Guglielmina Nadia Ranzani is full Professor of Genetics at the Faculty of Sciences of the University of Pavia since 2001, and current Director of the PhD program of the University of Pavia-Italy.
Educational background. She graduated in Biology at the University of Pavia-Italy in 1974 (cum laude). She received a PhD (PhD-equivalent) in Biophysics from the University of Pavia in 1977 (cum laude).
Faculty positions. Research assistant (1976-1981), and researcher (1981-1987) at the Department of Genetics and Microbiology of the University of Pavia; Associate Professor of Human Genetics at the University of Camerino-Italy (1987-1990) and at the University of Pavia (1990-2001). As from October 2001 she is Full Professor of Human Genetics in the Faculty of Sciences-University of Pavia.
Foreign research experience. Graduate student fellow for ten months (1976-1977) at the Department of Human Genetics-University of Leiden (the Netherlands); long-term EMBO fellow for two years (1981-1983) at the Department of Animal Biology- University of Geneva (Switzerland); "maître-assistant" (1983-1984) at the University of Geneva.
Scientific activity. After having studied genetic variability in humans, G.N. Ranzani focused on the genetics of cancer. Particularly, she is interested in the genetic lesions involved in genesis and progression of sporadic/hereditary tumors of the digestive system (gastric and colon cancer), and in the genetic characterization of Italian families with HNPPC (Hereditary Non Polyposis Colorectal Cancer), with FAP/MAP (hereditary polyposes) and with HDGC (Hereditary Diffuse Gastric Cancer). In 1998, as invited member of an expert panel, she attended the NCI-Bethesda meeting on consensus criteria to define tumor instability. She has published 82 papers in international scientific journals some of which with high impact factor, 6 reviews and 2 chapters in textbooks. She has presented about one hundred oral communications in national and international meetings, and has held numerous seminars and conferences as guest speaker both in Italy and abroad. From October 2000 to November 2004, she has been president of the A.I.F.E.G. (Italian Association for the study of familial and hereditary gastrointestinal tumors). From 2004 to 2006 she has been the principal investigator of an Italian research network on hereditary gastrointestinal tumors, granted by the Italian Ministry of Scientific Research (MIUR).
Research fundings. In the last ten years G.N. Ranzani received the following research grants: FAR (University of Pavia); PRIN (Italian Ministry for University and Research); Banca del Monte di Lombardia Foundation; Cariplo Foundation (as participant-NOBEL project); Policlinico San Matteo-Pavia research foundings; AIRC (Italian Association for Cancer Research). In addition, she received grants for personnel exchanges from CNR (INSERM-Unité 434, Paris-France) and from Ateneo Italo-Tedesco (GSF, Institut of Pathology, Munchen-Germany).
Directorships. Beginning with the Academic year 1999-2000, G.N. Ranzani directed for five years the Specialization School of Applied Genetics, Faculty of Sciences-University of Pavia. From November 2003 to November 2009 she has been Chairmen of the Department of Genetics and Microbiology of the University of Pavia. From November 2009 she is Director of the PhD program of the University of Pavia (Scuola di Alta Formazione Dottorale).

One of the aims of the research activity is the detection and the functional characterization of the genetic lesions associated with the development of gastrointestinal tumors in families with hereditary syndromes. These syndromes include HNPCC (Hereditary Non Polyposis Colorectal Cancer), FAP/MAP (Familial Adenomatous Polyposis/MUTYH-Associated Polyposis) and HDGC (Hereditary Diffuse Gastric Cancer). In particular, the research is focused on the pathogenic significance of MUTYH and CDH1 gene mutations that are identified in polyposis and gastric cancer patients, respectively; pathogenic significance is assessed by gene expression analysis, by cell-based functional assays, and by bioinformatics tools.
Findings from numerous studies have shown that the genetic component plays a crucial role not only in syndromic and familial cases, but also in the development of the so-called sporadic cancers. Genome Wide Association Studies (GWAS) have recently detected genetic variants at different loci that can modulate the risk of colorectal cancer. The research group is interested in investigating the functional significance of low-penetrance alleles that have been associated with an increased risk of colorectatal cancer; indeed, the association with risk is currently defined only at a statistic level.
Beside genetic factors predisposing to colorectal cancer, somatic lesions involved in colorectal cancer progression and development of metastasis are also investigated. The aim of the analysis is to identify possible prognostic markers that can be used in clinical practice.
Very recently, a collaborative study has started, dealing with the genetic components associated with the pain treatment response in oncologic patients.

De Gregori M, Garbin G, De Gregori S, Minella CE, Bugada D, Lisa A, Govoni S, Regazzi M, Allegri M, Ranzani GN. Genetic variability at COMT but not at OPMR1 and UGT2B7 loci modulates morphine analgesic response in acute postoperative pain. Eur J Clin Pharmacol. 2013; in press

De Gregori S, Minella CE, De Gregori M, Tinelli C, Ranzani GN, Govoni S, Allegri M, Regazzi M. Clinical pharmacokinetics of morphine and its metabolites during morphine dose titration for chronic cancer pain. Ther Drug Monit. 2013; in press

Venesio T, Balsamo A, Errichiello E, Ranzani GN, Risio M. Oxidative DNA damage drives carcinogenesis in MUTYH-associated-polyposis by specific mutations of mitochondrial and MAPK genes. Mod Pathol. 2013; Apr 19. doi: 10.1038/modpathol.2013.66. [Epub ahead of print]

Turco E, Ventura I, Minoprio A, Russo MT, Torreri P, Degan P, Molatore S, Ranzani GN, Bignami M, Mazzei F. Understanding the role of the Q338H MUTYH variant in oxidative damage repair. Nucleic Acids Res. 2013; 41: 4093-103

Lanni C, Garbin G, Lisa A, Biundo F, Ranzenigo A, Sinforiani E, Cuzzoni G, Govoni S, Ranzani GN, Racchi M. Influence of COMT Val158Met Polymorphism on Alzheimer's Disease and Mild Cognitive Impairment in Italian Patients. J Alzheimers Dis. 2012; 32:919-26

Venesio T, Balsamo A, D'Agostino VG, Ranzani GN. MUTYH-associated polyposis (MAP), the syndrome implicating base excision repair in inherited predisposition to colorectal tumors. Front Oncol. 2012; 2: 1-9 Art 83

De Gregori M, De Gregori S, Ranzani GN, Allegri M, Govoni S, Regazzi M. Individualizing pain therapy with opioids: the rational approach based on pharmacogenetics and pharmacokinetics. Eur J Pain. 2010; Suppl. 4: 245-250

D'Agostino VG, Minoprio A, Torreri P, Marinoni I, Bossa C, Petrucci TC, Albertini AM, Ranzani GN, Bignami M, Mazzei F. Functional analysis of MUTYH mutant proteins associated with familial adenomatous polyposis. DNA Repair. 2010; 9:700-7

De Gregori M, Allegri M, De Gregori S, Garbin G, Tinelli C, Regazzi M, Govoni S, Ranzani GN. How and why to screen for CYP2D6 interindividual variability in patients under pharmacological treatments. Curr Drug Metab. 2010; 11:276-82

Molatore S, Russo MT, D'Agostino VG, Barone F, Matsumoto Y, Albertini AM, Minoprio A, Degan P, Mazzei F, Bignami M, Ranzani GN. MUTYH mutations associated with familial adenomatous polyposis: functional characterization by a mammalian cell-based assay. Hum Mutat. 2010; 31:159-66

Klug SJ, Ressing M, Koenig J, Abba MC, Agorastos T, Brenna SM, Ciotti M, Das BR, Del Mistro A, Dybikowska A, Giuliano AR, Gudleviciene Z, Gyllensten U, Haws AL, Helland A, Herrington CS, Hildesheim A, Humbey O, Jee SH, Kim JW, Madeleine MM, Menczer J, Ngan HY, Nishikawa A, Niwa Y, Pegoraro R, Pillai MR, Ranzani G, et al. TP53 codon 72 polymorphism and cervical cancer: a pooled analysis of individual data from 49 studies. Lancet Oncol. 2009; 10:772-784

Govoni S, Regazzi M, RanzaniGN. Pain and the pharmacogenetics at the fuzzy border between pain physiopathology and pain treatment. Eur J Pain. 2008; Suppl. 2:5-12

Cattaneo F, Molatore S, Mihalatos M, Apessos A, Venesio T, Bione S, Grignani P, Nasioulas G, Ranzani GN. Heterogeneous molecular mechanisms underlie attenuated familial adenomatous polyposis. Genet Med. 2007; 9:836-841

Ponz de Leon M, Bertario L, Genuardi M, Lanza G, Oliani C, Ranzani GN, Rossi GB, Varesco L, Venesio T, Viel A. Identification and classification of HNPCC (Lynch Syndrome): adapting old concepts to recent advancements. Report from the Italian Association for the Study of Hereditary Colorectal Tumors Consensus Group. Dis Colon Rectum. 2007; 50:2126-2134

Venesio T, Balsamo A, Sfiligoi C, Fuso L, Molatore S, Ranzani GN, Risio M. Constitutional high expression of an APC mRNA isoform in a subset of Attenuated Familial Adenomatous Polyposis patients. J Mol Med. 2007; 85:301-308

Cattaneo F, Venesio T, Molatore S, Russo A, Fiocca R, Frattini M, Scovassi AI, Ottini L, Bertario L, Ranzani GN. Functional analysis and case-control study of -160C/A polymorphism in the E-cadherin gene promoter: association with cancer risk. Anticancer Res. 2006; 26:4627-4632

Perri F, Piepoli A, Bonvicini C, Gentile A, Quitadamo M, Di Candia M, Cotugno R, Cattaneo F, Zagari MR, Ricciardiello L, Gennarelli M, Bazzoli F, Ranzani GN, Andriulli A. Cytokine gene polymorphisms in gastric cancer patients from two Italian areas at high and low cancer prevalence. Cytokine. 2005; 30:293-302

Bardella C, Costa B, Maggiora P, Patane' S, Olivero M, Ranzani GN, De Bortoli M, Comoglio PM, Di Renzo MF. Truncated RON tyrosine kinase drives tumor cell progression and abrogates cell-cell adhesion through E-cadherin transcriptional repression. Cancer Res. 2004; 64:5154-5161

Venesio T, Molatore S, Cattaneo F, Arrigoni A, Risio M, Ranzani GN. High Frequency of MYH Gene Mutations in a Subset of Familial Adenomatous Polyposis Patients. Gastroenterology. 2004; 126:1681-1685

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