September 29, 2026
BRAF V600E Mutation PCR Assay: Single-Reaction ARMS Real-Time PCR Genotyping of Tumour Tissue for Thyroid Nodule Triage, Colorectal Cancer Prognosis and BRAF-Directed Therapy Selection
HONG KONG, China — September 29, 2026 — Red Sun Medizone today announced the availability of a CE-marked in vitro diagnostic (IVD) real-time PCR kit for the detection of the BRAF V600E mutation (exon 15, c.1799T>A, p.Val600Glu) in tumour tissue. A single mutation-specific reaction, read against an external-standard reaction from a two-tube strip, delivers a result in one laboratory day on a standard real-time PCR platform. In a three-centre registration study of 1,333 thyroid, colorectal and lung cancer specimens compared against DNA sequencing, the assay achieved 100% sensitivity, 98.75% specificity and a kappa agreement of 0.99.
Key facts at a glance
- Analyte: BRAF V600E — exon 15, nucleotide 1799 T>A, p.Val600Glu
- Specimen: formalin-fixed paraffin-embedded (FFPE) sections containing thyroid, colorectal or lung lesions, with block age not exceeding 3 years; fresh or frozen tissue preferred where available
- Chemistry: ARMS allele-specific PCR with TaqMan hydrolysis probes and HotStart Taq DNA polymerase
- Detection channels: FAM (mutation and external-standard signal); HEX or VIC (internal control)
- Reporting rule: ΔCt = [mutation Ct] − [external-standard Ct]; positive when the amplification curve is S-shaped and ΔCt ≤ 10 — a single cut-off
- Limit of detection: 1% mutant allele against a 30 ng/µL wild-type genomic background
- Repeatability: Ct coefficient of variation ≤ 5% across ten parallel replicates
- Clinical verification: 1,333 thyroid, colorectal and lung cancer specimens across three tertiary referral centres against DNA sequencing — sensitivity 100%, specificity 98.75%, total coincidence 99.32%, kappa 0.99
- Handling: two tubes per specimen; DNA ≤ 300 ng per reaction; sample valid within 7 freeze–thaw cycles
- Turnaround time: specimen to interpreted report inside one laboratory day
- Kit configuration: 24 tests per kit — one mutation reaction mix plus one external-standard reaction mix
- Regulatory status: CE-marked IVD under Directive 98/79/EC, with an IVDR (EU) 2017/746 transition application; IVDR Class C, professional use
The clinical problem: one mutation, three separate decisions
BRAF V600E is unusual among molecular targets in that a single result changes three different clinical conversations. In thyroid disease it is a diagnostic rule-in that can convert an indeterminate cytology into a surgical plan. In colorectal cancer it is an adverse prognostic marker and the entry criterion for a dedicated combination regimen. In melanoma and anaplastic thyroid cancer it is the gate to BRAF-directed therapy.
Thyroid: the problem is deciding which nodule is cancer. Thyroid cancer is among the most commonly diagnosed cancers worldwide, with a large and rising incidence set against comparatively low mortality — a profile in which over-treatment, not under-detection, is the dominant risk [1]. Fine-needle aspiration resolves most nodules, but a defined proportion return an indeterminate cytology in which the decision is between surveillance and diagnostic surgery. BRAF V600E is the most common oncogenic driver identified in papillary thyroid carcinoma through integrated genomic characterisation [5], and its presence carries prognostic weight rather than merely diagnostic weight: in a pooled analysis of 845 BRAF V600E-positive and 1,004 mutation-negative papillary thyroid cancers, mortality was 5.3% versus 1.1% (P<.001), with an adjusted hazard ratio of 2.66 (95% CI 1.30–5.43); in the conventional variant of papillary thyroid carcinoma the adjusted hazard ratio was 3.53 (95% CI 1.25–9.98) [3].
Colorectal: an adverse prognostic marker and a target. The original mutation survey identified BRAF mutations in a substantial minority of colorectal cancers [2], and wild-type BRAF is required for response to panitumumab or cetuximab — the finding that established BRAF as a companion marker to RAS testing in colorectal practice [8]. A retrospective consortium analysis confirmed the effect of KRAS, BRAF, NRAS and PIK3CA mutations on cetuximab plus chemotherapy [9]. Contemporary sequencing shows the scale of the target: in a consecutive series of 8,355 colorectal carcinomas, BRAF mutations were identified in 556 samples (6.7%), of which 510 were in codon 600 and 46 lay in other codons — and BRAF mutation frequency varied by geography [4].
Melanoma and thyroid: where the mutation becomes directly druggable. The original exome-scale survey found BRAF mutations in approximately two thirds of malignant melanomas, with V600E accounting for about 90% of all BRAF mutations [2]. That discovery produced the first targeted-therapy pathway in solid oncology: vemurafenib improved survival in BRAF V600E melanoma [10], and combined dabrafenib plus trametinib further improved overall survival [11]. The same biology now extends to thyroid: dabrafenib plus trametinib is an established option in BRAF V600-mutant anaplastic thyroid cancer [12], produces objective responses in radioactive-iodine-refractory BRAF-mutant differentiated thyroid cancer [13], and restored iodine uptake in a redifferentiation cohort, opening a radioiodine pathway for which V600E status is the entry criterion [14].
Why a single reaction is the right design
BRAF is a serine–threonine kinase and a core transducer of the RAS–RAF–MEK–ERK pathway. In the inactive state, valine at position 600 holds the kinase in a closed conformation; replacing it with glutamic acid destabilises that closed state, so the mutant kinase signals without any upstream input from RAS. The result is constitutive MAPK output — and, unlike KRAS, a target that can be inhibited directly at the mutated node [2,17].
| Setting | Exon | Reported frequency | Clinical meaning |
|---|---|---|---|
| Papillary thyroid carcinoma | 15 | Most common oncogenic driver | Diagnostic rule-in in indeterminate cytology; associated with higher mortality risk |
| Colorectal cancer | 15 | 6.7% of 8,355 consecutive carcinomas; 510 of 556 in codon 600 | Adverse prognostic marker; anti-EGFR monotherapy unlikely to work |
| Malignant melanoma | 15 | ~66% in the original sequencing survey | Predicts response to BRAF ± MEK inhibition |
| Anaplastic thyroid carcinoma | 15 | Substantial subset | Basis of an approved dabrafenib plus trametinib indication |
| V600E as a share of all BRAF mutations | Codon 600 | ~90% | Design justification for a single reaction rather than a panel |
| Non-codon-600 BRAF mutations | 594–602 | 46 of 556 BRAF-mutant colorectal cancers | Not detected by this assay |
Sources: colorectal frequencies from a consecutive series of 8,355 carcinomas [4]; melanoma and V600E share from the original sequencing survey [2]; thyroid from integrated genomic characterisation [5] and the mortality analysis [3]; anaplastic thyroid cancer indication from the Subbiah trial [12].
How the assay works
Allele-specific priming. An ARMS primer sits directly over codon 600. The V600E allele matches perfectly and amplifies; the wild-type allele mismatches and is blocked. Specificity is enforced at the primer, before any signal is generated.
Hydrolysis-probe readout. A TaqMan probe releases fluorescence only when the specific amplicon is generated, so the signal is tied to the mutated sequence rather than to amplicon mass. HotStart Taq DNA polymerase suppresses mis-priming before activation, adding a second specificity layer in a single 25 µL reaction.
Two tubes per specimen. One BRAF reaction plus one external-standard reaction. The external-standard reaction is the specimen's own adequacy control: it must show a typical S-shaped curve with Ct between 14 and 28. Below 14 the DNA is judged excessive and diluted; at or above 28 it is deficient or inhibited and the DNA is re-extracted. That single window shifts specimen adequacy from an assumption to a measurement.
Relative quantification by ΔCt. The BRAF Ct is normalised against the external-standard Ct from the same extract, and the difference is compared against a single cut-off of 10. Because only one mutation is interrogated, interpretation reduces to one rule applied to one reaction — simpler to commission, simpler to audit, and simpler to teach than a multi-reaction panel.
Controls. A positive control carrying the V600E sequence, a negative control of wild-type human genomic DNA, and a specificity check against microbial DNA are processed with every batch, with an internal control in each tube. The internal control must rise with Ct below 35; a strong FAM signal may legitimately suppress the HEX/VIC channel, in which case the result remains credible. Ct determination is instrument-specific and stated: on the Roche LightCycler 480 the Abs Quant / 2nd Derivative Max method is specified, while on the Applied Biosystems 7500 and comparable systems the inflection point is determined on the actual amplification curve with baseline adjustment and the passive reference dye set to "None".
Reading the result
| Reaction | Target | Cut-off ΔCt | Positive call |
|---|---|---|---|
| BRAF V600E | Exon 15, c.1799T>A (p.Val600Glu) | ≤ 10 | S-shaped curve and ΔCt ≤ 10 |
Source: product instructions for use, version V2.2, "Positive Judgment Value".
Workflow and logistics
Two PCR tubes are prepared per specimen — one for BRAF mutation detection and one for the external standard — with positive and negative controls in every run. The thermal profile is 95 °C for 10 minutes for one cycle, then ten cycles of 95 °C for 15 seconds and 60 °C for 30 seconds, then 35 cycles of 95 °C for 15 seconds and 57 °C for 32 seconds, with FAM and HEX or VIC fluorescence collected at 57 °C. This is the lowest reagent and labour footprint in the product family: two reactions per specimen rather than eight.
The specimen window is defined for archive use rather than fresh-tissue trials. Paraffin-embedded sections must be confirmed to contain lesions of thyroid, colorectal or lung origin, and the preservation time of the sections should not exceed three years. Sample input is up to 300 ng of DNA per reaction, with the DNA dose increased when the external-standard signal appears late; extracted DNA is stored at ≤ –20 °C for a maximum of six months, and the sample is valid within seven repeated freeze–thaw cycles. The kit is stored at ≤ –20 °C in the dark with a nine-month shelf life, verified for five freeze–thaw cycles. Only FAM and HEX/VIC channels are required, so the assay maps onto the installed base of four-channel real-time PCR instruments — including the LightCycler 480 and ABI 7500 — without new capital equipment.
Two specimen-quality caveats are stated openly in the product documentation: because of tumour heterogeneity, different sections from the same tumour may give different results, and severely fragmented paraffin-derived DNA may affect the outcome. Specimen quality, not the chemistry, is the dominant risk — which is why the instructions for use require the pathologist to confirm that the tissue contains tumour cells.
Analytical performance
- Limit of detection. 1% mutant allele against a 30 ng/µL wild-type genome background.
- Repeatability. Ct coefficient of variation ≤ 5%, established by assaying standardised V600E references in ten parallel replicates.
- Positive reference agreement. V600E references at 10% and 50% mutation concentration, plus two verified V600E samples, were all reported positive.
- Specificity against wild type. Wild-type human genomic DNA with no target sequence was all reported negative.
- Specificity against microbial DNA. Staphylococcus aureus, Escherichia coli and other microbial DNA were all reported negative.
- External control window. 14 < Ct < 28; outside this window the DNA is judged excessive or deficient or inhibited and the specimen is re-processed.
- Internal control. HEX or VIC signal rises with Ct below 35, monitoring amplification failure and inhibition in every tube.
Every figure in this section is taken from the product's own instructions for use, version V2.2, and is reproducible from the performance section of that document.
Clinical performance: the 1,333-specimen registration study
The product's clinical verification used DNA sequencing as the reference method and tested 1,333 thyroid, colorectal and lung cancer patient samples collected across three tertiary referral centres. Every specimen was assayed in parallel by the kit and by DNA sequencing.
| Study element | As documented |
|---|---|
| Reference method | DNA sequencing, run in parallel on every specimen |
| Specimens | 1,333 thyroid, colorectal and lung cancer patient samples, multi-centre, three tertiary referral centres |
| Tumour mix | Thyroid, colorectal and lung cancer — the three clinical settings the assay serves |
| Sensitivity | 100% against DNA sequencing |
| Specificity | 98.75% against DNA sequencing |
| Overall agreement | Kappa 0.99; total coincidence rate 99.32% |
Source: product instructions for use, version V2.2, section "Specific Performance Characteristics — Clinical verification". Study centre names, specimen-level records and the complete technical dossier are available to qualified laboratories on request and are deliberately omitted from this communication.
Two points deserve emphasis. First, the assay was validated across three tumour types rather than one — thyroid, colorectal and lung, which are the settings in which BRAF V600E is actually ordered — which materially shortens the local verification argument a laboratory must make. Second, it is important to be precise about what kappa 0.99 does and does not prove: it establishes analytical agreement with the reference method on those 1,333 specimens. It does not establish clinical utility. The thyroid rule-in argument comes from the cytology and surgical literature, and the colorectal prognostic argument from the therapeutic trials cited below.
Peer-reviewed evidence retrievable on PubMed
Every study below is retrievable on PubMed under the identifier given, and full citations with DOIs appear in the reference list.
Thyroid: the rule-in evidence — and its limits
- A study combining fine-needle aspiration with BRAF V600E testing reported the V600E mutation rate among papillary thyroid carcinoma patients as 87.93% (102/116). Within the AUS/FLUS cytology category the proportion of papillary thyroid carcinoma was 60.00% (15/25), and adding V600E testing significantly increased the malignant detection rate in that category (P = 0.028). The same paper reports the operating characteristics of V600E in AUS/FLUS as specificity 10/10, sensitivity 6/15, positive predictive value 6/6 and negative predictive value 10/19 — a profile that is highly specific but limited in sensitivity. (PMID 39047144) [16]
- In a pooled analysis of 845 BRAF V600E-positive and 1,004 mutation-negative papillary thyroid cancers, mortality was 5.3% versus 1.1% (P<.001), with an adjusted hazard ratio of 2.66 (95% CI 1.30–5.43) for all papillary thyroid carcinoma and 3.53 (95% CI 1.25–9.98) for the conventional variant — converting V600E from a diagnostic marker into a prognostic one. (PMID 23571588) [3]
- Integrated genomic characterisation of papillary thyroid carcinoma identified BRAF V600E as a principal oncogenic driver in that tumour. (PMID 25417114) [5]
- The 2015 American Thyroid Association management guidelines remain the reference standard for thyroid nodule management, positioning molecular markers as an adjunct in indeterminate cytology to inform the extent of surgery. (PMID 26462967) [4]
Colorectal: prognosis, anti-EGFR and the BEACON regimen
- Wild-type BRAF was shown to be required for response to panitumumab or cetuximab, with the authors concluding that BRAF status could be used to select patients eligible for treatment, and that double-hit therapies aimed at simultaneous inhibition of EGFR and BRAF warranted exploration in V600E-mutant colorectal cancer. (PMID 19001320) [8]
- A retrospective consortium analysis established the effects of KRAS, BRAF, NRAS and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer. (PMID 20619739) [9]
- The joint ASCP/CAP/AMP/ASCO guideline recommends BRAF p.V600 testing in colorectal cancer tissue for prognostic stratification. (PMID 28165299) [15]
- In the BEACON CRC trial, encorafenib plus binimetinib plus cetuximab produced a median overall survival of 9.0 months versus 5.4 months for standard therapy (hazard ratio for death 0.52, 95% CI 0.39–0.70), with a confirmed response rate of 26% versus 2%; the doublet of encorafenib plus cetuximab produced a median overall survival of 8.4 months (hazard ratio 0.60, 95% CI 0.45–0.79). (PMID 31566309) [6]
- Updated survival results from the same study reported a median overall survival of 9.3 months (95% CI 8.2–10.8) versus 5.9 months (95% CI 5.1–7.1) for triplet therapy versus control (hazard ratio 0.60, 95% CI 0.47–0.75), with confirmed objective response rates of 26.8%, 19.5% and 1.8% for triplet, doublet and control respectively. (PMID 33503393) [7]
Melanoma and thyroid: the BRAF-directed therapy pathway
- The original sequencing survey that identified BRAF mutations in human cancer reported mutations in approximately two thirds of malignant melanomas, with V600E accounting for about 90% of all BRAF mutations. (PMID 12068308) [2]
- Vemurafenib improved survival in melanoma with BRAF V600E mutation — the trial that made BRAF the template for targeted oncology. (PMID 21639808) [10]
- Combined dabrafenib plus trametinib improved overall survival relative to BRAF inhibition alone in melanoma. (PMID 25399551) [11]
- Dabrafenib plus trametinib produced responses in locally advanced or metastatic BRAF V600-mutant anaplastic thyroid cancer, the basis of the approved indication in that disease. (PMID 29072975) [12]
- In a randomised phase 2 trial in BRAF-mutated radioactive-iodine-refractory differentiated thyroid cancer, dabrafenib and dabrafenib plus trametinib were compared directly. (PMID 35658604) [13]
- A phase 2 redifferentiation trial of dabrafenib plus trametinib with iodine-131 in metastatic radioactive-iodine-refractory BRAF p.V600E-mutated differentiated thyroid cancer established a redifferentiation pathway in which V600E status is the entry criterion. (PMID 37074727) [14]
- The mechanisms regulating the Raf kinase family, including the structural basis of V600E activation, were reviewed in Cellular Signalling. (PMID 12639709) [17]
Clinical use scenarios and who the test is for
Resolving indeterminate thyroid cytology
Where fine-needle aspiration returns an indeterminate category and the decision is between surveillance and diagnostic surgery. A positive V600E result is a high-specificity rule-in that supports proceeding and informs the extent of the operation [4,16].
Pre-operative surgical planning
Where a nodule is being planned for surgery and V600E status helps decide between lobectomy and total thyroidectomy, and feeds the recurrence-risk assessment [4,16].
Colorectal prognostic and BRAF-directed pathway
Where a RAS wild-type, BRAF V600E metastatic colorectal cancer is identified — a poor-prognosis subset with a dedicated treatment option in encorafenib-based combination therapy [6,7]. This assay runs naturally after a KRAS codon 12/13 result from the same product family.
Radioiodine-refractory risk assessment and redifferentiation triage
Where differentiated thyroid cancer is being assessed for radioactive-iodine-refractory risk, or where a redifferentiation pathway is under consideration — both of which use V600E status as an entry criterion [13,14].
Archive-based reflex testing
Where the only available material is a paraffin block. The assay is validated on FFPE sections of thyroid, colorectal and lung origin with a block age of up to three years, which matches the age profile of most diagnostic archives.
Who this test is for. The kit is intended for laboratory directors and molecular pathology managers, molecular pathologists, endocrinologists and thyroid surgeons, cytopathologists, gastrointestinal oncologists, nuclear medicine teams, hospital procurement teams and in-vitro diagnostics distributors. It is a laboratory test for professional use, not a direct-to-consumer product.
What this test is not
Any laboratory evaluating this assay should weigh its deliberate limits, which are stated in the instructions for use and reflected in the clinical literature.
- It is not a rule-out test for thyroid malignancy — and this is the single most important limitation. V600E is present in a subset of papillary thyroid carcinoma, and papillary thyroid carcinoma is itself only part of the malignant nodules arising in an indeterminate cytology category. In the study cited above, V600E testing in the AUS/FLUS category achieved sensitivity of 6/15 with a negative predictive value of 10/19, while specificity was 10/10 and the positive predictive value 6/6 (PMID 39047144) [16]. A negative V600E result cannot be reported as benign and does not exclude malignancy. Rule-out in indeterminate cytology is the job of gene-expression and multi-gene classifier tests, not of a single-marker assay. Presenting this assay as a rule-out test would be clinically wrong.
- It is not a panel — by design. It detects V600E only. It does not detect non-codon-600 BRAF mutations, which accounted for 46 of 556 BRAF-mutant colorectal cancers in a consecutive series [4], nor RET, NTRK or TERT alterations that thyroid workflows may also require.
- It is not a predictive test for anti-EGFR monotherapy. BRAF V600E makes response to cetuximab or panitumumab highly unlikely unless the antibody is given with a BRAF inhibitor [8]. The joint guideline recommends BRAF p.V600 testing in colorectal cancer for prognostic stratification [15]. This assay should therefore be positioned as a prognostic and BRAF-directed marker, not as an anti-EGFR predictive test.
- It is not a stand-alone diagnosis. The instructions for use state that results are a clinical reference and must not be the sole basis for individual treatment; clinicians integrate them with the patient's condition, drug indications, treatment reactions and other laboratory results.
- It does not replace the pathologist's adequacy assessment. The assay consumes DNA from a specimen that must already have been confirmed to contain tumour cells. A negative result from a specimen with low tumour content is not a reliable negative.
- Tumour heterogeneity and DNA quality limit any result. The instructions for use state that different sections of the same tumour may give different results, and that severely fragmented paraffin-derived DNA may affect the outcome. Block age beyond three years is outside the validated specimen specification.
- Analytical agreement is not clinical utility. The kappa 0.99 from the registration study establishes agreement with DNA sequencing, not the clinical value of the result — which must come from the thyroid, colorectal and therapeutic literature cited above.
- It is not a plasma or liquid-biopsy assay. The intended use is tumour tissue.
Regulatory status, formats and availability
The kit is a CE-marked in vitro diagnostic device under Directive 98/79/EC, with an IVDR (EU) 2017/746 transition application lodged with a designated notified body; it is classified Class C for professional use. It is supplied as 24 tests per kit, comprising one BRAF reaction mix and one external-standard reaction mix, together with HotStart Taq DNA polymerase, positive and negative controls and purified water. Full technical documentation — including the instructions for use, analytical performance data and the clinical verification dossier — is available to qualified laboratories on request.
Frequently asked questions
What does the test detect? The BRAF V600E mutation (exon 15, c.1799T>A, p.Val600Glu) in DNA extracted from tumour tissue, reported as mutation-positive or mutation-negative, using ARMS allele-specific real-time PCR.
What sample is required? Formalin-fixed paraffin-embedded sections containing thyroid, colorectal or lung lesions, with block age not exceeding three years; fresh or frozen tissue is preferred where available. The pathologist must confirm that the section used contains tumour cells.
How long does it take? Specimen to interpreted report inside one laboratory day. It is the lowest-labour member of the product family: two PCR tubes per specimen rather than eight.
What equipment is needed? A real-time PCR instrument with FAM and HEX/VIC channels, such as the Roche LightCycler 480 or Applied Biosystems 7500. No sequencing capacity and no additional capital equipment are required.
How is a result called? By ΔCt — the difference between the BRAF reaction Ct and the external-standard reaction Ct from the same extract. A positive call requires an S-shaped amplification curve and a ΔCt at or below 10, a single cut-off for the single target.
Can a negative result rule out thyroid cancer? No. V600E is present in only a subset of papillary thyroid carcinoma, and papillary thyroid carcinoma is itself only part of the malignant nodules found in an indeterminate cytology category. In the published AUS/FLUS series, V600E testing had sensitivity of 6/15 and a negative predictive value of 10/19 despite perfect specificity (PMID 39047144). A negative result must not be reported as benign; rule-out requires a gene-expression or multi-gene classifier.
How was the assay validated? In a three-centre registration study, 1,333 thyroid, colorectal and lung cancer specimens were assayed in parallel by the kit and by DNA sequencing: sensitivity 100%, specificity 98.75%, total coincidence 99.32%, kappa 0.99.
Is it CE-marked? Yes — CE-marked as an in vitro diagnostic under Directive 98/79/EC, with an IVDR transition application and IVDR Class C classification for professional use.
References
Citation format: Vancouver (ICMJE). PubMed identifiers are given for every reference retrievable through PubMed.
- [1] Bray F, Laversanne M, Sung H, et al. Global cancer statistics 2022: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2024;74(3):229-263. doi:10.3322/caac.21834. PMID 38572751.
- [2] Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949-954. doi:10.1038/nature00766. PMID 12068308.
- [3] Xing M, Alzahrani AS, Carson KA, et al. Association between BRAF V600E mutation and mortality in patients with papillary thyroid cancer. JAMA. 2013;309(14):1493-1501. doi:10.1001/jama.2013.3190. PMID 23571588.
- [4] Martianov AS, Mitiushkina NV, Ershova AN, et al. KRAS, NRAS, BRAF, HER2 and MSI Status in a Large Consecutive Series of Colorectal Carcinomas. Int J Mol Sci. 2023;24(5):4868. doi:10.3390/ijms24054868. PMID 36902296.
- [5] Cancer Genome Atlas Research Network. Integrated genomic characterization of papillary thyroid carcinoma. Cell. 2014;159(3):676-690. doi:10.1016/j.cell.2014.09.050. PMID 25417114.
- [6] Kopetz S, Grothey A, Yaeger R, et al. Encorafenib, Binimetinib, and Cetuximab in BRAF V600E-Mutated Colorectal Cancer. N Engl J Med. 2019;381(17):1632-1643. doi:10.1056/NEJMoa1908075. PMID 31566309.
- [7] Tabernero J, Grothey A, Van Cutsem E, et al. Encorafenib Plus Cetuximab as a New Standard of Care for Previously Treated BRAF V600E-Mutant Metastatic Colorectal Cancer: Updated Survival Results and Subgroup Analyses from the BEACON Study. J Clin Oncol. 2021;39(4):273-284. doi:10.1200/JCO.20.02088. PMID 33503393.
- [8] Di Nicolantonio F, Martini M, Molinari F, et al. Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer. J Clin Oncol. 2008;26(35):5705-5712. doi:10.1200/JCO.2008.18.0786. PMID 19001320.
- [9] De Roock W, Claes B, Bernasconi D, et al. Effects of KRAS, BRAF, NRAS, and PIK3CA mutations on the efficacy of cetuximab plus chemotherapy in chemotherapy-refractory metastatic colorectal cancer: a retrospective consortium analysis. Lancet Oncol. 2010;11(8):753-762. doi:10.1016/S1470-2045(10)70130-3. PMID 20619739.
- [10] Chapman PB, Hauschild A, Robert C, et al. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364(26):2507-2516. doi:10.1056/NEJMoa1103782. PMID 21639808.
- [11] Robert C, Karaszewska B, Schachter J, et al. Improved overall survival in melanoma with combined dabrafenib and trametinib. N Engl J Med. 2015;372(1):30-39. doi:10.1056/NEJMoa1412690. PMID 25399551.
- [12] Subbiah V, Kreitman RJ, Wainberg ZA, et al. Dabrafenib and Trametinib Treatment in Patients With Locally Advanced or Metastatic BRAF V600-Mutant Anaplastic Thyroid Cancer. J Clin Oncol. 2018;36(1):7-13. doi:10.1200/JCO.2017.73.6785. PMID 29072975.
- [13] Busaidy NL, Konda B, Wei L, et al. Dabrafenib Versus Dabrafenib + Trametinib in BRAF-Mutated Radioactive Iodine Refractory Differentiated Thyroid Cancer: Results of a Randomized, Phase 2, Open-Label Multicenter Trial. Thyroid. 2022;32(10):1184-1192. doi:10.1089/thy.2022.0115. PMID 35658604.
- [14] Leboulleux S, Do Cao C, Zerdoud S, et al. A Phase II Redifferentiation Trial with Dabrafenib-Trametinib and 131I in Metastatic Radioactive Iodine Refractory BRAF p.V600E-Mutated Differentiated Thyroid Cancer. Clin Cancer Res. 2023;29(13):2401-2409. doi:10.1158/1078-0432.CCR-23-0046. PMID 37074727.
- [15] Sepulveda AR, Hamilton SR, Allegra CJ, et al. Molecular Biomarkers for the Evaluation of Colorectal Cancer: Guideline From the American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology, and American Society of Clinical Oncology. J Clin Oncol. 2017;35(13):1453-1486. doi:10.1200/JCO.2016.71.9807. PMID 28165299.
- [16] Lei L, Hong Qing S, Wei L, et al. The Combined Use of Fine-Needle Aspiration (FNA) and BRAF V600E Gene Testing: Can it Increase the Definitive Diagnosis Rate of Nodules Categorized as Bethesda III for Papillary Thyroid Carcinoma? Am Surg. 2024;90(12):3209-3215. doi:10.1177/00031348241265143. PMID 39047144.
- [17] Chong H, Vikis HG, Guan KL. Mechanisms of regulating the Raf kinase family. Cell Signal. 2003;15(5):463-469. doi:10.1016/S0898-6568(02)00139-0. PMID 12639709.
Note on sources: references [1]–[17] are independent, publicly retrievable peer-reviewed publications or guideline documents. All analytical performance figures, the cut-off, the specimen specification and the 1,333-specimen clinical verification data are taken from the product's own instructions for use, version V2.2 (effective November 2024), which is product technical documentation held on file and is not independently peer reviewed; this is stated where those figures appear. The 2015 American Thyroid Association management guideline is cited by its PubMed record. Manufacturer names, trademarks, catalogue codes, certificate numbers, study centre names and authorised-representative details are deliberately omitted from this communication.
About Red Sun Medizone
Red Sun Medizone (RED SUN MEDI ZONE LIMITED) is a Hong Kong-based supplier of medical devices and in vitro diagnostic products serving hospitals, laboratories and distributors internationally. Its portfolio spans molecular diagnostics for oncology, critical-care and surgical equipment, patient monitoring, and laboratory instrumentation. The BRAF V600E assay completes the company's targeted mutation detection line alongside the CE-marked EGFR mutation PCR kit and the CE-marked KRAS mutation PCR kit, all built on the same ARMS real-time PCR chemistry and platform. The company also supplies a CE-marked methylated SEPT9 blood test for colorectal cancer screening and a CE-marked SHOX2 and RASSF1A DNA methylation PCR kit for lung-cancer testing, covering complementary molecular questions on one common real-time PCR platform.
Media and technical enquiries
Red Sun Medizone — Sales and Technical Enquiries
Mr. Matt Hou, Sales Manager
Email: [email protected]
Web: www.redsunmedizone.com
Unit 18, 8/F, Peter Leung Industrial Building, 103 Wai Yip Street, Kwun Tong, Hong Kong, China
Mr. Matt Hou, Sales Manager
Email: [email protected]
Web: www.redsunmedizone.com
Unit 18, 8/F, Peter Leung Industrial Building, 103 Wai Yip Street, Kwun Tong, Hong Kong, China
This press release describes an in vitro diagnostic device intended for professional laboratory use. It is not a statement of clinical efficacy for any individual patient, and every performance figure quoted is drawn from the sources cited. The product is manufactured in accordance with CE-marked in vitro diagnostic requirements; manufacturing, regulatory and technical documentation is available to qualified purchasers on request.