TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis andprogression of pleomorphic adenomas.

Loredana Bruno, Rosa Maria Tomasino, Viviana Bazan, Aldo Gerbino, Patrizia Cammareri, Valentina Calo', Antonio Russo, Vincenza Morello, Valentina Agnese, Arianna Gullo, Antonio Russo, Marcella Macaluso, Sandra Cascio, Eva Surmacz, Claudia Augello, Rita Passantino, Sandra Cascio, Valter Gregorio

Risultato della ricerca: Article

18 Citazioni (Scopus)

Abstract

The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivarygland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case ofcarcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/SingleStrand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7%(2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutations in K-Ras. p16INK4A promoterhypermethylation was found in 14% (4/28) of PAs and 100% (5/5) carcinomas. All genetic and epigenetic alterations were detectedexclusively in the epithelial and transitional tumor components, and were absent in the mesenchymal parts. Our analysis suggeststhat TP53 mutations and p16INK4A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in themalignant progression of PA into carcinoma. J. Cell. Physiol. 207: 654–659, 2006. 2006 Wiley-Liss, Inc.
Lingua originaleEnglish
pagine (da-a)654-659
Numero di pagine6
RivistaJournal of Cellular Physiology
Volume207(3)
Stato di pubblicazionePublished - 2006

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Pleomorphic Adenoma
Carcinogenesis
Methylation
Genes
Carcinoma
Mutation
ras Genes
Tumors
Epigenomics
Polymerase chain reaction
Polymorphism
Polymerase Chain Reaction
Tumor Suppressor Genes
Neoplasms
Adenocarcinoma

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cita questo

TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis andprogression of pleomorphic adenomas. / Bruno, Loredana; Tomasino, Rosa Maria; Bazan, Viviana; Gerbino, Aldo; Cammareri, Patrizia; Calo', Valentina; Russo, Antonio; Morello, Vincenza; Agnese, Valentina; Gullo, Arianna; Russo, Antonio; Macaluso, Marcella; Cascio, Sandra; Surmacz, Eva; Augello, Claudia; Passantino, Rita; Cascio, Sandra; Gregorio, Valter.

In: Journal of Cellular Physiology, Vol. 207(3), 2006, pag. 654-659.

Risultato della ricerca: Article

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title = "TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis andprogression of pleomorphic adenomas.",
abstract = "The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivarygland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case ofcarcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/SingleStrand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53were found in 14{\%} (4/28) of PAs and in 60{\%} (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4{\%}(1/28) and7{\%}(2/28) of PAs, respectively. Only 20{\%} (1/5) of carcinomas screened displayed mutations in K-Ras. p16INK4A promoterhypermethylation was found in 14{\%} (4/28) of PAs and 100{\%} (5/5) carcinomas. All genetic and epigenetic alterations were detectedexclusively in the epithelial and transitional tumor components, and were absent in the mesenchymal parts. Our analysis suggeststhat TP53 mutations and p16INK4A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in themalignant progression of PA into carcinoma. J. Cell. Physiol. 207: 654–659, 2006. 2006 Wiley-Liss, Inc.",
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author = "Loredana Bruno and Tomasino, {Rosa Maria} and Viviana Bazan and Aldo Gerbino and Patrizia Cammareri and Valentina Calo' and Antonio Russo and Vincenza Morello and Valentina Agnese and Arianna Gullo and Antonio Russo and Marcella Macaluso and Sandra Cascio and Eva Surmacz and Claudia Augello and Rita Passantino and Sandra Cascio and Valter Gregorio",
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T1 - TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis andprogression of pleomorphic adenomas.

AU - Bruno, Loredana

AU - Tomasino, Rosa Maria

AU - Bazan, Viviana

AU - Gerbino, Aldo

AU - Cammareri, Patrizia

AU - Calo', Valentina

AU - Russo, Antonio

AU - Morello, Vincenza

AU - Agnese, Valentina

AU - Gullo, Arianna

AU - Russo, Antonio

AU - Macaluso, Marcella

AU - Cascio, Sandra

AU - Surmacz, Eva

AU - Augello, Claudia

AU - Passantino, Rita

AU - Cascio, Sandra

AU - Gregorio, Valter

PY - 2006

Y1 - 2006

N2 - The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivarygland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case ofcarcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/SingleStrand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7%(2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutations in K-Ras. p16INK4A promoterhypermethylation was found in 14% (4/28) of PAs and 100% (5/5) carcinomas. All genetic and epigenetic alterations were detectedexclusively in the epithelial and transitional tumor components, and were absent in the mesenchymal parts. Our analysis suggeststhat TP53 mutations and p16INK4A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in themalignant progression of PA into carcinoma. J. Cell. Physiol. 207: 654–659, 2006. 2006 Wiley-Liss, Inc.

AB - The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivarygland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case ofcarcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/SingleStrand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7%(2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutations in K-Ras. p16INK4A promoterhypermethylation was found in 14% (4/28) of PAs and 100% (5/5) carcinomas. All genetic and epigenetic alterations were detectedexclusively in the epithelial and transitional tumor components, and were absent in the mesenchymal parts. Our analysis suggeststhat TP53 mutations and p16INK4A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in themalignant progression of PA into carcinoma. J. Cell. Physiol. 207: 654–659, 2006. 2006 Wiley-Liss, Inc.

KW - TP53

UR - http://hdl.handle.net/10447/18943

M3 - Article

VL - 207(3)

SP - 654

EP - 659

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

ER -