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Sökning: WFRF:(Leone Isabella)

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1.
  • Guerini-Rocco, Elena, et al. (författare)
  • Genomic aberrations and late recurrence in postmenopausal women with hormone receptor-positive early breast cancer: Results from the SOLE Trial.
  • 2021
  • Ingår i: Clinical cancer research : an official journal of the American Association for Cancer Research. - 1078-0432. ; 27:2, s. 504-512
  • Tidskriftsartikel (refereegranskat)abstract
    • Women with hormone-receptor-positive early breast cancers have a persistent risk of relapse and biomarkers for late recurrence are needed. We sought to identify tumor genomic aberrations associated with increased late recurrence risk.In a secondary analysis of Study of Letrozole Extension (SOLE) trial, a case-cohort-like sampling selected 598 primary breast cancer for targeted next-generation sequencing (NGS) analysis of gene mutations and copy number gains (CNG). Correlations of genomic aberrations with clinicopathologic factors and breast and distant recurrence free-intervals (BCFI and DRFI) were analyzed using weighted Cox models.Analysis of mutations and CNG was successfully performed for 403 and 350 samples, including 148 and 134 patients with breast cancer recurrences (median follow-up time: 5.2 years), respectively. The most frequent alterations were PIK3CA mutations (42%) and CNGs of CCND1 (15%), ERBB2 (10%), FGFR1 (8%) and MYC (8%). PIK3CA mutations and MYC CNG were associated with lower (p=0.03) and higher (p=0.004) tumor grade respectively; a higher Ki67 was seen in tumor with CCND1, ERBB2 and MYC CNGs (p=0.01, <0.001 and 0.03 respectively). FGFR1 CNG was associated with an increased risk of late events in univariate analyses (17/29 patients; BCFI: HR=3.2, 95%CI: 1.48-6.92, p =0.003; DRFI: HR=3.5, 95%CI: 1.61-7.75, p=0.002) and in multivariable models adjusted for clinicopathologic factors.Postmenopausal women with hormone receptor-positive early breast cancer harboring FGFR1 CNG had an increased risk of late recurrence despite extended therapy. FGFR1 CNG may represent a useful prognostic biomarker for late recurrence and a therapeutic target.
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2.
  • Leone, Maria Isabella, et al. (författare)
  • License to learn : an investigation into thin and thick licensing contracts
  • 2016
  • Ingår i: R &D Management. - : Blackwell Publishing. - 0033-6807 .- 1467-9310. ; 46:2, s. 326-340
  • Tidskriftsartikel (refereegranskat)abstract
    • This article introduces the distinction between thin and thick contracts to the investigation of licensing-in as a mechanism for technological learning. Thick contracts include a clause specifying that the licensors are obligated to assist the licensees in assimilating and integrating the technology. Drawing on a sample of 133 licensees and an equal number of matched nonlicensees, we present empirical evidence that thick contracts propel the licensees' likelihood of introducing new inventions. It is also found that thick contracts act as a substitute for licensees' absorptive capacity. Licensees that are more familiar with the licensed technology are in less need of assistance from the licensors to assimilate and integrate the knowledge. However, this substitution effect is neutralized once the hurdle of invention has been overcome, meaning that the licensees have succeeded to ignite the invention process, suggesting the exploitation of the learning curve, triggered by their mutual understanding.
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3.
  • Sonnenschein-van der Voort, Agnes M. M, et al. (författare)
  • Preterm birth, infant weight gain, and childhood asthma risk: A meta-analysis of 147,000 European children
  • 2014
  • Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier. - 0091-6749 .- 1097-6825. ; 133:5, s. 1317-1329
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Preterm birth, low birth weight, and infant catch-up growth seem associated with an increased risk of respiratory diseases in later life, but individual studies showed conflicting results. Objectives: We performed an individual participant data meta-analysis for 147,252 children of 31 birth cohort studies to determine the associations of birth and infant growth characteristics with the risks of preschool wheezing (1-4 years) and school-age asthma (5-10 years). Methods: First, we performed an adjusted 1-stage random-effect meta-analysis to assess the combined associations of gestational age, birth weight, and infant weight gain with childhood asthma. Second, we performed an adjusted 2-stage random-effect meta-analysis to assess the associations of preterm birth (gestational age less than 37 weeks) and low birth weight (less than 2500 g) with childhood asthma outcomes. Results: Younger gestational age at birth and higher infant weight gain were independently associated with higher risks of preschool wheezing and school-age asthma (P less than. 05). The inverse associations of birth weight with childhood asthma were explained by gestational age at birth. Compared with term-born children with normal infant weight gain, we observed the highest risks of school-age asthma in children born preterm with high infant weight gain (odds ratio [OR], 4.47; 95% CI, 2.58-7.76). Preterm birth was positively associated with an increased risk of preschool wheezing (pooled odds ratio [pOR], 1.34; 95% CI, 1.25-1.43) and school-age asthma (pOR, 1.40; 95% CI, 1.18-1.67) independent of birth weight. Weaker effect estimates were observed for the associations of low birth weight adjusted for gestational age at birth with preschool wheezing (pOR, 1.10; 95% CI, 1.00-1.21) and school-age asthma (pOR, 1.13; 95% CI, 1.01-1.27). Conclusion: Younger gestational age at birth and higher infant weight gain were associated with childhood asthma outcomes. The associations of lower birth weight with childhood asthma were largely explained by gestational age at birth.
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