Contents
06 February 2019
Vol 11, Issue 478
Vol 11, Issue 478
Perspective
- Clinical implications of tumor-intrinsic mechanisms regulating PD-L1
Genetic changes modulate antitumor immune responses through the PD-1/PD-L1 axis, which should be considered when designing combinatory drug regimens.
Research Articles
- Tissue-specific regulation of p53 by PKM2 is redox dependent and provides a therapeutic target for anthracycline-induced cardiotoxicity
The redox status of tetrameric PKM2 defines its differential regulation of p53 activity and apoptosis.
- Suppressing fatty acid uptake has therapeutic effects in preclinical models of prostate cancer
Prostate cancer depends on fatty acid uptake and remodeling of the prostate lipidome, and blocking fatty acid uptake impairs prostate tumorigenesis.
- Recurrent group A Streptococcus tonsillitis is an immunosusceptibility disease involving antibody deficiency and aberrant TFH cells
Recurrent tonsillitis is a multifactorial disease associated with an aberrant tonsillar germinal center response to group A Streptococcus.
- Modulation of the sigma-1 receptor–IRE1 pathway is beneficial in preclinical models of inflammation and sepsis
Sigma-1 receptor is a critical inhibitor of endoplasmic reticulum–driven inflammation and a potential therapeutic target in septic shock.
Editors' Choice
- Raff-ining our understanding of pneumococcal invasion
Differential raffinose metabolism influences Streptococcus pneumoniae tissue tropism and disease phenotype.
- Cilial agitation prevents sperm agglutination
Agitating cilia produce fluid turbulence to prevent sperm from clogging testicular tubules.
- Transforming lung to treat type 1 diabetes
A tissue engineering strategy repurposes lung tissue for islet transplantation.
Erratum
About The Cover
ONLINE COVER The Heart of the Matter. This image of a glowing heart illustrates that the heart is an oxidized organ. This contrasts with the low oxidation state of tumors and is key to a cardioprotective approach that overcomes the cardiotoxic effects of anthracycline cancer chemotherapy (Saleme et al.). A redox-sensitive enzyme, PKM2, that suppresses the activity of proapoptotic protein p53, protected cardiomyocytes from dying under oxidized conditions in vitro. Conversely, in a low oxidation environment, the reduced form of PKM2 activated p53, resulting in cancer cell death. Treating mice with lung tumors with a compound that stabilizes PKM2 boosted the anticancer effects of anthracycline chemotherapy while protecting heart cells. [CREDIT: WOODOO007/123RF.COM]