Toxic pond scum goes airborne + Cancer driven by DNA outside chromosomes

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A dangerous toxin from pond scum can go airborne, study finds
https://gizmodo.com/a-dangerous-toxin-fr...1846619624

EXCERPT: Algae blooms and the toxins they produce have become an increasingly common problem. These blooms are showing up more often and more intensely than they did decades ago, often in lakes or freshwater sources, and when they do, they can cause mass poisonings and die-offs in the local ecosystem. People and their pets exposed to these toxins aren’t safe, either—dogs dying after swimming in or ingesting algae-contaminated freshwater has sadly become an annual event.

One particularly scary toxin is called anatoxin-a (ATX), also known by its edgier name, “Very Fast Death Factor.” ATX is produced by species of blue-green algae—a group of bacteria that survive through photosynthesis, like plants (the blue-green refers to the color they usually display in massive numbers). ATX is known to have killed birds, dogs, and other animals since its discovery in the 1960s; it’s also suspected of having poisoned people. In humans, it’s been linked to blurred vision, dizziness, headache, and gastrointestinal symptoms like vomiting and diarrhea.

Though ATX has never been observed to go airborne, the researchers behind this new study theorized that it could happen under the right conditions. Their study, published in Lake and Reservoir Management, seems to show that it can... (MORE - details)


Cancer May Be Driven by DNA Outside of Chromosomes
https://www.the-scientist.com/features/c...omes-68590

EXCERPTS: . . . The tumors had dramatically reduced the number of copies of the targeted epidermal growth factor receptor (EGFR) gene, presumably giving them an advantage to escape the drugs, and they had evolved these genetic differences at a rate that seemed to make no sense—within just one to two weeks.

Normally, we think of cancers evolving over many cell divisions, as the cells carrying genetic changes that provide a fitness advantage—such as an ability to resist a particular treatment—will be more likely to survive and divide. Here, we were noticing a change in the copy number of the gene within just a few generations. There was no way that we could explain how the tumors were altering their DNA so quickly.

Even stranger, we could take any cell from the tumor, and whether it had high or undetectable protein levels of EGFR, it would give rise to a new tumor when cultured in the lab or implanted into a mouse. Each of these new tumors would then display the full spectrum of cells found in the original tumor, varied in their EGFR copy number. This makes no sense according to what we know about classical genetics. We would have expected that tumors arising from a cell with low levels of EGFR would give rise to a tumor with low EGFR levels, whereas a tumor arising from a cell with high levels of EGFR would give rise to a tumor with high EGFR levels.

In 2012, in a project spearheaded by a graduate student in my lab named David Nathanson, who is now an associate professor at the University of California, Los Angeles, we set out to understand why. [...] We published our results in Science in 2014, but they were not immediately accepted by the community. Although we had only studied one tumor type, glioblastoma, we began to wonder whether this might be the tip of the iceberg.

Without realizing it, this study led us, and now others, to a series of discoveries that have changed the way that researchers view cancer in general, revealing frightening ways that tumors can evolve. We have learned that ecDNA [extrachromosomal DNA] is central to the behavior of some of the most aggressive forms of cancer, enabling remarkably elevated levels of oncogene transcription, creating new gene regulatory interactions, and providing a powerful mechanism for rapid change that can drive very high oncogene copy numbers or allow cancer cells to resist treatment.

Along the path of discovery, we found that we were not the first to have seen these extrachromosomal particles. But with new tools in hand, and new questions in mind, we saw them in a very different way. And when we took the time to peer deeply into the nucleus of cancer cells, we saw ecDNAs in abundance. We eagerly pursued studies to understand their importance in cancer progression and drug resistance, and even founded a biotech company, Boundless Bio, to identify and develop new ways to treat patients whose cancers are driven by ecDNA... (MORE - details)
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