Analysis of 1p, 19q, 9p, and 10q as prognostic markers for high-grade
astrocytomas using fluorescence in situ hybridization on tissue microarrays
from Radiation Therapy Oncology Group trials

Brat, Daniel J.; Seiferheld, W.; Perry, Arie; Hammond, Elizabeth H.; Murray, Kevin; Schulsinger, Alan; Mehta, Minesh P.; Curran, Walter J.

doi:10.1215/s1152851703000231

Cited by 59 publications

(51 citation statements)

References 29 publications

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“…10 In astrocytomas (grade II/III), LOH 1p and 19q is reported to range from 0 to 17%. 11 The current study revealed isolated 19q and combined 1p/19q LOH in 17.6% of DA, similar to the Western literature. LOH 1p/19q was encountered in a solitary case of AA, which could perhaps be attributed to the small sample size.…”

Section: Discussionsupporting

confidence: 89%

Correlation of histomorphologic prognostic markers and proliferative index with loss of heterozygosity 1p/19q and MGMT status in diffusely infiltrating gliomas

Deb

Mani

Sudumbrekar

et al. 2013

Medical Journal Armed Forces India

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LOH 1p/19qMGMT MIB-1LI a b s t r a c t Background: Loss of heterozygosity (LOH)1p/19q, and epigenetic silencing of O 6 -methylguanine-DNAmethyltransferase (MGMT ) gene, displayed promising role as predictive and prognostic markers in brain tumours. The present study correlated both with conventional histomorphologic prognostic markers and proliferative index in diffusely infiltrating gliomas (DIG). Methods:Tissues from 45 patients were evaluated for LOH1p/19q using polymerase chain reaction based microsatellite analysis; and for MGMT using immunohistochemistry. Results were correlated with age, histologic type, WHO grade, and proliferation index.Results: Mean MIB-1 LI showed significant correlation with tumour grade. MGMT-staining in grade II and IV tumours were 31.1% and 16.8%, respectively, while in DA and GBM it was 88.2% and 19.0%, respectively, which were statistically significant. Sixteen cases showed LOH 1p and/or 19q of which 10 (5 oligodendroglial, 3 GBM, AA, DA) had combined LOH; while three each showed 1p (all GBM) and 19q (2 DA and GBM) loss. In the MIB-1LI 5% and >5% groups LOH 1p and/or 19q was encountered in 6 and 10 cases, respectively. A significant inverse association was noted between LOH with MGMT. Available online at www.sciencedirect.com jo urn al ho mep age: www .e lsev ie r. co m/ lo cate/ mj afi m e d i c a l j o u r n a l a r m e d f o r c e s i n d i a 6 9 ( 2 0 1 3 ) 2 2 8 e2 3 6

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Section: Discussionsupporting

confidence: 89%

Correlation of histomorphologic prognostic markers and proliferative index with loss of heterozygosity 1p/19q and MGMT status in diffusely infiltrating gliomas

Deb

Mani

Sudumbrekar

et al. 2013

Medical Journal Armed Forces India

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“…3,24,26 In contrast, loss of 19q has been established to be a hallmark of glioblastomas that may develop through a secondary multistep transformation process, and this abnormality was associated with long-term survival. 3,16,24,26 Nevertheless, various aberrations of chromosome 19 were found in the small minority of tumors from our current series, suggesting that these molecular alterations play no significant role in the evolution of pediatric glioblastomas, as well as codeletion of 1p/19q loci that was identified only in one tumor specimen.…”

Section: Discussionmentioning

confidence: 53%

“…[16][17][18][19][20] In the current study, we applied FISH technique for molecular profiling of pediatric glioblastomas, keeping in the mind its applicability to paraffin-embedded specimens and the presence of well-established criteria for reproducible results interpretation. To the best of our knowledge, this is a first FISH analysis of a representative cohort of pediatric glioblastomas.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, approximately 40% of pediatric glioblastomas from the current series FISH in pediatric glioblastomas A Korshunov et al revealed loss of 1p36 locus, although the frequency of such alteration in adult high-grade astrocytic gliomas does not exceed 15%. [16][17][18][19][22][23][24][25][26] These findings allow one to suggest the presence of tumor suppressor gene(s) located on 1p36, an alteration that may be involved in carcinogenesis of pediatric glioblastomas, as it has been identified in embryonal neuroepithelial tumors of childhood. 3 Chromosome 19 is one of the most commonly altered chromosomes in glioblastomas, while gain of 19 was previously found closely related with older patients and adverse outcomes.…”

Section: Discussionmentioning

confidence: 99%

“…Signal detection was performed as described previously. [16][17][18][19][20] Briefly, samples showing sufficient FISH efficiency (490% nuclei with signals) were evaluated. Two independent referees (AK and RS) were unaware of clinical data.…”

Section: Patient Population and Pathological Analysismentioning

confidence: 99%

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Clinical utility of fluorescence in situ hybridization (FISH) in nonbrainstem glioblastomas of childhood

et al. 2005

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Astrocytic gliomas are the most common pediatric brain tumors; however, nonbrainstem glioblastomas are extremely rare compared with their adult counterparts. Little information is available on the clinical significance of various molecular markers in pediatric grade IV astrocytomas. The current study was focused on the molecular analysis and clinico-pathological correlations in a set of 44 tumor samples obtained from pediatric patients with nonbrainstem glioblastomas. Fluorescence in situ hybridization (FISH) with a set of 10 commercial chromosome probes (1p36, 1q25, centromere (CEP)7, EGFR, CEP9, 9p21/p16, CEP10, 10q23/PTEN, 19p13, and 19q13) was performed. Disclosed molecular abnormalities, in descending order of frequency, included polysomy 7 (72%), loss of 10q23 (61%), loss of 9p21 (52%), loss of 1p36 (41%), gain of 1q25 (25%), polysomy 9 (16%), EGFR amplification (9%), loss of 19q13 (5%), polysomy 19 (5%), and codeletion 1p36/19q13 (2%). The overall survival time was markedly shorter only for those patients whose lesions harbored deletion of 10q23/ PTEN locus (log-rank test; P ¼ 0.00007). By multivariate analysis, only loss of 10q23 locus reached an independent level of prognostic value (hazard ratio ¼ 2.88; P ¼ 0.01). There were no significant differences in patient survival for other molecular abnormalities. In conclusion, a FISH analysis of 10q23 dosage should be recommended as an ancillary laboratory method that allows further clinical subdivision of pediatric glioblastomas.

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The prognostic relevance of molecular alterations in glioblastomas for patients age < 50 years

Korshunov

Sycheva

Golanov

2005

Cancer

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BACKGROUNDIn patients with glioblastoma, age < 50 years was identified as a consistent prognostic variable. In addition, the prognosis for these patients may be determined by a complex interaction between age and genetic alterations. The objective of the current study was the molecular analysis of glioblastomas from adult patients age < 50 years (“young adults”).METHODSThe authors analyzed a set of 189 glioblastoma specimens. Fluorescence in situ hybridization was performed with a set of 10 chromosome probes (1p36, 1q25, centomere probe 7 [CEP7], 7p12/epidermal growth factor receptor gene (EGFR), CEP9, 9p21/p16, CEP10, 10q23/phosphatase and tesnin homolog gene (PTEN), 19p13, and 19q13).RESULTSPatient age < 40 years was associated strongly with a favorable prognosis. Patients age ≥ 40 years frequently showed EGFR amplification, loss of 9p, loss of 10q, and gain of chromosome 19. The patients with − 19q were age < 40 years. The survival was shorter for patients with EGFR amplification, gain of chromosome 7, loss of 9p, loss of 10q, and gain of chromosome 19. In contrast, the patients who had tumors with gain of chromosome 9 or loss of 19q had more favorable outcomes. In a multivariate analysis, gain of chromosome 9 (P = 0.026) and loss of 10q23 (P = 0.007) reached the level of independent prognostic value. In addition, the prognostic value of molecular alterations in patients age < 40 years and patients age > 40 years were examined separately. Consequently, EGFR amplification, − 9p, and + 9 were significant for both age groups, whereas gain of chromosome 7 and loss of 10q showed clinical importance only among patients age > 40 years.CONCLUSIONSAdult patients age < 50 years with glioblastoma had molecularly distinct disease, and the age‐dependent heterogeneity seen on the chromosomal level also applied at the clinical level. Cancer 2005. © 2005 American Cancer Society.

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Analysis of 1p, 19q, 9p, and 10q as prognostic markers for high-grade astrocytomas using fluorescence in situ hybridization on tissue microarrays from Radiation Therapy Oncology Group trials

Cited by 59 publications

References 29 publications

Correlation of histomorphologic prognostic markers and proliferative index with loss of heterozygosity 1p/19q and MGMT status in diffusely infiltrating gliomas

Correlation of histomorphologic prognostic markers and proliferative index with loss of heterozygosity 1p/19q and MGMT status in diffusely infiltrating gliomas

Clinical utility of fluorescence in situ hybridization (FISH) in nonbrainstem glioblastomas of childhood

The prognostic relevance of molecular alterations in glioblastomas for patients age < 50 years

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