Bacterial Assassin

 

Will this Chinese-engineered ‘bacterial assassin’ transform cancer treatment?


Cancer researchers in China who have been experimenting with bacteria may have cracked the deadliest puzzle hindering treatment of the disease: how to eliminate cancers while evading human immune responses.

A landmark study published in the peer-reviewed scientific journal Cell on March 4 revealed how lab-engineered “bacterial assassins” selectively destroyed tumours in mice – slashing colorectal, melanoma and bladder cancer volumes by 80 per cent with a 100 per cent survival rate, and even vaccinating the survivors against future tumour assaults.

A synthetic biological “kill switch” can bridge a major gap in immunotherapy: unleashing the lethal precision of bacteria against malignancies while taming their dangers, the study suggested.

According to researchers, most human tumours already carry a molecular “key” for this kind of therapy, but the findings by Liu’s team illuminated a fast-track path to turning bacterial armies into universal cancer cures.

“Unlike traditional medicines, bacteria are alive. Bacteria can survive in tumours, suggesting they can evade the immune system,” lead author Liu Chenli, a professor from the Shenzhen Institutes of Advanced Technology under the Chinese Academy of Sciences, said in an article published by China Science Daily on March 4.

“At the same time, the bacteria can inhibit tumour growth, indicating that they can activate anti-tumour immune responses.”

To prove their claim, the researchers engineered a strain of bacteria called Salmonella typhimurium, dubbed “Designer Bacterium 1” (DB1).

In studies of mice, DB1 survived and proliferated in tumour tissues due to the unique micro-environment of the malignancies. DB1 was rapidly cleared from healthy tissues, and achieved a “tumour-targeting” and “tumour-clearing” effect, the researchers said.

Three days after an injection, 99.9 per cent of DB1 cells were located within the tumour site of the mouse. The number of bacteria within the tumour remained high in the following days, according to the study.

In models of bladder cancer, melanoma and colon cancer, the researchers said their DB1 treatments in the lab animals reduced tumour volumes by more than 80 per cent, and produced survival rates of 100 per cent after 20 days.

Beyond tumour regression, the treatments also encouraged a robust immunity response. Additionally, the cured mice showed strong immunity against secondary challenges from the same type of tumour, with a 90 per cent reduction in pulmonary metastatic nodules.

In their subsequent studies with the bacteria, Liu’s team found that DB1’s therapeutic efficacy depended on enhancing the cytotoxicity of tumour-infiltrating CD8+ T cells.

They also found that the signalling molecule interleukin-10 (IL-10) played a crucial role in mediating these effects, with efficacy depending on the high levels of the IL-10 receptor on the CD8+ T cells and neutrophils in tumours only.

The treatment stemmed from the unique lag in the responses of the IL-10 receptor. In human solid tumour samples, for example, 82 per cent (or 22 out of 27) showed high levels of IL-10.

By detecting the IL-10 receptor expression level in tumour biopsies, the researchers believe it may be possible to screen a patient population to find the most suitable candidates for bacterial immunotherapy.

“Our findings illuminate a crucial, yet previously unresolved mechanism in bacterial cancer therapy. This mechanism not only provides valuable insights but also serves as a guiding principle for the design of engineered bacteria, enhancing safety and efficacy,” Liu said.

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