Hello Nature readers,
This week, scientists discover how to stop air pollution from causing lung cancer in mice, demonstrate the benefits of using younger, stem-like T cells for immunotherapy and explore how cell death is a growth strategy for cancer.

How air pollution causes cancer

Air pollution seems to cause lung cancer through an indirect route — inflammation — and halting this process could prevent cancer. Breathing in dirty air creates an inflammatory response in the lungs, which induces the growth of lung cells that have pre-existing mutations in the EGFR or KRAS genes. Treating mice carrying these mutations with an anti-inflammatory drug called an IL-1β-targeting antibody reduced the development of tumours after exposure to air pollution. It's not practical to give this expensive prophylactic to entire populations, but the finding might revitalize this area of research. The study also found that just three years of exposure to air pollution was enough to cause lung cancer in a group of around 33,000 non-smokers.

Younger CAR T cells attack solid tumours

Using younger, stem-like immune cells as opposed to older ones may be an effective strategy for fighting solid tumours. Younger T cells have stem-like qualities, which means they can transform and specialize into other types of cells. They are also more robust and persistent in their fight against cancer. Once genetically modified to express the cancer-recognizing chimeric antigen receptor (CAR) on their cell surface, and combined with an immune checkpoint inhibitor, younger T cells eradicated solid tumours in mice. Existing CAR T-cell therapies have low numbers of stem-like T cells, and are effective against blood cancers but not solid cancers.

Promising treatment for childhood cancer

Immunotherapy called chimeric antigen receptor (CAR) T-cell therapy has been successfully trialled in 27 children with a rare form of nerve cell cancer called neuroblastoma. In the trial, nine children had a complete response to treatment, and eight had a partial response. Eleven children were alive three years after the start of the study. "Those kids were all destined to die without that therapy," says immunologist Carl June. "No one's ever had patients responding like this before."

Cell death as a cancer growth strategy

Dying breast cancer cells encourage nearby cells to grow and spread by expelling a mixture of DNA and proteins called chromatin from the nucleus of the cell. This nuclear expulsion activates receptor for advanced glycation endproducts (RAGE) ligands in neighbouring tumour cells and stimulates the proliferation of those cells, mouse models suggest. Researchers found evidence of this process in people with breast, bladder and lung cancer, and it was associated with decreased survival.

Kidney cancer's unusual trait

Kidney cancer defies the norm by not having tumour mutational burden as a predictive biomarker for immunotherapy success. This unexpected finding has driven "intense scrutiny of the genomic architecture of clear-cell renal cell carcinoma, and a detailed search for drivers of immunogenicity", three cancer biologists write. In a review, they explore the factors that make kidney tumours susceptible to immunotherapy, including insertion or deletion of base pairs (INDELs) and the reactivation of endogenous retroviruses, which are evolutionary vestiges of retroviruses that have been incorporated into the genome.