Medical Policy

 

Subject: Genetic Testing for Endocrine Gland Cancer Susceptibility
Document #: GENE.00030 Publish Date:    12/27/2017
Status: Reviewed Last Review Date:    11/02/2017

Description/Scope

This document addresses genetic testing for individuals who are at higher than average risk for the development of endocrine gland cancer, including medullary thyroid cancer.  Genetic tests addressed in this document include, but are not limited to, the following:

Note: For additional information on genetic testing for other malignant conditions, please refer to:

Position Statement

Medically Necessary:

Genetic testing for RET proto-oncogene point mutations for the purposes of assessing multiple endocrine neoplasia type 2 (MEN 2) or medullary thyroid cancer risk is considered medically necessary in individuals who meet any one of the following criteria, A, B or C and all of criteria D: 

  1.  The individual is a member of a family with defined RET gene mutations; or
  2.  The individual is a member of a family known to be affected by inherited medullary thyroid cancer but not previously evaluated for RET mutations; or
  3.  The individual has sporadic medullary thyroid cancer; and
  4.  Genetic counseling, which encompasses all of the following components, has been performed
    1. Interpretation of family and medical histories to assess the probability of disease occurrence or recurrence; and
    2. Education about inheritance, genetic testing, disease management, prevention and resources; and
    3. Counseling to promote informed choices and adaptation to the risk or presence of a genetic condition; and
    4. Counseling for the psychological aspects of genetic testing.\

Investigational and Not Medically Necessary:

  1. Genetic testing for RET proto-oncogene point mutations is considered investigational and not medically necessary in individuals not meeting any of the criteria above.
  2.  Genetic testing for endocrine gland cancer susceptibility using panels of genes (with or without next-generation sequencing) is considered investigational and not medically necessary unless all components of the panel have been determined to be medically necessary based on the criteria above.  However, individual components of a panel may be considered medically necessary when criteria above are met.

Note: When a component of a genetic panel is separately identified, but a specific medical necessity statement is not found above or in another document, the criteria in GENE.00001 Genetic Testing for Cancer Susceptibility may be used to determine medical necessity.

Rationale

Based on histological findings, thyroid cancer includes the following categories: (1) differentiated (follicular, papillary and Hurthle); (2) medullary; and (3) anaplastic (aggressive undifferentiated tumor).  Medullary thyroid cancer (MTC) develops from the “C” or parafollicular cells of the thyroid gland which produce calcitonin.  Approximately 80% of the cases of MTC are sporadic.  The remaining inherited syndromes include multiple endocrine neoplasia (MEN) type 2A (also known as MEN 2A), MEN 2B and familial MTC (FMTC).  All three of these subtypes, MEN 2A, MEN 2B and FMTC are inherited in an autosomal dominant pattern and involve an elevated risk for the development of medullary carcinoma of the thyroid.  MEN 2A and MEN 2B have an increased risk for the development of pheochromocytoma.  MEN 2A has an elevated risk for parathyroid adenoma or hyperplasia.  Additional features in MEN 2B include distinctive facies with enlarged lips, mucosal neuromas of the lips and tongue and ganglioneuromatosis of the gastrointestinal tract.  MTC generally occurs in early childhood in MEN 2B, early adulthood in MEN 2A, and middle age in FMTC (Moline, 2013).

Mutations in the RET proto-oncogene are found in at least 95% of individuals with MEN 2A and 88% of FMTC.  Mutations associated with MEN 2A and familial MTC have been most frequently identified in several codons of the extracellular domains of exon 10, 11 and 13, while MEN 2B and some FMTC mutation have been identified within the intracellular exons 14 to 16.  Somatic mutations in exons 11, 13 and 16 have also been identified in at least 25% of sporadic MTC tumors.  Approximately 6% of individuals with clinical sporadic MTC are carriers of a RET germline mutation (National Comprehensive Cancer Network® [NCCN], 2017).   

Benej and colleagues (2011) evaluated the analytical validity of a high-resolution melting analysis for the identification of RET gene variants using a test developed for 28 RET sequence variants distributed among 9 exons (23 pathogenic variants and 5 variants of unknown significance).  The accuracy of the assay was measured in a blind study of 6 members of a family transmitting a p.Cys634Arg variant (5 positive and 1 negative).  The results for the unaffected noncarrier family members were distinguishable from those of the carrier relatives.  Intermediate precision of the assay was measured by having two different examiners test p.Cys634Arg-positive and p.Cys634Arg-negative samples on 2 different days.  The robustness of the assay was measured by doing two sets of experiments using modified test conditions.  Although these changes resulted in changes in melting curve shapes, the differences between normal and variant alleles remained.  The reproducibility of the melting curve analysis was assessed by performing the analysis on three different quantitative PCR instruments.  While the different instruments demonstrated variable degrees of sample differentiation (for a p.Ser649Leu variant), none yielded false-negative or false-positive results.

Several studies have evaluated the diagnostic yield of RET gene testing in individuals with the clinical manifestations of MEN2.  Eng and colleagues (1996) investigated the relationship between specific mutations and the presence of certain disease features in MEN 2 which could help in clinical decision making.  This study which included 477 MEN 2 families found that 440 (92%) had pathogenic variants in 1 of 8 RET codons (codons 609, 611, 618, 620, 634, 768, 804, and 918).  The diagnostic yield was 88% for FMTC families, 95% for MEN 2B families, and 98% for MEN 2A families, with 68% of all families carrying a sequence variant involving codon 634.  Other studies indicate that when the most commonly affected exons (10, 11, 12, 13, 14, 15, and 16) are analyzed, approximately 96.5% to 100% of individuals with clinically diagnosed MEN 2 are found to carry pathogenic RET gene variants; 98.8% to 100% for MEN 2A; 100% for MEN 2B; 96.5% to 100% for FMTC (Alvandi, 2011; Bugalho, 2007; Cascón, 2009; Elisei, 2007; Romei, 2010).  The diagnostic yield for RET gene testing in individuals with apparently sporadic MTC ranged from 3.9% to 14.3% (Alvandi, 2011; Bugalho, 2007; Elisei, 2007; Romei, 2011).  The diagnostic yield for RET gene testing among individuals with apparently sporadic pheochromocytoma (with or without paragangliomas) ranged from 0% to 19.2%, with the largest study of individuals with pheochromocytoma only (n≥340) showing a detection rate of 8% (Cascón, 2009; Iacobone, 2011; Krawczyk, 2010; Mannelli, 2009; Waldmann, 2009).

The management of MEN 2 depends on the type of MEN 2 diagnosed and whether the condition was identified prior to clinical signs and symptoms.  If treated prior to regional lymph node metastases, MEN2 can usually be cured surgically.  However, the majority of individuals (up to 75%) have lymph node involvement at the time of diagnosis.  Because the development of invasive MTC is usually preceded by C-cell hyperplasia and can be detected by the oversecretion of calcitonin in response to a chemical challenge, annual surveillance employing biochemical testing has been used to monitor those with inherited disease before it progresses beyond the earliest stages.  Genetic assays for RET mutations may be utilized as an alternative to annual biochemical testing for C-cell hyperplasia in individuals with a known family history of MEN 2A, 2B, or FMTC.  Annual biochemical screening can be discontinued in those individuals who test negative for RET mutations. Individuals who test positive for RET mutations may elect to undergo immediate thyroidectomy or defer thyroidectomy until biochemical tests suggest the development of MTC.  Genetic assays for RET oncogene mutations have also been used to determine if new cases of MTC without a known family history are truly sporadic in origin.  Positive test results in this setting may prompt the evaluation of family members or initiate screening for pheochromocytoma.

The American Thyroid Association (ATA) developed four MTC risk levels based on correlations between RET genotype and MEN 2 phenotype, and made specific recommendations regarding the ideal timing for prophylactic thyroidectomy (ATA, 2015).  For individuals with RET variants associated with MEN 2B, who have the highest risk for early-onset MTC, thyroidectomy is recommended within the first year of life.  For individuals at the next highest risk level (i.e., those with variants involving RET codon 634), thyroidectomy is recommended in the first 5 years of life.  For individuals with genotypes at the third highest level of risk, thyroidectomy should be considered prior to the age of 5 years, but may be delayed if stringent clinical criteria are met.  For individuals with genotypes in the lowest risk category, thyroidectomy may be delayed after age 5 in the context of normal screening results and a family history consistent with less aggressive MTC.

According to the recommendations set forth in the guidelines by the NCCN (NCCN, 2017), genetic testing for RET-proto-oncogene mutations is recommended for all newly diagnosed individuals with clinically apparent sporadic MTC, and for screening children and adults in known relatives with inherited forms of MTC. 

In summary, there is adequate data to show that genetic tests for point mutation in the RET gene can identify those with an inherited susceptibility for MTC prior to the onset of clinical manifestations.  Test results affect individual management by prompting age-appropriate prophylactic thyroidectomy, the early diagnosis and treatment of pheochromocytoma and/or hyperparathyroidism, continued biochemical monitoring in affected individuals, and by prompting discontinuation of monitoring in individuals who test negative.    

Background/Overview

Thyroid cancer (carcinoma) is relatively uncommon.  In the United States, the lifetime risk of being diagnosed with thyroid cancer is approximately 1%.  An estimated 64,300 cases of newly diagnosed thyroid cancer are expected in the United States in 2017 (National Cancer Institute[NCI]). 

MEN 2 is a genetic condition which can be passed from generation to generation in a family.  The gene associated with MEN 2 is called RET (RET proto-oncogene).  A mutation in the RET gene increases an individual’s risk of developing medullary thyroid cancer and other tumors associated with MEN 2. 

Three major types of tumors are associated with MEN 2: medullary thyroid cancer, parathyroid tumors, and pheochromocytoma.  MEN 2 is classified into three subtypes based on clinical features: MEN 2A, which affects 60% to 90% of MEN 2 families; MEN 2B, which affects 5% of MEN 2 families; and FMTC, which affects 5% to 35% of MEN 2 families (ASCO, 2013).  The most common sign of multiple endocrine neoplasia type 2 is medullary thyroid cancer.

Genetic Counseling

According to the National Society of Genetic Counselors (NSGC), genetic counseling is the process of assisting individuals to understand and adapt to the medical, psychological and familial ramifications of a genetic disease.  This process typically includes the guidance of a specially trained professional who:

  1. Integrates the interpretation of family and medical histories to assess the probability of disease occurrence or recurrence; and
  2. Provides education about inheritance, genetic testing, disease management, prevention and resources; and
  3. Provides counseling to promote informed choices and adaptation to the risk or presence of a genetic condition; and
  4. Provides counseling for the psychological aspects of genetic testing (NSGC, 2006).
Definitions

Genetic testing: A type of test that is used to determine the presence or absence of a specific gene or set of genes to help diagnose a disease, screen for specific health conditions, and for other purposes.

Medullary thyroid cancer: The type of thyroid cancer that develops from the C cells of the thyroid gland.

Multiple endocrine neoplasia Type 2 (MEN 2): A hereditary disorder in which individuals develop a type of thyroid cancer accompanied by recurring cancer of the adrenal glands.

Mutation: A change in DNA sequence.

Pheochromocytoma:  A tumor of the adrenal glands which is usually benign: 50% with MEN 2A affected.

Coding

The following codes for treatments and procedures applicable to this document are included below for informational purposes. Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy. Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage of these services as it applies to an individual member.

When Services may be Medically Necessary, when criteria are met:

CPT

 

81404

Molecular pathology procedure, Level 5 (eg, analysis of 2-5 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of 6-10 exons, or characterization of a dynamic mutation disorder/triplet repeat by Southern blot analysis)  [when specified as the following]:

  • RET (ret proto-oncogene) (eg, multiple endocrine neoplasia, type 2B and familial medullary thyroid carcinoma), common variants (eg, M918T, 2647_2648delinsTT, A883F) 

81405

Molecular pathology procedure, Level 6 (eg, analysis of 6-10 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of 11-25 exons, regionally targeted cytogenomic array analysis)  [when specified as the following]:

  • RET (ret proto-oncogene) (eg, multiple endocrine neoplasia, type 2A and familial medullary thyroid carcinoma), targeted sequence analysis (eg, exons 10, 11, 13-16)

 

 

HCPCS

 

S3840

DNA analysis for germline mutations of the RET proto-oncogene for susceptibility to multiple endocrine neoplasia type 2 [MEN 2]

 

 

ICD-10 Diagnosis

 

C73

Malignant neoplasm of thyroid gland

C74.00-C74.92

Malignant neoplasm of adrenal gland

C75.0

Malignant neoplasm of parathyroid gland

D35.00-D35.02

Benign neoplasm of adrenal gland

D35.1

Benign neoplasm of parathyroid gland

E21.0-E21.5

Hyperparathyroidism and other disorders of parathyroid gland

E31.20-E31.23

Multiple endocrine neoplasia (MEN) syndromes

Z15.81

Genetic susceptibility to multiple endocrine neoplasia (MEN)

Z80.8

Family history of malignant neoplasm of other organs or systems [endocrine]

Z83.41-Z83.49

Family history of other endocrine, nutritional and metabolic diseases

When services are Investigational and Not Medically Necessary:
For the procedure codes listed above when criteria are not met or for all other diagnoses not listed, or when the code describes a procedure indicated in the Position Statement section as investigational and not medically necessary.

When services are also Investigational and Not Medically Necessary:
When the code describes a procedure indicated in the Position Statement section as investigational and not medically necessary.

CPT

 

81445

Targeted genomic sequence analysis panel, solid organ neoplasm, DNA analysis, and RNA analysis when performed, 5-50 genes (eg, ALK, BRAF, CDKN2A, EGFR, ERBB2, KIT, KRAS, NRAS, MET, PDGFRA, PDGFRB, PGR, PIK3CA, PTEN, RET), interrogation for sequence variants and copy number variants or rearrangements, if performed

81455

Targeted genomic sequence analysis panel, solid organ or hematolymphoid neoplasm, DNA analysis, and RNA analysis when performed, 51 or greater genes (eg, ALK, BRAF, CDKN2A, CEBPA, DNMT3A, EGFR, ERBB2, EZH2, FLT3, IDH1, IDH2, JAK2, KIT, KRAS, MLL, NPM1, NRAS, MET, NOTCH1, PDGFRA, PDGFRB, PGR, PIK3CA, PTEN, RET), interrogation for sequence variants and copy number variants or rearrangements, if performed

81479

Unlisted molecular pathology procedure [when specified as testing for endocrine cancer syndrome susceptibility using panels of genes (with or without next generation sequencing)]

 

 

ICD-10 Diagnosis

 

C73

Malignant neoplasm of thyroid gland

C74.00-C74.92

Malignant neoplasm of adrenal gland

C75.0

Malignant neoplasm of parathyroid gland

D35.00-D35.02

Benign neoplasm of adrenal gland

D35.1

Benign neoplasm of parathyroid gland

E21.0-E21.5

Hyperparathyroidism and other disorders of parathyroid gland

E31.20-E31.23

Multiple endocrine neoplasia (MEN) syndromes

Z15.81

Genetic susceptibility to multiple endocrine neoplasia (MEN)

Z80.8

Family history of malignant neoplasm of other organs or systems [endocrine]

Z83.41-Z83.49

Family history of other endocrine, nutritional and metabolic diseases

References

Peer Reviewed Publications:

  1. Alvandi E, Akrami SM, Chiani M, et al. Molecular analysis of the RET proto-oncogene key exons in patients with medullary thyroid carcinoma: a comprehensive study of the Iranian population. Thyroid. 2011; 21(4):373-382.
  2. Benej M, Bendlova B, Vaclavikova E, Poturnajova M. Establishing high resolution melting analysis: method validation and evaluation for c-RET proto-oncogene mutation screening. Clin Chem Lab Med. 2011; 50(1):51-60.
  3. Bugalho MJ, Domingues R, Santos JR, et al. Mutation analysis of the RET proto-oncogene and early thyroidectomy: results of a Portuguese cancer centre. Surgery. 2007; 141(1):90-95.
  4. Cascón A, Pita G, Burnichon N, et al. Genetics of pheochromocytoma and paraganglioma in Spanish patients. J Clin Endocrinol Metab. 2009; 94(5):1701-1705.
  5. Elisei R, Romei C, Cosci B, et al. RET genetic screening in patients with medullary thyroid cancer and their relatives: experience with 807 individuals at one center. J Clin Endocrinol Metab. 2007; 92(12):4725-4729.
  6. Eng C, Clayton D, Schuffenecker I, et al. The relationship between specific RET proto-oncogene mutations and disease phenotype in multiple endocrine neoplasia type 2. International RET mutation consortium analysis. JAMA. 1996; 276(19):1575-1579.
  7. Frank-Raue K, Buhr H, Dralle H, et al. Long-term outcome in 46 gene carriers of hereditary medullary thyroid carcinoma after prophylactic thyroidectomy: impact of individual RET genotype. Eur J Endocrinol. 2006; 155(2):229-236. 
  8. Gertner ME, Kebebew E. Multiple endocrine neoplasia type 2. Curr Treat Options Oncol. 2004; 5(4):315-325.
  9. Huang SM, Tao BL, Tzeng CC, et al Prenatal molecular diagnosis of RET proto-oncogene mutation in multiple endocrine neoplasia type 2A. J Formos Med Assoc. 1997; 96:542-544.
  10. Iacobone M, Schiavi F, Bottussi M, et al. Is genetic screening indicated in apparently sporadic pheochromocytomas and paragangliomas? Surgery. 2011; 150(6):1194-1201.
  11. Jimenez C, Cote G, Arnold A, Gagel RF. Review: Should patients with apparently sporadic pheochromocytomas or paragangliomas be screened for hereditary syndromes? J Clin Endocrinol Metab. 2006; 91(8):2851-2858.
  12. Krawczyk A, Hasse-Lazar K, Pawlaczek A, et al. Germinal mutations of RET, SDHB, SDHD, and VHL genes in patients with apparently sporadic pheochromocytomas and paragangliomas. Endokrynol Pol. 2010; 61(1):43-48.
  13. Leboulleux S, Baudin E, Travagli JP, et al. Medullary thyroid carcinoma. Clin Endocrinol. 2004; 61(3):299-310.
  14. Mannelli M, Castellano M, Schiavi F, et al.; Italian Pheochromocytoma/Paraganglioma Network. Clinically guided genetic screening in a large cohort of Italian patients with pheochromocytomas and/or functional or nonfunctional paragangliomas. J Clin Endocrinol Metab. 2009; 94(5):1541-1547.
  15. Martinelli P, Maruotti GM, Pasquali D, et al. Genetic prenatal RET testing and pregnancy management of multiple endocrine neoplasia Type II A (MEN2A): a case report. J Endocrinol Invest. 2004; 27(4):357-360.
  16. Offit K, Kohut K, Clagett B, et al. Cancer genetic testing and assisted reproduction. J Clin Oncol. 2006; 24:4775-4782.
  17. Offit K, Sagi M, Hurley K. Preimplantation genetic diagnosis for cancer syndromes: a new challenge for preventive medicine. JAMA. 2006; 296(22):2727–2730.
  18. Plaza-Menacho I, Burzynski GM, de Groot JW, et al. Current concepts in RET-related genetics, signaling and therapeutics. Trends Genet. 2006; 22(11):627-636.
  19. Romei C, Mariotti S, Fugazzola L, et al.; ItaMEN network. Multiple endocrine neoplasia type 2 syndromes (MEN 2): results from the ItaMEN network analysis on the prevalence of different genotypes and phenotypes. Eur J Endocrinol. 2010; 163(2):301-308.
  20. Romei C, Tacito A, Molinaro E, et al. Twenty years of lesson learning: how does the RET genetic screening test impact the clinical management of medullary thyroid cancer? Clin Endocrinol (Oxf). 2015; 82(6):892-899.
  21. Siegel R, Ward E, Brawley O, Jemal A. Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin. 2011; 61(4):212-236.
  22. Waldmann J, Langer P, Habbe N, et al. Mutations and polymorphisms in the SDHB, SDHD, VHL, and RET genes in sporadic and familial pheochromocytomas. Endocrine. 2009; 35(3):347-355.

Government Agency, Medical Society, and Other Authoritative Publications:

  1. American Association of Clinical Endocrinologists. AACE/AAES medical/surgical guidelines for clinical practice: Management of thyroid carcinoma. 2001. Available at: https://www.aace.com/files/thyroid-carcinoma.pdf. Accessed on September 29, 2017.  
  2. American Thyroid Association (ATA) Guidelines Task Force, Wells S, Asa S, et al. Revised Medullary thyroid cancer: management guidelines of the American Thyroid Association. March 26, 2015. Available at: http://online.liebertpub.com/doi/pdf/10.1089/thy.2014.0335. Accessed on September 29, 2017.
  3. Moline J, Eng C. GeneReviews™. Multiple Endocrine Neoplasia Type 2. Last updated June 25, 2015. Available at: http://www.ncbi.nlm.nih.gov/books/NBK1257/#men2.REF.americansocietyofclinica.2003.1. Accessed on September 29, 2017.
  4. National Society of Genetic Counselors' Definition Task Force, Resta R, Biesecker BB, et al. A new definition of Genetic Counseling: National Society of Genetic Counselors' Task Force report. J Genet Couns. 2006 ; 5(2):77-83.
  5. NCCN Clinical Practice Guidelines in Oncology®. © 2017 National Comprehensive Cancer Network, Inc. For additional information visit the NCCN website: http://www.nccn.org/index.asp. Accessed on September 29, 2017.
    • Neurodendocrine Tumors (V3.2017). Revised June 13, 2017.
    • Thyroid Carcinoma (V2.2017). Revised May 17, 2017.
  6. Robson ME, Storm CD, Weitzel J, et al. American Society of Clinical Oncology position statement update: genetic and genomic testing for cancer susceptibility. J Clin Oncol. 2010; 28(5):893-901.
  7. Romei C, Cosci B, Renzini G, et al. RET genetic screening of sporadic medullary thyroid cancer (MTC) allows the preclinical diagnosis of unsuspected gene carriers and the identification of a relevant percentage of hidden familial MTC (FMTC). Clin Endocrinol (Oxf). 2011; 74(2):241-247.
  8. Romei C, Mariotti S, Fugazzola L, et al. ItaMEN network. Multiple endocrine neoplasia type 2 syndromes (MEN 2): results from the ItaMEN network analysis on the prevalence of different genotypes and phenotypes. Eur J Endocrinol. 2010; 163(2):301-308.
  9. Szinnai G, Meier C, Komminoth P, Zumsteg UW. Review of multiple endocrine neoplasia type 2A in children: therapeutic results of early thyroidectomy and prognostic value of codon analysis. Pediatrics. 2003; 111(2):E132-E139.  
Websites for Additional Information
  1. American Society of Clinical Oncology. Multiple Endocrine Neoplasia Type 2. Last reviewed November, 2015. Available at: http://www.cancer.net/cancer-types/multiple-endocrine-neoplasia-type-2. Accessed on September 29, 2017.
  2.  National Cancer Institute. Genetics of Endocrine and Neuroendocrine Neoplasias–for health professionals (PDQ®). Last updated July 19, 2017. Available at: http://www.cancer.gov/types/thyroid/hp/medullary-thyroid-genetics-pdq. Acessed on September 29, 2017.
  3. National Library of Medicine (NLM). Genetics Home Reference: Multiple endocrine neoplasia. Reviewed Marcy 2017. Available at: http://ghr.nlm.nih.gov/condition/multiple-endocrine-neoplasia. Accessed on September 29, 2017.
  4. SEER Stat Fact Sheets: Thyroid. National Cancer Institute. Available at: http://seer.cancer.gov/statfacts/html/thyro.html. Accessed on September 29, 2017.
Index

Endocrine gland cancer
Medullary Thyroid Cancer
MEN2
Multiple Endocrine Neoplasia
RET gene
RET proto-oncogene

The use of specific product names is illustrative only. It is not intended to be a recommendation of one product over another, and is not intended to represent a complete listing of all products available.

Document History

Status

Date

Action

Reviewed

11/02/2017

Medical Policy & Technology Assessment Committee (MPTAC) review.

Reviewed

11/01/2017

Hematology/Oncology Subcommittee review. Updated header language from “Current Effective Date” to “Publish Date.” Updated References section.

Revised

05/04/2017

MPTAC review.

Revised

05/03/2017

Hematology/Oncology Subcommittee review. Added genetic counseling to the Medically Necessary criteria. Updated Rationale, Background/Overview and References sections.

Reviewed

11/03/2016

MPTAC review.

Reviewed

11/02/2016

Hematology/Oncology Subcommittee review. Updated formatting in Position Statement section. Updated References section.

Reviewed

11/05/2015

MPTAC review.

Reviewed

11/04/2015

Hematology/Oncology Subcommittee review. Updated Reference section. Updated Coding section with 01/01/2016 CPT descriptor changes; also removed ICD-9 codes.

Reviewed

11/13/2014

MPTAC review.

Reviewed

11/12/2014

 

Hematology/Oncology Subcommittee review.  Updated Reference section.  Updated Coding section with 01/01/2015 CPT changes.

New

11/14/2013

MPTAC review.

New

11/13/2013

 

Hematology/Oncology Subcommittee review. Initial document development. Clinical content relevant to endocrine gland cancer including multiple endocrine neoplasia type 2 (MEN2) and medullary thyroid cancer, moved from GENE.00001 to this document.