Nano electron guns can help zap cancers and drive new classes of lasers.

A cholesterol-lowering drug may help reduce the risk of heart failure in people with lymphoma who receive chemotherapy drugs called anthracyclines, results from a clinical trial suggest.

Anthracyclines, such as doxorubicin, are used to treat many types of cancer. But these drugs may affect the heart’s ability to pump blood, potentially leading to heart failure.

In the trial, atorvastatin (Lipitor) was found to reduce the risk of some cardiac changes linked to heart failure among patients treated with anthracyclines.

The anti–PD-1 agent tislelizumab was noninferior, but not superior, to the tyrosine kinase inhibitor sorafenib for unresectable hepatocellular cancer.

First-line treatment for patients with unresectable hepatocellular cancer (HCC) is either combination immunotherapy with bevacizumab and atezolizumab or tremelimumab and durvalumab. Although immunotherapy-based combination therapy has replaced tyrosine kinase inhibitors (TKIs) as initial therapy, randomized trials have not indicated superiority of single agent anti–PD-1 or PD-L1 therapy over TKIs.

Investigators have now conducted an industry-sponsored, global, open-label, randomized, phase 3 trial (RATIONALE-301) to compare first-line treatment with the anti–PD-1 agent tislelizumab versus the TKI sorafenib in 674 patients with Child-Pugh class A unresectable HCC. Of the patients, 85% were men, 58% had distant metastases, 76% had received prior locoregional therapy, 60% had hepatitis B, 13% had hepatitis C, and 3% had hepatitis B and C.

The primary endpoint of noninferiority for overall survival (OS) was achieved with tislelizumab compared with sorafenib (median 15.9 vs. 14.1 months; hazard ratio, 0.85; 95% confidence interval, 0.71–1.02), reaching the noninferiority margin upper limit of a hazard ratio 1.08. Superiority for OS with tislelizumab was not met. Antitumor response was numerically higher with tislelizumab than with sorafenib (14.3% vs. 5.4%), and median duration of response was longer with tislelizumab than with sorafenib (36.1 vs. 11.0 months). Median progression-free survival was similar with tislelizumab and sorafenib (2.1 and 3.4 months, respectively). Grade 3–4 treatment-related adverse events were more common with sorafenib than with tislelizumab (53.4% vs. 22.2%).

An international research consortium led by Ludwig Maximilian University of Munich (LMU) has tested a rapid new analytical tool which needs just a blood sample from the fingertip.

About 240,000 children worldwide die of tuberculosis every year. The disease is among the top 10 causes of death in children under the age of 5. One of the main reasons for this mortality is that tuberculosis is often misdiagnosed or not diagnosed in time, particularly in regions with limited resources.

A new diagnostic tool, which an international research consortium led by LMU medical scientists Laura Olbrich and Norbert Heinrich from the Division of Infectious Diseases and Tropical Medicine at LMU University Hospital Munich has tested as part of a large-scale study in five countries, offers significant progress in this area. The authors report on their findings in The Lancet Infectious Diseases.

A team led by researchers at Baylor College of Medicine is coming closer to delivering on the promise of personalized breast cancer therapy with a strategy to predict the most likely response of a cancer to a specific less toxic treatment regimen.

In this study published in Clinical Cancer Research, a journal of the American Association for Cancer Research, the scientists developed and validated in clinical trials a multiparameter molecular classifier test to predict with a high degree of confidence which patients with HER2-positive (HER2+) breast cancer would be candidates for anti-HER2 therapy alone without the need for chemotherapy. The molecular classifier also accurately identifies patients whose tumors may need chemo or other targeted therapies.

“HER2+ breast cancer, which represents about one of every five breast cancers, expresses high levels of HER2 proteins and is physiologically dependent on the abundance of this protein to grow fast and metastasize or spread to other organs,” said co-corresponding author Dr. Rachel Schiff, professor of medicine and molecular and cellular biology and member of the Lester and Sue Smith Breast Center and the Dan L Duncan Comprehensive Cancer Center at Baylor. “Historically, HER2+ breast cancer was treated only by chemotherapy, but patient outcomes were poor. This changed in the late 1990s when the introduction of anti-HER2 therapy, drugs that block the growth effects of HER2, transformed the treatment of this disease.”