Shingrix now available for over 18s
The non-live recombinant Varicella Zoster Virus vaccine Shingrix is now available on the private market for the prevention of shingles (herpes zoster) and post-herpetic neuralgia (PHN) in people aged 18 years who are at increased risk of shingles.
In June 2021 Shingrix was made available to people over the age of 50. According to GSK, the new approval of Shingrix was supported by a range of clinical trials in highly immunocompromised populations aged 18 years and older, including patients with solid tumours, haematological malignancies, HIV infection, autologous hematopoietic stem cell transplant recipients, and renal transplant patients on chronic immunosuppressive treatment.
The TGA has previously warned of the risks of live zoster vaccines in immunocompromised people after receiving reports of two deaths. Shingrix is given intramuscularly in two doses, six months apart.
Microbiota biomarker for pancreatic cancer
A faecal microbiota signature panel may help identify pancreatic ductal adenocarcinoma (PDAC) at an earlier stage.
A Spanish case-control study analysed 100 saliva and 212 stool samples from 57 adults newly diagnosed with either early stage and advanced disease, 50 healthy controls, and 29 people with chronic pancreatitis, a known risk factor for pancreatic cancer.
The study found faecal microbiota-based screening predicted PDAC with high accuracy and specificity and irrespective of cancer stage. The predictive ability of the microbial profile was also validated in a separate German cohort.
Faecal microbiota-based screening was found to be superior to salivary microbiota-based screening.
“In summary, the described faecal microbiome signatures enabled robust metagenomic classifiers for PDAC detection at high disease specificity, complementary to existing markers, and with potential towards cost-effective PDAC screening and monitoring,” the researchers concluded.
Read more in Gut
New clues to cancer resistance and relapse
Cancer researchers have identified a pathway by which drug-induced cellular adaptation leads to the development of resistance to treatments and relapse.
The research, led by a team from the Peter MacCallum Cancer Centre, uncovered mRNA transport and translation pathways as regulators of metabolic response to BRAFi in BRAFv600 melanoma cells.
“We propose inactivation of this pathway may provide therapeutic opportunities to interfere with adaptive metabolic reprogramming following oncogene targeted therapy, and delay resistance in melanoma patients,” they said.
Specifically, “Our data identify a key role for UHMK1 in this process, and importantly, the inactivation of UHMK1 delays resistance and improves survival following combined BRAF and MEK inhibition in vivo.”
Read more in Nature Communications