20q13 and cyclin D1 in ovarian carcinomas. Analysis by fluorescencein situ hybridization

Diebold, Joachim; Mösinger, Kerstin; Peiró, Gloria; Pannekamp, Uwe; Kaltz, Christine; Baretton, Gustavo; Meier, W.; Löhrs, U.

doi:10.1002/(sici)1096-9896(200004)190:5<564::aid-path569>3.0.co;2-l

Cited by 42 publications

(22 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…20q13.2 Gain has been identified as an independent prognostic marker that indicate reduced survival in breast and ovarian cancer (25,26). Intravesical recurrence after UUT-TCC reportedly occurred in 16% to 50% cases (2 -8), which is in agreement with our results.…”

Section: Resultssupporting

confidence: 92%

Chromosome 20q13.2 Gain May Predict Intravesical Recurrence after Nephroureterectomy in Upper Urinary Tract Urothelial Tumors

Akao

Matsuyama²,

Yamamoto³

et al. 2006

Clinical Cancer Research

View full text Add to dashboard Cite

Purpose: Amplification or gain of copy number of chromosome 20q13.2 has been implicated as a causal factor for chromosome instability.We investigated the impact of chromosomal instability and its causative molecular markers, 20q13.2 gain and centrosome amplification, on patient outcome in upper urinary tract transitional cell carcinoma (UUT-TCC). Experimental Design: The number of centrosomes was assessed by immunohistochemistry. Numerical aberrations of chromosomes 7, 9, and 17 that allowed the estimation of chromosomal instability and 20q13.2 gain were evaluated by fluorescence in situ hybridization in 96 frozen specimens from UUT-TCC and compared with clinicopathologic background and patient outcome. Results: Chromosomal instability, 20q13.2 gain, and centrosome amplification were detected in 62 of 96 (64.6%), 61of 96 (63.5%), and 45 of 90 (50.0%) tumors, respectively. 20q13.2 Gain was significantly associated with tumor stage (P = 0.042), chromosomal instability (P < 0.0001), and centrosome amplification (P < 0.0001). Kaplan-Meier analysis showed that 20q13.2 gain was strongly associated with intravesical recurrence-free survival in all patients (P = 0.0050), as well as in patients with grade 2 tumors (P = 0.0011, log-rank test). On multivariate analysis, 20q13.2 gain was found to be the sole independent prognostic factor predicting subsequent intravesical recurrence (hazard ratio, 1.65; 95% confidence interval, 1.03^2.90; P = 0.036). Conclusions: 20q13.2 gain was strongly associated with a reduced time to intravesical recurrence in all patients. Our data suggest that 20q13.2 gain may be a predictive marker of intravesical recurrence in patients with UUT-TCC.

show abstract

Section: Resultssupporting

confidence: 92%

Chromosome 20q13.2 Gain May Predict Intravesical Recurrence after Nephroureterectomy in Upper Urinary Tract Urothelial Tumors

Akao

Matsuyama²,

Yamamoto³

et al. 2006

Clinical Cancer Research

View full text Add to dashboard Cite

show abstract

“…In comparison, some other genes showed higher rates of amplifications in these cancers. For example, the amplification of ERBB2 ranges (0-66%), 25,26 EGFR (3.65-12%), 27,28 CCND1 (0-19%), [29][30][31] C-MYC up to 54.5, 25,32,33 and KRAS (31%). 33 The significant frequency of estrogen receptor positivity in ovarian cancers had prompted treatment efforts using hormonal therapy early on.…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor gene amplification occurs rarely in ovarian cancer

et al. 2009

View full text Add to dashboard Cite

Amplification of the gene encoding estrogen receptor-a occurs in about 20% of breast cancers and is an important mechanism for estrogen receptor overexpression in this tumor type. In ovarian cancer, overexpression of estrogen receptor protein has been described in more than two thirds of cases. To study a potential role of estrogen receptor-a gene amplification for estrogen receptor overexpression in ovarian cancer, a tumor tissue microarray containing 428 ovarian cancers was analyzed by fluorescence in situ hybridization for estrogen receptor-a gene amplification and immunohistochemistry for estrogen receptor expression. The estrogen receptor-a gene status was successfully determined in 243 of 428 arrayed cancers. Estrogen receptor gene amplification was found in 5 of 243 (2%) of tumors. Amplification levels were usually low, with 4-8 estrogen receptor-a gene copies. However, one case had a high-level amplification, with more than 30 estrogen receptor-a gene copies. Keywords: ovarian cancers; estrogen receptor-a gene; estrogen receptors; fluorescence in situ hybridization; immunohistochemistry Worldwide, ovarian cancer is the fifth most frequent malignant tumor in women and the most common cause of death among cancers of the reproductive system.1 Prognosis is generally poor as these cancers are often detected in late stage. The median overall survival in these patients is 24-38 months after diagnosis. 2Treatment options include surgical removal of the tumor mass with a maximal reduction of the peritoneal cancer mass in case of local tumor extension. In addition, topical and systemic cytotoxic therapy is applied. Ovarian cancer belongs to the group of cancers with frequent expression of steroid hormone receptors. Depending on the study estrogen receptor expression has been reported in 25-86% of ovarian cancers with the highest percentages reported in endometroid and serous subtypes.3-16 Accordingly, endocrine therapy is a recognized option in the treatment of chemoresistant ovarian cancer after the failure of first-and second-line therapies. However, not all estrogen receptor-positive ovarian cancers respond to antiestrogen therapy, and it was suggested that it might be because of the facts that most of the studies have been retrospective, small in size without adequate selection of the patients and generally used hormonal therapy as a last-line therapy for the refractory or resistant ovarian cancers. Moreover, concerning tamoxifen, it has not been definitely clarified whether it only acts as a pure estrogen antagonist in ovarian tissue, or it has also an agonist effects. 17-21In breast cancer, we had recently described estrogen receptor-a (ESR1) gene amplification as a frequent mechanism for estrogen receptor overexpression. More than 20% of breast cancers showed ESR1 gene amplification and more than 15% additional cases low-level ESR1 gene copy number gains.22 Preliminary data also suggested that ESR1 amplified breast cancers may exhibit a high responsiveness to tamoxifen. To determine, whether ESR1 amplificat...

show abstract

“…Under microscopic control, excess normal tissue was removed by microdissection, and tumor cell nuclei were extracted by the method of Hyytinen et al (25). The in situ hybridization was performed as described previously (26). The hybridization mix was prepared according to the manufacturer's protocol with DNA-specific probes for chromosomes 12, 17, 22, and X (Vysis, Downers Grove, IL).…”

Section: Fluorescence In Situ Hybridizationmentioning

confidence: 99%

Characteristic Pattern of Genetic Aberrations in Ovarian Granulosa Cell Tumors

Mayr¹,

Kaltz-Wittmer²,

Arbogast³

et al. 2002

Mod Pathol

View full text Add to dashboard Cite

The cytogenetic abnormalities of granulosa cell tumors (GCT) of the ovary are only partially known. Up to now, mainly numerical chromosomal aberrations have been described. Therefore we performed a comprehensive study on paraffin-embedded material of 20 GCT (17 adult, 3 juvenile; patient age between 16 and 78 y) combining comparative genomic hybridization (CGH); fluorescence in situ hybridization (FISH) using DNA-specific probes for chromosome 12, 17, 22, and X; DNA cytometry; and immunohistochemistry (inhibin, p53, Ki67).By DNA cytometry, 16 of 20 tumors (80%) were diploid. However, 6 of 16 diploid tumors (37%) showed aberrations by FISH. FISH revealed monosomy 22 in 8/18 cases (40%); trisomy 12 in 5/20 (25%); monosomy X in 2/20 (10%); and loss of chromosome 17 in one case (5%). The main findings by CGH were gains of chromosomes 12 (6 cases, 33%) and 14 (6 cases, 33%) and losses of chromosomes 22 (7 cases, 35%) and X (1 case, 5%), mostly comprising whole chromosomes or chromosome arms. Inhibin and p53 were expressed in 100% and 95% of the tumors, respectively. The Ki67 index ranged from 0% to 61%. Neither immunohistochemistry, nor DNA cytometry and molecular genetic analysis, provided statistically significant prognostic information.In summary, our study reveals a distinctive pattern of cytogenetic alterations in GCT. Our observations confirm earlier reports that trisomy 12 and 14 are frequent aberrations; however, monosomy 22 seemingly is even more prevalent. Granulosa cell tumors of the ovary (GCT) are much less common than epithelial ovarian cancer. These tumors account for 1.5% of all ovarian neoplasms and for 6% of malignant ovarian tumors. Sixty-five percent of patients are postmenopausal; Ͻ5% are prepubertal. The juvenile granulosa cell tumor is a distinctive form of GCT that occurs almost exclusively in children and young adults. More than 95% of the GCT are unilateral and confined to the ovary.

show abstract

20q13 and cyclin D1 in ovarian carcinomas. Analysis by fluorescencein situ hybridization

Cited by 42 publications

References 42 publications

Chromosome 20q13.2 Gain May Predict Intravesical Recurrence after Nephroureterectomy in Upper Urinary Tract Urothelial Tumors

Chromosome 20q13.2 Gain May Predict Intravesical Recurrence after Nephroureterectomy in Upper Urinary Tract Urothelial Tumors

Estrogen receptor gene amplification occurs rarely in ovarian cancer

Characteristic Pattern of Genetic Aberrations in Ovarian Granulosa Cell Tumors

Contact Info

Product

Resources

About