BIRC2 amplification in squamous cell carcinomas of the uterine cervix.
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BIRC2 amplification in squamous cell carcinomas of the uterine cervix. / Choschzick, Matthias; Tabibzada, A M; Gieseking, Frederike; Wölber, Linn; Jänicke, Fritz; Sauter, Guido; Simon, Ronald.
in: VIRCHOWS ARCH, Jahrgang 461, Nr. 2, 2, 2012, S. 123-128.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - BIRC2 amplification in squamous cell carcinomas of the uterine cervix.
AU - Choschzick, Matthias
AU - Tabibzada, A M
AU - Gieseking, Frederike
AU - Wölber, Linn
AU - Jänicke, Fritz
AU - Sauter, Guido
AU - Simon, Ronald
PY - 2012
Y1 - 2012
N2 - Oncogene amplification is a key step in cell transformation towards malignancy. Chromosomal aberrations involving the long arm of chromosome 11, including amplifications at 11q13 and 11q22, have been previously reported in cervical cancer. While the role of the CCND1 gene as the driver gene for 11q13 amplification is well established in different tumor types, the significance of the 11q22 amplicon is less clear. The 11q22 amplicon corresponds to several putative target genes including the apoptose inhibitor BIRC2, recently detected as amplified in cervical cancer cell lines. To better understand the distribution and frequency of 11q amplification sites in uterine cervical carcinomas, we analyzed BIRC2 and CCND1 copy number changes using fluorescence in situ hybridization in a tissue microarray containing 238 cervical cancers. High-level amplification of BIRC2 was found in 12.9 % of tumors. Amplification of BIRC2 in cervical carcinomas was homogeneous as shown in corresponding whole tissue sections of amplified tumors at the tissue microarray. BIRC2 amplification was significantly more frequent than CCND1 amplification (2.1 %) in our cohort (p?<?0.01), and amplification of both genes were independent from each other. BIRC2 amplification was associated with younger-patient age (p?<?0.05) and squamous cell differentiation (p?=?0.025) of cervix carcinomas. However, BIRC2 copy number changes were not related to tumor stage, grading and nodal status of cervical cancers. In conclusion, BIRC2 is amplified in a subset of squamous cell carcinoma of the uterine cervix. Further studies are necessary to evaluate possible prognostic effects of BIRC2 copy number gains in cervical carcinomas.
AB - Oncogene amplification is a key step in cell transformation towards malignancy. Chromosomal aberrations involving the long arm of chromosome 11, including amplifications at 11q13 and 11q22, have been previously reported in cervical cancer. While the role of the CCND1 gene as the driver gene for 11q13 amplification is well established in different tumor types, the significance of the 11q22 amplicon is less clear. The 11q22 amplicon corresponds to several putative target genes including the apoptose inhibitor BIRC2, recently detected as amplified in cervical cancer cell lines. To better understand the distribution and frequency of 11q amplification sites in uterine cervical carcinomas, we analyzed BIRC2 and CCND1 copy number changes using fluorescence in situ hybridization in a tissue microarray containing 238 cervical cancers. High-level amplification of BIRC2 was found in 12.9 % of tumors. Amplification of BIRC2 in cervical carcinomas was homogeneous as shown in corresponding whole tissue sections of amplified tumors at the tissue microarray. BIRC2 amplification was significantly more frequent than CCND1 amplification (2.1 %) in our cohort (p?<?0.01), and amplification of both genes were independent from each other. BIRC2 amplification was associated with younger-patient age (p?<?0.05) and squamous cell differentiation (p?=?0.025) of cervix carcinomas. However, BIRC2 copy number changes were not related to tumor stage, grading and nodal status of cervical cancers. In conclusion, BIRC2 is amplified in a subset of squamous cell carcinoma of the uterine cervix. Further studies are necessary to evaluate possible prognostic effects of BIRC2 copy number gains in cervical carcinomas.
KW - Adult
KW - Humans
KW - Aged
KW - Female
KW - Middle Aged
KW - Aged, 80 and over
KW - Young Adult
KW - Immunohistochemistry
KW - Neoplasm Staging
KW - In Situ Hybridization, Fluorescence
KW - Tissue Array Analysis
KW - Gene Amplification
KW - Neoplasm Grading
KW - Carcinoma, Squamous Cell/genetics/pathology
KW - Cyclin D1/genetics
KW - Inhibitor of Apoptosis Proteins/genetics
KW - Uterine Cervical Neoplasms/genetics/pathology
KW - Adult
KW - Humans
KW - Aged
KW - Female
KW - Middle Aged
KW - Aged, 80 and over
KW - Young Adult
KW - Immunohistochemistry
KW - Neoplasm Staging
KW - In Situ Hybridization, Fluorescence
KW - Tissue Array Analysis
KW - Gene Amplification
KW - Neoplasm Grading
KW - Carcinoma, Squamous Cell/genetics/pathology
KW - Cyclin D1/genetics
KW - Inhibitor of Apoptosis Proteins/genetics
KW - Uterine Cervical Neoplasms/genetics/pathology
M3 - SCORING: Journal article
VL - 461
SP - 123
EP - 128
JO - VIRCHOWS ARCH
JF - VIRCHOWS ARCH
SN - 0945-6317
IS - 2
M1 - 2
ER -
