Imaging Features of Non-Small Cell Lung Cancer with Targetable Oncogenic Driver Mutations

Dexter P. Mendoza1, Subba R. Digumarthy1*

1Department of Radiology, Division of Thoracic Imaging and Intervention, Massachusetts General Hospital, USA


The overall 5-year survival rate and prognosis for advanced non-small lung cancer (NSCLC) continue to be dismal despite significant advances in diagnosis and treatment. In the last decade, however, significant improvements in outcomes have been achieved for a select group of patients with NSCLC harboring certain targetable mutations treated with specific tyrosine kinase inhibitors (TKI)1–8. Based on the results of several randomized controlled trials, the National Comprehensive Cancer Network (NCCN) recommends routine testing for targetable mutation in advanced NSCLC9. The mutations that are routinely tested include those involving the EGFR, ALK, and ROS1 genes that account for approximately 12% of advanced adenocarcinoma of the lung9,10. While these mutations have been associated with adenocarcinoma pathology, it is notable that these mutations are typically not seen in cases of mucinous adenocarcinoma, which has been associated with KRAS mutations11. There are many other targetable mutations such as alterations in the BRAF, RET, and MET genes that can be treated with specific drugs with completed or ongoing clinical trials.

The clinical features of NSCLC that harbor established targetable mutations are distinct and are most commonly seen in non-smokers and in relatively young individuals. The imaging features and distribution of metastases in cancers with targetable mutations can also provide clues to the presence of underlying driver mutations and can help triage patients for molecular testing and selection of mutation panel. The purpose of this review article is to highlight the imaging and clinical features of common driver mutations of NSCLC that can be treated with targeted therapy.

Epidermal growth factor receptor (EGFR) mutations are the most common targetable mutation in the treatment of NSCLC12. These mutations are more commonly seen in younger patients with little or no smoking history12. Several targeted agents, which have been shown to improve survival in this subset of patients, are now FDA-approved as front-line therapy in the treatment of advanced EGFR-mutant NSCLC1,2.

Several researchers have investigated the imaging features of EGFR-mutant NSCLC. Compared to EGFR-wild type NSCLC, the primary tumors harboring EGFR mutations have been reported to more likely to have groundglass components and more tumoral cavitations and air-bronchograms13–16. Several groups have reported the increased frequency of diffuse “miliary” lung metastases (Figure 1)17–19. Our group has previously reported up to a six-fold increased incidence of diffuse lung metastases in EGFR-mutant NSCLC compared to EGFR-wild type NSCLC19. While diffuse lung metastases are typically associated with worse prognosis, the presence of an EGFR mutation can potentially improve outcomes in these patients.

JCTD-19-1174-Fig1

Figure 1: 54-year-old female non-smoker with EGFR-mutant NSCLC. (A) Coronal chest CT image shows a consolidative mass with air-bronchograms in the right upper lobe with diffuse lung metastases bilaterally. (B) Follow up chest CT obtained 3 months following initiation of EGFR-targeted tyrosine kinase inhibitor shows marked decrease in extent of the mass with a residual cavitation and marked decrease in bilateral lung metastases. EGFR-mutant NSCLC are associated with increased propensity for diffuse “miliary” lung metastases and are responsive to targeted therapy.

Using 18FDG-PET (18-fluorodeoxyglucose positron emission tomography), Mak et al. reported a high maximum standardized uptake value of primary tumor in wild type compared to EGFR mutant lung adenocarcinoma20. The emerging technique of radiomics identifies the quantitative image parameters that are beyond the resolution of the human eye. Several studies have shown the potential of predicting EGFR mutations in NSCLC by using radiomics21, although these techniques are not yet fully standardized and have not been validated for routine clinical use.

Anaplastic lymphoma kinase (ALK) gene rearrangements, often with fusion of ALK to echinoderm microtubule-associated protein-like 4, is the second most common driver mutation with targetable treatment and is reported in approximately 5% of NSCLC22. Similar to EGFR mutations, ALK rearrangements are more common in younger patients with minimal or no smoking history22,23. Several ALK-targeted TKIs have been shown to be highly effective in treating ALK-rearranged NSCLC and are now FDA-approved, with alectinib being the current standard initial therapy in advanced ALK-positive3–7.

Several authors have also investigated the imaging features of ALK-rearranged NSCLC, although most of these studies have been on small sample sizes due to the relative rarity of the mutation15,24–30. A recent meta-analysis of these studies found several common imaging patterns in ALK-positive NSCLC31. Compared to the primary tumors in EGFR-mutant NSCLC, the primary tumors in ALK-rearranged NSCLC tend to be more solid and less likely to have air bronchograms or cavitations31. More recently, Mendoza et al. also reported that the primary tumors tend to occur in the lower lobes in ALK-rearranged NSCLC, compared to EGFR-wild type and ALK/EGFR-negative tumors32.

With respect to patterns of metastasis, ALK-rearranged NSCLC have a predilection for lymphatic spread, with increased frequencies of intrathoracic lymphadenopathy and lymphangitic carcinomatosis (Figure 2)31. The extensive lymphadenopathy seen in ALK-rearranged NSCLC can be misinterpreted initially on imaging as representing lymphoma28,30. There is also an increased propensity for pleural and pericardial metastases (Figure 2) 31. The same study by Mendoza, et al reported that osseous metastases, when present, tend to be sclerotic or blastic in nature and may be a useful feature for identifying these mutations32. Prior to this report, osseous metastases in NSCLC had been thought to be predominantly lytic in nature. ALK-rearranged NSCLC has also been associated with high rates of metastases to the brain, which is also a common site of disease progression33,34.

JCTD-19-1174-Fig2

Figure 2: 46-year-old male non-smoker with ALK-rearranged NSCLC. (A) Fused FDG-PET/CT image shows extensive FDG-avid mediastinal, hilar, and supraclavicular lymphadenopathy. (B) Axial CT lung window image shows lymphangitic carcinomatosis in the right lower lobe with nodular septal thickening and ground glass opacities. (C) Axial CT mediastinal window shows pleural thickening and a small pleural effusion consistent with pleural metastasis. Extensive lymphadenopathy, lymphangitic carcinomatosis, and pleural metastases are features that have been associated with the presence of an underlying ALK rearrangement in NSCLC.

ROS proto-oncogene 1 (ROS1) rearrangements represent another targetable driver alteration identified in 1-2% of NSCLC35,36. Similar to EGFR mutations and ALK rearrangements, ROS1 rearrangements are associated with younger age, little to no smoking history, and adenocarcinoma histology35,36. Crizotinib is currently the standard first-line treatment for advanced ROS1-rearranged NSCLC8.

Less data is available regarding the imaging features of ROS1-rearranged NSCLC. Two small studies have previously reported that the primary tumors in ROS1-rearranged NSCLC tend to be peripheral rather than central in location37,38. A larger, more recent study, however, did not support these findings and suggested that ROS1-rearranged NSCLC share several imaging features to those of ALK-rearranged NSCLC, including increased propensity for lymphangitic carcinomatosis and distant lymphadenopathy and tendency to have sclerotic rather than lytic bone metastases (Figure 3)39. Similar to the primary tumors in ALK-rearranged NSCLC, the primary tumors in ROS1-rearranged NSCLC were also less likely to air bronchograms compared to EGFR-mutant NSCLC39.

JCTD-19-1174-Fig3

Figure 3: 56-year-old female non-smoker with ROS1-rearranged NSCLC. (A) Sagittal CT image shows sclerotic lesions involving several thoracic vertebral bodies. (B) Axial CT image shows a large left upper lobe mass associated with bilateral mediastinal and left axillary lymphadenopathy. Distant metastatic lymphadenopathy and sclerotic metastases have been associated with underlying ROS1 rearrangements.

Other oncogenic driver mutations have emerged as promising targets in the treatment of NSCLC. These, among others, include rearranged during transfection proto-oncogene (RET), mesenchymal-epithelial transition gene exon 14 (METex14) skipping, and BRAF gene mutations. Less data is available regarding the imaging features of NSCLC harboring these mutations.

RET fusions are seen in 1-2% of NSCLC and are also more commonly seen in younger patients with minimal to no smoking history and adenocarcinoma histologic subtype40,41. Recently, two highly potent, RET-selective TKIs have demonstrated promising preliminary safety and efficacy profiles in patients with advanced NSCLC harboring RET alterations42–44. Small studies investigating the imaging features of RET-rearranged NSCLC have reported the increased tendency of the primary tumors RET-rearranged NSCLC to be more peripheral rather than central in location38,45. In addition, RET-rearranged NSCLC has been associated with a higher frequency of brain metastases46. This underscores the importance of developing therapies that can cross the blood-brain barrier and that have robust CNS activity.

This high propensity for brain metastases has also been reported in NSCLC harboring METex14 skipping mutations47. These mutations are reported in up to 4% of NSCLC and are typically encountered in slightly older patients compared to the other common targetable driver mutations48,49. At this time, the imaging features and metastatic patterns in METex14-positive NSCLC have not been extensively studied.

Finally, BRAF mutations are another promising target in NSCLC50. BRAF mutations have historically been classified as either V600-mutant or non-V600-mutant, but emerging evidence regarding biological differences among those with non-v600 mutations has allowed for further stratification into functional classes, which have been shown to have differences in clinical outcomes51. Previous studies, including one by our group, failed to show differences in the imaging features of the primary tumor among these functional classes, with tumors from all groups typically presenting as solid masses or nodules30,52. We did find, however, that V600-mutant NSCLC may be more likely to have intrathoracic metastases while non-V600-mutant NSCLC may have more intra-abdominal metastases at the time of presentation52.

Current evidence supports that there are differences in the imaging features and patterns of metastases among NSCLC harboring different targetable oncogenic driver mutations. The mechanism behind the morphological differences of the primary tumor and the differences in metastatic tropisms among these molecular subgroups remain unclear, but they suggest differences in their respective underlying biology.

While these imaging features and metastatic patterns may suggest the presence of specific targetable mutations, they are unlikely to replace molecular genotyping in identifying these mutations and guiding therapy. They may, however, assist in selecting patients who may benefit from expedited pathways for molecular testing or repeat testing when the initial genotyping results are discordant with the clinical and imaging presentation. More study is necessary to elucidate the mechanism behind these differences and their implication to treatment and prognosis.

Funding: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

The authors have no conflicts of interest related to this work. Other disclosures (not related to this work) are below:

DPM: No relevant disclosures.

SRD: Provides independent image analysis for hospital contracted clinical research trials programs for Merck, Pfizer, Bristol Mayer Squibb, Novartis, Roche, Polaris, Cascadian, Abbvie, Gradalis, Clinical Bay, Zai laboratories. Received honorarium from: Siemens, not related to work.

  1. Sequist LV, Yang JCH, Yamamoto N, et al. Phase III study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations. J Clin Oncol. 2013; 31(27): 3327-3334. doi:10.1200/JCO.2012.44.2806
  2. Soria JC, Ohe Y, Vansteenkiste J, et al. Osimertinib in Untreated EGFR-Mutated Advanced Non-Small-Cell Lung Cancer. N Engl J Med. 2018; 378(2): 113-125. doi:10.1056/NEJMoa1713137
  3. Peters S, Camidge DR, Shaw AT, et al. Alectinib versus Crizotinib in Untreated ALK-Positive Non–Small-Cell Lung Cancer. New England Journal of Medicine. 2017; 377(9): 829-838. doi:10.1056/NEJMoa1704795
  4. Soria JC, Tan DSW, Chiari R, et al. First-line ceritinib versus platinum-based chemotherapy in advanced ALK-rearranged non-small-cell lung cancer (ASCEND-4): a randomised, open-label, phase 3 study. The Lancet. 2017; 389(10072): 917-929. doi:10.1016/S0140-6736(17)30123-X
  5. Shaw AT, Gandhi L, Gadgeel S, et al. Alectinib in ALK-positive, crizotinib-resistant, non-small-cell lung cancer: a single-group, multicentre, phase 2 trial. The Lancet Oncology. 2016; 17(2): 234-242. doi:10.1016/S1470-2045(15)00488-X
  6. Solomon BJ, Besse B, Bauer TM, et al. Lorlatinib in patients with ALK-positive non-small-cell lung cancer: results from a global phase 2 study. Lancet Oncol. 2018; 19(12): 1654-1667. doi:10.1016/S1470-2045(18)30649-1
  7. Lin JJ, Jiang GY, Joshipura N, et al. Efficacy of Alectinib in Patients with ALK-Positive NSCLC and Symptomatic or Large CNS Metastases. J Thorac Oncol. 2019; 14(4): 683-690. doi:10.1016/j.jtho.2018.12.002
  8. Shaw AT, Ou SHI, Bang YJ, et al. Crizotinib in ROS1-rearranged non-small-cell lung cancer. N Engl J Med. 2014; 371(21): 1963-1971. doi:10.1056/NEJMoa1406766
  9. National Comprehensive Cancer Network. NCCN practice guidelines in oncology: Non-small cell lung cancer. National Comprehensive Cancer Network. https://www.nccn.org/professionals/physician_gls/pdf/nscl.pdf. Accessed April 24, 2019.
  10. Kalemkerian GP, Narula N, Kennedy EB, et al. Molecular Testing Guideline for the Selection of Patients With Lung Cancer for Treatment With Targeted Tyrosine Kinase Inhibitors: American Society of Clinical Oncology Endorsement of the College of American Pathologists/International Association for the Study of Lung Cancer/Association for Molecular Pathology Clinical Practice Guideline Update. J Clin Oncol. 2018; 36(9): 911-919. doi:10.1200/JCO.2017.76.7293
  11. Kadota K, Yeh YC, D’Angelo SP, et al. Associations between mutations and histologic patterns of mucin in lung adenocarcinoma: invasive mucinous pattern and extracellular mucin are associated with KRAS mutation. Am J Surg Pathol. 2014; 38(8): 1118-1127.
  12. Paez JG, Jänne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science. 2004; 304(5676): 1497-1500. doi:10.1126/science.1099314
  13. Hasegawa M, Sakai F, Ishikawa R, et al. CT Features of Epidermal Growth Factor Receptor-Mutated Adenocarcinoma of the Lung: Comparison with Nonmutated Adenocarcinoma. J Thorac Oncol. 2016; 11(6): 819-826. doi:10.1016/j.jtho.2016.02.010
  14. Lee HJ, Kim YT, Kang CH, et al. Epidermal growth factor receptor mutation in lung adenocarcinomas: relationship with CT characteristics and histologic subtypes. Radiology. 2013; 268(1): 254-264. doi:10.1148/radiol.13112553
  15. Rizzo S, Petrella F, Buscarino V, et al. CT Radiogenomic Characterization of EGFR, K-RAS, and ALK Mutations in Non-Small Cell Lung Cancer. Eur Radiol. 2016; 26(1): 32-42. doi:10.1007/s00330-015-3814-0
  16. Zhang H, Cai W, Wang Y, et al. CT and clinical characteristics that predict risk of EGFR mutation in non-small cell lung cancer: a systematic review and meta-analysis. Int J Clin Oncol. March 2019. doi:10.1007/s10147-019-01403-3
  17. Okuma Y, Kashima J, Watanabe K, et al. Survival analysis and pathological features of advanced non-small cell lung cancer with miliary pulmonary metastases in patients harboring epidermal growth factor receptor mutations. J Cancer Res Clin Oncol. 2018; 144(8): 1601-1611. doi:10.1007/s00432-018-2681-x
  18. Hsu F, Nichol A, Toriumi T, et al. Miliary metastases are associated with epidermal growth factor receptor mutations in non-small cell lung cancer: a population-based study. Acta Oncologica. 2017; 56(9): 1175-1180. doi:10.1080/0284186X.2017.1328128
  19. Digumarthy SR, Mendoza DP, Padole A, et al. Diffuse Lung Metastases in EGFR-Mutant Non-Small Cell Lung Cancer. Cancers. 2019; 11(9): 1360. doi:10.3390/cancers11091360
  20. Mak RH, Digumarthy SR, Muzikansky A, et al. Role of 18F-fluorodeoxyglucose positron emission tomography in predicting epidermal growth factor receptor mutations in non-small cell lung cancer. Oncologist. 2011; 16(3): 319-326. doi:10.1634/theoncologist.2010-0300
  21. Digumarthy SR, Padole AM, Gullo RL, et al. Can CT radiomic analysis in NSCLC predict histology and EGFR mutation status? Medicine (Baltimore). 2019; 98(1): e13963. doi:10.1097/MD.0000000000013963
  22. Shaw AT, Hsu PP, Awad MM, et al. Tyrosine kinase gene rearrangements in epithelial malignancies. Nature reviews Cancer. 2013; 13(11): 772. doi:10.1038/nrc3612
  23. Wong DWS, Leung ELH, So KKT, et al. The EML4-ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS. Cancer. 2009; 115(8): 1723-1733. doi:10.1002/cncr.24181
  24. Miao Y, Zhu S, Li H, et al. Comparison of clinical and radiological characteristics between anaplastic lymphoma kinase rearrangement and epidermal growth factor receptor mutation in treatment naïve advanced lung adenocarcinoma. J Thorac Dis. 2017; 9(10): 3927-3937. doi:10.21037/jtd.2017.08.134
  25. Wang H, Schabath MB, Liu Y, et al. Clinical and CT characteristics of surgically resected lung adenocarcinomas harboring ALK rearrangements or EGFR mutations. Eur J Radiol. 2016; 85(11): 1934-1940. doi:10.1016/j.ejrad.2016.08.023
  26. Park J, Kobayashi Y, Urayama KY, et al. Imaging Characteristics of Driver Mutations in EGFR, KRAS, and ALK among Treatment-Naïve Patients with Advanced Lung Adenocarcinoma. PLoS ONE. 2016; 11(8): e0161081. doi:10.1371/journal.pone.0161081
  27. Kim TJ, Lee CT, Jheon SH, et al. Radiologic Characteristics of Surgically Resected Non-Small Cell Lung Cancer With ALK Rearrangement or EGFR Mutations. Ann Thorac Surg. 2016; 101(2): 473-480. doi:10.1016/j.athoracsur.2015.07.062
  28. Choi CM, Kim MY, Hwang HJ, et al. Advanced adenocarcinoma of the lung: comparison of CT characteristics of patients with anaplastic lymphoma kinase gene rearrangement and those with epidermal growth factor receptor mutation. Radiology. 2015; 275(1): 272-279. doi:10.1148/radiol.14140848
  29. Nakada T, Okumura S, Kuroda H, et al. Imaging Characteristics in ALK Fusion-Positive Lung Adenocarcinomas by Using HRCT. Ann Thorac Cardiovasc Surg. 2015; 21(2): 102-108. doi:10.5761/atcs.oa.14-00093
  30. Halpenny DF, Plodkowski A, Riely G, et al. Radiogenomic Evaluation Of Lung Cancer – Are There Imaging Characteristics Associated With Lung Adenocarcinomas Harboring BRAF Mutations? Clin Imaging. 2017; 42: 147-151. doi:10.1016/j.clinimag.2016.11.015
  31. Mendoza DP, Stowell J, Muzikansky A, et al. Computed Tomography Imaging Characteristics of Non-Small-Cell Lung Cancer With Anaplastic Lymphoma Kinase Rearrangements: A Systematic Review and Meta-Analysis. Clin Lung Cancer. May 2019. doi:10.1016/j.cllc.2019.05.006
  32. Mendoza DP, Lin JJ, Rooney MM, et al. Imaging features and metastatic patterns of advanced ALK-positive non-small cell lung cancer. American Journal of Roentgenology. (in press).
  33. Gainor JF, Tseng D, Yoda S, et al. Patterns of Metastatic Spread and Mechanisms of Resistance to Crizotinib in ROS1-Positive Non–Small-Cell Lung Cancer. JCO Precis Oncol. 2017; 2017.
  34. Xing P, Wang S, Wang Q, et al. Efficacy of Crizotinib for Advanced ALK-Rearranged Non-Small-Cell Lung Cancer Patients with Brain Metastasis: A Multicenter, Retrospective Study in China. Target Oncol. 2019; 14(3): 325-333. doi:10.1007/s11523-019-00637-5
  35. Bergethon K, Shaw AT, Ignatius Ou SH, et al. ROS1 Rearrangements Define a Unique Molecular Class of Lung Cancers. J Clin Oncol. 2012; 30(8): 863-870. doi:10.1200/JCO.2011.35.6345
  36. Zhang Q, Wu C, Ding W, et al. Prevalence of ROS1 fusion in Chinese patients with non-small cell lung cancer. Thorac Cancer. November 2018. doi:10.1111/1759-7714.12899
  37. Yoon HJ, Sohn I, Cho JH, et al. Decoding Tumor Phenotypes for ALK, ROS1, and RET Fusions in Lung Adenocarcinoma Using a Radiomics Approach. Medicine Baltimore. 2015; 94(41). doi:10.1097/MD.0000000000001753
  38. Plodkowski AJ, Drilon A, Halpenny DF, et al. From genotype to phenotype: Are there imaging characteristics associated with lung adenocarcinomas harboring RET and ROS1 rearrangements? Lung Cancer. 2015; 90(2): 321-325. doi:10.1016/j.lungcan.2015.09.018
  39. Digumarthy SR, Mendoza DP, Lin JJ, et al. CT imaging features and distribution of metastases in ROS1-rearranged non-small cell lung cancer. Clin Lung Cancer. (in press).
  40. Wang R, Hu H, Pan Y, et al. RET fusions define a unique molecular and clinicopathologic subtype of non-small-cell lung cancer. J Clin Oncol. 2012; 30(35): 4352-4359. doi:10.1200/JCO.2012.44.1477
  41. Gautschi O, Milia J, Filleron T, et al. Targeting RET in Patients With RET-Rearranged Lung Cancers: Results From the Global, Multicenter RET Registry. J Clin Oncol. 2017; 35(13): 1403-1410. doi:10.1200/JCO.2016.70.9352
  42. Subbiah V, Velcheti V, Tuch BB, et al. Selective RET kinase inhibition for patients with RET-altered cancers. Ann Oncol. 2018; 29(8): 1869-1876. doi:10.1093/annonc/mdy137
  43. Gainor JF, Lee DH, Curigliano G, et al. Clinical activity and tolerability of BLU-667, a highly potent and selective RET inhibitor, in patients (pts) with advanced RET-fusion+ non-small cell lung cancer (NSCLC). JCO. 2019; 37(15_suppl): 9008-9008. doi:10.1200/JCO.2019.37.15_suppl.9008
  44. Drilon AE, Subbiah V, Oxnard GR, et al. A phase 1 study of LOXO-292, a potent and highly selective RET inhibitor, in patients with RET-altered cancers. Journal of Clinical Oncology. 2018; 36(15_suppl): 102.
  45. Saiki M, Kitazono S, Yoshizawa T, et al. Characterization of Computed Tomography Imaging of Rearranged During Transfection-rearranged Lung Cancer. Clin Lung Cancer. 2018; 19(5): 435-440.e1. doi:10.1016/j.cllc.2018.04.006
  46. Drilon A, Lin JJ, Filleron T, et al. Frequency of Brain Metastases and Multikinase Inhibitor Outcomes in Patients With RET-Rearranged Lung Cancers. J Thorac Oncol. 2018; 13(10): 1595-1601. doi:10.1016/j.jtho.2018.07.004
  47. Song Z, Wang H, Yu Z, et al. De Novo MET Amplification in Chinese Patients With Non-Small-Cell Lung Cancer and Treatment Efficacy With Crizotinib: A Multicenter Retrospective Study. Clin Lung Cancer. 2019; 20(2): e171-e176. doi:10.1016/j.cllc.2018.11.007
  48. Cancer Genome Atlas Research Network. Comprehensive molecular profiling of lung adenocarcinoma. Nature. 2014; 511(7511): 543-550. doi:10.1038/nature13385
  49. Awad MM, Oxnard GR, Jackman DM, et al. MET Exon 14 Mutations in Non-Small-Cell Lung Cancer Are Associated With Advanced Age and Stage-Dependent MET Genomic Amplification and c-Met Overexpression. J Clin Oncol. 2016; 34(7): 721-730. doi:10.1200/JCO.2015.63.4600
  50. Baik CS, Myall NJ, Wakelee HA. Targeting BRAF-Mutant Non-Small Cell Lung Cancer: From Molecular Profiling to Rationally Designed Therapy. Oncologist. 2017; 22(7): 786-796. doi:10.1634/theoncologist.2016-0458
  51. Dagogo-Jack I, Martinez P, Yeap BY, et al. Impact of BRAF Mutation Class on Disease Characteristics and Clinical Outcomes in BRAF-Mutant Lung Cancer. Clin Cancer Res. January 2018:clincanres.2062.2018. doi:10.1158/1078-0432.CCR-18-2062
  52. Mendoza DP, Dagogo-Jack I, Chen T, et al. Imaging characteristics of BRAF-mutant non-small cell lung cancer by functional class. Lung Cancer. 2019; 129: 80-84. doi:10.1016/j.lungcan.2019.01.007
 

Article Info

Article Notes

  • Published on: November 28, 2019

Keywords

  • Non-Small Cell Lung Cancer

  • Mutations
  • EGFR
  • ALK
  • ROS1
  • Imaging
  • Radiology

*Correspondence:

Dr. Subba R. Digumarthy
Department of Radiology, Massachusetts General Hospital, 55 Fruit Street, Founders 202, Boston, MA 02114, USA; Telephone No: 617-724-4254; Fax No: 617-724-0046
Email: sdigumarthy@mgh.harvard.edu.