Expression and Alteration of p16 in Diffuse Large B Cell Lymphoma

Objectives: This study aimed to examine (1) the expression of P16 protein relative to sites of presentation, immunophenotypic subgroups and proliferative indices of tumour cells, and (2) the relationship between p16 gene alterations and P16 protein overexpression in 70 cases of diffuse large B cell...

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Veröffentlicht in:Pathobiology (Basel) 2010-01, Vol.77 (2), p.96-105
Hauptverfasser: Lee, Ee-Soo, Kim, Lian-Hua, Abdullah, Wan Ariffin, Peh, Suat-Cheng
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creator Lee, Ee-Soo
Kim, Lian-Hua
Abdullah, Wan Ariffin
Peh, Suat-Cheng
description Objectives: This study aimed to examine (1) the expression of P16 protein relative to sites of presentation, immunophenotypic subgroups and proliferative indices of tumour cells, and (2) the relationship between p16 gene alterations and P16 protein overexpression in 70 cases of diffuse large B cell lymphoma (DLBCL). Methods: Expression of P16, CD10, BCL-6, MUM-1 and proliferation marker (Ki-67) was demonstrated by immunohistochemistry. Fluorescence in situ hybridization (FISH) was employed to detect p16 alterations. Results: P16 overexpression was shown in 45.7% (32/70) of the DLBCL cases, and was significantly correlated with CD10 (p = 0.022) and germinal centre B-cell-like (GCB) phenotype (p = 0.022). High expression of P16 was inversely associated with high proliferative activity (Ki-67 index greater than 75%) (p = 0.020). Of the 47 cases that yielded interpretable FISH results, 57.4% (27/47) showed deletions of p16 and 27.7% (13/47) showed gains of p16. P16 overexpression and p16 deletions were mutually exclusive (p = 0.019). There was no correlation between P16 overexpression and p16 gains (p = 0.621). Conclusions: The GCB and non-GCB subgroups of DLBCLs show different patterns of P16 expression. High levels of P16 may mitigate tumour cell proliferation. Gains of p16 do not necessarily increase P16 protein expression.
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Methods: Expression of P16, CD10, BCL-6, MUM-1 and proliferation marker (Ki-67) was demonstrated by immunohistochemistry. Fluorescence in situ hybridization (FISH) was employed to detect p16 alterations. Results: P16 overexpression was shown in 45.7% (32/70) of the DLBCL cases, and was significantly correlated with CD10 (p = 0.022) and germinal centre B-cell-like (GCB) phenotype (p = 0.022). High expression of P16 was inversely associated with high proliferative activity (Ki-67 index greater than 75%) (p = 0.020). Of the 47 cases that yielded interpretable FISH results, 57.4% (27/47) showed deletions of p16 and 27.7% (13/47) showed gains of p16. P16 overexpression and p16 deletions were mutually exclusive (p = 0.019). There was no correlation between P16 overexpression and p16 gains (p = 0.621). Conclusions: The GCB and non-GCB subgroups of DLBCLs show different patterns of P16 expression. High levels of P16 may mitigate tumour cell proliferation. 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Karger AG</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Cell Proliferation ; Cells ; Child ; Child, Preschool ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Female ; Fluorescence in situ hybridization ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes, p16 ; Genotype &amp; phenotype ; Humans ; Immunoenzyme Techniques ; In Situ Hybridization, Fluorescence ; Lymphoma ; Lymphoma, Large B-Cell, Diffuse - genetics ; Lymphoma, Large B-Cell, Diffuse - metabolism ; Lymphoma, Large B-Cell, Diffuse - pathology ; Male ; Middle Aged ; Original Paper ; Proteins ; Tumors</subject><ispartof>Pathobiology (Basel), 2010-01, Vol.77 (2), p.96-105</ispartof><rights>2010 S. Karger AG, Basel</rights><rights>Copyright (c) 2010 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-a22d46ff200094abff3ae4405d41a43db8aaf2ccc8ab3b2a3a8c00e125ea85ba3</citedby><cites>FETCH-LOGICAL-c399t-a22d46ff200094abff3ae4405d41a43db8aaf2ccc8ab3b2a3a8c00e125ea85ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2429,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20332669$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Ee-Soo</creatorcontrib><creatorcontrib>Kim, Lian-Hua</creatorcontrib><creatorcontrib>Abdullah, Wan Ariffin</creatorcontrib><creatorcontrib>Peh, Suat-Cheng</creatorcontrib><title>Expression and Alteration of p16 in Diffuse Large B Cell Lymphoma</title><title>Pathobiology (Basel)</title><addtitle>Pathobiology</addtitle><description>Objectives: This study aimed to examine (1) the expression of P16 protein relative to sites of presentation, immunophenotypic subgroups and proliferative indices of tumour cells, and (2) the relationship between p16 gene alterations and P16 protein overexpression in 70 cases of diffuse large B cell lymphoma (DLBCL). 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Methods: Expression of P16, CD10, BCL-6, MUM-1 and proliferation marker (Ki-67) was demonstrated by immunohistochemistry. Fluorescence in situ hybridization (FISH) was employed to detect p16 alterations. Results: P16 overexpression was shown in 45.7% (32/70) of the DLBCL cases, and was significantly correlated with CD10 (p = 0.022) and germinal centre B-cell-like (GCB) phenotype (p = 0.022). High expression of P16 was inversely associated with high proliferative activity (Ki-67 index greater than 75%) (p = 0.020). Of the 47 cases that yielded interpretable FISH results, 57.4% (27/47) showed deletions of p16 and 27.7% (13/47) showed gains of p16. P16 overexpression and p16 deletions were mutually exclusive (p = 0.019). There was no correlation between P16 overexpression and p16 gains (p = 0.621). Conclusions: The GCB and non-GCB subgroups of DLBCLs show different patterns of P16 expression. High levels of P16 may mitigate tumour cell proliferation. Gains of p16 do not necessarily increase P16 protein expression.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>20332669</pmid><doi>10.1159/000278291</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Aged
Aged, 80 and over
Cell Proliferation
Cells
Child
Child, Preschool
Cyclin-Dependent Kinase Inhibitor p16 - genetics
Cyclin-Dependent Kinase Inhibitor p16 - metabolism
Female
Fluorescence in situ hybridization
Gene expression
Gene Expression Regulation, Neoplastic
Genes, p16
Genotype & phenotype
Humans
Immunoenzyme Techniques
In Situ Hybridization, Fluorescence
Lymphoma
Lymphoma, Large B-Cell, Diffuse - genetics
Lymphoma, Large B-Cell, Diffuse - metabolism
Lymphoma, Large B-Cell, Diffuse - pathology
Male
Middle Aged
Original Paper
Proteins
Tumors
title Expression and Alteration of p16 in Diffuse Large B Cell Lymphoma
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