Not All KRAS is the Same: Shifting from the Overall KRAS Status to Exon, Codon, and Point KRAS Mutations

Erlotinib plus gemcitabine is one of the standard chemotherapies for unresectable pancreatic cancer. Pancreatic cancer has the highest frequency of KRAS gene mutations among human cancers, and some studies suggest that KRAS status might be a predictive biomarker for anti-epidermal growth factor receptor treatment. However, the reliability of this biomarker has not been confirmed. Here, we evaluated the impact of KRAS mutations in pancreatic cancer patients treated with first line gemcitabine-based chemotherapy. 23 patients treated with gemcitabine-based chemotherapy whose KRAS status could be examined from primary or metastatic lesions were enrolled. KRAS mutations were analyzed by sequencing codons 12 and 13. We retrospectively evaluated the correlation between KRAS status, and prognosis and treatment efficacy. Patient characteristics were as follows: median age 68 years, male/female=6/17, PS 0/1=9/14, TNM stage III/IV=1/22, and gemcitabine alone/erlotinib plus gemcitabine=13/10. Among the 23 patients, KRAS codon 12 was mutated in 15, one of whom also had mutation on codon 13. Median progression-free survival (PFS) and overall survival (OS) of all patients were 4.3 months (95% confidence interval (CI): 3.1 to 5.4) and 8.1 months (95% CI: 5.9 to 10.0; events in 96%), respectively. KRAS status showed no association with PFS (p=0.310), OS (p=0.934), or the efficacy of treatment with (p=0.833) or without erlotinib (p=0.478). Thus, in this study, there was no correlation between KRAS status and the efficacy of first line chemotherapy with gemcitabine with or without erlotinib. Identification of a rationale for personalized medicine in pancreatic cancer will require further exploratory prospective studies.

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In Situ Detection and Quantification of AR-V7, AR-FL, PSA, and KRAS Point Mutations in Circulating Tumor Cells

Clinical Chemistry ◽

10.1373/clinchem.2017.281295 ◽

2018 ◽

Vol 64 (3) ◽

pp. 536-546 ◽

Cited By ~ 40

Author(s):

Amin El-Heliebi ◽

Claudia Hille ◽

Navya Laxman ◽

Jessica Svedlund ◽

Christoph Haudum ◽

...

Keyword(s):

Androgen Receptor ◽

Tumor Cells ◽

Circulating Tumor Cells ◽

Specific Antigen ◽

Padlock Probe ◽

Castration Resistant Prostate Cancer ◽

Kras Mutations ◽

Padlock Probes ◽

Kras Status

Abstract BACKGROUND Liquid biopsies can be used in castration-resistant prostate cancer (CRPC) to detect androgen receptor splice variant 7 (AR-V7), a splicing product of the androgen receptor. Patients with AR-V7-positive circulating tumor cells (CTCs) have greater benefit of taxane chemotherapy compared with novel hormonal therapies, indicating a treatment-selection biomarker. Likewise, in those with pancreatic cancer (PaCa), KRAS mutations act as prognostic biomarkers. Thus, there is an urgent need for technology investigating the expression and mutation status of CTCs. Here, we report an approach that adds AR-V7 or KRAS status to CTC enumeration, compatible with multiple CTC-isolation platforms. METHODS We studied 3 independent CTC-isolation devices (CellCollector, Parsortix, CellSearch) for the evaluation of AR-V7 or KRAS status of CTCs with in situ padlock probe technology. Padlock probes allow highly specific detection and visualization of transcripts on a cellular level. We applied padlock probes for detecting AR-V7, androgen receptor full length (AR-FL), and prostate-specific antigen (PSA) in CRPC and KRAS wild-type (wt) and mutant (mut) transcripts in PaCa in CTCs from 46 patients. RESULTS In situ analysis showed that 71% (22 of 31) of CRPC patients had detectable AR-V7 expression ranging from low to high expression [1–76 rolling circle products (RCPs)/CTC]. In PaCa patients, 40% (6 of 15) had KRAS mut expressing CTCs with 1 to 8 RCPs/CTC. In situ padlock probe analysis revealed CTCs with no detectable cytokeratin expression but positivity for AR-V7 or KRAS mut transcripts. CONCLUSIONS Padlock probe technology enables quantification of AR-V7, AR-FL, PSA, and KRAS mut/wt transcripts in CTCs. The technology is easily applicable in routine laboratories and compatible with multiple CTC-isolation devices.

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KRAS mutation analysis in cetuximab-treated advanced stage non-small cell lung cancer (NSCLC): SWOG experience with S0342 and S0536

Journal of Clinical Oncology ◽

10.1200/jco.2009.27.15_suppl.8022 ◽

2009 ◽

Vol 27 (15_suppl) ◽

pp. 8022-8022 ◽

Cited By ~ 3

Author(s):

P. C. Mack ◽

W. S. Holland ◽

M. Redman ◽

P. N. Lara ◽

L. J. Snyder ◽

...

Keyword(s):

Colorectal Cancer ◽

Copy Number ◽

Kinase Inhibitors ◽

Response Rate ◽

Poor Response ◽

Phase Iii ◽

Phase Ii Trials ◽

Kras Mutations ◽

Kras Status ◽

Predictive Role

8022 Background: KRAS mutations occur in NSCLC with a frequency of 15–25% and have been associated with a poor response to EGFR tyrosine kinase inhibitors. In colorectal cancer, benefit from the EGFR-targeted monoclonal antibody cetuximab is largely limited to patients (pts) whose tumors are KRAS wild-type (WT). However, in cetuximab-treated NSCLC, a predictive role for KRAS mutations has not been established. We evaluated KRAS status in specimens from two cetuximab-based front-line multicenter SWOG phase II trials in advanced NSCLC. Methods: DNA extracted from archival tumor and plasma specimens from S0342 (carboplatin-paclitaxel plus sequential vs. concurrent cetuximab) and S0536 (carboplatin-paclitaxel-cetuximab-bevacizumab) was analyzed for KRAS mutations by micro-dissection/sequencing and/or Scorpion-ARMS (DxS LTD). Results: For S0342, 45 archival tissues and 90 plasma specimens were analyzed. Combined, KRAS mutations were detected in 24% of pts. No differences between mutant and WT tumors were observed for response rate (p=0.62) or progression-free survival (PFS; p=0.65). Overall survival (OS) was non-significantly higher for pts with WT vs. mutant KRAS [median OS: 11 vs. 8 mo.; p=0.39]. When evaluated with EGFR copy number analysis conducted previously (JCO 10:3351, 2008), pts with both low EGFR copy number and mutant KRAS trended towards a worse OS [7 mo. vs. 17 mo. for all others, p=0.08, n=31]. For S0536, 6/26 pt specimens (23%) harbored KRAS mutations. In the limited sample set available from S0536, no associations were observed between KRAS status and clinical outcome [response rate: p=0.83; PFS: p=0.93; OS p=0.89]. Conclusions: These data suggest that KRAS mutations may not play a significant predictive role for cetuximab-based therapy in NSCLC, contrary to colorectal cancer. KRAS analysis in recently completed phase III trials of chemotherapy ± cetuximab will be of interest to confirm these observations. Trends in favorable OS in pts with WT KRAS may reflect prognostic effects of KRAS mutations. [Table: see text]

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KRAS mutations and relation to prognosis in patients operated for localized pancreatic cancer and other periampullary cancers

Journal of Clinical Oncology ◽

10.1200/jco.2009.27.15_suppl.e15618 ◽

2009 ◽

Vol 27 (15_suppl) ◽

pp. e15618-e15618

Author(s):

N. A. Schultz ◽

A. Roslind ◽

I. J. Christensen ◽

M. Gaustadnes ◽

J. S. Johansen ◽

...

Keyword(s):

Pancreatic Cancer ◽

Ampullary Cancer ◽

Duodenal Cancer ◽

Cancer Tissue ◽

Kras Mutations ◽

T Stage ◽

Kras Status ◽

Exon 1 ◽

N Stage ◽

Cox Analysis

e15618 Background: Prognostic biomarkers in patients with pancreatic cancer might direct patients to optimal treatment. We studied the prognostic value of KRAS mutations in patients operated for pancreatic and other periampullary cancers. Methods: Retrospective study of 328 patients who were operated with a Whipples procedure at a single HBP-center during the period August 1976 to May 2008. For the present pilot study cancer tissue blocks were collected from 58 patients (31 men, 27 women, median age 64, range 33–81 years, ASA 1–3). All had localized pancreatic (n=26), ampullary (n=26) or duodenal cancer (n=6) and were operated during the period June 2001 to May 2008. 32 patients died (3 within the first month after operation and were excluded). Median follow-up time was 41 months (range 7–90). KRAS mutations in exon 1 and 2 were determined by LightScanner analysis (Idaho Technology). Results: KRAS mutations were found in 32 (55%) of the patients; 16 (62%) patients with pancreatic cancer, 13 (50%) with ampullary cancer and in 3 (50%) with duodenal cancer. KRAS status was neither associated with type of cancer (p=0.68), TNM stage (T stage p=0.64, N stage p=0.31). The median survival time for all patients was 22 months (KRAS mutation: 21, 95% CI: 10–40; Wildtype: not reached yet). Univariate Cox analysis showed that T stage (TNM) (1: HR=0.09, 95% CI: 0.02–0.48 p=0.004; 2: HR=0.18, 0.06- 0.51, p=0.0013; 3: HR=0.26, 0.09–0.71, p=0.0089) was a prognostic factor of OS. KRAS status (HR=0.70, 0.33–1.49, p=0.36) and N stage (TNM) (HR=0.53, 0.25–1.11, p=0.09) were not significant factors of OS, but there is a strong tendency for both factors. Conclusions: KRAS mutations are frequent in patients with localized pancreatic, ampullary and duodenal cancers. Preliminary analysis of 58 patients out of our cohort of 328 patients indicate that KRAS mutations may be a marker of overall survival and time to progression. No significant financial relationships to disclose.

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Colorectal cancer (CRC) KRAS mutational status and response to chemotherapy in absence of influence of epidermal growth factor receptor (EGFR) monoclonal antibody (MAb) therapy.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.4_suppl.504 ◽

2012 ◽

Vol 30 (4_suppl) ◽

pp. 504-504

Author(s):

Nirit Yarom ◽

Nana Boame ◽

Gillian Gresham ◽

David Hill ◽

Derek J. Jonker

Keyword(s):

Small Sample Size ◽

Tumour Response ◽

Stage Iv ◽

Small Sample ◽

Kras Mutations ◽

Triple Combination Therapy ◽

Mutational Status ◽

Response To Chemotherapy ◽

Kras Status ◽

Refractory State

504 Background: KRAS mutations (MUT), present in ~40% of CRC, predict benefit from EGFR MAb treatment. The effect of mutation status on benefit from chemotherapy alone is less clear. Methods: Following ethics approval, 223 CRC patients with known KRAS status treated at a single institution were retrospectively analyzed for response to chemotherapy prior to initiation of EGFR MAb therapy. Tumour response rate and progression-free survival (PFS) were determined retrospectively. Given chemotherapy sequencing variability, a measure of the time to chemotherapy-refractory state (TTCR) was defined as time from start of first line therapy to progression on all drugs; ie fluoropyrimidines (F), irinotecan (I), and oxaliplatin (O), +/- bevacizumab (B). Results: Patients were median age 60 years (25-86), 58/42% male/female, 38% rectal or rectosigmoid, 18% liver-only metastases, 45.6% stage I-III and 54.4% stage IV at initial diagnosis, 43% prior adjuvant chemotherapy, 43/57% KRAS MUT/wild-type(WT) status. With a median follow-up of 27 months, 64 (29%) are alive. TTCR did not vary by KRAS status, with median 16.7 vs 14.8 months in WT vs MUT status patients, respectively, HR 0.85 [0.65-1.12], p=0.26. Overall survival (which now includes influence of any subsequent EGFR MAb therapy, received by 76/126 (60%) of KRAS WT status patients) did not differ significantly by KRAS status, with median survival 34.3 vs 29.2 months for WT vs MUT status, respectively, 0.79 [0.58-1.08], p=0.14. Conclusions: For most treatment strategies KRAS status did not affect 1st line PFS or time to chemotherapy-refractory state. However, for patients who received triple combination therapy, MUT status was associated with early progression. Small sample size, chance or some yet-to-be-elucidated molecular interaction may account for this finding. [Table: see text]

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Two parallel randomized phase II studies of selumetinib (S) and erlotinib (E) in advanced non-small cell lung cancer selected by KRAS mutations.

Journal of Clinical Oncology ◽

10.1200/jco.2013.31.15_suppl.8026 ◽

2013 ◽

Vol 31 (15_suppl) ◽

pp. 8026-8026 ◽

Cited By ~ 15

Author(s):

Corey Allan Carter ◽

Arun Rajan ◽

Eva Szabo ◽

Sean Khozin ◽

Anish Thomas ◽

...

Keyword(s):

Combination Therapy ◽

Single Agent ◽

Objective Response ◽

Standard Of Care ◽

Primary Resistance ◽

Kras Mutations ◽

Phase Ii Studies ◽

Platinum Based Chemotherapy ◽

Kras Status ◽

Never Smokers

8026 Background: KRAS mutations are present in 20% of NSCLC and are associated with primary resistance to erlotinib (E). KRAS mutations result in constitutive activation of the Ras/Raf/MEK/ERK pathway. Selumetinib (S) (AZD6244, ARRY-142886) is a selective and uncompetitive inhibitor of MEK kinase. Preclinical studies demonstrated increased activity in NSCLC cell lines using S+E regardless of KRAS status. Methods: Advanced NSCLC patients with progressive disease after platinum based chemotherapy +/- one other treatment were stratified by KRAS status, which was centrally assessed using macrodissection and pyrosequencing for all mutations involving codons 12, 13, and 61. Patients were randomized to receive either the standard of care E or a combination of S+E in KRAS wild type (wt) and S alone or S+E in patients with KRAS mutations. Single agent E and S were administered orally at 150 mg daily and 75 mg twice daily respectively. Combination dosing were S 150 mg every morning and E 100 mg every evening. The primary endpoint for the KRAS wt group was PFS and for the KRAS mutant group objective response rate. Results: From March 2010 to January 2013, 79 patients screened; 78 enrolled: KRAS mutant, 39; KRAS wt, 40; M/F (39:39); median age: 64 years (33-84); median WHO PS 1(0-2); 66 former and 13 never smokers; 67 adenocarcinoma, 9 squamous cell. Three patients died of complications prior to first evaluation (1 coronary disease, 1 pulmonary fibrosis, and 1 disease progression) of which none were related to S. Dose reductions occurred in 5% E, 40% S, and 56% E+S. Most grade 3/4 AEs occurred in combination therapy; diarrhea (23%), fatigue (23%) lymphopenia (13%), myositis (10%), dyspnea (10%), rash (7%). Discontinuation due to AEs was 8% all occurring in S+E cohorts. Conclusions: This study failed to show improvement of combination therapy over single agent in KRAS wt and mutant patients. Toxicity was increased in the combination arms. Interestingly, the KRAS mutant cohort had longer PFS than KRAS wt patients, although not statistically significant (p=0.11). Clinical trial information: NCT01229150. [Table: see text]

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Phase I study of RAD001 (everolimus), cetuximab, and irinotecan as second-line therapy in metastatic colorectal cancer (mCRC)

Journal of Clinical Oncology ◽

10.1200/jco.2009.27.15_suppl.e15115 ◽

2009 ◽

Vol 27 (15_suppl) ◽

pp. e15115-e15115

Author(s):

S. Sharma ◽

T. Reid ◽

S. Hoosen ◽

C. Garrett ◽

J. Beck ◽

...

Keyword(s):

Colorectal Cancer ◽

Phase I ◽

Clin Oncol ◽

Dose Level ◽

Phase I Study ◽

Open Label ◽

Kras Mutations ◽

Kras Status ◽

Dose Limiting Toxicity ◽

Unacceptable Toxicity

e15115 Background: The PI3K/AKT/mTOR pathway is frequently dysregulated in colorectal cancer (Cancer Res 2005;65:11227). In a phase I study in patients with advanced solid tumors, everolimus an oral mTOR inhibitor demonstrated clinical benefit including a partial response in pts with colorectal cancer (J Clin Oncol 2008;26:1603–10; J Clin Oncol 2008; 26:1588–95). Methods: This open-label, multicenter phase I study uses a Bayesian logistic model to identify feasible doses of everolimus + irinotecan + cetuximab. Adult pts with mCRC progressing despite prior 5-FU/oxaliplatin (FOLFOX) or capecitabine/oxaliplatin (XELOX) plus bevacizumab (if standard practice) were treated using a sequential dose escalation scheme (Table). Dose decisions were driven by the probability of dose-limiting toxicity (DLT) in the first 2 cycles. Dose level decisions were based on maximizing the probability that end-of-cycle-2 DLT rate would be within the targeted toxicity interval (20% to <35%) and minimizing the risk of over-dosing (< 5% risk of unacceptable toxicity and < 25% risk of excessive/unacceptable toxicity). Results: 18 pts were treated from April ‘07 to August ‘08, 5 pts at dose level A1 and 13 pts at dose level B1. Two DLTs (G3 rash on cycle 2 day 1 lasting > 7 days and G3 mucositis on cycle 1 day 14 lasting > 7 days, 1 pt each) were reported in 4 evaluable pts at dose level A1. No DLTs were reported in 7 evaluable patients at dose level B1. Conclusions: At dose level B1 everolimus in combination with irinotecan and cetuximab was generally well tolerated. The study was stopped due to changes in clinical practice based on emerging data indicating that cetuximab has limited efficacy in mCRC patients with KRAS mutations and that efficacy data favors daily RAD001 over weekly dosing. Patients in this study were treated with cetuximab irrespective of KRAS status. [Table: see text] [Table: see text]

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BRAF and KRAS mutations in penile cancer and their correlation with clinical features.

Journal of Clinical Oncology ◽

10.1200/jco.2011.29.7_suppl.221 ◽

2011 ◽

Vol 29 (7_suppl) ◽

pp. 221-221 ◽

Cited By ~ 1

Author(s):

C. M. Valverde ◽

J. Hernandez-Losa ◽

C. Ferrandiz-Pulido ◽

R. Morales ◽

C. Suarez ◽

...

Keyword(s):

Penile Cancer ◽

Developed Countries ◽

Advanced Stage ◽

Clinicopathologic Features ◽

Braf Mutations ◽

Kras Mutations ◽

Histologic Subtype ◽

Small Series ◽

Kras Status

221 Background: Penile cancer is a rare disease in developed countries. While surgery may be curative for patients with localized disease, for metastatic patients systemic chemotherapy may offer palliation with usually short-lived responses. Thus, new options in this setting are needed. Retrospective series have reported EGFR overexpression in more than 90% of the cases and also interesting results of EGFR directed therapies in these patients have been comunicated. The role of KRAS status or other molecular markers as prognostic or predictive factors remains unclear. The aim of this study was to determine the prevalence of BRAF and KRAS somatic mutations in penile cancer and their correlation with clinicopathologic features. Methods: We analyzed 28 samples collected from de archives of the Pathology Department at our institution from 1996 to 2009. The DNAs were extracted from FFPE blocks by Biorobot EZ1 following the manufacturer protocol of the EZ1-DNA Tissue kit (Qiagen). KRAS and BRAF mutations were amplified with specific primers, and sequenced by Sanger with Bigdye terminator v3.1 Cycle Sequencing Kit. Medical records were reviewed for clinical data. Results: No BRAF mutations were found, but we identified somatic missense mutations in the KRAS gene (all activating G12D mutations) in 6/27 samples (22%, one not evaluable). Median age at diagnosis (73 vs. 71), grade and histologic subtype did not differ between wt and mutated (mt) patients. There was a trend toward a more advanced stage at diagnosis in mt versus wt : 33 versus 47% stage I, 16 versus 9% stage II and 50 versus 38% stage III respectively. 2/6 mt patients died (due to other causes) as did 5/21 wt patients (3 of them because of disease progression). Conclusions: BRAF mutations seem not involved in the EGFR pathway in penile carcinomas. The prevalence of KRAS mutations was unexpectedly high in our series and mt patients tended to be diagnosed at a more advanced stage. Unfortunately, no correlation was found with other clinicopathologic features, including overall survival in our small series. These results suggest a role of KRAS mutation in the development of these carcinomas and support the importance to determine KRAS status in patients to be treated with anti-EGFR based therapies. No significant financial relationships to disclose.

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Retrospective cohort study on the safety and efficacy of cetuximab for metastatic colorectal cancer patients: HGCSG0901—Analysis of predictive markers.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.4_suppl.683 ◽

2012 ◽

Vol 30 (4_suppl) ◽

pp. 683-683

Author(s):

Kazuteru Hatanaka ◽

Satoshi Yuki ◽

Hiroshi Nakatsumi ◽

Takahiro Kogawa ◽

Hiraku Fukushima ◽

...

Keyword(s):

Overall Survival ◽

Statistical Tests ◽

Progression Free Survival ◽

Predictive Marker ◽

Skin Toxicity ◽

Kras Mutations ◽

Free Survival ◽

Egfr Expression ◽

Kras Status ◽

Expression Status

683 Background: The anti-EGFR antibody Cetuximab (Cmab) do not provide therapeutic effect to patients with KRAS mutations. It has been reported that there is no correlation between the staining intensity of EGFR and efficacy of Cmab. Moreover, the previous studies have suggested that the intensity of skin toxicity that occurs after the administration is a predictive marker of Cmab. Methods: Of 269 cases registered in the multi-institutional retrospective study (HGCSG0901) treated with Cmab, 252 patients for 3rd line or after treatment line were analyzed. Each degree of skin toxicity, KRAS mutation status and EGFR expression status, respectively, were analyzed for response rates, progression-free survival (PFS) and overall survival (OS). The Response Evaluation in Solid Tumors (RECIST) criteria version 1.0 was used to assess tumor response. The Kaplan–Meier method was used to determine PFS and OS. Log-rank test was used to compare each regimen in terms of PFS and OS. All statistical tests were performed using SPSS. Results: KRAS status: wild type (WT)/mutant type (MT): 135/32, EGFR status: positive/negative: 210/38, Skin toxicity: Grade 0/1/2/3: 31/50/128/43. Analysis of KRAS status: Response rate: WT 23.7%/MT 6.3% (p=0.028), Progression-free survival: WT 4.8 months /MT 2.1 months (p<0.001), Overall survival: WT 9.9 months/MT 5.3 months (p=0.003). There was a significant correlation between the degree of skin toxicity and efficacy. However, EGFR expression status showed no differences in efficacy. Conclusions: Here, we reported the results of efficacy analysis for each predictive marker of Cmab. As with previous reports, patients with KRAS mutations did not benefit from Cmab. Degree of skin toxicity was a useful indicator of effectiveness after starting treatment, whereas EGFR status was not effective predictor in daily practice setting.

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Determina KRAS: A consolidated project.

Journal of Clinical Oncology ◽

10.1200/jco.2012.30.4_suppl.428 ◽

2012 ◽

Vol 30 (4_suppl) ◽

pp. 428-428 ◽

Cited By ~ 1

Author(s):

Jesus Garcia-Foncillas

Keyword(s):

Kras Mutation ◽

Treatment Decision ◽

Predictive Biomarker ◽

Major Advance ◽

Kras Mutations ◽

Nccn Guidelines ◽

Treatment Decision Making ◽

Kras Status ◽

Patient Will ◽

National Networks

428 Background: The identification of KRAS mutation status as a predictive biomarker for the activity of anti-EGFR in mCRC patients, was the start of the personalize medicine. ASCO recognized it as a major advance in 2008 and it also gave a clinical opinion so every candidate for anti-EGFR therapy should be tested for KRAS mutations. NCCN guidelines recommends to do it at the first diagnose of metastatic disease. KRAS status testing was no widely available in Spain by 2008. The project Determina KRAS was developed in order to provide access to this test throughout the country to any mCRC patient. Methods: Five well known Spanish centres were trained and provided with equipment so they could analyze KRAS status in a five working day period. First centre was initiated in July 2008, being the last one in October 2008. A validated KRAS mutation kit (DxS Ltd, Manchester, UK) which identifies 7 different somatic mutations located in codons 12 and 13 using allele-specific real-time polymerase chain reaction was used. Results: 15.330 samples from mCRC patients have been analyzed since July 2008. 53,7% samples showed wild type KRAS status. G12D mutation was the most frequent mutation observed in general (35,1% of all mutation). G13D mutation was the most frequent of the codon 13 mutation, with a 20,2% of the global mutations. Conclusions: KRAS status testing allows to patients with mCRC receive a personalized medicine. KRAS status testing is essencial for treatment decision-making in mCRC and access to it must be guaranteed for any patient. The determination of biomarkers to choose the most effective treatment for each patient will be the future of oncology. These futures assessments must be available for all patients through national Networks, as the Determina KRAS project has made with KRAS testing.

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