Saverio Caini

Dr. Saverio Caini

Institute for Cancer Research, Prevention and Clinical Network (ISPRO), Via Cosimo il Vecchio 2, 50139 Florence, Italy
orcid

Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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9 April 2008 in International Journal of Cancer
Verified
Journal Article
Open access
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SRSara Raimondi
Sara Raimondi
FSFrancesco Sera
Francesco Sera
Sara GandiniSara Gandini
Sara Gandini
SISimona Iodice
Simona Iodice
Saverio CainiSaverio Caini
Saverio Caini
MFMaria Concetta Fargnoli
Maria Concetta Fargnoli
Melanocortin‐1‐receptor (MC1R) is one of the major genes that determine skin pigmentation. MC1R variants were suggested to be associated with red hair, fair skin, and an increased risk of melanoma. We performed a meta‐analysis on the association between the 9 most studied MC1R variants (p.V60L, p.D84E, p.V92M, p.R142H, p.R151C, p.I155T, p.R160W, p.R163Q and p.D294H) and melanoma and/or red hair, fair skin phenotype. Eleven studies on MC1R and melanoma, and 9 on MC1R and phenotype were included in the analysis. The 7 variants p.D84E, p.R142H, p.R151C, p.I155T, p.R160W, p. R163Q and p.D294H were significantly associated with melanoma development, with ORs (95%CI) ranging from 1.42 (1.09–1.85) for p.R163Q to 2.45 (1.32–4.55) for p.I155T. The MC1R variants p.R160W and p.D294H were associated both with red hair and fair skin, while p.D84E, p.R142H, and p.R151C were strongly associated with red hair only‐ ORs (95%CI) ranged from 2.99 (1.51–5.91) for p.D84E to 8.10 (5.82–11.28) for p.R151C. No association with melanoma or phenotype was found for p.V60L and p.V92M variants. In conclusion this meta‐analysis provided evidence that some MC1R variants are associated both with melanoma and phenotype, while other are only associated with melanoma development. These results suggest that MC1R variants could play a role in melanoma development both via pigmentary and non‐pigmentary pathways.

10 August 2015 in Influenza and Other Respiratory Viruses
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Journal Article
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Saverio CainiSaverio Caini
Saverio Caini
QHQ. Sue Huang
Q. Sue Huang
MCMeral A. Ciblak
Meral A. Ciblak
GKGabriela Kusznierz
Gabriela Kusznierz
RORhonda Owen
Rhonda Owen
TSthe Global Influenza B Study
the Global Influenza B Study
Introduction: Literature on influenza focuses on influenza A, despite influenza B having a large public health impact. The Global Influenza B Study aims to collect information on global epidemiology and burden of disease of influenza B since 2000.Methods: Twenty‐six countries in the Southern (n = 5) and Northern (n = 7) hemispheres and intertropical belt (n = 14) provided virological and epidemiological data. We calculated the proportion of influenza cases due to type B and Victoria and Yamagata lineages in each country and season; tested the correlation between proportion of influenza B and maximum weekly influenza‐like illness (ILI) rate during the same season; determined the frequency of vaccine mismatches; and described the age distribution of cases by virus type.Results: The database included 935 673 influenza cases (2000–2013). Overall median proportion of influenza B was 22·6%, with no statistically significant differences across seasons. During seasons where influenza B was dominant or co‐circulated (>20% of total detections), Victoria and Yamagata lineages predominated during 64% and 36% of seasons, respectively, and a vaccine mismatch was observed in ≈25% of seasons. Proportion of influenza B was inversely correlated with maximum ILI rate in the same season in the Northern and (with borderline significance) Southern hemispheres. Patients infected with influenza B were usually younger (5–17 years) than patients infected with influenza A.Conclusion: Influenza B is a common disease with some epidemiological differences from influenza A. This should be considered when optimizing control/prevention strategies in different regions and reducing the global burden of disease due to influenza.

12 September 2019 in PLOS ONE
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Journal Article
Open access
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Saverio CainiSaverio Caini
Saverio Caini
GKGabriela Kusznierz
Gabriela Kusznierz
VGVerònica Vera Garate
Verònica Vera Garate
SWSonam Wangchuk
Sonam Wangchuk
BTBinay Thapa
Binay Thapa
TTthe Global Influenza B Study team
the Global Influenza B Study team
We describe the epidemiological characteristics, pattern of circulation, and geographical distribution of influenza B viruses and its lineages using data from the Global Influenza B Study. We included over 1.8 million influenza cases occurred in thirty-one countries during 2000–2018. We calculated the proportion of cases caused by influenza B and its lineages; determined the timing of influenza A and B epidemics; compared the age distribution of B/Victoria and B/Yamagata cases; and evaluated the frequency of lineage-level mismatch for the trivalent vaccine. The median proportion of influenza cases caused by influenza B virus was 23.4%, with a tendency (borderline statistical significance, p = 0.060) to be higher in tropical vs. temperate countries. Influenza B was the dominant virus type in about one every seven seasons. In temperate countries, influenza B epidemics occurred on average three weeks later than influenza A epidemics; no consistent pattern emerged in the tropics. The two B lineages caused a comparable proportion of influenza B cases globally, however the B/Yamagata was more frequent in temperate countries, and the B/Victoria in the tropics (p = 0.048). B/Yamagata patients were significantly older than B/Victoria patients in almost all countries. A lineage-level vaccine mismatch was observed in over 40% of seasons in temperate countries and in 30% of seasons in the tropics. The type B virus caused a substantial proportion of influenza infections globally in the 21st century, and its two virus lineages differed in terms of age and geographical distribution of patients. These findings will help inform health policy decisions aiming to reduce disease burden associated with seasonal influenza.

1 August 2014 in Cancer Epidemiology
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Journal Article
Closed access
Saverio CainiSaverio Caini
Saverio Caini
Sara GandiniSara Gandini
Sara Gandini
MDMaria Dudas
Maria Dudas
VBViviane Bremer
Viviane Bremer
ESEttore Severi
Ettore Severi
AGAlin Gherasim
Alin Gherasim

1 November 2009 in European Journal of Cancer
Verified
Journal Article
Closed access
Saverio CainiSaverio Caini
Saverio Caini
Sara GandiniSara Gandini
Sara Gandini
FSFrancesco Sera
Francesco Sera
SRSara Raimondi
Sara Raimondi
MFMaria Concetta Fargnoli
Maria Concetta Fargnoli
BABruce K. Armstrong
Bruce K. Armstrong

1 October 2014 in European Journal of Cancer
Verified
Journal Article
Closed access
Saverio CainiSaverio Caini
Saverio Caini
MBMathieu Boniol
Mathieu Boniol
GTGiulio Tosti
Giulio Tosti
SMSerena Magi
Serena Magi
MMMatelda Medri
Matelda Medri
Sara GandiniSara Gandini
Sara Gandini