Martins, C. | Search bioRxiv

bioRxiv2018

High-sensitivity c-reactive protein and total and saturated fat intake in adolescent students: a longitudinal study

ObjectiveThe present study aimed to assess the relationship between hs-CRP concentrations and total and saturated fat intake in adolescents after a year of follow-up.\n\nMethodsA longitudinal study carried out in the years 2014 and 2015 evaluated 408 adolescents from the municipal and state public schools of Joao Pessoa, Paraiba, between 10 and 14 years of age, who participated in the Longitudinal Study on Sedentary Behavior, Physical Activity, Eating Habits and Adolescent Health (LONCAAFS). Data were obtained on sociodemographic data, anthropometric nutritional status, physical activity and hs-CRP concentration. The consumption of total and saturated fats was evaluated from the 24 hour recall.\n\nResultsThe associations between concentrations of hs-CRP and total and saturated fat intake were performed by linear regression considering panel data, individual fixed effect, balanced bank, stratified by sex and BMI. The mean values of the hs-CRP variable were significantly different between the analyzed years (p = 0.024). The percentage of total and saturated fat consumption is within the recommended level in both years, with no significant difference (p> 0.05). No statistically significant associations were found between hs-CRP and total fat consumption ({beta} = -0.19p = 0.582) and saturated fat ({beta} = 0.20, p = 0.282).\n\nConclusionThe study did not present significant evidence on the relationship between the concentrations of hs-CRP and the consumption of total and saturated fats, as one year of follow-up may not have promoted evident changes in the levels of hs-CRP in adolescents.

epidemiology↗

bioRxiv2018

The ERBB network facilitates KRAS-driven lung tumorigenesis

KRAS is the most frequently mutated driver oncogene in human adenocarcinoma of the lung. There are presently no clinically proven strategies for treatment of KRAS-driven lung cancer. Activating mutations in KRAS are thought to confer independence from upstream signaling, however recent data suggest that this independence may not be absolute. Here we show that initiation and progression of KRAS-driven lung tumors requires input from ERBB family RTKs: Multiple ERBB RTKs are expressed and active from the earliest stages of KRAS driven lung tumor development, and treatment with a multi-ERBB inhibitor suppresses formation of KRasG12D-driven lung tumors. We present evidence that ERBB activity amplifies signaling through the core RAS pathway, supporting proliferation of KRAS mutant tumor cells in culture and progression to invasive disease in vivo. Importantly, brief pharmacological inhibition of the ERBB network significantly enhances the therapeutic benefit of MEK inhibition in an autochthonous tumor setting. Our data suggest that lung cancer patients with KRAS-driven disease may benefit from inclusion of multi-ERBB inhibitors in rationally designed treatment strategies.\n\nOne Sentence SummaryG12 Mutant KRAS requires tonic ERBB network activity for initiation and maintenance of lung cancer

cancer biology↗