Look deeper with Signatera
The personalized, tumor-informed surveillance test that detects molecular residual disease (MRD)
earlier than previously possible to optimize clinical decision making across the continuum of cancer care.
Signatera is the first and only personalized, tumor-informed assay for early MRD detection
Deciding what comes next after definitive therapy for CRC can be a dilemma. Did resection get all the cancer, or might molecular residual disease be lurking? Is adjuvant treatment working? How likely is the cancer to recur?
Imagine knowing about the presence or absence of residual disease, down to the molecular level, at any time along the continuum of care. And imagine how awareness of MRD status might empower committed patients to share in the decisions made on that journey.
This is what the Signatera residual disease test provides — a predictive marker of relapse risk, available to you and every patient many months earlier than standard imaging or monitoring can reveal.
Watch how Signatera looks deeper to detect circulating tumor DNA (ctDNA)
Signatera is the only commercially available test to detect MRD in solid tumors1-4
Personalized,
tumor-informed assay
One-time, primary tissue sample and matched normal tissue is required for whole exome sequencing and personalized test design.
Ultrasensitive
ctDNA detection
Signatera is designed to detect ctDNA of somatic and truncal variants to optimize sensitivity. Tumor-informed method enables filtering of CHIP mutations to decrease false positive rates.
Optimized for
longitudinal monitoring
Once the patient’s personalized test has been designed, only a blood sample is needed each subsequent time Signatera is ordered for the program or Surveillance program.
Test report indicates the presence or absence of detectable ctDNA
Signatera is not designed for early cancer screening, nor to identify actionable mutations for cancer therapy selection.
Unlike ctDNA assays used for liquid biopsies, Signatera detects ctDNA to indicate the presence of MRD.
Signatera looks deeper — so you can know sooner
Risk stratification validated across multiple tumor types1-4*
88% sensitivity to relapse
Average lead time 8.7 mos
89% sensitivity to relapse
Average lead time 9.5 mos
92% sensitivity to relapse
Average lead time 4.0 mos
100% sensitivity to relapse
Average lead time 2.8 mos
*ctDNA positive is defined as positive at any time point at or before clinical relapse.
ctDNA negative is defined as negative in all longitudinal time points.
Use Signatera after surgery to evaluate need for adjuvant chemotherapy or to avoid unnecessary treatment
Signatera MRD status outperforms known clinicopathologic risk factors in predicting relapse1
Signatera is better than staging, tumor grade, and DNA mismatch repair (MMR) status in identifying patients who may potentially benefit from additional therapy versus continued observation.1,5-7
*ctDNA positive is defined as positive at any time point at or before clinical relapse.
ctDNA negative is defined as negative in all longitudinal time points.
Signatera was clinically validated in a study with 125 patients (Stage I-III CRC). A total of 795 plasma samples were collected before surgery, postoperatively at day 30, and every 3 months.
Plasma samples were collected for up to 3 years after surgery (median 12.5 months).
Signatera helps you optimize risk stratification after surgery and monitor treatment response during adjuvant chemotherapy
of patients with a positive
Signatera result will relapse
without additional treatment1
Determine recurrence with confidence during routine follow-up testing
Identifying recurrence while interventions can still be curative remains a challenge in CRC.8
With current surveillance tools and biomarkers, only 10% of metastases are treated with curative intent.9
Signatera looks deeper
The only personalized, tumor informed assay for detecting MRD to provide an early predictive marker of relapse to inform each milestone throughout a patient’s continuum of care.
References
1.Reinert T, Henriksen TV, Christensen E, et al. Analysis of plasma cell-free DNA by ultradeep sequencing in patients with stages I to III colorectal cancer. JAMA Oncol. 2019;5(8):1124-1131. 2.Coombes RC, Page K, Salari R, et al. Personalized detection of circulating tumor DNA antedates breast cancer metastatic recurrence. Clin Cancer Res. 2019;25(14):4255-4263. 3.Abbosh C, Birkbak NJ, Wilson GA, et al. Phylogenetic ctDNA analysis depicts early-stage lung cancer evolution. Nature. 2017;545:446-451. 4.Christensen E, Birkenskamp-Demtroder K, Sethi H, et al. Early detection of metastatic relapse and monitoring of therapeutic efficacy by ultra-deep sequencing of plasma cell-free DNA in patients with urothelial bladder carcinoma. J Clin Oncol. 2019;37(18):1547-1557. 5.Sinicrope FA, Foster NR, Thibodeau SN, et al. DNA mismatch repair status and colon cancer recurrence and survival in clinical trials of 5 Fluorouracil-based adjuvant therapy. J Natl Cancer Inst. 2011;103(11):863–875. 6.Yothers G, O’Connell MJ, Lopatin M, et al. Validation of the 12-gene colon cancer recurrence score in NSABP C-07 as a predictor of recurrence in patients with stage II and III colon cancer treated with fluorouracil and leucovorin (FU/LV) and FU/LV plus oxaliplatin. J Clin Oncol. 2013;31(36):4512-4519. 7.Aoyama, Oba K, Honda M, et al. Impact of postoperative complications on the colorectal cancer survival and recurrence: analyses of pooled individual patients’ data from three large phase III randomized trials. Cancer Med. 2017;6(7):1573–1580. 8.Young PE, Womeldorph CM, Johnson EK, et al. Early detection of colorectal cancer recurrence in patients undergoing surgery with curative intent: current status and challenges. J Cancer. 2014;5(4):262-271. 9.Elferink MA, de Jong KP, Klaase JM, et al. Metachronous metastases from colorectal cancer: a population-based study in North-East Netherlands. Int J Colorectal Dis. 2015;30(2):205-212. 10.Purandare NC, Dua SG, Arora A, et al. Colorectal cancer — patterns of locoregional recurrence and distant metastases as demonstrated by FDG PET/CT. Indian J Radiol Imaging. 2010;20(4):284-288.