scholarly journals Private Payer and Medicare Coverage for Circulating Tumor DNA Testing: A Historical Analysis of Coverage Policies From 2015 to 2019

2020 ◽  
Vol 18 (7) ◽  
pp. 866-872
Author(s):  
Michael P. Douglas ◽  
Stacy W. Gray ◽  
Kathryn A. Phillips
Keyword(s):  
Clinical Care ◽  
Genomic Medicine ◽  
Circulating Tumor Dna ◽  
Significant Shift ◽  
Study Objective ◽  
Panel Testing ◽  
Medicare Coverage ◽  
Pan Cancer ◽  
Tumor Dna ◽  
Private Payer

Background: Clinical adoption of the sequencing of circulating tumor DNA (ctDNA) for cancer has rapidly increased in recent years. This sequencing is used to select targeted therapy and monitor nonresponding or progressive tumors to identify mechanisms of therapeutic resistance. Our study objective was to review available coverage policies for cancer ctDNA–based testing panels to examine trends from 2015 to 2019. Methods: We analyzed publicly available private payer policies and Medicare national coverage determinations and local coverage determinations (LCDs) for ctDNA-based panel tests for cancer. We coded variables for each year representing policy existence, covered clinical scenario, and specific ctDNA test covered. Descriptive analyses were performed. Results: We found that 38% of private payer coverage policies provided coverage of ctDNA-based panel testing as of July 2019. Most private payer policy coverage was highly specific: 87% for non–small cell lung cancer, 47% for EGFR gene testing, and 79% for specific brand-name tests. There were 8 final, 2 draft, and 2 future effective final LCDs (February 3 and March 15, 2020) that covered non–FDA-approved ctDNA-based tests. The draft and future effective LCDs were the first policies to cover pan-cancer use. Conclusions: Coverage of ctDNA-based panel testing for cancer indications increased from 2015 to 2019. The trend in private payer and Medicare coverage is an increasing number of coverage policies, number of positive policies, and scope of coverage. We found that Medicare coverage policies are evolving to pan-cancer uses, signifying a significant shift in coverage frameworks. Given that genomic medicine is rapidly changing, payers and policymakers (eg, guideline developers) will need to continue to evolve policies to keep pace with emerging science and standards in clinical care.

scholarly journals Clinical Utilization, Utility, and Reimbursement for Expanded Genomic Panel Testing in Adult Oncology

2020 ◽  
pp. 1038-1048
Author(s):  
Susan J. Hsiao ◽  
Anthony N. Sireci ◽  
Danielle Pendrick ◽  
Christopher Freeman ◽  
Helen Fernandes ◽  
...  
Keyword(s):  
Clinical Practice ◽  
High Risk ◽  
Clinical Utility ◽  
Medical Center ◽  
Clinical Care ◽  
Genomic Medicine ◽  
Tumor Board ◽  
Panel Testing ◽  
Pan Cancer ◽  
Cancer Panel

PURPOSE The routine use of large next-generation sequencing (NGS) pan-cancer panels is required to identify the increasing number of, but often uncommon, actionable alterations to guide therapy. Inconsistent coverage and variable payment is hindering NGS adoption into clinical practice. A review of test utilization, clinical utility, coverage, and reimbursement was conducted in a cohort of patients diagnosed with high-risk cancer who received pan-cancer panel testing as part of their clinical care. MATERIALS AND METHODS The Columbia Combined Cancer Panel (CCCP), a 467-gene panel designed to detect DNA variations in solid and liquid tumors, was performed in the Laboratory of Personalized Genomic Medicine at Columbia University Irving Medical Center. Utilization was characterized at test order. Results were reviewed by a molecular pathologist, followed by a multidisciplinary molecular tumor board where clinical utility was classified by consensus. Reimbursement was reviewed after payers provided final coverage decisions. RESULTS NGS was performed on 359 high-risk tumors from 349 patients. Reimbursement data were available for 246 cases. The most common reason providers ordered CCCP testing was for patients diagnosed with a treatment-resistant or recurrent tumor (n = 214; 61%). Findings were clinically impactful for 229 cases (64%). Molecular alterations that may inform future therapy in the event of progression or relapse were found in 42% of cases, and a targeted therapy was initiated in 23 cases (6.6%). The majority of tests were denied coverage by payers (n = 190; 77%). On average, insurers reimbursed 10.75% of the total NGS service charge. CONCLUSION CCCP testing identified clinically impactful alterations in 64% of cases. Limited coverage and low reimbursement remain barriers, and broader reimbursement policies are needed to adopt pan-cancer NGS testing that benefits patients into clinical practice.

scholarly journals Pan-cancer circulating tumor DNA detection in over 10,000 Chinese patients

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yongliang Zhang ◽  
Yu Yao ◽  
Yaping Xu ◽  
Lifeng Li ◽  
Yan Gong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Circulating Tumor Dna ◽  
Small Cell ◽  
Chinese Patients ◽  
Plasma Samples ◽  
Small Cell Lung ◽  
Pan Cancer ◽  
Tumor Dna

AbstractCirculating tumor DNA (ctDNA) provides a noninvasive approach to elucidate a patient’s genomic landscape and actionable information. Here, we design a ctDNA-based study of over 10,000 pan-cancer Chinese patients. Using parallel sequencing between plasma and white blood cells, 14% of plasma cell-free DNA samples contain clonal hematopoiesis (CH) variants, for which detectability increases with age. After eliminating CH variants, ctDNA is detected in 73.5% of plasma samples, with small cell lung cancer (91.1%) and prostate cancer (87.9%) showing the highest detectability. The landscape of putative driver genes revealed by ctDNA profiling is similar to that in a tissue-based database (R2 = 0.87, p < 0.001) but also shows some discrepancies, such as higher EGFR (44.8% versus 25.2%) and lower KRAS (6.8% versus 27.2%) frequencies in non-small cell lung cancer, and a higher TP53 frequency in hepatocellular carcinoma (53.1% versus 28.6%). Up to 41.2% of plasma samples harbor drug-sensitive alterations. These findings may be helpful for identifying therapeutic targets and combined treatment strategies.

Comparative circulating tumor DNA levels for KRAS mutations in patients with nonresectable pancreatic cancer.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 288-288 ◽  
Author(s):  
Julia S. Johansen ◽  
Cecile Rose T. Vibat ◽  
Dan Calatayud ◽  
Benny Vittrup Jensen ◽  
Jane Preuss Hasselby ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Pancreatic Cancer ◽  
Cancer Patients ◽  
Kras Mutation ◽  
Circulating Tumor Dna ◽  
Resectable Pancreatic Cancer ◽  
Kras Mutations ◽  
Study Objective ◽  
Wide Range ◽  
Tumor Dna

288 Background: Non-resectable pancreatic cancer patients have a wide range of median time for overall survival (OS). Currently there is a lack of diagnostic tools to predict patient outcome at diagnosis. KRAS mutations are present in the vast majority of pancreatic tumors. The study objective was to determine if quantitative baseline and longitudinal monitoring of KRAS mutations from plasma circulating tumor DNA (ctDNA) could be used to stratify patients for predicting outcome. Methods: Plasma was prospectively collected from the Danish BIOPAC study for non-resectable pancreatic cancer patients undergoing treatment with gemcitabine or FOLFIRINOX. Feasibility of monitoring ctDNA KRAS mutations was assessed in 10 patients with long OS (median 493 days; range 360-1031) and 10 patients with short OS (median 66 days; range 21-136). KRAS G12A/C/D/R/S/V, and G13D mutations were PCR enriched, sequenced by massively parallel deep sequencing, quantitated and standardized by reporting number of copies detected per 105 genome equivalents (GE). Results: In a pilot study of 20 patients, all 18 patients with evaluable DNA had detectable KRAS mutations. Of 18 patients, 12 had baseline plus longitudinal time points (7 short, 5 long OS). Mutant KRAS copies were higher for short OS (median=994; range 0-34305 copies/105 GE) vs. with long OS (median 196; range, 34-278 copies/105 GE). Longitudinally, KRAS mutation levels remained mostly low with long OS (last time point median 204; range 8-873 copies/105 GE) vs. short OS where levels increased or remained high (median 2363; range 71-47919 copies/105 GE). Identical KRAS mutations were consistently detected for a given patient with short OS. However, long OS patients had variable KRAS mutations in longitudinal analysis. Conclusions: High levels of ctDNA KRAS mutations at diagnosis and post-treatment elevation of KRAS mutations were more associated with short OS. Different levels of KRAS mutation at diagnosis may predict patient outcome and could reflect distinct underlying tumor biology. Expansion of this prospective-retrospective biomarker cohort will be reported.

scholarly journals Association of circulating tumor DNA (ctDNA) detection in metastatic renal cell carcinoma (mRCC) with tumor burden.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 4582-4582 ◽  
Author(s):  
Manuel Caitano Maia ◽  
Paulo Gustavo Bergerot ◽  
Nazli Dizman ◽  
JoAnn Hsu ◽  
Jeremy Jones ◽  
...  
Keyword(s):  
Checkpoint Inhibitors ◽  
Clinical Care ◽  
Stage Iv ◽  
Circulating Tumor Dna ◽  
Continuous Variable ◽  
Tumor Burden ◽  
Variable Number ◽  
Clinical Annotation ◽  
Scan Data ◽  
Tumor Dna

4582 Background: In a series of 224 pts with advanced RCC, we have previously reported ctDNA detection in 79% of pts (Pal SK et al ASCO GU 2017). Clinical factors associated with detection are unknown. Methods: Data was obtained from pts with radiographically confirmed stage IV RCC who received ctDNA profiling as a part of routine clinical care using a CLIAA-certified platform evaluating 73 genes. Detailed clinical annotation was performed, including assessment of Heng risk score, previous and current treatments and calculation of tumor burden using scan data most proximal to ctDNA assessment. Tumor burden was equated to the sum of longest diameter (SLD) of all measurable lesions. Results: 32 pts were assessed (M:F 19:13) with a median age of 62 (range, 34-84). 25 pts, 4 pts and 3 pts had clear cell, sarcomatoid and papillary histology, respectively. Heng risk was good, intermediate and poor in 13, 18 and 1 pt, respectively. Pts received a median of 2 lines of prior tx. Specifically, 4 pts were not on active therapy (tx), 16 pts were receiving VEGF-directed tx, 6 pts were receiving checkpoint inhibitors (CPIs) and 6 pts were receiving combined VEGF/CPI tx. ctDNA was detected in 16 pts (50%) with a median of 2 genomic alterations (GAs) per pt. No associations were found between Heng risk, histology or tx type and presence/absence of ctDNA. However, pts with detectable ctDNA had a higher SLD compared to pts with no detectable ctDNA (99.6 vs 50.0 mm; P = 0.041). Furthermore, when evaluated as a continuous variable, number of GAs was correlated with SLD (P = 0.023). TP53 and VHL alterations were the most frequent GAs in this series, each occurring in 25% of the cohort. All 3 pts with brain metastases had ctDNA detected. Conclusions: With the caveat of a limited sample size, it appears that SLD (a surrogate for tumor burden) is higher in mRCC pts with detectable ctDNA, and increasing SLD may be associated with a higher number of GAs. Further validation of these findings may help identify appropriate pts for ctDNA assessment and maximize yield in clinical practice.

scholarly journals Evaluation of the Oncomine Pan-Cancer Cell-Free Assay for Analyzing Circulating Tumor DNA in the Cerebrospinal Fluid in Patients with Central Nervous System Malignancies

2021 ◽  
Vol 23 (2) ◽  
pp. 171-180
Author(s):  
Mauli Shah ◽  
Takeshi Takayasu ◽  
Soheil Zorofchian Moghadamtousi ◽  
Octavio Arevalo ◽  
Melissa Chen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Cancer Cell ◽  
Circulating Tumor Dna ◽  
Pan Cancer ◽  
Tumor Dna

scholarly journals KRAS A146 Mutations Are Associated With Distinct Clinical Behavior in Patients With Colorectal Liver Metastases

2021 ◽  
pp. 1758-1767
Author(s):  
Iris van 't Erve ◽  
Nina J. Wesdorp ◽  
Jamie E. Medina ◽  
Leonardo Ferreira ◽  
Alessandro Leal ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Kras Mutation ◽  
Clinical Care ◽  
Prospective Trial ◽  
Predictive Biomarker ◽  
Circulating Tumor Dna ◽  
Kras Mutations ◽  
Molecular Subgroup ◽  
Computed Tomography Images ◽  
Tumor Dna

PURPOSE Somatic KRAS mutations occur in approximately half of the patients with metastatic colorectal cancer (mCRC). Biologic tumor characteristics differ on the basis of the KRAS mutation variant. KRAS mutations are known to influence patient prognosis and are used as predictive biomarker for treatment decisions. This study examined clinical features of patients with mCRC with a somatic mutation in KRAS G12, G13, Q61, K117, or A146. METHODS A total of 419 patients with colorectal cancer with initially unresectable liver-limited metastases, who participated in a multicenter prospective trial, were evaluated for tumor tissue KRAS mutation status. For the subgroup of patients who carried a KRAS mutation and were treated with bevacizumab and doublet or triplet chemotherapy (N = 156), pretreatment circulating tumor DNA levels were analyzed, and total tumor volume (TTV) was quantified on the pretreatment computed tomography images. RESULTS Most patients carried a KRAS G12 mutation (N = 112), followed by mutations in G13 (N = 15), A146 (N = 12), Q61 (N = 9), and K117 (N = 5). High plasma circulating tumor DNA levels were observed for patients carrying a KRAS A146 mutation versus those with a KRAS G12 mutation, with median mutant allele frequencies of 48% versus 19%, respectively. Radiologic TTV revealed this difference to be associated with a higher tumor load in patients harboring a KRAS A146 mutation (median TTV 672 cm3 [A146] v 74 cm3 [G12], P = .036). Moreover, KRAS A146 mutation carriers showed inferior overall survival compared with patients with mutations in KRAS G12 (median 10.7 v 26.4 months; hazard ratio = 2.5; P = .003). CONCLUSION Patients with mCRC with a KRAS A146 mutation represent a distinct molecular subgroup of patients with higher tumor burden and worse clinical outcomes, who might benefit from more intensive treatments. These results highlight the importance of testing colorectal cancer for all KRAS mutations in routine clinical care.

Abstract B028: Pan-cancer landscape of somaticBRCA1andBRCA2mutations detected in circulating tumor DNA

2019 ◽  
Author(s):  
Carin R Espenschied ◽  
Jennifer L Yen ◽  
Tracy Nance ◽  
Richard B Lanman ◽  
Kimberly C Banks
Keyword(s):  
Circulating Tumor Dna ◽  
Pan Cancer ◽  
Tumor Dna
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