| Coverage Policy Manual | |
| Policy #: | 2007011 |
| Category: | Laboratory |
| Initiated: | July 2007 |
| Last Review: | December 2023 |
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| Genetic Test: KIT (c-KIT, CD117) | |
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| Description: |
CPT-4 manual coding instructions, in the header prior to the listing of Genetic Testing Code Modifiers: “This listing of modifiers is intended for reporting with molecular laboratory procedures related to genetic testing. Genetic testing modifiers should be used in conjunction with CPT and HCPCS codes to provide diagnostic granularity of service to enable providers to submit complete and precise genetic testing information without altering test descriptors. These two-character modifiers are categorized by mutation. The first (numeric) character indicates the disease category and the second (alpha) character denotes gene type. Introductory guidelines in the molecular diagnostic and molecular cytogenetic code sections of the CPT codebook provide further guidance in interpretation and application of genetic testing modifiers.”
These modifiers are appended to the molecular diagnostics codes 83890-83913 when molecular diagnostic procedures are performed to test for infectious disease, oncology, hematology, neurology, or inherited disorders to specify the probe type or condition tested. The new genetic modifiers may also be appended to the cytogenetic studies codes 88245-88291 when molecular diagnostic procedures are performed to test for oncologic or inherited disorders to specify the probe type or condition tested.
Genetic modifier ‘-0P’ is to identify testing for the c-kit receptor tyrosine kinase (KIT). The ability to molecularly classify individual cases of a specific disease that manifest different mutations of this gene allows for molecularly targeted therapy.
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Policy/ Coverage: |
Meets Primary Coverage Criteria Or Is Covered For Contracts Without Primary Coverage Criteria
Genetic testing for determination of the presence or absence of the c-KIT gene or mutations thereof meets member benefit certificate primary coverage criteria that there be scientific evidence of effectiveness for the diagnosis of:
Does Not Meet Primary Coverage Criteria Or Is Investigational For Contracts Without Primary Coverage Criteria
Molecular diagnostic testing for the c-KIT gene does not meet member benefit certificate primary coverage criteria that there be scientific evidence of effectiveness for, but not limited to, the following conditions: melanoma, dermatofibrosarcoma protuberans, hypereosinophilic syndrome, multiple myeloma, plasma cell leukemia, breast cancer, brain cancer, monoclonal gammopathy of unknown significance, retinoblastoma.
For members with contracts without primary coverage criteria, molecular diagnostic testing for the c-KIT gene is considered investigational for, but not limited to, the following conditions: melanoma, dermatofibrosarcoma protuberans, hypereosinophilic syndrome, multiple myeloma, plasma cell leukemia, breast cancer, brain cancer, monoclonal gammopathy of unknown significance, retinoblastoma. Investigational services are specific contract exclusions in most member benefit certificates of coverage.
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| Rationale: |
2011 Update
A review of the literature has been conducted through December 2010. There was no new literature identified that would prompt a change in the coverage statement.
Clinical Utility:
The clinical utility of a direct diagnostic genetic test for the determination of the presence or absence of the c-KIT gene or mutations thereof has been found to have little, if any, risks associated with it, and the benefits of this test can be invaluable in this selected population of patients.
New York State Validation Program:
Currently there is no evidence that any of the four laboratories, three of which are outside of the USA, currently performing genetic testing for the determination of the presence or absence or the c-KIT gene or mutations thereof have been validated by the New York State Validation program (Wadsworth).
Clinical Appropriateness:
Genetic testing for the determination of the presence or absence of the c-KIT gene or mutations thereof in applicable patients is deemed appropriate and necessary at this juncture.
EGAPP:
Genetic testing for the determination of the presence or absence of the c-KIT gene or mutations thereof has not been evaluated by EGAPP. It has been identified as a topic of interest, and it is currently on the list of tests to be evaluated in the future.
Gene Reviews:
Gene testing for the determination of the presence or absence of the c-KIT gene or mutations thereof has been evaluated by Gene Reviews, and currently, there is a full complement of information on this testing modality available on the Gene Reviews web site.
American College of Medical Genetics:
Gene testing for the determination of the presence or absence of the c-KIT gene or mutations thereof is not currently listed on the website of the American College of Medical Genetics.
Hayes Inc Assessment:
Hayes Inc. Assessment states that gene testing for determination of the presence or absence of the c-KIT gene or mutations thereof, has been evaluated and assessed, and it was concluded there is enough information available for a Technology Evaluation Assessment to be conducted. This will be done as soon as time allows in the future.
2012 Update
A literature search was conducted through May 2012. There was no new literature identified that would prompt a change in the coverage statement.
2015 Update
A literature search conducted through May 2015 did not reveal any new information that would prompt a change in the coverage statement.
2017 Update
A literature search conducted using the MEDLINE database through October 2017 did not reveal any new information that would prompt a change in the coverage statement.
2018 Update
A literature search was conducted through November 2018. There was no new information identified that would prompt a change in the coverage statement.
2021 Update
Annual policy review completed with a literature search using the MEDLINE database through November 2021. No new literature was identified that would prompt a change in the coverage statement.
2022 Update
Annual policy review completed with a literature search using the MEDLINE database through November 2022. No new literature was identified that would prompt a change in the coverage statement.
2023 Update
Annual policy review completed with a literature search using the MEDLINE database through November 2023. No new literature was identified that would prompt a change in the coverage statement.
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| References: |
Aslan DL, Oprea GM, et al.(2005) c-kit expression in adenoid cystic carcinoma does not have an impact on local or distant tumor recurrence. Head Neck, 2005; 27:1028-34. Barry RJ, Moura LR, et al.(2007) Expression of C-kit in retinoblastoma: a potential therapeutic target. Br J Ophthalmol, 2007; [Epub ahead of print]. Biermann K, Klingmuller D, et al.(2006) Diagnostic value of markers M2A, OCT 3/4, AP-2gamma, PLAP and c-KIT in the detection of extragonadal seminomas. Histopathology, 2006; 49:290-7. Droogendijk HJ, Kluin-Nelemans HJ, et al.(2006) Imatinib mesylate in the treatment of systemic mastocytosis: a phase II trial. Cancer, 2006; 107:345-51. Haberier C, Geipi E, et al.(2006) Immunohistochemical analysis of platelet-derived growth factor receptor -alpha, -beta, c-kit, c-abi, and arg proteins in glioblastoma: possible implications for patient selection for imatinib mesylate therapy. J Neurooncol, 2006; 76:105-9. Horny HP, Sotlar K, Valent P.(2007) Mastocytosis: state of the art. Pathobiology, 2007; 74:121-32. Hungness SI, Akin C.(2007) Mastocytosis: advances in diagnosis and treatment. Curr Allergy Asthma Rep, 2007; 7:248-54. Joensuu H, Puputti M, et al.(2005) Amplification of genes encoding KIT, PDGFRalpha and VEGFR2 receptor tyrosine kinases is frequent in glioblastoma multiforme. J Pathol, 2005; 207:224-31. Pardanani A, Akin C, Valent P.(2006) Pathogenesis, clinical features, and treatment advances in mastocytosis. Best Pract Res Clin Haematol, 2006; 19:595-615. Patnaik MM, Rindos M, et al.(2007) Systemic mastocytosis: a concise clinical and laboratory review. Arch Pathol Lab Med, 2007; 131:784-91. Sihto H, Tynninen O, et al.(2007) Endothelial cell KIT expression in human tumours. J Pathol, 2007; 211:481-8. Sorensen KB, Godballe C, et al.(2006) Parotid carcinoma: expression of kit protein and epidermal growth factor receptor. J Oral Pathol Med, 2006; 35:286-91. Tefferi A, Pardanani A.(2004) Clinical, genetic, and therapeutic insights into systemic mast cell disease. Curr Opin Hematol, 2004; 11:58-64. Wang-rodriguez J, Lopez JP, et al.(2006) STI-571 (Gleevec) potentiates the effect of cisplatin in inhibiting the proliferation of head and neck squamous cell carcinoma in vitro. Laryngoscope, 2006; 116:1409-16. Went PT, Dirnhofer S, et al.(2004) Prevalence of KIT expression in human tumors. J Clin Oncol, 2004; 22:4514-22. Wiseman SM, Masoudi H, et al.(2007) Anaplastic thyroid carcinoma: expression profile of targets for therapy offers new insights for disease treatment. Ann Surg Oncol, 2007; 14:719-29. |
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Group specific policy will supersede this policy when applicable. This policy does not apply to the Wal-Mart Associates Group Health Plan participants or to the Tyson Group Health Plan participants.
CPT Codes Copyright © 2024 American Medical Association. |
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