Luigi Panza

Dr. Luigi Panza

Dept. of Pharmaceutical Sciences, University of Eastern Piedmont
orcid

Research Focus & Metrics

Academic Career Length

43Years (1984-Present)

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

Representative Publications

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1 December 1999 in Tetrahedron
Verified
Journal Article
Closed access
GGGiovanni Battista Giovenzana
Giovanni Battista Giovenzana
LLLuigi Lay
Luigi Lay
DMDiego Monti
Diego Monti
GPGiovanni Palmisano
Giovanni Palmisano
Luigi PanzaLuigi Panza
Luigi Panza

30 October 2009 in Journal of Medicinal Chemistry
Verified
Journal Article
Closed access
Saverio AltieriSaverio Altieri
Saverio Altieri
MBM. Balzi
M. Balzi
Silva BortolussiSilva Bortolussi
Silva Bortolussi
PBP. Bruschi
P. Bruschi
LCL. Ciani
L. Ciani
Sandra RistoriSandra Ristori
Sandra Ristori

10 April 2021 in Life
Verified
Journal Article
Open access
PDF file
Wolfgang SauerweinWolfgang Sauerwein
Wolfgang Sauerwein
Lucie SANCEYLucie SANCEY
Lucie SANCEY
Evamarie Hey-HawkinsEvamarie Hey-Hawkins
Evamarie Hey-Hawkins
MKMartin Kellert
Martin Kellert
Luigi PanzaLuigi Panza
Luigi Panza
AWAndrea Wittig
Andrea Wittig
Boron neutron capture therapy (BNCT) has the potential to specifically destroy tumor cells without damaging the tissues infiltrated by the tumor. BNCT is a binary treatment method based on the combination of two agents that have no effect when applied individually: 10B and thermal neutrons. Exclusively, the combination of both produces an effect, whose extent depends on the amount of 10B in the tumor but also on the organs at risk. It is not yet possible to determine the 10B concentration in a specific tissue using non-invasive methods. At present, it is only possible to measure the 10B concentration in blood and to estimate the boron concentration in tissues based on the assumption that there is a fixed uptake of 10B from the blood into tissues. On this imprecise assumption, BNCT can hardly be developed further. A therapeutic approach, combining the boron carrier for therapeutic purposes with an imaging tool, might allow us to determine the 10B concentration in a specific tissue using a non-invasive method. This review provides an overview of the current clinical protocols and preclinical experiments and results on how innovative drug development for boron delivery systems can also incorporate concurrent imaging. The last section focuses on the importance of proteomics for further optimization of BNCT, a highly precise and personalized therapeutic approach.

15 August 2011 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
FFFederica Facciotti
Federica Facciotti
MCMarco Cavallari
Marco Cavallari
CACatherine Angénieux
Catherine Angénieux
LGLuis F. Garcia-Alles
Luis F. Garcia-Alles
FSFrançois Signorino-Gelo
François Signorino-Gelo
GLGennaro De Libero
Gennaro De Libero
CD1e is a member of the CD1 family that participates in lipid antigen presentation without interacting with the T-cell receptor. It binds lipids in lysosomes and facilitates processing of complex glycolipids, thus promoting editing of lipid antigens. We find that CD1e may positively or negatively affect lipid presentation by CD1b, CD1c, and CD1d. This effect is caused by the capacity of CD1e to facilitate rapid formation of CD1–lipid complexes, as shown for CD1d, and also to accelerate their turnover. Similar results were obtained with antigen-presenting cells from CD1e transgenic mice in which lipid complexes are assembled more efficiently and show faster turnover than in WT antigen-presenting cells. These effects maximize and temporally narrow CD1-restricted responses, as shown by reactivity to Sphingomonas paucimobilis -derived lipid antigens. CD1e is therefore an important modulator of both group 1 and group 2 CD1-restricted responses influencing the lipid antigen availability as well as the generation and persistence of CD1–lipid complexes.

24 May 2007 in European Journal of Immunology
Verified
Journal Article
Open access
PDF file
JSJens Schümann
Jens Schümann
FFFederica Facciotti
Federica Facciotti
Luigi PanzaLuigi Panza
Luigi Panza
MMMario Michieletti
Mario Michieletti
Federica CompostellaFederica Compostella
Federica Compostella
GLGennaro De Libero
Gennaro De Libero
Deficiencies in enzymes of the lysosomal glycosphingolipid degradation pathway or in lysosomal lipid transfer proteins cause an imbalance in lipid metabolism and induce accumulation of certain lipids. A possible impact of such an imbalance on the presentation of lipid antigens to lipid‐reactive T cells has only been hypothesized but not extensively studied so far. Here we demonstrate that presentation of lipid antigens to, and development of, lipid‐reactive CD1d‐restricted NKT cells, are impaired in mice deficient in the lysosomal enzyme β‐galactosidase (βGal) or the lysosomal lipid transfer protein Niemann‐Pick C (NPC) 2. Importantly, the residual populations of NKT cells selected in βGal–/– and NPC2–/– mice showed differential TCR and CD4 repertoire characteristics, suggesting that differential selecting CD1d:lipid antigen complexes are formed. Furthermore, we provide direct evidence that accumulation of lipids impairs lipid antigen presentation in both cases. However, the mechanisms by which imbalanced lipid metabolism affected lipid antigen presentation were different. Based on these results, the impact of lipid accumulation should be generally considered in the interpretation of immunological deficiencies found in mice suffering from lipid metabolic disorders.

19 January 2007 in Biomacromolecules
Verified
Journal Article
Closed access
CMChiara Di Meo
Chiara Di Meo
Luigi PanzaLuigi Panza
Luigi Panza
DCDonatella Capitani
Donatella Capitani
Luisa ManninaLuisa Mannina
Luisa Mannina
ABAlessandra Banzato
Alessandra Banzato
VCVittorio Crescenzi
Vittorio Crescenzi