Inherited cancer mutations may drive tumor growth, study shows

Share on facebook
Share on twitter
Share on linkedin
Share on email
Share on print

Most cancer genome studies have focused on mutations in the tumor itself and how such gene variants allow a tumor to grow unchecked. A study led by researchers at Washington University School of Medicine in St. Louis takes a deep dive into inherited cancer mutations measured in a healthy blood sample and reports how those mutations might take a toll on the body’s cells starting at birth, perhaps predisposing a person to develop cancers at various stages of life.

To access this subscriber-only content please log in or subscribe.

If your institution has a site license, log in with IP-login or register for a sponsored account.*
*Not all site licenses are enrolled in sponsored accounts.

Login Subscribe
Table of Contents

YOU MAY BE INTERESTED IN

Throughout my career as a physician and scientist, I’ve seen ideas once considered impossible become breakthroughs that save lives. They happened because talented scientists had the resources, institutions, and sustained support to pursue ambitious ideas. Most importantly, they knew patients could not afford to wait. 
Intismeran autogene (intismeran; V940 or mRNA-4157), a novel investigational mRNA-based individualized neoantigen therapy, plus Keytruda (pembrolizumab) improved recurrence-free survival and distant metastasis-free survival as an adjuvant treatment for patients with completely resected stage 2B-4 melanoma, according to results of the phase III INTerpath-001 trial. 
Rasonque (daraxonrasib) consistently provided an overall survival benefit compared with chemotherapy across all evaluated RAS genotype subgroups among patients with previously treated metastatic pancreatic adenocarcinoma, including those with no identified tumor RAS mutation, according to exploratory subgroup analyses from the phase III RASolute 302 trial.
Camupepimut (ELI-002 7P) demonstrated consistent and favorable treatment-effect trends in patients with and without detectable baseline ctDNA and in patients without prior radiation across multiple pre-specified analyses, according to the results of a randomized phase II study of patients with resected pancreatic ductal adenocarcinoma called AMPLIFY-7P. 

Never miss an issue!

Get alerts for our award-winning coverage in your inbox.

Login