12 research outputs found
Supplementary Tables S1 and S2 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplementary Table 1. Demographic, clinical, and plasma cfDNA data for the patients included in the study deconvoluted by Sun et al. (3) and Moss et al. (43) by QP and NNLS. NA, not available.
Supplementary Table 2. Demographic, clinical, and plasma cfDNA data for the patients included in the study deconvoluted by Loyfer et al. (44) NA, not available.</p
Figure S8 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 8. The relative contribution of cfDNA from various tissues before and ~24 hours after surgery for pancreatic cancer. * p < 0.05, ** p < 0.01, *** p < 0.001</p
Figure S3 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 3. Fraction of plasma cfDNA that could be attributed to high molecular weight genomic DNA in samples analyzed by RealSeqS.</p
Figure S9 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 9. Plasma AST and ALT levels before and ~24 hours after surgery for pancreatic cancer. AST and ALT levels substantially increased in all five patients.</p
Figure S7 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 7. The amount of total cfDNA before and after surgery in patients with pancreatic cancer.</p
Figure S5 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 5. Methylation profiles using quadratic programming vs. non-negative least- squares regression using the reference matrix described in Moss et al. (43). Pearson’s correlation coefficient and p values are presented at the bottom of this figure, showing the derived contributions from each of the 25 tissue types that could be assessed.</p
Figure S1 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 1. Overview of the patient samples included in the present study.</p
Figure S10 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 10. In silico mixing experiments (N = 10) of buffy coat bisulfite sequencing data with liver (A), lung (B), colon epithelial cell (C), and left atrium (D) bisulfite sequencing data deconvoluted using the Moss et al. (43) reference matrix and quadratic programming shows excellent agreement between predicted and actual fractional contribution.</p
Supplementary Notes 1-5 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplementary Notes 1-5. Supplementary Note 1: Origins of cell-free DNA. Supplementary Note 2: Leukocyte Lysis. Supplementary Note 3: Reference datasets and deconvolution algorithms used to interpret whole genome bisulfite sequencing data. Supplementary Note 4: Turnover rates. Supplementary Note 5: Relationships between ctDNA and tissue specific cfDNA in cancer patients.</p
Figure S4 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
Supplemental Figure 4. Methylation profiles using quadratic programming vs. non-negative least- squares regression using the reference matrix described in Sun et al. (3). Pearson’s correlation coefficient and p values are presented at the bottom of this figure, showing the derived contributions from each of the 12 tissue types that could be assessed.</p