Implementing Biomarker-Informed Cancer Care in NSCLC

Non-Small Cell Lung Cancer

Most cases (47.6%) of non–small cell lung cancer (NSCLC) cases are advanced or metastatic at diagnosis,¹ and 54% of early-stage cases will eventually progress to stage IV.²

Patients with advanced or metastatic NSCLC may be eligible to receive targeted therapy and should have comprehensive genomic profiling performed to test for actionable biomarkers.³

However, less than 40% of eligible patients with NSCLC receive targeted therapy.⁴ Practice gaps in the NSCLC treatment journey contribute to this patient loss.⁴ Implementing strategic solutions to standardize and optimize protocols in key workflow areas may help improve overall patient access to targeted therapies. Click below to learn more about each step of the NSCLC treatment journey.

Patient Identification

Sample Collection

Tissue Stewardship

Selecting a Molecular Test

Multidisciplinary Communication

Treatment Decision

Managing Disease Progression

Patient Identification

Identifying patients who will benefit from precision medicine and selecting the right first-line therapy is essential to optimizing patient outcomes in NSCLC.^5,6 Inappropriate first-line therapies based on incomplete testing are unlikely to be effective and can lead to increased toxicity with subsequent targeted treatments. To optimize selection of the most appropriate first-line therapy, comprehensive molecular testing, in combination with conservative use of IHC, should be performed at diagnosis before initiating treatment in all patients with advanced or metastatic NSCLC.

Actionable Genomic Alterations in NSCLC

More than half of all patients with NSCLC harbor potentially actionable genomic alterations; however, many of these individual alterations occur with relatively low frequency.⁷ Thus, identifying patients who will benefit from precision medicine often involves detecting relatively rare gene alterations. Successfully doing so allows for targeting of actionable alterations with precision medicine, which potentially improves survival in patients with NSCLC.^5,6

The use of targeted therapy has been associated with a more favorable outcome in advanced NSCLC, with a 31% reduction in risk of death and improved survival duration that was approximately 1.5-fold longer compared with patients with an identified mutational driver but did not receive targeted therapy.⁸ Comprehensive testing is recommended to identify potentially actionable biomarkers and optimize choice of therapy in patients with NSCLC.⁹

Frequency of Genomic Alterations in NSCLC Adenocarcinoma¹

View image description

Immune Checkpoint Inhibitors in NSCLC

PD-1 and PD-L1 Testing

PD-L1 expression is the currently available biomarker to assess whether patients are responsive to PD-1 or PD-L1 inhibitors.^64,65 However, it is important to obtain molecular test results for actionable genomic biomarkers before administering immune checkpoint inhibitors (ICIs) in the first line, because when given alone, ICIs have low efficacy in patients with oncogenic-driven metastatic NSCLC.^9,66 Multiple anti-PD-L1 IHC assays have been developed for different ICIs. Definition of a positive or negative PD-L1 test result depends on the individual antibody, clone, and platform, which may be unique to each ICI.^64,65

Microsatellite Instability and DNA Mismatch Repair

DNA MMR pathways play a key role in identifying and repairing mismatched nucleotides that arise during genetic recombination or because of damage caused by extrinsic physical or chemical insults. If one or more MMR proteins are not expressed or are dysfunctional, the tissue is considered dMMR.⁶⁷ Inactivation of MMR genes can result in microsatellite instability.⁶⁷ ICI therapy has been shown to be effective in dMMR/MSI-high GI and endometrial tumors, but there is limited evidence in NSCLC.⁶⁸

Tumor Mutational Burden

TMB is the total number of somatic mutations in a defined region of a tumor genome and varies according to tumor type as well as among patients.⁶⁹ Some clinical data demonstrate that tumors with high TMB are more likely to achieve clinical benefit from treatment with ICIs.⁷⁰ However, several other trials have shown that high TMB levels do not correlate with PD-L1 expression levels in patients with NSCLC.⁷⁰ Moreover, some patients with low TMB levels respond to immunotherapy, and others with high levels do not respond to immunotherapy.⁷⁰

Sample Collection

Collection Technique

Collection technique affects diagnostic yield and downstream success of genomic testing (molecular yield). Identifying the reason for biopsy can help choose the best method to optimize yield.^71-73

Thoughtful selection of the appropriate biopsy approach (eg, technique, needle gauge) for specimen collection can ensure sufficient material is available to render a diagnosis and provide comprehensive biomarker testing from a single procedure.⁷⁴

If initial biopsy reveals lung adenocarcinoma, but limited tissue remains after diagnostic workup⁷⁵:

Communicate presence of limited testing material to the ordering provider
- Prioritize testing for targets most likely to be identified and/or smaller panels that are less likely to be QNS
- Consider ordering a liquid biopsy (ctDNA assay)
- Consider repeat biopsy, and communicate “molecular priority” protocol for known diagnosis
- Consider testing alternative specimens (see “Tissue Stewardship”)

Approximate Diagnostic Yield of Tissue Collection Techniques^71-73

View image description

ROSE has the potential to positively impact outcomes.^76-80

View image description

Rapid OnSite Evaluation (ROSE) has the potential to positively impact outcomes by increasing diagnostic accuracy and yield. Cytopathologic diagnostic assessment of individual biopsy passes performed during a biopsy procedure can help distinguish between diagnostic adequacy and ancillary molecular testing adequacy.^76-80

Each molecular laboratory will have a minimal amount and concentration of tumor cells required for accurate detection of molecular alterations, based on the specific tumor enrichment protocols available and assay platforms used for testing.⁸¹ Most NGS platforms require a sample size of ≥25 mm² tumor surface area and ≥20% viable tumor nuclei per sample.^82,

Tissue blocks that are adequate for molecular testing should be tracked and by flagging in the report for the tissue navigator and/or lab technician.⁸⁴

Tissue Stewardship

While resection specimens have abundant tissue available for testing, they are available only in a small subset of patients with NSCLC.⁸¹ Thus, it is necessary to consider other types of specimens that might require testing.⁸¹ The majority of patients with lung cancer are diagnosed after examination of a small biopsy or cytology specimen of the primary lesion or a suspected metastasis.⁸¹ It has been well documented that small biopsy specimens, cytology cell blocks, and cytology touch imprints or aspirate slides are suitable for molecular testing.⁸¹

Impact of Acquisition Method on Sequencing Success⁸⁵

View image description

These specimens should be handled prudently with as much material as possible preserved for molecular testing, keeping in mind that they may be the only specimen available.^81,84,86 A limited number of immunohistochemical preparations (rather than a “shotgun” panel) is preferable to confirm a pulmonary origin and identify adenocarcinoma.^81,84,86 Where possible, limit IHC to PD-L1 status (for fist-line immunotherapy), 1 adenocarcinoma marker, and 1 squamous carcinoma marker.^81,84,86

Implementing standardized tissue-specific procedures and optimizing pre-analytic conditions by processing samples according to lab specifications via a preferred vendor may help reduce quantity not sufficient (QNS) rates and downstream sequencing failure.^85,87

View image description

Specific methods that can be used to preserve tissue include cutting 15-20 unstained slides up front (which may provide enough slides for molecular testing and leave several unstained slides available if immunostains are needed).⁸¹ Although it requires additional time and effort in the histologic processing laboratory, all tissue cut from the block should be picked up onto glass slides (no sections should be discarded from the water bath).⁸¹

Selecting a Molecular Test

Next-Generation Sequencing Approach

Although a single gene test (SGT) may have a shorter turnaround time than NGS, NGS is faster than sequential testing with SGTs.⁸⁸ Upfront NGS testing in metastatic NSCLC is associated with reduced cost and time-to-results for commercial and CMS payers.⁸⁹

Additionally, with a sequential single-gene approach, tumor tissue may be insufficient, and some biomarkers may come back without results, which may impact treatment strategy and patient outcomes.⁸⁶

Single Gene Test vs Comprehensive Profiling⁸⁶

View image description

Comprehensive tumor profiling can be achieved with NGS-based testing. All the recommended biomarkers for NSCLC can be analyzed by broad molecular profiling with NGS sequencing of tumor tissue or circulating tumor DNA.⁹⁰

Molecular Testing Options to Identify Targetable, Sensitizing Alterations in NSCLC^{9,14,47,55,68,90-94}

View image description

Concurrent Tissue and ctDNA Testing^89,95

Use of tissue- and plasma-based (ctDNA) testing are acceptable in the advanced/metastatic NSCLC setting, whether used sequentially or concurrently. Concurrent testing has the potential to reduce TAT if a protracted wait is anticipated for tissue-based results or may also be indicated in cases where there is limited tumor tissue available and QNS is probable. The identification of an actionable driver mutation by either method is sufficient to start therapy. Conversely, the absence of an actionable driver mutation in either assay does warrant the use of a complementary method. Additional advantages and disadvantages to both testing approaches are outlined below.

Tissue

Advantages: Pathology information, assessment of DNA and non-DNA biomarkers, PD-L1 assessment

Disadvantages: Longer TAT, limited tissue quantity/quality, invasive at disease progression, re-biopsy not always feasible, tumor heterogeneity

ctDNA

Advantages: Rapid TAT, minimally invasive, repeatable overtime, better capture of tumor heterogeneity and clonal evolution

Disadvantages: Non-DNA biomarkers are not evaluable, Low tumor fraction, presence of mutations from sites other than the target lesion, most commonly ChIP

Tissue + ctDNA

Advantages: All included in ctDNA and tissue testing

Disadvantages: Potential increased costs

Diagnostic Algorithm for ctDNA Testing Use in Treatment-naïve Advanced/Metastatic NSCLC^89,95

View image description

The algorithm above is applicable to advanced/metastatic NSCLC. However, there are currently no consensus guidelines in early-stage NSCLC regarding the use of ctDNA testing. When available, a tissue sample should be used if molecular testing is required, and this can be either the diagnostic specimen (if sufficient) or the post-resection specimen. If tissue is unavailable, ctDNA can be considered, but the limitations of the assay must be understood prior to ordering.

Multidisciplinary Communication

Doctor Jill Kolesar and Doctor Ravneet Thind

Learn from Drs. Jill Kolesar and Ravneet Thind about how the multidisciplinary communication facilitated by a molecular tumor board can enable biomarker-informed decision-making and optimize therapeutic options for patients.

Molecular Tumor Boards

As molecular diagnostic testing is becoming increasingly sophisticated and complex, molecular tumor boards can bring relevant expertise to this rapidly emerging field and are crucial for patient care.

>16% increase in recommended treatment choice^96,97

~30% decrease in time to treatment initiation^96-98

~40% absolute increase in overall patient survival rate⁹⁹

Expanding Molecular Tumor Boards to Community Settings with Drs Jill Kolesar and Ravneet Thind

QUESTION 02: What are the advantages of an MTB?

Dr. Kolesar: We implemented a molecular tumor board with the intention of increasing the rates of molecular testing, which we anticipated would decrease turnaround time for testing, increase access to clinical trials, and ultimately, more patients receiving biomarker-informed treatment decisions.

Dr. Thind: Due to the general cytotoxicity of conventional chemotherapy, focus has now shifted to novel therapeutic targets that can be exploited based on genomic data and molecular tumor board recommendations. So as Jill mentioned previously, molecular tumor boards can increase guideline-concordant testing and decrease turnaround time for molecular testing, which enables biomarker-informed decision-making and optimizes therapeutic options for our patients.

Dr. Kolesar: Dr. Thind, as you can see in this figure from our case-control study, we showed that patients with non–small cell lung cancer who had their cases reviewed by a molecular tumor board had improved overall survival compared to those who did not, regardless of whether they were treated in an academic setting or a community.

MTB Coordinators and Patient Navigators

Academic centers can expand molecular tumor boards to reach community sites by:

Hosting virtual meetings
Providing a molecular tumor board-dedicated navigator

Expanding Molecular Tumor Boards to Community Settings with Drs Jill Kolesar and Ravneet Thind

QUESTION 02: What elements were necessary for extension of the MTB to rural community sites?

Dr. Kolesar: I think the most important part was really to make it easy for sites to participate. So to do that, we held a virtual meeting, and we had a molecular tumor board coordinator that managed the cases referred from the community sites.

Our coordinator interacts with clinic staff from the treating physician office to gather up the notes and NGS reports for review and to provide the written recommendations back. They also coordinate the virtual meeting.

Dr. Thind: Yes, I agree. I think having a molecular tumor board–dedicated navigator has been a game changer. Along with excellent communication and support from the University of Kentucky, with clear and precise explanation of the entire process.

Dr. Kolesar: I think it was also really helpful to demonstrate the clinical benefit showing that patients with molecular tumor board review had better outcomes.

And having wide clinical and genomic expertise, with evidence grading were also critical to the success of the molecular tumor board.

Dedicated molecular tumor board coordinators and patient navigators can help with¹⁰⁰:

Consolidation of reports and upload into EMR
Follow-up of results and communication of findings
Facilitation of multidisciplinary discussions

View image description

Treatment Decision

RET-Positive NSCLC Patient Case Studies

Test for certain molecular and immune biomarkers in all appropriate patients with NSCLC
Have molecular testing results for the actionable oncogenic mutations before starting systemic therapy combined with immunotherapy
Treat patients with oncogenic driver mutations with targeted first-line therapy for that oncogene rather than first-line ICIs

Move image slider tool to see the after treatment scan

Judicious use of IHC to conserve tumor tissue for molecular studies, especially in patients with advanced disease
Broad molecular profiling using a validated test to minimize tissue use and potential wastage and assess all recommended biomarkers in all appropriate patients with NSCLC
Patients with these oncogenic mutations should receive treatment with targeted agents

Move image slider tool to see the after treatment scan

Perform broad molecular profiling using a validated test to minimize tissue use and potential wastage and assess a for actionable genetic biomarkers
Have molecular testing results for the actionable oncogenic mutations before starting systemic therapy combined with immunotherapy
Treat patients with oncogenic driver mutations with targeted first-line therapy for that oncogene

PET scan of patient after treatment (front view)

PET scan of patient before treatment (side view)

Move image slider tool to see the after treatment scan

Treatment Roadmap for HCPs

The roadmap is designed to be used in discussions HCPs and their patients with NSCLC to facilitate informative and meaningful conversations that will help prepare patients to begin their treatment journeys. Discussion topics include guideline-concordant molecular biomarker testing, as well as recommendations on traditional chemotherapy, chemoimmunotherapy, and oncogene-targeted therapy treatment options for these patients. See the “Related Resources” section to download the roadmap, discussion guide, and accompanying video for your patients.

Every patient diagnosed with non-small cell lung cancer is embarking on a personal treatment journey.

The decisions they make can impact not only their outcomes, but the kinds of obstacles they will face along the way.

While providing medical explanations and trusted advice, you are often your patient’s main source of information. The tone you set and guidance you provide impacts patient decision making.

One way to help patients make the best decision for themselves is to provide as much insight and data as possible. Molecular biomarker testing can provide the most appropriate roadmap to navigate treatment options, but the wait time for results can be difficult.

One way to help patients make the best decision for themselves is to provide as much insight and data as possible. Molecular biomarker testing can provide the most appropriate roadmap to navigate treatment options, but the wait time for results can be difficult.

Do they stay on this route and wait for traffic to clear or do they take an exit and search for a path around the backup?

For a patient, waiting to receive molecular biomarker test results may seem as frustrating as the wait in traffic. But with much higher stakes. When multiple treatment paths can be taken, each requires careful planning for optimal outcomes.

Let’s look at three possible scenarios.

When the dark blue car encounters the traffic jam, they’re anxious and feel the need to begin treatment immediately, instead of waiting for biomarker results.

For the driver, feeling like they need to refuel may lead them to exit and fill up at a nearby gas station before returning to the highway.

Similarly, starting a patient on a round of chemotherapy while waiting for biomarker results may achieve a compromise on treatment path with minimum impact on the efficacy of potential targeted therapies later.

Here, the light blue car also exits the highway to search for an alternate route. To keep moving, they choose a winding path through the city before eventually re-entering the highway later.

However, city streets come with their own obstacles, which can be as frustrating as waiting in the traffic jam and are not necessarily better routes to the driver’s destination.

Similarly, patients may want to explore treatment paths they can begin immediately instead of waiting for biomarker results. For patients eligible for immunotherapy, that treatment route may initially look better because it can be started quickly, but it may make them ineligible for later targeted therapy.

The red car, however, stays on the highway and waits through the traffic jam. It may seem tedious, but sometimes waiting for traffic to clear is the fastest way through.

Although molecular biomarker testing may come with a wait, results provide the most complete roadmap for navigating treatment.

Patients who are positive for an actionable biomarker can be given a targeted therapy, which tend to be better tolerated and have greater efficacy, for a clear path ahead as they navigate their cancer journey.

There are no “right” answers. But your guidance can help patients feel supported as they make difficult decisions.

You can find This Treatment Roadmap and other patient resources to help facilitate discussions with patients about treatment plans by scanning the QR codes.

Download the Let's Talk About Targeted Therapies in Non–Small Cell Lung Cancer Roadmap.

Managing Disease Progression

Both intrinsic and acquired resistance remains a challenge when patients are treated with TKIs, with most patients experiencing disease progression. Intrinsic mechanisms are present before therapy, whereas acquired mechanisms are induced after therapy is initiated. Common mechanisms of resistance to TKIs include^101-104:

TKI domain or other drug-binding site mutations
Downstream signaling effector mutations
Bypass signaling pathways

For patients with a documented prior actionable alteration in whom the disease has progressed with therapy, retesting should be done exclusively on rebiopsy specimens of a progressing lesion. If a biopsy is performed on a suspected bony metastasis, it is critical that decalcification be avoided because some methods of decalcification can preclude any subsequent molecular testing.⁸¹

Post-diagnostic Use of Biopsies¹⁰⁵

View image description

ADC=antibody drug conjugate; AKT=protein kinase B; ALK=anaplastic lymphoma kinase; ARAF=A-rapidly accelerated fibrosarcoma; ATP=adenosine triphosphate; ATR=ataxia telangiectasia and Rad3-related protein; AXL=tyrosine-protein kinase receptor UFO; BAD=B-cell lymphoma-extra large/-2 associated death promoter; BCL-X=B-cell lymphoma-extra large; BRAF=B-rapidly accelerated fibrosarcoma; ChIP=chromatin immunoprecipitation; CMS=Centers for Medicare & Medicaid Services; CNV=copy number variation; CR=conserved region; CRAF=C-rapidly accelerated fibrosarcoma; ctDNA=circulating tumor deoxyribonucleic acid; DAG=diacylglycerol; dMMR=MMR deficient; EBUS=endobronchial ultrasound bronchoscopy; EGFR=epidermal growth factor receptor; EML4=echinoderm microtubule-associated protein-like 4; EMR= electronic medical records; ERBB2=erythroblastic oncogene B 2; ERK=extracellular signal-related kinase; FISH=fluorescence in situ hybridization; FNA=fine needle aspiration; FN3=fibronectin type III; GAB=Grb2-associated binding scaffold protein; GDNF=glial cell line-derived neurotrophic factor; GDP=guanosine diphosphate; GF=growth factor; GFRα=GDNF family receptor-α; GI=gastrointestinal; GTP=guanosine triphosphate; HCP=healthcare professional; HER2=human epidermal growth factor receptor 2; HGF=hepatocyte growth factor; ICI=immune checkpoint inhibitor; IHC=immunohistochemistry; IPT=immunoglobulins, plexins, and transcription factors; IP3=inositol trisphosphate; JAK=Janus kinase; JNK=JUN N-terminal kinase; KIF5B=kinesin family member 5b; KRAS=Kirsten rat sarcoma; LDL=low-density lipoprotein; LRR=leucine-rich repeat; MAM=meprin/A5/Mu; MAPK=mitogen-activated protein kinase; MEK=mitogen-activated protein kinase; MET=mesenchymal-epithelial transition; MMR=mismatch repair; MSI=microsatellite instability; mTOR=mammalian target of rapamycin; NCOA4=nuclear receptor coactivator 4; NF-κB=nuclear factor kappa B; NGS=next-generation sequencing; NSCLC=non–small cell lung cancer; NT=neurotrophic; NTRK=neurotrophic tyrosine receptor kinase; PAK=P21-activated kinase; PCR=polymerase chain reaction; PDK1=pyruvate dehydrogenase lipoamide kinase isozyme 1; PD-L1=programmed death-ligand 1; PIP2=phosphatidylinositol biphosphate; PI3K=phosphatidylinositol 3-kinase; PKA=protein kinase A; PKC=protein kinase C; PLC=phospholipase C; PSI=plexins, semaphorins, and integrins; QNS = quantity not sufficient; RAC1=Ras-related c3 botulinum toxin substrate 1; RAF=rapidly accelerated fibrosarcoma; RAS=rat sarcoma; RET=rearranged during transfection; RHO=rhodopsin; ROSE=Rapid OnSite Evaluation; ROS1=ROS proto-oncogene 1; SGT= single gene test; SNV=single-nucleotide variant; SOS=Son of Sevenless; STAT=signal transducer and activator of transcription; TAT=turnaround time; TFG=tropomyosin-receptor kinase-fused gene; TIAM1=T-lymphoma invasion and metastasis-inducing protein 1; TKI = targeted kinase inhibitor; TM=transmembrane; TMB=tumor mutation burden; TRIM=ectodermin homolog and tripartite motif-containing; TRK=tropomyosin receptor kinase; TSC=tuberous sclerosis protein; VEGFA = vascular endothelial growth factor A.

GlobalData. Non-Small Cell Lung Cancer: Epidemiology Forecast to 2029. GlobalData; 2020.
Karacz CM, Yan J, Zhu H, Gerber DE. Timing, sites, and correlates of lung cancer recurrence. Clin Lung Cancer. 2020;21(2):127-135.e3.
Hendriks LE, Kerr K, Menis J, et al; ESMO Guidelines Committee. Oncogene-addicted metastatic non-small-cell lung cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up. Ann Oncol. 2023;34(4):339-357.
Sadik H, Pritchard D, Keeling DM, et al. Impact of clinical practice gaps on the implementation of personalized medicine in advanced non-small-cell lung cancer. JCO Precis Oncol. 2022;6:e2200246.
Frampton GM, Fichtenholtz A, Otto GA, et al. Development and validation of a clinical cancer genomic profiling test based on massively parallel DNA sequencing. Nat Biotechnol. 2013;31(11):1023-1031.
Singal G, Miller PG, Agarwala V, et al. Association of patient characteristics and tumor genomics with clinical outcomes among patients with non-small cell lung cancer using a clinicogenomic database. JAMA. 2019;321(14):1391-1399.
Chen R, Manochakian R, James L, et al. Emerging therapeutic agents for advanced non-small cell lung cancer. J Hematol Oncol. 2020;13(1):58.
Kris MG, Johnson BE, Berry LD, et al. Using multiplexed assays of oncogenic drivers in lung cancers to select targeted drugs. JAMA. 2014;311(19):1998-2006.
Ettinger DS, Wood DE, Aisner DL, et al. NCCN guidelines insights: non-small cell lung cancer, version 2.2021. J Natl Compr Canc Netw. 2021;19(3):254-266.
Gimple RC, Wang X. RAS: Striking at the core of the oncogenic circuitry. Front Oncol. 2019;9:965.
Cheng L, Alexander RE, Maclennan GT, et al. Molecular pathology of lung cancer: key to personalized medicine. Mod Pathol. 2012;25(3):347-369.
Salgia R, Pharaon R, Mambetsariev I, Nam A, Sattler M. The improbable targeted therapy: KRAS as an emerging target in non-small cell lung cancer (NSCLC). Cell Rep Med. 2021;2(1):100186.
Awad MM, Liu S, Rybkin II, et al. Acquired resistance to KRASG12C inhibition in cancer. N Engl J Med. 2021;384(25):2382-2393.
Lindeman NI, Cagle PT, Aisner DL, et al. Updated molecular testing guideline for the selection of lung cancer patients for treatment with targeted tyrosine kinase inhibitors: guideline from the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology. J Mol Diagn. 2018;20(2):129-159.
Lim TKH, Skoulidis F, Kerr KM, et al. KRAS G12C in advanced NSCLC: prevalence, co-mutations, and testing. Lung Cancer. 2023;184:107293.
Cai X, Sheng J, Tang C, et al. Frequent mutations in EGFR, KRAS and TP53 genes in human lung cancer tumors detected by ion torrent DNA sequencing. PLoS One. 2014;9(4):e95228.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) - KRAS. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=KRAS&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Gazdar AF. Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors. Oncogene. 2009;28(suppl 1):S24-S31.
Shah P, Sands J, Normanno N. The expanding capability and clinical relevance of molecular diagnostic technology to identify and evaluate EGFR mutations in advanced/metastatic NSCLC. Lung Cancer. 2021;160:118-126.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) - EGFR. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=EGFR&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Takita J. The role of anaplastic lymphoma kinase in pediatric cancers. Cancer Sci. 2017;108(10):1913-1920.
Shaw AT, Engelman JA. ALK in lung cancer: past, present, and future. J Clin Oncol. 2013;31(8):1105-1111.
Peters S, Taron M, Bubendorf L, Blackhall F, Stahel R. Treatment and detection of ALK-rearranged NSCLC. Lung Cancer. 2013;81(2):145-154.
Chuang TP, Lai WY, Gabre JL, et al. ALK fusion NSCLC oncogenes promote survival and inhibit NK cell responses via SERPINB4 expression. Proc Natl Acad Sci. 2023;120(8):e2216479120.
Holla VR, Elamin YY, Bailey AM, et al. ALK: a tyrosine kinase target for cancer therapy. Cold Spring Harb Mol Case Stud. 2017;3(1):a001115.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): Samples with mutation and CNA data (915 samples / 860 patients) - ALK. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=ALK&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Hernandez S, Conde E, Alonso M, et al. A narrative review of methods for the identification of ALK fusions in patients with non-small cell lung carcinoma. Transl Lung Cancer Res. 2023;12(7):1549-1562.
Fiesco JAM, Durrant DE, Morrison DK, Zhang P. Structural insights into the BRAF monomer-to-dimer transition mediated by RAS binding. Nat Commun. 2022;13(1):486.
Ascierto PA, Kirkwood JM, Grob JJ, et al. The role of BRAF V600 mutation in melanoma. J Transl Med. 2012;10:85.
Mazieres J, Cropet C, Montané L, et al. Vemurafenib in non-small-cell lung cancer patients with BRAFV600 and BRAFnonV600 mutations. Ann Oncol. 2020;31(2):289-294.
Degirmenci U, Yap J, Sim YRM, Qin S, Hu J. Drug resistance in targeted cancer therapies with RAF inhibitors. Cancer Drug Resist. 2021;4(3):665-683.
Guaitoli G, Zullo L, Tiseo M, Dankner M, Rose AA, Facchinetti F. Non-small-cell lung cancer: how to manage BRAF-mutated disease. Drugs Context. 2023;12:2022-11-3.
Laud K, Kannengiesser C, Avril MF, et al. BRAF as a melanoma susceptibility candidate gene? Cancer Res. 2003;63(12):3061-3065.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) - BRAF. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=BRAF&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Drilon A, Cappuzzo F, Ou SI, Camidge DR. Targeting MET in lung cancer: Will expectations finally be MET? J Thorac Oncol. 2017;12(1):15-26.
Comoglio PM, Trusolino L, Boccaccio C. Known and novel roles of the MET oncogene in cancer: a coherent approach to targeted therapy. Nat Rev Cancer. 2018;18(6):341-358.
Yao HP, Tong XM, Wang MH. Oncogenic mechanism-based pharmaceutical validation of therapeutics targeting MET receptor tyrosine kinase. Ther Adv Med Oncol. 2021;13:17588359211006957.
Recondo G, Bahcall M, Spurr LF, et al. Molecular mechanisms of acquired resistance to MET tyrosine kinase inhibitors in patients with MET exon 14-mutant NSCLC. Clin Cancer Res. 2020;26(11):2615-2625.
Michaels E, Bestvina CM. Meeting an un-MET need: targeting MET in non-small cell lung cancer. Front Oncol. 2022;12:1004198.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) - MET. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=MET&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Chin LP, Soo RA, Soong R, Ou SH. Targeting ROS1 with anaplastic lymphoma kinase inhibitors: a promising therapeutic strategy for a newly defined molecular subset of non-small-cell lung cancer. J Thorac Oncol. 2012;7(11):1625-1630.
Lin JJ, Choudhury NJ, Yoda S, et al. Spectrum of mechanisms of resistance to crizotinib and lorlatinib in ROS1 fusion-positive lung cancer. Clin Cancer Res. 2021;27(10):2899-2909.
Gendarme S, Bylicki O, Chouaid C, Guisier F. ROS-1 Fusions in non-small-cell lung cancer: evidence to date. Curr Oncol. 2022;29(2):641-658.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) – ROS1. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=ROS1&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Arteaga CL, Sliwkowski MX, Osborne CK, Perez EA, Puglisi F, Gianni L. Treatment of HER2-positive breast cancer: current status and future perspectives. Nat Rev Clin Oncol. 2011;9(1):16-32.
Zeng J, Ma W, Young RB, Li T. Targeting HER2 genomic alterations in non-small cell lung cancer. JNCC. 2021;1(2):58-73.
Ren S, Wang J, Ying J, et al. Consensus for HER2 alterations testing in non-small-cell lung cancer [published correction appears in ESMO Open. 2022 Jun;7(3):100482]. ESMO Open. 2022;7(1):100395.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) – ERBB2. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=ERBB2&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Subbiah V, Cote GJ. Advances in targeting RET-dependent cancers. Cancer Discov. 2020;10(4):498-505.
Mulligan LM. RET revisited: expanding the oncogenic portfolio. Nat Rev Cancer. 2014;14(3):173-186.
Liu F, Wei Y, Zhang H, Jiang J, Zhang P, Chu Q. NTRK fusion in non-small cell lung cancer: diagnosis, therapy, and TRK inhibitor resistance. Front Oncol. 2022;12:864666.
Ferrara R, Auger N, Auclin E, Besse B. Clinical and translational implications of RET rearrangements in non-small cell lung cancer. J Thorac Oncol. 2018;13(1):27-45.
Drilon A, Oxnard G, Wirth L, et al. Registrational results of LIBRETTO-001: a phase 1/2 trial of LOXO-292 in patients with RET fusion-positive lung cancers. Oral presentation at: World Conference on Lung Cancer; September 7-10, 2019; Barcelona, Spain. Abstract 964
Rosen EY, Won HH, Zheng Y, et al. The evolution of RET inhibitor resistance in RET-driven lung and thyroid cancers [published correction appears in Nat Commun. 2022;13(1):1936]. Nat Commun. 2022;13(1):1450.
Belli C, Penault-Llorca F, Ladanyi M, et al. ESMO recommendations on the standard methods to detect RET fusions and mutations in daily practice and clinical research. Ann Oncol. 2021;32(3):337-350.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) – RET. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=RET&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Cocco E, Scaltriti M, Drilon A. NTRK fusion-positive cancers and TRK inhibitor therapy. Nat Rev Clin Oncol. 2018;15(12):731-747.
Marchiò C, Scaltriti M, Ladanyi M, et al. ESMO recommendations on the standard methods to detect NTRK fusions in daily practice and clinical research. Ann Oncol. 2019;30(9):1417-1427.
Zito Marino F, Pagliuca F, Ronchi A, et al. NTRK fusions, from the diagnostic algorithm to innovative treatment in the era of precision medicine. Int J Mol Sci. 2020;21(10):3718.
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) – NTRK1. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=NTRK1&geneset_list=%20&tab_index=tab_visualize&Action=Submit
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) – NTRK2. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=NTRK2&geneset_list=%20&tab_index=tab_visualize&Action=Submit
UniProt. Q16620 · NTRK2_HUMAN. Accessed May 09, 2023. https://www.uniprot.org/uniprotkb/Q16620/entry#subcellular_location
cBioPortal for Cancer Genomics. Non-small cell cancer (MSK, Cancer Discov 2017): samples with mutation and CNA data (915 samples / 860 patients) – NTRK3. Accessed May 8, 2023. https://www.cbioportal.org/results/mutations?cancer_study_list=lung_msk_2017&Z_SCORE_THRESHOLD=2.0&RPPA_SCORE_THRESHOLD=2.0&profileFilter=mutations%2Cstructural_variants%2Ccna&case_set_id=lung_msk_2017_cnaseq&gene_list=NTRK3&geneset_list=%20&tab_index=tab_visualize&Action=Submit
Udall M, Rizzo M, Kenny J, et al. PD-L1 diagnostic tests: a systematic literature review of scoring algorithms and test-validation metrics. Diagn Pathol. 2018;13(1):12.
Doroshow DB, Bhalla S, Beasley MB, et al. PD-L1 as a biomarker of response to immune-checkpoint inhibitors. Nat Rev Clin Oncol. 2021;18(6):345-362.
Calles A, Riess JW, Brahmer JR. Checkpoint blockade in lung cancer with driver mutation: choose the road wisely. Am Soc Clin Oncol Educ Book. 2020;40:372-384.
Zhao P, Li L, Jiang X, Li Q. Mismatch repair deficiency/microsatellite instability-high as a predictor for anti-PD-1/PD-L1 immunotherapy efficacy. J Hematol Oncol. 2019;12(1):54.
Giustini N, Bazhenova L. Recognizing prognostic and predictive biomarkers in the treatment of non-small cell lung cancer (NSCLC) with immune checkpoint inhibitors (ICIs). Lung Cancer (Auckl). 2021;12:21-34.
Stenzinger A, Allen JD, Maas J, et al. Tumor mutational burden standardization initiatives: recommendations for consistent tumor mutational burden assessment in clinical samples to guide immunotherapy treatment decisions. Genes Chromosomes Cancer. 2019;58(8):578-588.
Galvano A, Gristina V, Malapelle U, et al. The prognostic impact of tumor mutational burden (TMB) in the first-line management of advanced non-oncogene addicted non-small-cell lung cancer (NSCLC): a systematic review and meta-analysis of randomized controlled trials. ESMO Open. 2021;6(3):100124.
Penault-Llorca F, Kerr KM, Garrido P, et al. Expert opinion on NSCLC small specimen biomarker testing - Part 1: Tissue collection and management. Virchows Arch. 2022;481(3):335-350.
Jain D, Allen TC, Aisner DL, et al. Rapid on-site evaluation of endobronchial ultrasound-guided transbronchial needle aspirations for the diagnosis of lung cancer: a perspective from members of the Pulmonary Pathology Society. Arch Pathol Lab Med. 2018;142(2):253-262.
Roy-Chowdhuri S, Dacic S, Ghofrani M, et al. Collection and handling of thoracic small biopsy and cytology specimens for ancillary studies: guideline from the College of American Pathologists in collaboration with the American College of Chest Physicians, Association for Molecular Pathology, American Society of Cytopathology, American Thoracic Society, Pulmonary Pathology Society, Papanicolaou Society of Cytopathology, Society of Interventional Radiology, and Society of Thoracic Radiology. Arch Pathol Lab Med. 2020;144(8):933-958.
Fox AH, Nishino M, Osarogiagbon RU, et al. Acquiring tissue for advanced lung cancer diagnosis and comprehensive biomarker testing: a National Lung Cancer roundtable best-practice guide. CA Cancer J Clin. 2023;73(4):3658-375.
Molecular In My PocketTM. Oncology: NSCLC Test Ordering - clinical and laboratory aspects in small specimen processing. Association for Molecular Pathology; 2023. Accessed February 28, 2024. https://www.amp.org/education/amp-review-resources/molecular-in-my-pocket-guides/
Cardoso AV, Neves I, Magalhães A, Sucena M, Barroca H, Fernandes G. The value of rapid on-site evaluation during EBUS-TBNA. Rev Port Pneumol. 2015;21(5):253-258.
Wu D, Liu YY, Wang T, Huang YY, Xia P. Computed tomography-guided lung biopsy with rapid on-site evaluation for diagnosis of lung lesions: a meta-analysis. J Cardiothorac Surg. 2023;18(1):122.
Yiminniyaze R, Zhang X, Zhang Y, et al. Diagnostic efficiency and safety of rapid on-site evaluation combined with CT-guided transthoracic core needle biopsy in suspected lung cancer patients. Cytopathology. 2022;33(4):439-444.
Uchida J, Imamura F, Takenaka A, et al. Improved diagnostic efficacy by rapid cytology test in fluoroscopy-guided bronchoscopy. J Thorac Oncol. 2001;1(4):314-318.
Guo H, Liu S, Guo J, et al. Rapid on-site evaluation during endobronchial ultrasound-guided transbronchial needle aspiration for the diagnosis of hilar and mediastinal lymphadenopathy in patients with lung cancer. Cancer Lett. 2016;371(2):182-186.
Alsner DL, Marshall CB. Molecular pathology of non-small cell lung cancer: a practical guide. Am J Clin Pathol. 2012;138(3):332-346.
Tomlins SA, Hovelson DH, Suga JM, et al. Real-world performance of a comprehensive genomic profiling test optimized for small tumor samples. JCO Precis Oncol. 2021;5:1312-1324.
Smits AJ, Kummer JA, de Bruin PC, et al. The estimation of tumor cell percentage for molecular testing by pathologists is not accurate. Mod Pathol. 2014;27(2):168-174.
Fintelmann FL, Martin NA, Tahir I, et al. Optimizing molecular testing of lung cancer needle biopsy specimens: potential solutions from an interdisciplinary qualitative study. Respir Res. 2023;24(1):17.
Mata DA, Harries L, Williams EA, et al. Method of tissue acquisition affects success of comprehensive genomic profiling in lung cancer. Arch Pathol Lab Med. 2023;147(3):338-347.
Gregg JP, Li T, Yoneda KY. Molecular testing strategies in non-small cell lung cancer: optimizing the diagnostic journey. Transl Lung Cancer Res. 2019;8(3)286-301.
Compton CC, Robb JA, Anderson MW, et al. Preanalytics and precision pathology: pathology practices to ensure molecular integrity of cancer patient biospecimens for precision medicine. Arch Pathol Lab Med. 2019;143(11):1346-1363
Zheng Y, Vioix H, Liu FX, Singh B, Sharma S, Sharda D. Diagnostic and economic value of biomarker testing for targetable mutations in non-small-cell lung cancer: a literature review. Future Oncol. 2022;18(4):505-518.
Pennell NA, Mutebi A, Zhou ZY, et al. Economic impact of next-generation sequencing versus single-gene testing to detect genomic alterations in metastatic non-small-cell lung cancer using a decision analytic model. JCO Precis Oncol. 2019;3:1-9.
Naidoo J. Molecular diagnostic testing in non-small cell lung cancer. Am J Hematol Oncol. 2014;10(4):4-11.
Yan N, Guo S, Zhang H, Zhang Z, Shen S, Li X. BRAF-mutated non-small cell lung cancer: current treatment status and future perspectives. Front Oncol. 2022;12:863943.
Socinski MA, Pennell NA, Davies KD. MET exon 14 skipping mutations in non-small-cell lung cancer: an overview of biology, clinical outcomes, and testing considerations. JCO Precision Oncol. 2021;5(5):653-663.
Heyer EE, Deveson IW, Wooi D, et al. Diagnosis of fusion genes using targeted RNA sequencing. Nat Commun. 2019:10(1):1388.
Luchini C, Bibeau F, Ligtenberg MJL, et al. ESMO recommendations on microsatellite instability testing for immunotherapy in cancer, and its relationship with PD-1/PD-L1 expression and tumour mutational burden: a systematic review-based approach. Ann Oncol. 2019;30(8):1232-1243.
Rolfo C, Mack P, Scagliotti GV, et al. Liquid biopsy for advanced NSCLC: a consensus statement from the international association for the study of lung cancer. J Thorac Oncol. 2021;16(10):1647-1662
Friedman EL, Kruklitis RJ, Patson BJ, Sopka DM, Weiss MJ. Effectiveness of a thoracic multidisciplinary clinic in the treatment of stage III non-small-cell lung cancer. J Multidiscip Healthc. 2016;9:267-274.
Freeman RK, Van Woerkom JM, Vyverberg A, Ascioti AJ. The effect of a multidisciplinary thoracic malignancy conference on the treatment of patients with lung cancer. Eur J Cardiothorac Surg. 2010;38(1):1-5.
Senter J, Hooker C, Lang M Voong KR, Hales RK. Thoracic multidisciplinary clinic improves survival in patients with lung cancer. Int J Radiat Oncol Biol Phys. 2016;96(2):S134.
Huang B, Chen Q, Allison D, et al. Molecular tumor board review and improved overall survival in non–small-cell lung cancer. JCO Precis Oncol. 2021;5:1530-1539.
Doerfler-Evans RE, et al. Shifting paradigms continued-the emergence and the role of nurse navigator. J Thorac Dis. 2016;8(suppl 6):S498-S500.
Waarts MR, Stonestrom AJ, Park YC, et al. Targeting mutations in cancer. J Clin Invest. 2022;132(8):e154943.
Boumahdi S, de Sauvage FJ. The great escape: tumour cell plasticity in resistance to targeted therapy. Nat Rev Drug Discov. 2020;19:39-56.
Shen Z, Qiu B, Li L, et al. Targeted therapy of RET fusion-positive non-small cell lung cancer. Front Oncol. 2022;12:1033484.
Wang X, Zhang H, Chen X. Drug resistance and combating drug resistance in cancer. Cancer Drug Resist. 2019;2:141-160.
Brown NA, Aisner DL, Oxnard GR. Precision medicine in non–small cell lung cancer: current standards in pathology and biomarker interpretation. Am Soc Clin Oncol Educ Book. 2018;38:708-715.

VV-MED-156089

Non-Small Cell Lung Cancer

Patient Identification

KRAS Exons^12-17

EGFR Exons^14,16,18-20

ALK Exons^14,23-27

BRAF Exons^14,30-34

MET Exons^14,35,37-40

ROS1 Exons^14,41-44

HER2 Exons^{14, 46-48}

RET Exons^14,52-56

NTRK Exons^{51, 58-63}

Sample Collection

ROSE has the potential to positively impact outcomes.^76-80

Tissue Stewardship

Impact of Acquisition Method on Sequencing Success⁸⁵

Selecting a Molecular Test

Single Gene Test vs Comprehensive Profiling⁸⁶

Molecular Testing Options to Identify Targetable, Sensitizing Alterations in NSCLC^{9,14,47,55,68,90-94}

Diagnostic Algorithm for ctDNA Testing Use in Treatment-naïve Advanced/Metastatic NSCLC^89,95

Multidisciplinary Communication

Learn from Drs. Jill Kolesar and Ravneet Thind about how the multidisciplinary communication facilitated by a molecular tumor board can enable biomarker-informed decision-making and optimize therapeutic options for patients.

Treatment Decision

Managing Disease Progression

Post-diagnostic Use of Biopsies¹⁰⁵

Insourcing Rapid NGS in a Community Hospital with Dr. Brandon Sheffield

Expanding Molecular Tumor Boards to Community Settings with Drs Jill Kolesar and Ravneet Thind

Minimizing Turnaround Time for Molecular Testing Among Patients With NSCLC

PMDx NSCLC Roadmap HCP Overview Video

PMDx NSCLC Roadmap Patient Overview Video

Please rate your satisfaction with the content on the following statements:

Please rate your satisfaction with the content on the following statements:

Non-Small Cell Lung Cancer

Patient Identification

Expand accordion KRAS - 27%

KRAS Exons12-17

Expand accordion EGFR - 21%

EGFR Exons14,16,18-20

Expand accordion ALK - 5%

ALK Exons14,23-27

Expand accordion BRAF - 3%

BRAF Exons14,30-34

Expand accordion MET - 3%

MET Exons14,35,37-40

Expand accordion ROS1 - 2%

ROS1 Exons14,41-44

Expand accordion ERBB2 (HER2) - 2%

HER2 Exons14, 46-48

Expand accordion RET - 2%

RET Exons14,52-56

Expand accordion NTRK1/2/3 - 1%

NTRK Exons51, 58-63

Sample Collection

ROSE has the potential to positively impact outcomes.76-80

Tissue Stewardship

Impact of Acquisition Method on Sequencing Success85

Selecting a Molecular Test

Single Gene Test vs Comprehensive Profiling86

Molecular Testing Options to Identify Targetable, Sensitizing Alterations in NSCLC9,14,47,55,68,90-94

Diagnostic Algorithm for ctDNA Testing Use in Treatment-naïve Advanced/Metastatic NSCLC89,95

Multidisciplinary Communication

Learn from Drs. Jill Kolesar and Ravneet Thind about how the multidisciplinary communication facilitated by a molecular tumor board can enable biomarker-informed decision-making and optimize therapeutic options for patients.

Treatment Decision

Managing Disease Progression

Post-diagnostic Use of Biopsies105

Related Resources

Downloadable PDFs

Insourcing Rapid NGS in a Community Hospital with Dr. Brandon Sheffield

Expanding Molecular Tumor Boards to Community Settings with Drs Jill Kolesar and Ravneet Thind

Minimizing Turnaround Time for Molecular Testing Among Patients With NSCLC

PMDx NSCLC Roadmap HCP Overview Video

PMDx NSCLC Roadmap Patient Overview Video

Expand accordion References

Please rate your satisfaction with the content on the following statements:

Please rate your satisfaction with the content on the following statements:

KRAS Exons^12-17

EGFR Exons^14,16,18-20

ALK Exons^14,23-27

BRAF Exons^14,30-34

MET Exons^14,35,37-40

ROS1 Exons^14,41-44

HER2 Exons^{14, 46-48}

RET Exons^14,52-56

NTRK Exons^{51, 58-63}

ROSE has the potential to positively impact outcomes.^76-80

Impact of Acquisition Method on Sequencing Success⁸⁵

Single Gene Test vs Comprehensive Profiling⁸⁶

Molecular Testing Options to Identify Targetable, Sensitizing Alterations in NSCLC^{9,14,47,55,68,90-94}

Diagnostic Algorithm for ctDNA Testing Use in Treatment-naïve Advanced/Metastatic NSCLC^89,95

Post-diagnostic Use of Biopsies¹⁰⁵