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Cancer cells can ward off immune cells by persistently activating the STING signalling pathway. (Juan Gaertner/Science Photo Library) | |||||
Cancer's STING operationTumour cells trick the immune system into complacency by persistently activating the stimulator of interferon genes (STING) pathway. This pathway normally alerts the body to foreign or damaged cells, but it becomes desensitized when overstimulated. Researchers tracked interactions between cells using a new computational method called ContactTracing. Chronic activation of the STING pathway led to the rewiring of downstream signalling, stifling the immune response and allowing cancer cells to spread. The finding might explain why drugs that stimulate this pathway have so far failed as cancer treatments. Reference: Nature paper (23 August) | |||||
How γδ T cells get their super powersResearchers have discovered what triggers immune cells called gamma delta (γδ) T cells to fight a broad range of cancers. Using a CRISPR screen to tweak thousands of genes, the team found that, when a cancer cell is under stress, the number of butyrophilins on its surface increases. Butyrophilins are part of a protein complex that γδ T cells recognize, triggering them to kill the cancer. If cancer cells can be manipulated to overexpress butyrophilins, this could improve the performance of γδ T cells. People with more γδ T cells tend to have better cancer outcomes. Reference: Nature paper (30 August) | |||||
Microdevices test nine drugs inside gliomasInserting tiny devices into brain tumours for a few hours during surgery might help oncologists to determine which chemotherapy will be most effective for each patient. In a proof-of-concept study, microdevices smaller than the tip of a pen were implanted into the brain tumours of six adults for up to 3 hours during surgery. The devices released nine chemotherapies into different parts of the tumours. After surgery, the response of cancer cells to each chemotherapy was analysed, revealing that some drugs were more effective than others at damaging and killing the tumours, and that each patient had a different response to each chemotherapy. Reference: Science Translational Medicine paper (6 September) | |||||
Possible immunotherapy for ovarian cancerA protein called interferon-ε could be the first effective immunotherapy for ovarian cancer. Experiments using tumour-cell lines and mice revealed that this cytokine is expressed in the fallopian tube, where some types of ovarian cancer originate, and that tumours occur when the protein is absent. Reference: Nature paper (16 August) | |||||
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T cells with six base edits melt solid tumoursSolid tumours in eight mice disappeared after treatment with chimeric antigen receptor (CAR) T cells that had been base edited six times. Base editing creates a single alteration in the genetic code. Three of these base edits allowed the T cells to survive transfer from a donor to a recipient; the other three helped the immune cells to fight solid tumours. Alyssa, a teenage girl with leukaemia, was successfully treated last year with CAR T cells that had been base-edited four times. "Six, I think, is the most that we've ever seen," says molecular biologist and co-author Ryan Murray. New Scientist | 4 min read (paywall)Reference: bioRxiv preprint (4 August - not yet peer reviewed) | |||||
In the news
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The US Food and Drug Administration has approved sotorasib and adagrasib, which target a single KRAS mutation: G12C. They belong to the class of KRAS inhibitors (left) that target specific mutations but not healthy KRAS proteins. This makes them potentially less toxic than other types of KRAS inhibitor that harm healthy cells. The next class is the pan-KRAS inhibitors (middle), which are in clinical trials. These hit normal KRAS and all KRAS mutants, but not the healthy versions of the proteins created by the NRAS or HRAS genes, which are involved in cell division. The third class (right) targets all KRAS, NRAS and HRAS mutations. These have the highest toxicity risk because they also block healthy protein signalling. (Nature Cancer | 8 min read) (R. B. Corcoran/Nat. Cancer) | |||||
Quote of the week"'You have cancer.' Ask anyone who has been told this: It's terrifying. That's one reason we need to rethink what we call cancer."Tumours that are unlikely to change the quality or length of a person's life should be called something other than the "dreaded C-word", argue oncologists Laura Esserman and Scott Eggener. (The New York Times | 6 min read) | |||||
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