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MP 2.04.45 Epidermal Growth Factor Receptor (EGFR) Mutation Analysis for Patients with Non-Small Cell Lung Cancer (NSCLC)

Medical Policy    
Section
Medicine
 
Original Policy Date
4/25/06
Last Review Status/Date
Reviewed with literature search/1:2013
Issue
1:2013
  Return to Medical Policy Index

Disclaimer

Our medical policies are designed for informational purposes only and are not an authorization, or an explanation of benefits, or a contract.  Receipt of benefits is subject to satisfaction of all terms and conditions of the coverage.  Medical technology is constantly changing, and we reserve the right to review and update our policies periodically.


Description

Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase (TK) frequently overexpressed and activated in non-small cell lung cancer (NSCLC). Mutations in two regions of the EGFR gene (exons 18-24) --small deletions in exon 19 and a point mutation in exon 21 (L858R) -- appear to predict tumor response to tyrosine kinase inhibitors (TKIs) such as erlotinib. This policy summarizes the evidence for using EGFR mutations to decide which patients with advanced NSCLC should be considered for erlotinib therapy and which are better suited for alternative therapies.


Policy

Except as noted below, analysis of two types of somatic mutation within the EGFR gene -- small deletions in exon 19 and a point mutation in exon 21 (L858R) – may be considered medically necessary to predict treatment response to erlotinib in patients with advanced NSCLC.

Analysis of two types of somatic mutation within the EGFR gene – small deletions in exon 19 and a point mutation in exon 21 (L858R) is considered investigational for patients with advanced NSCLC of squamous cell-type.

Analysis for other mutations within exons 18-24, or other applications related to NSCLC, is considered investigational.


Policy Guidelines

The test is intended for use in patients with advanced NSCLC. Patients with either small deletions in exon 19 or a point mutation in exon 21 (L858R) of the tyrosine kinase domain of the epidermal growth factor gene are considered good candidates for treatment with erlotinib. Patients found to be wild type are unlikely to respond to erlotinib; other treatment options should be considered.

Effective in 2013, there is a specific CPT code for testing for common variants of EGFR:

81235: EGFR (epidermal growth factor receptor) (e.g., non-small cell lung cancer) gene analysis, common variants (e.g., exon 19 LREA deletion L858R, T790M, G719A, G719S, L861Q)

Prior to the creation of code 81235, no specific CPT codes were available, and this laboratory test would likely have been coded using a series of nonspecific genetic testing codes. One laboratory website listed the following group of CPT codes for this testing: 83907, 83900(x2), 83901(x18), 83891, 83896(x29), 83898(x6), 88381, 83914(x29), 83912-26.

If the testing is done by immunohistochemical assay, CPT code 88342 would likely be reported. If the testing is done by fluorescence in situ hybridization (FISH), CPT code 88365 would likely be reported. 


Benefit Application
BlueCard/National Account Issues 

Currently, epidermal growth factor receptor mutational analysis is commercially available at several commercial reference laboratories.


Rationale

Treatment options for NSCLC depend on disease stage and include various combinations of surgery, radiation therapy, chemotherapy and best supportive care. Unfortunately in up to 85% of cases the cancer has spread locally beyond the lungs at diagnosis, precluding surgical eradication. In addition, up to 40% of patients with NSCLC present with metastatic disease (1). When treated with standard platinum-based chemotherapy, patients with advanced NSCLC have a median survival of 8 to 11 months and a 1-year survival of 30 to 45% (2,3).

Laboratory and animal experiments have shown that therapeutic interdiction of the EGFR pathway could be used to halt tumor growth in solid tumors that express EGFR (4). These observations led to the development of two main classes of anti-EGFR agents for use in various types of cancer: small molecule TKIs and monoclonal antibodies (MAbs) that block EGFR-ligand interaction (5).

Two orally administered EGFR-selective small molecules (quinazolinamine derivatives) have been identified for use in treating NSCLC: gefitinib (Iressa®, AstraZeneca) and erlotinib (Tarceva®, Genentech BioOncology). While both are available for use in Europe, Canada and Asia, only erlotinib is available for use in new patients in the U.S.

Two publications (6,7) demonstrated that the underlying molecular mechanism underpinning dramatic responses in these favorably prognostic groups appeared to be the presence of activating somatic mutations in the tyrosine kinase domain of the EGFR gene, notably small deletions in exon 19 and a point mutation in exon 21 (L858R). These can be detected by direct sequencing or polymerase chain reaction technologies.

A TEC Assessment on this topic was first published in November 2007 (8). The 2007 Assessment concluded that there was insufficient evidence to permit conclusions about the clinical validity or utility of EGFR mutation testing to predict erlotinib sensitivity or to guide treatment in patients with NSCLC. This Assessment has recently been revised (9) with new conclusions indicating EGFR mutation testing has clinical utility in selecting or deselecting patients for treatment with erlotinib.

Thirteen publications have been published providing data on EGFR mutations in tumor samples obtained from NSCLC patients in erlotinib treatment studies. Nine of these (10-18) were nonconcurrent-prospective studies of patients treated with erlotinib and then studied for the presence or absence of mutations. Four (Table 1) were prospective one-arm enrichment studies of mutation-positive (3 studies) (19-21) or wild-type (1 study) (22) patients treated with erlotinib.

Table 1. Clinical Response in Prospective Studies of Erlotinib Therapy in Patients with EGFR Gene Mutation-Positive Advanced NSCLC* 

Study
(Yr)

No. Mutated. No. Tested (%)

Mutation Positive
Objective Radiologic
Response (%)

Median Progression-freeSurvival (mos.)
[95% CI]

Median Overall Survival (mos.)
[95% CI]

Jackman et al. (2009) Prospective 1-arm treatment EGFR-positive patients with erlotinib, chemotherapy naïve (19)

84 enrolled

70

13

28.7

Rosell et al. (2009) Prospective 1-arm treatment EGFR-positive patients with erlotinib in treatment failure and chemotherapy naïve (20)

350-2105

(16.6)

70

14

[11.3-16.7]

27

[24.9-33.1]

Sun et al. (2010) Prospective 1-arm treatment EGFR-positive patients with erlotinib in treatment failures (21)  

144/164

(32)

40

8

15.8

Yoshioka et al. (2010) Prospective 1-arm treatment EGFR wild-type patients with erlotinib in treatment failures (22)

30 enrolled

3.3

2.1

9.2

* all patients had stage IIIA/IV NSCLC

Abbreviation: CI, confidence interval

In a Phase 3 prospective clinical trial in China, Zhou et al. (23) reported the results of first-line treatment of patients with EGFR-mutation positive NSCLC randomized to treatment with erlotinib (n=83) versus standard chemotherapy (gemcitabine plus carboplatin) [n=82]). They observed a significant increase in progression-free survival (PFS) compared to treatment with chemotherapy (13.1 vs. 4.5 months; hazard ratio [HR] 0.16 (p<0.0001). Patients treated with erlotinib experienced fewer grade 3 and 4 toxic effects than those on chemotherapy. These results were duplicated in a European population in the EURTAC trial (NCT00446225), a multicenter, open-label, randomized Phase 3 trial. Adult patients with EGFR-mutations (exon 19 deletion or L858R mutation in exon 21) with NSCLC were randomized. Eighty-six received erlotinib, and 87 received standard chemotherapy. A planned interim analysis showed that the primary endpoint had been met. At the time the study was halted (Jan 26, 2011), median PFS was 9.7 (8.4-12.3) months versus 5.2 (4.5-5.8) in the erlotinib and standard chemotherapy groups, respectively, hazard ratio 0.37 (0.25-0.54); p<0.0001). (24) Six percent of patients on erlotinib had treatment-related severe adverse events compared to 20% of those receiving a standard chemotherapy regimen.

Petrelli et al. (25) reported a meta-analysis of 13 randomized trials of 1,260 patients receiving tyrosine kinase inhibitors (TKIs) for first-line, second-line, or maintenance therapy and compared outcomes to standard therapy. Overall, they noted that in patients with EGFR mutations, use of EGFR TKIs increased the chance of obtaining an objective response almost 2-fold when compared to chemotherapy. Response rates were 70% vs. 33% in first-line trials and 47% versus 28.5% in second-line trials. Tyrosine kinase inhibitors reduced the hazard of progression by 70% in all trials and by 65% in first-line trials; however, overall they did not improve survival.

In a pooled analysis of studies, EGFR mutations appear to demonstrate improved patient outcomes for patients treated with erlotinib, as compared to standard chemotherapy (median PFS of 13.2 versus 5.9 months, respectively). (26) Patients with EGFR mutations appear to be ideal candidates for treatment with erlotinib. Identification of patients likely to respond or to fail to respond to erlotinib treatment leads to tailored choices of treatment likely to result in predictable and desirable outcomes.

Data comparing erlotinib results in EGFR mutation-positive versus wild-type patients have also been reported in 9 other studies totaling 630 patients (Table 2). In studies of treatment with erlotinib, objective radiologic response rates in patients with EGFR-mutation-positive tumors ranged from 0% to 83% (median 45%) compared to objective radiologic response rates in patients with wild-type tumors of between 0% and 18% (median 5.5%). In the 5 studies statistically evaluating results, patients with EGFR-mutation-positive tumors always demonstrated statistically significant increases in objective radiologic response.

Progression-free survival (PFS) in patients with EGFR-mutation-positive tumors ranged from 6.8 to 13.1 months (median 12.5) and in wild-type tumors ranged from 1.4 to 5 months (median 2.5) (Table 2). In all cases in which these data were reported, EGFR-mutation-positive tumors showed a trend or a statistically significant increase in PFS rate

Overall survival (OS) in patients with EGFR-mutation-positive tumors ranged from 10 to 35 months (median 21) and in wild-type tumors ranged from 3 to 12 months (median 8.1) (Table 2). In all cases in which these data were reported, EGFR-mutation-positive tumors showed a trend or a statistically significant increase in survival rate.

In the 3 prospective studies of EGFR mutation-positive patients (Table 1), (19-21) objective radiologic response rates were 40% to 70%, PFS times were 8 to 14 months, and OS times were 16 to 29 months. This performance was distinctly different than that observed in wild-type patients (22) (Table 2) who exhibited an objective radiologic response of 3.3%, a PFS of 2.1 months, and an OS of 9.2 months.

Of note, EGFR mutations appear to provide prognostic, as well as predictive information about the behavior of tumors. In the study by Eberhard et al., (15) improved outcome parameters were observed in EGFR-positive patients compared to wild-type patients for the population as a whole (standard chemotherapy and standard chemotherapy with erlotinib) in all measurement categories with objective radiologic response of 38% versus 23% (p=0.01), time to progression of 8 months versus 5 months (p<0.001), and OS (not reached versus 10 months [p<0.001]).

Table 2. Outcomes in Patients According to EGFR Mutation Status in Response to Treatment with Erlotinib (9studies of 630 patients)

Endpoint

Overall Radiologic response Rate- Median (range) %

Progression-free Survival- Median (range) mos.

Overall Survival-Median (range) mos.

EGFR-Positive Patients

45 (0-83)

12.5 (6.8-13.1)

21 (10-35)

Wild-Type patients

5.5 (0-18)

2.5 (1.4-5)

8.1 (3-12)

Untested Patients (intent to Treat) – FDA Label

 

2.8

12

Rosell et al. (20) reported mutations in 16.6% of the total patients studied but noted these were found more frequently in women (69.7%), in patients who had never smoked (66.6%), and in patients with adenocarcinomas (80.9%). Based on these findings, Rosell et al. recommended EGFR-mutation screening in women with lung cancer with nonsquamous cell tumors who have never smoked. Other reports on the frequency of mutations have also revealed a higher prevalence in East Asians when compared to other ethnicities (38% versus 15%, respectively).(18) An increased incidence of mutations is clearly seen in these special populations (women, patients with adenocarcinoma, nonsmokers, and/or Asians); however, it does appear that a substantial number of patients without these selected demographics still exhibit EGFR mutations and would benefit from erlotinib treatment.

In a comprehensive analysis of 14 studies involving 2,880 patients, Mitsudomi et al. (24) noted mutations were observed in 10% of men, 7% of non-Asian patients, and 7% of current or former smokers, but only 2% of patients with nonadenocarcinoma histologies. While histology appears to be the strongest discriminating factor, results are diverse across studies. Eberhard et al.(15) observed mutations in 6.4% of patients with squamous cell carcinomas (SCCs) and Rosell et al.(20) in 11.5% of patients with large cell carcinomas. Numbers in these studies were small.

The National Comprehensive Cancer Network (NCCN) (28) has recently recommended testing not be performed in SCCs because of the low incidence identified in the Catalogue of Somatic Mutations in Cancer (COSMIC) maintained by the Sanger Institute. (26) This database of 1,873 samples of squamous cell lung cancers was noted to contain EGFR mutations in 2.7% of samples with an upper confidence interval (CI) for the true incidence of mutations reported to be 3.6% or less.

Park et al. (30) in a preselected set of Korean patients treated with gefitinib, reported EGFR mutations to be present in 3 out of 20 (15%) male smokers with SCC, a patient subgroup that based on demographics should have a low yield of EGFR mutations. Two of the 3 patients identified with the mutation exhibited a response to the drug versus a response in 1 of 17 wild-type patients. The PFS in patients with EGFR was 5.8 months, compared to 2.4 months in the wild-type group (not statistically significant, p=0.07, but suggesting a trend favoring a treatment response in patients with the mutation).

In vivo studies by Dobashi et al.(28) have recently been reported showing that in tumors in Japanese patients with both adenocarcinomas and SCCs, EGFR mutations are associated with downstream phosphorylation of EGFR and constitutive activation of the EGFR pathway.

Both of these studies appear to support the potential value of testing in patients with tumors of squamous cell histology, particularly in Asians. However, similar studies have not been reported in non-Asian populations or in populations treated with erlotinib.

Gene sequencing is generally considered an analytical gold standard. A rapid response report on EGFR-mutation analysis has recently been published by the Canadian Agency for Drugs and Technologies in Health. (32) Based on an analysis of 11 observational studies evaluating the use of PCR-based strategies to detect mutations in the EGFR gene, this report concluded PCR-based approaches are capable of identifying mutations in the EGFR gene with a sensitivity equivalent to that of direct sequencing.

 

Summary

Two randomized controlled trials, non-concurrent prospective studies, and single-arm enrichment studies demonstrate that the detection of epidermal growth factor receptor (EGFR) gene mutations identifies patients who are likely to benefit from use of erlotinib and who therefore represent ideal candidates for treatment with this drug. These observations have been made in a population composed primarily of tumors with adenocarcinoma histology. There is currently no evidence to indicate whether this behavior is also seen in patients with squamous cell histology.

Patients who are found to have wild-type tumors are unlikely to respond to erlotinib. They should be considered candidates for alternative therapies.

EGFR mutational analysis may be considered medically necessary to predict treatment response to erlotinib in patients with advanced non-small cell lung cancer (NSCLC); however, EGFR mutational analysis is investigational in patients with NSCLC of squamous-cell type.

National Comprehensive Cancer Network (NCCN) Guidelines

The National Comprehensive Cancer Network (NCCN) in the V1.2013 guidelines on non-small-cell lung cancer (33) recommends EGFR mutational analysis in patients with advanced NSCLC. It does suggest testing be deferred in patients with squamous cell carcinomas because of the low incidence of mutation in this histopathology type, except in never smokers and small biopsy specimens.

ASCO Publication Recommendations

In a 2011 publication, (34) the American Society of Clinical Oncology (ASCO) issued a provisional clinical opinion on EGFR mutation testing for patients with advanced non-small-cell lung cancer considering first-line EGFR tyrosine kinase inhibitor therapy. It concludes patients with NSCLC being considered for first-line therapy with an EGFR tyrosine kinase inhibitor should have their tumor tested for EGFR mutations to determine whether an EGFR tyrosine kinase inhibitor or chemotherapy is the appropriate first-line therapy.

References:

 

  1. Fathi AT, Brahmer JR. Chemotherapy for advanced stage non-small cell lung cancer. Semin Thorac Cardiovasc Surg 2008; 20(3):210-6.
  2. Martoni A, Marino A, Sperandi F et al. Multicentre randomised phase III study comparing the same dose and schedule of cisplatin plus the same schedule of vinorelbine or gemcitabine in advanced non-small cell lung cancer. Eur J Cancer 2005; 41(1):81-92.
  3. Rudd RM, Gower NH, Spiro SG et al. Gemcitabine plus carboplatin versus mitomycin, ifosfamide, and cisplatin in patients with stage IIIB or IV non-small-cell lung cancer: a phase III randomized study of the London Lung Cancer Group. J Clin Oncol 2005; 23(1):142-53.
  4. Fruehauf J. EGFR function and detection in cancer therapy. J Exp Ther Oncol 2006; 5(3):231-46.
  5. Heymach JV. ZD6474--clinical experience to date. Br J Cancer 2005; 92 Suppl 1:S14-20.
  6. Lynch TJ, Bell DW, Sordella R et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004; 350(21):2129-39.
  7. Paez JG, Janne PA, Lee JC et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004; 304(5676):1497-500.
  8. Blue Cross and Blue Shield Association Technology Evaluation Center (TEC). Epidermal growth factor receptor (EGFR) mutations and tyrosine kinase inhibitor therapy in advanced non-small-cell lung cancer. TEC Assessments 2007.
  9. Garrido P, de Castro J, Concha A et al. Guidelines for biomarker testing in advanced non-small-cell lung cancer. A national consensus of the Spanish Society of Medical Oncology (SEOM) and the Spanish Society of Pathology (SEAP). Clin Transl Oncol 2012; 14(5):338-49.
  10. Ahn MJ, Park BB, Ahn JS et al. Are there any ethnic differences in molecular predictors of erlotinib efficacy in advanced non-small cell lung cancer? Clin Cancer Res 2008; 14(12):3860-6.
  11. Amann JM, Lee JW, Roder H et al. Genetic and proteomic features associated with survival after treatment with erlotinib in first-line therapy of non-small cell lung cancer in Eastern Cooperative Oncology Group 3503. J Thorac Oncol 2010; 5(2):169-78.
  12. Felip E, Rojo F, Reck M et al. A phase II pharmacodynamic study of erlotinib in patients with advanced non-small cell lung cancer previously treated with platinum-based chemotherapy. Clin Cancer Res 2008; 14(12):3867-74.
  13. Miller VA, Riely GJ, Zakowski MF et al. Molecular characteristics of bronchioloalveolar carcinoma and adenocarcinoma, bronchioloalveolar carcinoma subtype, predict response to erlotinib. J Clin Oncol 2008; 26(9):1472-8.
  14. Schneider CP, Heigener D, Schott-von-Romer K et al. Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study. J Thorac Oncol 2008; 3(12):1446-53.
  15. Eberhard DA, Johnson BE, Amler LC et al. Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib. J Clin Oncol 2005; 23(25):5900-9.
  16. Giaccone G, Gallegos Ruiz M, Le Chevalier T et al. Erlotinib for frontline treatment of advanced non-small cell lung cancer: a phase II study. Clin Cancer Res 2006; 12(20 Pt 1):6049-55.
  17. Jackman DM, Yeap BY, Lindeman NI et al. Phase II clinical trial of chemotherapy-naive patients > or = 70 years of age treated with erlotinib for advanced non-small-cell lung cancer. J Clin Oncol 2007; 25(7):760-6.
  18. Zhu CQ, da Cunha Santos G, Ding K et al. Role of KRAS and EGFR as biomarkers of response to erlotinib in National Cancer Institute of Canada Clinical Trials Group Study BR.21. J Clin Oncol 2008; 26(26):4268-75.
  19. Jackman DM, Miller VA, Cioffredi LA et al. Impact of epidermal growth factor receptor and KRAS mutations on clinical outcomes in previously untreated non-small cell lung cancer patients: results of an online tumor registry of clinical trials. Clin Cancer Res 2009; 15(16):5267-73.
  20. Rosell R, Moran T, Queralt C et al. Screening for epidermal growth factor receptor mutations in lung cancer. N Engl J Med 2009; 361(10):958-67.
  21. Sun JM, Won YW, Kim ST et al. The different efficacy of gefitinib or erlotinib according to epidermal growth factor receptor exon 19 and exon 21 mutations in Korean non-small cell lung cancer patients. J Cancer Res Clin Oncol 2010.
  22. Yoshioka H, Hotta K, Kiura K et al. A phase II trial of erlotinib monotherapy in pretreated patients with advanced non-small cell lung cancer who do not possess active EGFR mutations: Okayama Lung Cancer Study Group trial 0705. J Thorac Oncol 2010; 5(1):99-104.
  23. Zhou C, Wu YL, Chen G et al. Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study. Lancet Oncol 2011; 12(8):735-42.
  24. Rosell R, Carcereny E, Gervais R et al. Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial. Lancet Oncol 2012; 13(3):239-46.
  25. Petrelli F, Borgonovo K, Cabiddu M et al. Efficacy of EGFR Tyrosine Kinase Inhibitors in Patients With EGFR-Mutated Non-Small Cell-Lung Cancer: A Meta-Analysis of 13 Randomized Trials. Clin Lung Cancer 2011.
  26. Paz-Ares L, Soulieres D, Melezinek I et al. Clinical outcomes in non-small-cell lung cancer patients with EGFR mutations: pooled analysis. J Cell Mol Med 2010; 14(1-2):51-69.
  27. Mitsudomi T, Kosaka T, Yatabe Y. Biological and clinical implications of EGFR mutations in lung cancer. Int J Clin Oncol 2006; 11(3):190-8.
  28. Grossi F. Management of non-small cell lung in cancer patients with stable disease. Drugs 2012; 72 Suppl 1:20-7.
  29. Forbes SA, Bhamra G, Bamford S et al. The Catalogue of Somatic Mutations in Cancer (COSMIC). Curr Protoc Hum Genet 2008; Chapter 10:Unit 10 11.
  30. Park SH, Ha SY, Lee JI et al. Epidermal growth factor receptor mutations and the clinical outcome in male smokers with squamous cell carcinoma of lung. J Korean Med Sci 2009; 24(3):448-52.
  31. Dobashi Y, Suzuki S, Kimura M et al. Paradigm of kinase-driven pathway downstream of epidermal growth factor receptor/Akt in human lung carcinomas. Hum Pathol 2011; 42(2):214-26.
  32. Mujoomdar ML, Mouton K, Spry C. Epidermal growth factor receptor mutation analysis in Advanced non-small cell lung cancer: a review of the clinical effectiveness and guidelines. . Canadian Agency for Drugs and Technologies in Health 2010.
  33. National Comprehensive Cancer Network (NCCN). NCCN Guidelines: Non-small cell lung cancer. 2012. Version 1.2013. Available oneline at http://www.nccn.org/professionals/physician_gls/PDF/nscl.pdf. Last accessed December 28, 2012.
  34. Keedy VL, Temin S, Somerfield MR et al. American Society of Clinical Oncology provisional clinical opinion: epidermal growth factor receptor (EGFR) Mutation testing for patients with advanced non-small-cell lung cancer considering first-line EGFR tyrosine kinase inhibitor therapy. J Clin Oncol 2011; 29(15):2121-7.

Codes

Number

Description

CPT 81235 EGFR (epidermal growth factor receptor) (eg, non-small cell lung cancer) gene analysis, common variants (eg, exon 19 LREA deletion, L858R, T790M, G719A, G719S, L861Q) (new code 1/1/13)

ICD-9 Diagnosis 

 

ICD-9-CM does not have specific coding for non-small cell lung cancer. The following malignant neoplasm of lung codes would be used.

  162.3 -162.9 Malignant neoplasm of lung code range
ICD-10-CM (effective 10/1/14)   ICD-10-CM does not have specific coding for non-small cell lung cancer. The following malignant neoplasm of lung codes would be used.
  C34.0 -C34.92 Malignant neoplasm of bronchus and lung
ICD-10-PCS (effective 10/1/14)    Not applicable. ICD-10-PCS codes are only used for inpatient services. There are no ICD procedure codes for laboratory tests.

Type of Service 

Medicine 

Place of Service 

Reference laboratory 


Index

EGFR Mutation Analysis
Epidermal Growth Factor Receptor Mutation Analysis


Policy History

Date Action Reason
4/25/06 Add policy New policy
7/20/06 Replace policy – correction only Corrected original policy date and issue number in header
12/11/08 Update policy Literature search performed, reference (34) added, NCCN guidelines position updated. No change to policy statement
01/13/11 Replace policy Revised extensively, based on 2010 TEC Assessment, policy statement changed from investigational to medically necessary for two types of mutations in NSCLC that is not of squamous cell type
1/12/12 Replace policy Policy updated with literature search. References 30-32 added; reference 25 updated. No change in policy statements.
11/8/12 Replace policy - coding update only CPT coding added
1/10/13 Update policy Policy updated with literature search. Reference 23 added; reference 32 updated. No change in policy statements.