University of Turin

education📍 Turin, Italy
University of Turin
2
Alpha-gal Syndrome Publications
1
Alpha-gal Syndrome Researchers

Associated Institutions

CTO Hospital
related
Azienda Ospedaliera Citta' della Salute e della Scienza di Torino
related
Azienda Ospedaliero Universitaria San Giovanni Battista
related
Istituto Nazionale di Fisica Nucleare, Sezione di Torino
related
Multi-Modal Molecular Imaging Italian Node
child

Alpha-gal Syndrome Researchers

Publications

[Not Available].

Aiuto B, Cirrincione S, Giuffrida MG, Cavallarin L, Portesi C, et al.
Molecular nutrition & food research •

Alpha-gal syndrome (AGS) is a mammalian meat allergy associated with tick bites and specific IgE to the oligosaccharide galactose-α-1,3-galactose (α-gal). Recent studies have shown that 10-20% of AGS patients also react to the dairy proteins. Considering the already described role of the meat lipid fraction in AGS manifestations, the aim of this work has been to investigate whether the milk fat globule proteins (MFGPs) could be involved in AGS. The MFGPs are extracted and their recognition by the IgE of AGS patients is proved through immunoblotting experiments. The identification of the immunoreactive proteins by LC-HRMS analysis allows to demonstrate for the first time that butyrophillin, lactadherin, and xanthine oxidase (XO) are α-gal glycosylated. The role of xanthine oxidase seems to be prevalent since it is highly recognized by both the anti-α-gal antibody and AGS patient sera. The results obtained in this study provide novel insights in the characterization of α-Gal carrying glycoproteins in bovine milk, supporting the possibility that milk, especially in its whole form, may give reactions in AGS patients. Although additional factors are probably associated with the clinical manifestations, the avoidance of milk and milk products should be considered in individuals with AGS showing symptoms related to milk consumption.

Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance.

Ali M, Kaltenbrun E, Anderson GR, Stephens SJ, Arena S, et al.
Nature communications •

KRAS mutations drive resistance to targeted therapies, including EGFR inhibitors in colorectal cancer (CRC). Through genetic screens, we unexpectedly find that mutant HRAS, which is rarely found in CRC, is a stronger driver of resistance than mutant KRAS. This difference is ascribed to common codon bias in HRAS, which leads to much higher protein expression, and implies that the inherent poor expression of KRAS due to rare codons must be surmounted during drug resistance. In agreement, we demonstrate that primary resistance to cetuximab is dependent upon both KRAS mutational status and protein expression level, and acquired resistance is often associated with KRAS mutations that function even when protein expression is low. Finally, cancer cells upregulate translation to facilitate KRAS-driven acquired resistance, resulting in hypersensitivity to translational inhibitors. These findings demonstrate that codon bias plays a critical role in KRAS-driven resistance and provide a rationale for targeting translation to overcome resistance.