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Article: Genetica ed oncogenesi dei tumori renali.

Viel, Alessandra

Giornale italiano di nefrologia : organo ufficiale della Societa italiana di nefrologia

2010 Volume 27 Suppl 50, Page(s) S3–9

Abstract: The development and progression of cancer requires several genetic modifications. Multiple transformation and progression events such as point mutations, deletions/insertions, chromosomal abnormalities, and epigenetic deregulation contribute to renal ... ...

Title translation	Genetics and oncogenesis of renal cancer.
Abstract	The development and progression of cancer requires several genetic modifications. Multiple transformation and progression events such as point mutations, deletions/insertions, chromosomal abnormalities, and epigenetic deregulation contribute to renal oncogenesis. Three types of genes are involved in this multistep process: oncogenes, tumor suppressor genes, and DNA repair genes. About 4% of renal tumors are hereditary, i.e., the first mutation is present at the constitutive level in all cells of an individual, leading to an increased lifetime risk of cancer. Sporadic tumors are mainly single and of late onset, while hereditary tumors are usually multiple and of early onset in the presence of a positive family history for kidney cancer. Moreover, hereditary tumors are often associated with specific syndromic signs. The main hereditary syndromes that include renal tumors are Von Hippel- Lindau disease, hereditary papillary renal clear cell carcinoma, hereditary leiomyomatosis renal cell carcinoma, and the Birt-Hogg-Dube' syndrome. Other rarer conditions are chromosome 3 translocation, tuberous sclerosis, and the Lynch syndrome. Study of these diseases and identification of the responsible genes have been extremely useful in understanding several molecular issues of renal oncogenesis. Genetic testing makes it possible to diagnose hereditary cancer and confirm a clinical suspicion, as well as to identify at-risk individuals within a family. It is extremely important for nephrologists to be aware of these hereditary conditions, as this will allow early recognition and improved clinical management.
MeSH term(s)	Genetic Predisposition to Disease ; Humans ; Kidney Neoplasms/genetics
Language	Italian
Publishing date	2010-09
Publishing country	Italy
Document type	English Abstract ; Journal Article
ZDB-ID	1237110-5
ISSN	0393-5590
ISSN	0393-5590
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Article ; Online: Hereditary Cancer Syndromes: A Comprehensive Review with a Visual Tool.

Garutti, Mattia / Foffano, Lorenzo / Mazzeo, Roberta / Michelotti, Anna / Da Ros, Lucia / Viel, Alessandra / Miolo, Gianmaria / Zambelli, Alberto / Puglisi, Fabio

Genes

2023 Volume 14, Issue 5

Abstract: Hereditary cancer syndromes account for nearly 10% of cancers even though they are often underdiagnosed. Finding a pathogenic gene variant could have dramatic implications in terms of pharmacologic treatments, tailored preventive programs, and familiar ... ...

Abstract	Hereditary cancer syndromes account for nearly 10% of cancers even though they are often underdiagnosed. Finding a pathogenic gene variant could have dramatic implications in terms of pharmacologic treatments, tailored preventive programs, and familiar cascade testing. However, diagnosing a hereditary cancer syndrome could be challenging because of a lack of validated testing criteria or because of their suboptimal performance. In addition, many clinicians are not sufficiently well trained to identify and select patients that could benefit from a genetic test. Herein, we searched the available literature to comprehensively review and categorize hereditary cancer syndromes affecting adults with the aim of helping clinicians in their daily clinical practice through a visual tool.
MeSH term(s)	Adult ; Humans ; Genetic Predisposition to Disease ; Neoplastic Syndromes, Hereditary/diagnosis ; Neoplastic Syndromes, Hereditary/genetics ; Genetic Testing
Language	English
Publishing date	2023-04-30
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14051025
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Article ; Online: MLH1

Carnevali, Ileana Wanda / Cini, Giulia / Libera, Laura / Sahnane, Nora / Facchi, Sofia / Viel, Alessandra / Sessa, Fausto / Tibiletti, Maria Grazia

Genes

2023 Volume 14, Issue 11

Abstract: 1) Background: ...

Abstract	(1) Background:
MeSH term(s)	Female ; Humans ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis/pathology ; MutL Protein Homolog 1/genetics ; Microsatellite Instability ; Genetic Predisposition to Disease ; DNA Methylation/genetics ; Endometrial Neoplasms/diagnosis ; Carcinogenesis/genetics
Chemical Substances	MutL Protein Homolog 1 (EC 3.6.1.3) ; MLH1 protein, human
Language	English
Publishing date	2023-11-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14112060
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Article ; Online: Hereditary Cancer Syndromes: A Comprehensive Review with a Visual Tool

Garutti, Mattia / Foffano, Lorenzo / Mazzeo, Roberta / Michelotti, Anna / Da Ros, Lucia / Viel, Alessandra / Miolo, Gianmaria / Zambelli, Alberto / Puglisi, Fabio

Genes (Basel). 2023 Apr. 30, v. 14, no. 5

2023

Abstract	Hereditary cancer syndromes account for nearly 10% of cancers even though they are often underdiagnosed. Finding a pathogenic gene variant could have dramatic implications in terms of pharmacologic treatments, tailored preventive programs, and familiar cascade testing. However, diagnosing a hereditary cancer syndrome could be challenging because of a lack of validated testing criteria or because of their suboptimal performance. In addition, many clinicians are not sufficiently well trained to identify and select patients that could benefit from a genetic test. Herein, we searched the available literature to comprehensively review and categorize hereditary cancer syndromes affecting adults with the aim of helping clinicians in their daily clinical practice through a visual tool.
Keywords	adults ; genes ; genetic testing ; neoplasms ; patients
Language	English
Dates of publication	2023-0430
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article ; Online
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14051025
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Article ; Online: Biallelic

Pedroni, Monica / Ponz de Leon, Maurizio / Reggiani Bonetti, Luca / Rossi, Giuseppina / Viel, Alessandra / Urso, Emanuele Damiano Luca / Roncucci, Luca

Genes

2022 Volume 13, Issue 11

Abstract: We describe a patient with constitutional mismatch repair-deficiency (CMMR-D) in whom the syndrome started at age 10 with the development of multiple adenomas in the large bowel. In the successive 25 years, four malignancies developed in different organs ...

Abstract	We describe a patient with constitutional mismatch repair-deficiency (CMMR-D) in whom the syndrome started at age 10 with the development of multiple adenomas in the large bowel. In the successive 25 years, four malignancies developed in different organs (rectum, ileum, duodenum, and lymphoid tissue). The patient had biallelic constitutional pathogenic variants in the
MeSH term(s)	Male ; Humans ; Mismatch Repair Endonuclease PMS2/genetics ; DNA Repair Enzymes/genetics ; Adenosine Triphosphatases/genetics ; DNA-Binding Proteins/genetics ; Neoplastic Syndromes, Hereditary/genetics ; Microsatellite Instability
Chemical Substances	Mismatch Repair Endonuclease PMS2 (EC 3.6.1.3) ; DNA Repair Enzymes (EC 6.5.1.-) ; Adenosine Triphosphatases (EC 3.6.1.-) ; DNA-Binding Proteins ; PMS2 protein, human (EC 3.6.1.-)
Language	English
Publishing date	2022-10-26
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13111953
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Article ; Online: Male with an apparently normal phenotype carrying a BRCA1 exon 20 duplication in trans to a BRCA1 frameshift variant.

Breast cancer research : BCR

2024 Volume 26, Issue 1, Page(s) 6

Abstract: Background: Reports of dual carriers of pathogenic BRCA1 variants in trans are extremely rare, and so far, most individuals have been associated with a Fanconi Anemia-like phenotype.: Methods: We identified two families with a BRCA1 in-frame exon 20 ... ...

Abstract	Background: Reports of dual carriers of pathogenic BRCA1 variants in trans are extremely rare, and so far, most individuals have been associated with a Fanconi Anemia-like phenotype. Methods: We identified two families with a BRCA1 in-frame exon 20 duplication (Ex20dup). In one male individual, the variant was in trans with the BRCA1 frameshift variant c.2475delC p.(Asp825Glufs21). We performed splicing analysis and used a transcription activation domain (TAD) assay to assess the functional impact of Ex20dup. We collected pedigrees and mapped the breakpoints of the duplication by long- and short-read genome sequencing. In addition, we performed a mitomycin C (MMC) assay from the dual carrier using cultured lymphoblastoid cells. Results:* Genome sequencing and RNA analysis revealed the BRCA1 exon 20 duplication to be in tandem. The duplication was expressed without skipping any one of the two exon 20 copies, resulting in a lack of wild-type transcripts from this allele. TAD assay indicated that the Ex20dup variant has a functional level similar to the well-known moderate penetrant pathogenic BRCA1 variant c.5096G > A p.(Arg1699Gln). MMC assay of the dual carrier indicated a slightly impaired chromosomal repair ability. Conclusions: This is the first reported case where two BRCA1 variants with demonstrated functional impact are identified in trans in a male patient with an apparently normal clinical phenotype and no BRCA1-associated cancer. The results pinpoint a minimum necessary BRCA1 protein activity to avoid a Fanconi Anemia-like phenotype in compound heterozygous status and yet still predispose carriers to hormone-related cancers. These findings urge caution when counseling families regarding potential Fanconi Anemia risk. Furthermore, prudence should be taken when classifying individual variants as benign based on co-occurrence in trans with well-established pathogenic variants.
MeSH term(s)	Humans ; Male ; BRCA1 Protein/genetics ; Breast Neoplasms ; Exons/genetics ; Fanconi Anemia/genetics ; Mitomycin ; Phenotype
Chemical Substances	BRCA1 Protein ; BRCA1 protein, human ; Mitomycin (50SG953SK6)
Language	English
Publishing date	2024-01-09
Publishing country	England
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-023-01755-9
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Zs.A 5494: Show issues

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Article ; Online: An Exceptional Response to Dostarlimab in Mismatch Repair Deficient, Microsatellite Instability-High and Platinum Refractory Endometrial Cancer.

Bartoletti, Michele / Giorda, Giorgio / Viel, Alessandra / Fornasarig, Mara / Zdjelar, Adrian / Segatto, Enrica / Sorio, Roberto / Corsetti, Serena / Scalone, Simona / Nicoloso, Milena Sabrina / Pivetta, Tania / Lucia, Emilio / Clemente, Nicolò / Palazzari, Elisa / Canzonieri, Vincenzo / Puglisi, Fabio

Current oncology (Toronto, Ont.)

2022 Volume 29, Issue 8, Page(s) 5209–5212

Abstract: Until recently, effective therapies for advanced endometrial cancer progressing to a platinum-based combination were lacking. In this setting, immunotherapy with anti PD-1/PDL-1 monoclonal antibodies is rising as a new paradigm in particular for patients ...

Abstract	Until recently, effective therapies for advanced endometrial cancer progressing to a platinum-based combination were lacking. In this setting, immunotherapy with anti PD-1/PDL-1 monoclonal antibodies is rising as a new paradigm in particular for patients with microsatellites instability/mismatch repair deficiency. In this case report, we describe an exceptional and rapid response to dostarlimab in a platinum refractory endometrial cancer patient with high disease burden harboring a mismatch repair deficiency.
MeSH term(s)	Antibodies, Monoclonal, Humanized ; Brain Neoplasms ; Colorectal Neoplasms ; DNA Mismatch Repair ; Endometrial Neoplasms/drug therapy ; Endometrial Neoplasms/genetics ; Female ; Humans ; Immune Checkpoint Inhibitors ; Microsatellite Instability ; Neoplastic Syndromes, Hereditary ; Platinum/therapeutic use ; Programmed Cell Death 1 Receptor
Chemical Substances	Antibodies, Monoclonal, Humanized ; Immune Checkpoint Inhibitors ; Programmed Cell Death 1 Receptor ; dostarlimab ; Platinum (49DFR088MY)
Language	English
Publishing date	2022-07-22
Publishing country	Switzerland
Document type	Case Reports ; Research Support, Non-U.S. Gov't
ZDB-ID	1236972-x
ISSN	1718-7729 ; 1198-0052
ISSN (online)	1718-7729
ISSN	1198-0052
DOI	10.3390/curroncol29080413
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Article: Role of MUTYH in human cancer.

Mazzei, Filomena / Viel, Alessandra / Bignami, Margherita

Mutation research

2013 Volume 743-744, Page(s) 33–43

Abstract: MUTYH, a human ortholog of MutY, is a post-replicative DNA glycosylase, highly conserved throughout evolution, involved in the correction of mismatches resulting from a faulty replication of the oxidized base 8-hydroxyguanine (8-oxodG). In particular ... ...

Abstract	MUTYH, a human ortholog of MutY, is a post-replicative DNA glycosylase, highly conserved throughout evolution, involved in the correction of mismatches resulting from a faulty replication of the oxidized base 8-hydroxyguanine (8-oxodG). In particular removal of adenine from A:8-oxodG mispairs by MUTYH activity is followed by error-free base excision repair (BER) events, leading to the formation of C:8-oxodG base pairs. These are the substrate of another BER enzyme, the OGG1 DNA glycosylase, which then removes 8-oxodG from DNA. Thus the combined action of OGG1 and MUTYH prevents oxidative damage-induced mutations, i.e. GC->TA transversions. Germline mutations in MUTYH are associated with a recessively heritable colorectal polyposis, now referred to as MUTYH-associated polyposis (MAP). Here we will review the phenotype(s) associated with MUTYH inactivation from bacteria to mammals, the structure of the MUTYH protein, the molecular mechanisms of its enzymatic activity and the functional characterization of MUTYH variants. The relevance of these results will be discussed to define the role of specific human mutations in colorectal cancer risk together with the possible role of MUTYH inactivation in sporadic cancer.
MeSH term(s)	Animals ; DNA Glycosylases/genetics ; DNA Glycosylases/metabolism ; DNA Repair ; Humans ; Mutation ; Neoplasms/enzymology ; Neoplasms/genetics ; Phenotype
Chemical Substances	DNA Glycosylases (EC 3.2.2.-) ; mutY adenine glycosylase (EC 3.2.2.-)
Language	English
Publishing date	2013-03-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	206607-5
ISSN	1873-135X ; 0027-5107 ; 1383-5718 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
ISSN (online)	1873-135X
ISSN	0027-5107 ; 1383-5718 ; 0165-1110 ; 0165-1161 ; 0165-7992 ; 0921-8777 ; 0165-1218 ; 1383-5726 ; 0167-8817 ; 0921-8734 ; 1383-5742
DOI	10.1016/j.mrfmmm.2013.03.003
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Article ; Online: Definition and management of colorectal polyposis not associated with APC/MUTYH germline pathogenic variants: AIFEG consensus statement.

Urso, Emanuele Damiano Luca / Ponz de Leon, Maurizio / Vitellaro, Marco / Piozzi, Guglielmo Niccolò / Bao, Quoc Riccardo / Martayan, Aline / Remo, Andrea / Stigliano, Vittoria / Oliani, Cristina / Lucci Cordisco, Emanuela / Pucciarelli, Salvatore / Ranzani, Guglielmina Nadia / Viel, Alessandra

Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

2021 Volume 53, Issue 4, Page(s) 409–417

Abstract: An expert consensus panel convened by the Italian Association for Inherited and Familial Gastrointestinal Tumors (Associazione Italiana per lo Studio della Familiarità ed Ereditarietà dei Tumori Gastrointestinali, AIFEG) reviewed the literature and ... ...

Abstract	An expert consensus panel convened by the Italian Association for Inherited and Familial Gastrointestinal Tumors (Associazione Italiana per lo Studio della Familiarità ed Ereditarietà dei Tumori Gastrointestinali, AIFEG) reviewed the literature and agreed on a number of position statements regarding the definition and management of polyposis coli without an identified pathogenic mutation on the APC or MUTYH genes, defined in the document as NAMP (non-APC/MUTYH polyposis).
MeSH term(s)	Adenomatous Polyposis Coli/diagnosis ; Adenomatous Polyposis Coli/therapy ; Adenomatous Polyposis Coli Protein/genetics ; Consensus ; DNA Glycosylases/genetics ; Germ Cells ; Humans ; Italy ; Societies, Medical
Chemical Substances	APC protein, human ; Adenomatous Polyposis Coli Protein ; DNA Glycosylases (EC 3.2.2.-) ; mutY adenine glycosylase (EC 3.2.2.-)
Language	English
Publishing date	2021-01-25
Publishing country	Netherlands
Document type	Practice Guideline ; Journal Article
ZDB-ID	1459373-7
ISSN	1878-3562 ; 1125-8055
ISSN (online)	1878-3562
ISSN	1125-8055
DOI	10.1016/j.dld.2020.11.018
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Article: Lynch syndrome and Muir-Torre phenotype associated with a recurrent variant in the 3'UTR of the MSH6 gene.

Cini, Giulia / Carnevali, Ileana / Sahnane, Nora / Chiaravalli, Anna Maria / Dell'Elice, Anastasia / Maestro, Roberta / Pin, Elisa / Bestetti, Ilaria / Radovic, Slobodanka / Armelao, Franco / Viel, Alessandra / Tibiletti, Maria Grazia

Cancer genetics

2021 Volume 254-255, Page(s) 1–10

Abstract: A MSH6 3'UTR variant (c.*23_26dup) was found in 13 unrelated families consulted for Lynch/Muir-Torre Syndrome. This variant, which is very rare in the genomic databases, was absent in healthy controls and strongly segregated with the disease in the ... ...

Abstract	A MSH6 3'UTR variant (c.23_26dup) was found in 13 unrelated families consulted for Lynch/Muir-Torre Syndrome. This variant, which is very rare in the genomic databases, was absent in healthy controls and strongly segregated with the disease in the studied pedigrees. All tumors were defective for MSH2/MSH6/MSH3 proteins expression, but only MSH2 somatic pathogenic mutations were found in 5 of the 12 sequenced tumors. Moreover, we had no evidence of MSH6 transcript decrease in carriers, whereas MSH2 transcript was downregulated. Additional evaluations performed in representative carriers, including karyotype, arrayCGH and Linked-Reads whole genome sequencing, failed to evidence any MSH2 germline pathogenic variant. Posterior probability of pathogenicity for MSH6 c.23_26dup was obtained from a multifactorial analysis incorporating segregation and phenotypic data and resulted >0.999, allowing to classify the variant as pathogenic (InSiGHT Class 5). Carriers shared a common haplotype involving MSH2/MSH6 loci, then a cryptic disease-associated variant, linked with MSH6 c.*23_26dup, cannot be completely excluded. Even if it is not clear whether the MSH6 variant is pathogenic per se or simply a marker of a disease-associated MSH2/MSH6 haplotype, all data collected on patients and pedigrees prompted us to manage the variant as pathogenic and to offer predictive testing within these families.
MeSH term(s)	3' Untranslated Regions/genetics ; Base Sequence ; Case-Control Studies ; Colorectal Neoplasms, Hereditary Nonpolyposis/genetics ; Colorectal Neoplasms, Hereditary Nonpolyposis/pathology ; DNA-Binding Proteins/genetics ; Female ; Gene Expression Regulation ; Germ-Line Mutation/genetics ; Heterozygote ; Humans ; Male ; Muir-Torre Syndrome/genetics ; Muir-Torre Syndrome/pathology ; MutS Homolog 2 Protein/genetics ; Pedigree ; Phenotype ; Probability ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	3' Untranslated Regions ; DNA-Binding Proteins ; G-T mismatch-binding protein ; RNA, Messenger ; MutS Homolog 2 Protein (EC 3.6.1.3)
Language	English
Publishing date	2021-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2599227-2
ISSN	2210-7762
ISSN	2210-7762
DOI	10.1016/j.cancergen.2021.01.005
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