p16INK4a Is Selectively Silenced in the Tumoral Progression of Mycosis Fungoides View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2002-02-01

AUTHORS

Inmaculada C Navas, Patrocinio Algara, Marisol Mateo, Pedro Martínez, Carmen García, Jose L Rodriguez, Francisco Vanaclocha, Nuria Barrientos, Luis Iglesias, Lydia Sánchez, Miguel A Piris, Pablo Ortiz-Romero

ABSTRACT

Knowledge about the molecular mechanisms involved in the pathogenesis of tumoral progression in mycosis fungoides (MF) is still scarce. Because the 9p21 locus seems to be a good target for a detailed study in MF, this prompted us to compare the mechanisms of inactivation of the p16INK4a, p15INK4b, and p14ARF genes in aggressive and stable forms of MF, performing microsatellite analysis, methylation-specific polymerase chain reaction, direct sequencing, and p16INK4a protein expression by immunohistochemistry. Additionally, the p53 gene was also sequenced in tumoral lesions. Thirty-nine patients with stable MF were studied. Alterations in p16INK4a and p15INK4b genes were detected in 18% and 5% of the cases, respectively. None of the cases analyzed showed alterations of the p14ARF gene. In contrast with these findings, in the 11 patients with aggressive MF, alterations of the p16INK4a, p15INK4b, or p14ARF genes were found in 8 (73%), 3 (27%), and 2 (18%) cases, respectively. A significant proportion (4/11) of these alterations were already present in the p16INK4a gene in the initial plaque lesions in these aggressive forms of MF. Alterations in the p16INK4a gene, either methylation or loss of heterozygosity, were clearly more frequent than those in the p15INK4b and p14ARF genes. These p16INK4A alterations were confirmed using immunohistochemistry. None of the nine tumoral lesions analyzed showed mutations in exons 1-2 of the p16INK4a gene or in exons 5-8 of the p53 gene. These results seem to suggest that 9p21 alterations, and selectively p16INK4a silencing, could be a characteristic phenomenon in MF progression. More... »

PAGES

123-132

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/labinvest.3780405

DOI

http://dx.doi.org/10.1038/labinvest.3780405

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1052631066

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/11850526


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33 schema:description Knowledge about the molecular mechanisms involved in the pathogenesis of tumoral progression in mycosis fungoides (MF) is still scarce. Because the 9p21 locus seems to be a good target for a detailed study in MF, this prompted us to compare the mechanisms of inactivation of the p16INK4a, p15INK4b, and p14ARF genes in aggressive and stable forms of MF, performing microsatellite analysis, methylation-specific polymerase chain reaction, direct sequencing, and p16INK4a protein expression by immunohistochemistry. Additionally, the p53 gene was also sequenced in tumoral lesions. Thirty-nine patients with stable MF were studied. Alterations in p16INK4a and p15INK4b genes were detected in 18% and 5% of the cases, respectively. None of the cases analyzed showed alterations of the p14ARF gene. In contrast with these findings, in the 11 patients with aggressive MF, alterations of the p16INK4a, p15INK4b, or p14ARF genes were found in 8 (73%), 3 (27%), and 2 (18%) cases, respectively. A significant proportion (4/11) of these alterations were already present in the p16INK4a gene in the initial plaque lesions in these aggressive forms of MF. Alterations in the p16INK4a gene, either methylation or loss of heterozygosity, were clearly more frequent than those in the p15INK4b and p14ARF genes. These p16INK4A alterations were confirmed using immunohistochemistry. None of the nine tumoral lesions analyzed showed mutations in exons 1-2 of the p16INK4a gene or in exons 5-8 of the p53 gene. These results seem to suggest that 9p21 alterations, and selectively p16INK4a silencing, could be a characteristic phenomenon in MF progression.
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40 schema:keywords MF progression
41 aggressive MF
42 aggressive form
43 alterations
44 analysis
45 cases
46 chain reaction
47 characteristic phenomena
48 contrast
49 detailed study
50 direct sequencing
51 exon 1
52 exon 5
53 expression
54 findings
55 form
56 fungoides
57 genes
58 good target
59 heterozygosity
60 immunohistochemistry
61 inactivation
62 initial plaque lesions
63 knowledge
64 lesions
65 loci
66 loss
67 loss of heterozygosity
68 mechanism
69 mechanism of inactivation
70 methylation
71 methylation-specific polymerase chain reaction
72 microsatellite analysis
73 molecular mechanisms
74 mutations
75 mycosis fungoides
76 p14ARF gene
77 p15INK4B
78 p15INK4B gene
79 p16INK4a
80 p16INK4a alterations
81 p16INK4a gene
82 p53 gene
83 pathogenesis
84 patients
85 phenomenon
86 plaque lesions
87 polymerase chain reaction
88 progression
89 proportion
90 protein expression
91 reaction
92 results
93 sequencing
94 significant proportion
95 stable MF
96 stable form
97 study
98 target
99 tumoral lesions
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