Long story short:  cancer is not always the patient’s fault, and a lack of cancer is not always indicative of a healthy lifestyle.

In Texas Hold’em poker, you begin with just two cards. Being dealt a 2 and 7, offsuit, is considered the worst possible hand you can get. In contrast, being dealt two aces is one of the best starting hands. The genes that combined to form your DNA are analogous to the cards you would be dealt at a poker table. Unlike the poker game, though, you can’t win by bluffing.

Researchers have found plenty of environmental agents that can mutate DNA. For example, exposure to UV radiation is one of the more notorious risk factors for skin cancer. But there are a few people who worship the sun and never get skin cancer. In addition, most children have not had extensive exposure to environmental carcinogens, yet, tragically, they can still get cancer. In 2014, it was estimated that 15,780 children and adolescents ages 0 to 19 years would be diagnosed with cancer and nearly 2,000 would not survive. Facts such as these support the notion that cancer is largely due to bad genes, not necessarily the environment.

Scientists at Johns Hopkins recently set out to tackle the question by constructing mathematical models of the disease. Their findings might take you by surprise:  in the majority of cases, the reason why a cell starts running all the red lights is due to a random mutation that occurs during cell division. In other words, lifestyle choices and even your genetic makeup play a lesser role in your chances in getting cancer. Let that sink in for a moment: RANDOM mutation - not mutation caused by UV light, engine exhaust, or some other carcinogen. Since the mutation appears to be a random mistake made by cell division enzymes, the authors dubbed this "bad luck".

DNA replication is a complex process in which the two strands are separated and used as a template to make a complementary second strand. But replication enzymes are not perfect (if they were, there'd be no evolution) and sometimes insert the wrong DNA base, causing a mutation.

 

This new study reminds us that every cell division contains an inherent risk that the daughter cell acquires a mutation that makes it divide like gangbusters. This doesn’t mean you should grab a carton of Marlboros to smoke as you suntan on the beach while devouring a couple extra-charred burgers for lunch.

Highlighted in this study was the finding that not all cell types give rise to cancer equally. Not surprisingly, tissues with a higher number of stem cell divisions are more prone to cancer, which explains why we don’t hear a lot about duodenum cancer. Importantly, the researchers identified several types of cancer that are influenced more by our lifestyle choices or inherited mutations: colon cancer, basal cell carcinoma, and lung cancer.

The findings essentially assert that since cells divide they are veritable time bombs. Somewhere down the line a mistake is going to happen regardless of environmental insults, and if that mistake occurs in the wrong gene, cancer can ensue. These are noncontroversial statements and not news to most people. However, the idea that "most" cancers are due to "bad luck" is a more controversial conclusion. A major limitation is that the model did not incorporate some of the most common cancers, such as breast and prostate cancer, because the frequency of stem cell divisions is unclear. Readers would be wise to check out this article by David Gorski at Science-Based Medicine, which provides detailed insight into the strengths and weaknesses of the experimental design. The World Health Organization was so opposed to the message this study sends that they issued a press release critical of the study.



Obi-Wan (Ben) Kenobi famously said, “In my experience, there’s no such thing as luck.” Some scientists who take issue with the Hopkins study would agree with Ben. 

 

At the end of the day, since we don’t yet know how all genes operate, much less which ones you might have in your DNA, it is wise to take common sense steps to minimize your exposure to known carcinogens and take advantage of tests designed to detect cancer at its earliest stage. Bad luck may be a major factor in cancer, but there are plenty of simple lifestyle changes you can make to try and beat the odds.

Contributed by: Bill Sullivan

Follow Bill on Twitter.





Tomasetti, C., & Vogelstein, B. (2015). Variation in cancer risk among tissues can be explained by the number of stem cell divisions Science, 347 (6217), 78-81 DOI: 10.1126/science.1260825

Ward E, DeSantis C, Robbins A, Kohler B, & Jemal A (2014). Childhood and adolescent cancer statistics, 2014. CA: a cancer journal for clinicians, 64 (2), 83-103 PMID: 24488779

The Friday Five

Highlighting some of the coolest science news we’ve seen lately.

1. The coffee plant (Coffea canephora) genome has finally been sequenced! Interestingly, the study revealed that the enzymes synthesizing caffeine evidently arose independently from others found in tea and cacao. The question that remains:  how many cups of coffee were required to get the data? Learn more, including why some plants make caffeine, in Carl Zimmer’s article. It took millions of years for plants to evolve the ability to manufacture caffeine, so it is no wonder we freak out when there’s no coffee:

 

2. Scientists were able to correct the genetic aberration in mice that causes muscular dystrophy using a new type of genome editing technique called CRISPR/Cas9. In the future, this strategy may be used to correct disease-causing mutations in the muscle tissue of humans. Learn more about CRISPR/Cas9 in the video below.

3. More big medical breakthroughs: one of the most promising medications for melanoma was fast-tracked by the FDA last week.

4. This doesn’t happen every day! Check out this live volcanic eruption and sonic boom of Mount Tarvurvur located in Papua New Guinea.

5. In a previous Friday Five, we highlighted a study on how to make the perfect pizza. So how about a little perfect dessert to go with that perfect pizza? Read on to discover the science behind the best chocolate chip cookie for you.

 

 

BONUS!

We recently wrote about species having names inspired by celebrities. Now we have a new one to add to the list. “A swamp-dwelling, plant-munching creature that lived 19 million years ago in Africa has been named after Rolling Stones lead singer Sir Mick Jagger, because of its big, sensitive lips and snout. The name of the animal, Jaggermeryx naida, translates to 'Jagger's water nymph.'”

Science quote of the week:

“The saddest aspect of life right now is that science gathers knowledge faster than society gathers wisdom.” –Isaac Asimov

 

Contributed by:  Bill Sullivan

Follow Bill on Twitter: @wjsullivan

Denoeud, F., Carretero-Paulet, L., Dereeper, A., Droc, G., Guyot, R., Pietrella, M., Zheng, C., Alberti, A., Anthony, F., Aprea, G., Aury, J., Bento, P., Bernard, M., Bocs, S., Campa, C., Cenci, A., Combes, M., Crouzillat, D., Da Silva, C., Daddiego, L., De Bellis, F., Dussert, S., Garsmeur, O., Gayraud, T., Guignon, V., Jahn, K., Jamilloux, V., Joet, T., Labadie, K., Lan, T., Leclercq, J., Lepelley, M., Leroy, T., Li, L., Librado, P., Lopez, L., Munoz, A., Noel, B., Pallavicini, A., Perrotta, G., Poncet, V., Pot, D., Priyono, ., Rigoreau, M., Rouard, M., Rozas, J., Tranchant-Dubreuil, C., VanBuren, R., Zhang, Q., Andrade, A., Argout, X., Bertrand, B., de Kochko, A., Graziosi, G., Henry, R., Jayarama, ., Ming, R., Nagai, C., Rounsley, S., Sankoff, D., Giuliano, G., Albert, V., Wincker, P., & Lashermes, P. (2014). The coffee genome provides insight into the convergent evolution of caffeine biosynthesis Science, 345 (6201), 1181-1184 DOI: 10.1126/science.1255274

Long, C., McAnally, J., Shelton, J., Mireault, A., Bassel-Duby, R., & Olson, E. (2014). Prevention of muscular dystrophy in mice by CRISPR/Cas9-mediated editing of germline DNA Science, 345 (6201), 1184-1188 DOI: 10.1126/science.1254445