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Sanford Burnham Prebys


Gut microbiome directs the immune system to fight cancer

Researchers have discovered a causal link between the gut microbiome and anti-tumor immunity, identifying key bacterial strains that activate the immune system to slow melanoma growth. The study also reveals the role of unfolded protein response (UPR) in this process, providing potential markers for patient stratification.

SourceSanford Burnham Prebys·JournalNature Communications·DateApr 2, 2019

Helping infants survive brain cancer

Researchers at Sanford Burnham Prebys have created a mouse model of choroid plexus carcinoma (CPC), a challenging type of brain cancer that affects young children. The study identified three promising drug compounds with biological activity, including dinaciclib and flavopiridol.

SourceSanford Burnham Prebys·JournalCancer Research·DateMar 27, 2019

How prostate cancer becomes treatment resistant

Scientists from Sanford Burnham Prebys Medical Discovery Institute identified how prostate cancer becomes treatment-resistant NEPC following targeted treatment. They found that an FDA-approved drug holds potential as a NEPC treatment and uncovered new therapeutic avenues to prevent transformation.

SourceSanford Burnham Prebys·JournalCancer Cell·DateFeb 28, 2019

Solving the gut inflammation puzzle

Researchers have discovered a protein called RNF5 that drives intestinal inflammation in inflammatory bowel disease (IBD). High levels of S100A8, another protein regulated by RNF5, are linked to disease severity and may serve as a potential diagnostic marker.

SourceSanford Burnham Prebys·JournalCell Reports·DateSep 18, 2018

Malicious brain cell identified

Researchers at Sanford Burnham Prebys Medical Discovery Institute have identified a previously unknown astrocyte subpopulation that plays a key role in driving brain inflammation. The newly discovered 'ieAstrocytes' are activated early in neuroinflammatory diseases, such as multiple sclerosis and Alzheimer's disease.

SourceSanford Burnham Prebys·JournaleNeuro·DateSep 13, 2018

Shedding light on 100-year-old cancer mystery

Researchers at Sanford Burnham Prebys Medical Discovery Institute found that cancer cells redirect energy production when lactate dehydrogenase is inhibited, instead relying on glutamine to sustain growth and survival. This discovery identifies a potential new target for melanoma treatment by targeting the ATF4-signaling pathway.

SourceSanford Burnham Prebys·JournalThe EMBO Journal·DateSep 12, 2018

How colorectal cancer cells spread to the liver

Researchers at Sanford Burnham Prebys Medical Discovery Institute discovered that PKC zeta deficiency promotes liver metastasis through the inactivation of enzyme ADAR2, leading to increased secretion of miR-200s. Treatment with a compound inhibiting miR-200s reduced liver metastasis in mice with colorectal cancer.

SourceSanford Burnham Prebys·JournalCell Reports·DateApr 24, 2018

Study finds how fat tissue shunts energy to tumors

Researchers at Sanford Burnham Prebys Medical Discovery Institute reveal that the loss of p62 in fat cells fuels aggressive prostate cancer by inhibiting energy-consuming processes. This discovery opens new avenues for therapeutic targeting and highlights the importance of considering whole-body metabolism in cancer treatment.

SourceSanford Burnham Prebys·JournalCancer Cell·DateApr 9, 2018

Research suggests new pathways for hyperaldosteronism

A study by Sanford Burnham Prebys Medical Discovery Institute founds a previously unknown regulatory axis that controls aldosterone levels, offering new avenues for drug discovery of secondary hypertension. The findings suggest that the adrenal glands' structure and cholesterol biosynthesis play a crucial role in hyperaldosteronism.

SourceSanford Burnham Prebys·JournalJCI Insight·DateDec 7, 2017

Scientists find key to regenerating blood vessels

A new study by Sanford Burnham Prebys Medical Discovery Institute identifies a crucial signaling pathway for angiogenesis, the growth of new blood vessels from pre-existing ones. The findings may improve current strategies to increase blood flow in ischemic tissues associated with atherosclerosis and diabetes.

SourceSanford Burnham Prebys·JournalNature Communications·DateNov 23, 2017

New player in Alzheimer's disease pathogenesis identified

A study published in Nature Communications reveals that membralin plays a crucial role in regulating the cell's machinery for producing beta-amyloid, the protein responsible for neuronal death in Alzheimer's disease. The researchers found that membranes with lower levels of this protein are associated with increased neurodegeneration a...

SourceSanford Burnham Prebys·JournalNature Communications·DateNov 14, 2017

Biomarker may predict early Alzheimer's disease

Researchers at Sanford Burnham Prebys Medical Discovery Institute have identified a peptide that can predict early Alzheimer's disease by recognizing vasculature associated with brain inflammation. The discovery may provide a means of homing drugs to diseased areas of the brain, targeting treatments before amyloid plaques appear.

SourceSanford Burnham Prebys·JournalNature Communications·DateNov 10, 2017

How SORLA protects against Alzheimer's disease

Researchers at Sanford Burnham Prebys Medical Discovery Institute identified a new protective function for the brain protein SORLA, which limits amyloid beta's toxic signaling. The study suggests that increasing levels of SORLA in mice reduced cognitive impairments caused by amyloid beta.

SourceSanford Burnham Prebys·JournalJournal of Experimental Medicine·DateNov 7, 2017

New clues to treat Alagille Syndrome from zebrafish

A new study published in Nature Communications identifies the cells and genes necessary to make liver ducts in zebrafish, which could lead to the development of new treatments for Alagille syndrome. The research team discovered that Jagged signals come from an unexpected cell type, endoderm-derived cells within the liver itself, stimul...

SourceSanford Burnham Prebys·JournalNature Communications·DateOct 18, 2017

Alternative splicing, an important mechanism for cancer

Researchers analyze data from over 4,000 cancer patients and discover that changes in alternative splicing lead to a loss of functional protein domains, affecting gene function in a manner similar to genetic mutations. This study reveals the potential oncogenic power of these changes, enabling healthy cells to become cancerous.

SourceSanford Burnham Prebys·JournalCell Reports·DateSep 21, 2017