Improving cancer treatment by exploiting mtDNA mutations
For the first time, mitochondrial DNA mutations could be used with immunotherapy to increase the chances of successful treatments.
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For the first time, mitochondrial DNA mutations could be used with immunotherapy to increase the chances of successful treatments.
A new learning-based framework enables patients and caregivers to predict the timing of any of the five clinical groups of AD development.
The Ku70 protein prevents cancer cells from becoming more aggressive and metastasising. It could also be used as an immune biomarker.
Low dose ionising radiation reduced lesion size and reversed motor deficits in traumatic brain injury and ischemic stroke mice.
Using CRISPRa to activate genes in readily accessible cells provides an effective and accurate diagnosis of genetic diseases.
The discovery that HIV capsids are importin-like transporters could be exploited for improved AIDS therapies.
Researchers observed significant upregulation of Siglec-15 in the tumour microenvironment in bone tumour samples from breast cancer patients.
Researchers discover that blocking PD-L2 in senescent cells increases the efficacy of chemotherapy in mouse models.
PLK4 inhibition could be a novel therapeutic for an acute myeloid leukaemia subtype carrying the TP53 mutation.
A patient-specific organ-on-a-chip model of cholangiocarcinoma, with its tumour microenvironment, helps to predict therapy response.
Inhibiting mTOR signalling and neutralising mtROS suppressed MCC-PD-1-mediated tumour proliferation in mice.
AcrlC8 and AcrlC9 prevent the CRISPR-Cas3 machine from binding to its DNA target site, providing a safer way to engineer the genome.
Inhibition of FAM3C expression in cancer-associated adipocytes during early tumour development holds promise as a novel treatment approach.
Researchers explored the effects of loops and 3D genome organisation on gene silencing, and found that ‘cohesinopathies’ may be linked it.
The ML algorithm explores how genetic mutations collectively influence a tumour’s reaction to drugs impeding DNA replication.