Article Figures & Data
Figures
- Figure 1.
LOH-based hierarchical clustering of HGSC. A, LOH-based clustering of 47 ovarian cancers. The clustering dendrogram is depicted at the top, and each column represents the genome-wide status of heterozygosity; yellow, region of retained heterozygosity; blue, region of LOH. Chromosome location is indicated on the vertical axis. B, box plots depicting fraction of LOH (FLOH) for HGSC in cluster Lo and cluster HiA and HiB from A. The horizontal line within the box is the median value of FLOH. C, box plots showing number of chromosomal segments containing allelic imbalance (AI) per cancer genome.
- Figure 2.
Genome-wide prevalence of LOH in HGSC. Chromosome location is on the horizontal axis. Horizontal red lines represent a threshold P value ≤ 0.05 by genome-wide permutation. A, genome-wide prevalence of LOH. B, frequency of genome-wide copy number gain and loss. Frequency of absolute copy gain ≥3 (red) and copy loss ≤1.4 (blue) for each SNP is shown on the vertical axis. The light vertical lines separate the short and long arms.
- Figure 3.
BRCA1 promoter methylation, FLOH and BRCA1 transcript levels in HGSC. A, frequency of BRCA1 promoter methylation in HGSC. P value was obtained by using 2-way contingency analysis and Chi square. B, BRCA1 promoter methylation and FLOH in HGSC. FLOH was compared between cases with BRCA1 promoter methylation (B1M) and cases without BRCA1 methylation (B1UM). C, BRCA1 promoter methylation and BRCA1 mRNA levels. P value is determined by Mann–Whitney U tests.
- Figure 4.
Genomic profiles of HGSC in AOCS and TCGA SNP array datasets. A, hierarchical clustering and visualization based on LOH patterns in the AOCS dataset. B, hierarchical clustering in the TCGA dataset.
- Figure 5.
FLOH and rate of resistance to platinum-based chemotherapy in subclusters of HGSC from three independent cohorts. A and B, chemotherapy resistance and mean FLOH in tumors from subclusters Lo, HiA, and HiB for patients with stage III disease and residual disease ≤1 cm after optimal debulking, pooled from the 3 cohorts. C and D, results from all patients including those with stages II and IV cancer and residual disease >1 cm. P values are derived from Chi square analysis using 2-way contingency tables in A and C, and from t test in B and D. *, **, and *** represent P values <0.05, <0.001, and <0.00001, respectively.
- Figure 6.
Progression-free survival (PFS) after surgery and chemotherapy. Kaplan–Meier analysis was done in patients with stage III disease and 1 cm or less residual cancer after surgery; all patients received platinum and taxane combination chemotherapy. A, the AOCS cohort; B, the Boston cohort. Patients were divided into quartiles of FLOH (from low to high) in their tumors. P values are calculated by log-rank test. Patients who were progression-free at the time of last follow-up were censored (+).
Additional Files
Supplementary Data
Files in this Data Supplement:
- Supplementary Figures 1 - 9 - PDF file, 366K, Supplementary Figures 1-9: 1. LOH patterns on different array platforms, 2. Allelic imbalance in LOH clusters, 3. LOH clustering breast cancer, 4. LOH and copy number prevalence in breast cancer, 5. Chemotherapy resistance and FLOH in three cohorts, 6. Chemotherapy resistance and FLOH with or without BRCA mutations, 7. PFS regardless of stage and residual disease, 8. PFS with or without BRCA mutations, 9. BRCA1 expression and FLOH.
- Supplementary Tables 4 - 8 - PDF file, 80K, Supplementary Tables 4-8: 4. LOH patterns in three cohorts, 5A&B. FLOH and chemotherapy resistance in three cohorts, 6. BRCA mutations in the AOCS, 7. Univariate and multivariate analysis of platinum resistantce, 8. PFS in LOH subclusters and patients with BRCA mutations.
- Supplementary Tables 1 - 3 - XLS file, 509K, supplementary Tables 1-3: 1. Information from the Boston cohort, 2. Information from AOCS cohort, 3. Information from TCGA.
Volume 18, Issue 20
