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The California Institute for Regenerative Medicine awarded Stanford researcher Crystal Mackall a grant to study immune cells genetically modified to attack two proteins on leukemia and lymphoma cells.

In mice, a fatal brainstem tumor was cleared by injecting it with engineered T cells that recognized the cancer and targeted it for destruction. The Stanford discovery is moving to human trials.

Analyzing individual cancer cells has enabled Stanford researchers to identify the small population of cells that spur relapse in some children with leukemia.

Priming the immune system with induced pluripotent stem cells prevented or slowed the development of cancer in mice, Stanford researchers found.

CD47 is an important inhibitor of cancer-killing immune cells called macrophages. Now Stanford researchers have identified another, similar way to activate macrophages to destroy cancer cells.

High-grade gliomas, a group of aggressive brain tumors, cease growing in mice if a signaling molecule called neuroligin-3 is absent or its activity is blocked with drugs, a Stanford team has shown.

Targeting backup biological pathways often used by cancers can lead to more efficient drug development and less-toxic therapies. Stanford researchers have developed a new way to identify these pathways.

An antibody to the cell receptor PD-1 may launch a two-pronged assault on cancer by initiating attacks by both T cells and macrophages, a Stanford study has found.

A common signaling pathway unites diverse fibrotic diseases in humans, Stanford researchers have found. An antibody called anti-CD47, which is being tested as an anti-cancer agent, reverses fibrosis in mice.

Antibodies against the CD47 “don’t eat me” signal were shown in mice to be a safe and effective way to target five kinds of pediatric brain tumors, according to Stanford researchers.