Melanoma

Melanoma is a malignancy of the melanocytes. Because of the rising incidence worldwide, it now ranks second to adult leukemia in loss of years of potential life per death. Histology is the gold standard for diagnosis. Molecular testing is helpful when planning targeted therapy.

Tabs Content

Clinical Overview

Key Points

Disseminated melanoma is generally unresponsive to traditional chemotherapy and/or radiotherapy. With the advent of targeted therapy, molecular testing in melanoma has gained importance.

Mutation^a	Biology	Targeted Therapy	Comments
BRAF gene BRAF Codon 600 Mutation Detection by Pyrosequencing 2002498 BRAF V600E Mutation Detection in Circulating Cell-Free DNA by Digital Droplet PCR 2013921	BRAF is a protein involved in the MAPK pathway, which includes BRAF/MEK/ERK signaling Activates pathway, mediates growth signaling, links with factor receptors (eg, tyrosine kinases), leading to cell growth and depression of immune regulation of cancer cells >80% mutations substitute glutamic acid for valine at codon 600, resulting in V600E mutation Other mutations – V600K, V600R, V600D	Combining BRAF with MEK inhibition may improve outcome BRAF V600E inhibitors Vemurafenib Dabrafenib MEK inhibitors Trametinib Selumetinib Cobimetinib Binimetinib	~50% of melanomas (Long, 2011) Molecular genetic testing required if therapy directed at BRAF V600E mutation is being considered Most common in cutaneous melanomas derived from intermittent, acute sun-damaged skin, younger age (<55 yrs), and poorer prognosis compared to BRAF and NRAS wild-type melanomas Resistance develops in all patients Resistance to BRAF inhibitors develops downstream, not at the initial mutation site
RAS family of genes(NRAS, KRAS, HRAS) NRAS Mutation Detection by Pyrosequencing 2003123	NRAS is a protein involved in the RAS/RAF/MAPK pathway Most mutations are in NRAS gene Mutation leads to defective GTPase activity with uncontrolled cell proliferation Most common mutations are located in codons 12, 13,61 Mutation is generally mutually exclusive of BRAF mutation	Phase I and II clinical trials combining BRAF inhibitors with MEK, ATK, and PI3K inhibitors	15-20% of melanomas (Solus, 2013) Associated with thicker tumors, higher mitotic rate, and worse prognosis than BRAF mutation or wild-type BRAF/NRAS genes
KIT gene KIT Mutations, Melanoma 2002695	KIT gene encodes for type III transmembrane receptor tyrosine kinase, which is involved in regulation of MAPK and PI3K pathways Mutations function as oncogene Exons 9, 11, 13, 14, 17, 18	For specific treatment recommendations refer to NCCN Clinical Practice Guidelines in Oncology, Melanoma	Up to 15% of melanomas (Jiang, 2008) Rate of occurrence dependent on type of melanoma Most common in acral lentiginous, sun-damaged skin, or mucosal melanomas KIT mutation testing is important for prediction of response to targeted therapy Immunohistochemistry for c-kit (CD117) should not be used to predict response to targeted therapy
PTEN gene	Functions as lipid phosphatase regulating PI3K/AKT pathways Mutation causes high-level activation of pathway with unregulated cell growth and proliferation Mutation is generally mutually exclusive of NRAS gene mutations, but usually inclusive for BRAF gene mutations	Multiple classes of inhibitors in phase I and II trials – PI3K, AKT, mTORC1, dual PI3K/mTOR inhibitors
^aTests listed are available at ARUP Laboratories.

Diagnosis

Indications for Testing

Atypical melanocytic lesion (mole) requires histologic evaluation.

Histology

Gold standard for diagnosis
- Immunohistochemistry may be required to distinguish poorly differentiated lesions of carcinoma, sarcoma, or lymphoma (B cell or T cell) from melanoma
- Stains to consider include cytokeratin 8,18 low molecular weight (CAM 5.2); melanoma antibody, HMB45; Ki-67 (Mib-1); melan A; S-100 protein; vimentin; and MITF
Architectural and cytologic features of biopsy are interpreted in the context of clinical information
- Architecture – large, asymmetrical, poorly circumscribed lesion; pagetoid spread of melanocytes; effaced rete ridges and underlying dermal architecture; perineural invasion
- Cytology – large nuclei with prominent nucleoli; atypical mitosis (especially in dermis); lack of melanocyte maturation in deep portion of lesion
Metaplastic differentiation (nonmelanocytic cells or tissues) may be identified that may not be melanoma
Molecular testing – refer to Key Points
- Testing for BRAF and KIT mutations recommended by National comprehensive Cancer Network (NCCN, 2017) to guide choice of therapy
- PD-1 is being investigated as predictive marker for response to anti-PD-1 therapy (recommended first line at some centers)

Imaging Studies

Routine cross-sectional imaging (CT, PET, MRI) is not recommended in patients with localized melanoma due to low yield

Genetic Testing

Should be offered to individuals with (ACMG, 2015)
- ≥3 diagnoses of melanoma and/or pancreatic cancer in close relatives
- ≥3 primary melanomas in the same person
- Melanoma and pancreatic cancer in the same person
- Melanoma and astrocytoma in the same person or in 2 first-degree relatives

Prognosis

Depth of tumor invasion – used to determine prognosis
- Breslow thickness – most important factor contributing to T status in tumor, nodes, and metastasis staging
  - Measured from top of epidermal granular cell layer to deepest malignant melanocyte
  - 5-year survival rate – 95.3% with Breslow thickness ≤1.0 mm (corresponds to T1 lesion), 45.1% with Breslow thickness >4.0 mm
- Clark level – important in T1 lesions (<1 mm thick) (corresponds to 95% or better survival)
  - Clark I – melanoma in situ; does not cross basement membrane
  - Clark II – invasion of papillary dermis
  - Clark III – expansion of papillary dermis
  - Clark IV – invasion of reticular dermis
  - Clark V – invasion of subcutaneous fat
Additional histologic features used to determine prognosis
- Involvement of regional lymph nodes (regional nodal dissection or sentinel node testing)
  - Sentinel lymph node biopsy or other diagnostic tests for the evaluation of early, thin melanoma are not recommended as routine testing – these tests do not improve survival (Choosing Wisely, American Society for Clinical Pathology, 2016)
- Metastasis
- Growth phase
- Mitotic count
- Regression
- Ulceration
Additional serum testing
- Lactate dehydrogenase – prognostic factor in late-stage melanoma
  - Elevated levels likely correlate with tumor burden (NCCN, 2017)
  - Independent predictor of poor outcome
- S-100B, serum – elevated level associated with poor prognosis

Differential Diagnosis

Clinical – melanocytic nevi
Histologic
- Well differentiated – melanocytic nevi
- Poorly differentiated – carcinoma, sarcoma, lymphoma (T cell, B cell)

Screening

The American Academy of Dermatology (AAD) and American Cancer Society (ACS) recommend regular skin exams in all patients
The U.S. Preventive Services Task Force finds insufficient evidence to recommend regular skin exams

Monitoring

The National Comprehensive Cancer Network (NCCN) recommends skin examination at least once per year for life for melanoma patients (including those with stage 0, in situ melanoma)
- Patients with stage IA-IIA melanoma, no evidence of disease
  - Comprehensive exam every 3-12 months for five years and annually thereafter as clinically indicated
- Patients with stage IIB-IV melanoma, no evidence of disease
  - Comprehensive exam every 3-6 months for two years, then every 3-12 months for three years, and annually thereafter as clinically indicated
- Although not recommended at baseline, x-ray, CT/MRI, and/or PET/CT every 6-12 months can be considered to screen for recurrent or metastatic disease at discretion of physician
  - Most recurrences manifest within first five years – routine imaging not recommended beyond this period
S-100B, serum
- Rising concentrations after treatment indicate disease recurrence

Background

Epidemiology

Incidence – 22.3/100,000 (SEER, 2017)
- ~87,110 new melanomas in 2017 (estimated) (SEER, 2017)
- Tripled over the last 20 years
- Highest incidence worldwide is in Australia
Age – median is 64 years; rare in children (SEER, 2017)
Sex – M>F, 1.5:1
Ethnic – 10-fold increased incidence in Caucasians
- Acral lentiginous melanoma has equal distribution across all ethnic groups

Inheritance

Gene mutations associated with hereditary melanoma

Gene Symbol^a	Germline Mutations Increase Risk for the Following Cancer Types	Percentage of Hereditary Melanoma^bAttributed to Gene
BAP1	Mesothelioma, melanoma of the eye	Rare
CDK4	Melanoma	2%
CDKN2A	Melanoma, pancreatic	20-40%
PTEN	Thyroid, breast, renal, colorectal, endometrial, melanoma	Rare
RB1	Retinoblastoma, pinealoblastoma, sarcomas, melanoma	Rare
TP53	Li-Fraumeni syndrome, sarcoma, leukemia, breast, brain, adrenocortical, hepatocellular, melanoma	Rare
^aAll genes have autosomal dominant inheritance ^b~5-10% of melanomas are hereditary

Classification

Superficial spreading melanoma (~70%)
Nodular melanoma (10-15%)
Lentigo maligna melanoma (10%)
Acral lentiginous melanoma (~5%)
Mucosal lentiginous melanoma (3%)

Risk Factors

Sunlight – sunburns in childhood, intermittent UV exposure associated with higher risk
Blue or green eyes
Red or blond hair
Melanocytic nevus, dysplastic nevus
Family history – 2-fold risk if first-degree relative had melanoma
- Clustering of melanoma in familial retinoblastoma and Li-Fraumeni syndrome
- Increased risk of familial melanoma in the presence of family history of pancreatic cancer or astrocytoma
Immunosuppression
Prior melanoma

Clinical Presentation

82-85% of melanoma patients present with localized disease; 10-30% present with regional disease; 2-5% with distant metastatic disease
Nevus with Asymmetry, Border irregularity, Color variation, Diameter >6 mm, and Evolving changes (ABCDE criteria)
Head and neck most common sites
Ulceration, pigment loss
Rare sites – eye (iris, ciliochoroidal), mucosa, unknown primary

Pediatrics

Epidemiology

Incidence – 300-425 cases annually in the U.S. (SEER, 2017)
Age – 15-19 years most common
Sex – F>M (minimal)

Risk Factors

Family history – 2-fold risk if first-degree relative had melanoma
- Clustering of melanoma in familial retinoblastoma and Li-Fraumeni syndrome
- Increased risk of familial melanoma in the presence of family history of pancreatic cancer or astrocytoma
History of severe sunburns (>3 before 20 years)
Xeroderma pigmentosa
Immunosuppression
Dysplastic nevi (3- to 6-fold increased risk)

Clinical Presentation

Lesions frequently amelanotic or nodular
ABCDE criteria (Asymmetry, Border irregularity, Color variation, Diameter >6 mm, and Evolving changes) less reliable than in adults

Histology

Congenital nevus has slightly different histologic appearance
Refer to Histology in Diagnosis

Differential Diagnosis

Spitz nevus
Blue nevus
Congenital nevus

ARUP Lab Tests

Detect activating BRAF mutations at codon 600, which can indicate responsiveness to BRAF inhibitors in melanomas

Single gene assay

Oncogenic mutations outside of codon 600 will not be detected

BRAF Codon 600 Mutation Detection by Pyrosequencing 2002498

Method: Polymerase Chain Reaction/Pyrosequencing

Determine BRAF V600E mutation status in patients with solid tumors to select candidates for targeted therapy with kinase (BRAF and/or MEK) inhibitors

Monitor response to therapy and disease progression in patients carrying BRAF V600E mutation

BRAF V600E Mutation Detection in Circulating Cell-Free DNA by Digital Droplet PCR 2013921

Method: Polymerase Chain Reaction

Predict response to anti-EGFR and MAPK pathway therapies in melanoma

NRAS Mutation Detection by Pyrosequencing 2003123

Method: Polymerase Chain Reaction/Pyrosequencing

Detect activating mutations in KIT and PDGFRA

Predict response to targeted therapy

Refer to Additional Technical Information document for further content

Mutations outside of targeted exons are not detected

Test alone cannot be used for diagnosis of malignancy

Variants below the limit of detection (LOD) of 5% variant allele frequency may not be detected

10 ng input DNA from extracted tissue sample is minimally required, but 50 ng input DNA is recommended for optimal results

Large variants (>60bp) may not be detected

Not intended to detect minimal residual disease

Does not distinguish between somatic and germline variants

KIT Mutations, Melanoma 2002695

Method: Massively Parallel Sequencing

Assess for targeted variants that are useful for prognosis and/or treatment of individuals with solid tumor cancers, including melanoma, gastrointestinal stromal tumor (GIST), colorectal, bladder, and hepatocellular carcinomas, at initial diagnosis or in the presence of refractory disease

If the clinical indication is lung cancer, additional molecular genetic testing may be considered for detection of gene rearrangements and/or c-MET exon 14-skipping alterations

For evaluation of microsatellite instability, additional molecular testing should be considered

Refer to Additional Technical Information document for further content

Does not detect translocations, gene rearrangements, copy number alterations, microsatellite instability, or tumor mutational burden

Variants present below the limit of detection of 5% variant allele frequency may not be detected

10 ng input DNA from extracted tissue sample is minimally required, but 50 ng input DNA is recommended for optimal results

Large variants (>60 bp) may not be detected

Variants in known pseudogenes, homologous genomic regions, and/or low mappability regions may not be detected

Not intended to detect minimal residual disease

Does not distinguish between somatic and germline variants

Solid Tumor Mutation Panel by Next Generation Sequencing 2007991

Method: Massively Parallel Sequencing

Genes included: AKT1, ALK, APC, ATM, BRAF, CDH1, CDKN2A, CTNNB1, DDR2, EGFR, ERBB2, ERBB4, EZH2, FBXW7, FGFR1, FGFR2, FGFR3, GNA11, GNAQ, GNAS, HRAS, IDH1, IDH2, KDR, KIT, KRAS, MAP2K1, MET, MTOR, NOTCH1, NRAS, NTRK1, PDGFRA, PIK3CA, PTEN, RB1, RET, ROS1, SMAD4, SMO, STK11, TERT promoter, TP53, VHL

Aid in histologic diagnosis of melanoma

Stained and returned to client pathologist; consultation available if needed

Cytokeratin 8,18 Low Molecular Weight (CAM 5.2) by Immunohistochemistry 2003493

Method: Immunohistochemistry

Melanoma Antibody, HMB45 by Immunohistochemistry 2003935

Method: Immunohistochemistry

Melan A by Immunohistochemistry 2003996

Method: Immunohistochemistry

S-100 Protein by Immunohistochemistry 2004127

Method: Immunohistochemistry

Vimentin by Immunohistochemistry 2004181

Method: Immunohistochemistry

MITF by Immunohistochemistry 2011998

Method: Immunohistochemistry

Aid in histologic diagnosis of melanoma

Stained and resulted by ARUP

Ki-67 with Interpretation by Immunohistochemistry 2007182

Method: Immunohistochemistry

Monitor treatment and determine prognosis of patients with malignant melanoma

Not used for diagnosis

Lactate Dehydrogenase, Serum or Plasma 0020006

Method: Quantitative Enzymatic

Test may be useful as a biomarker of various central nervous system (CNS) pathologies and as a tumor marker for malignant melanoma

S-100B Protein, Serum 2001766

Method: Quantitative Enzyme-Linked Immunosorbent Assay

Aids in prediction of response to nivolumab (OPDIVO) for patients with melanoma

FDA-approved test

PD-L1 28-8 pharmDx by Immunohistochemistry with Interpretation, nivolumab (OPDIVO) 2013684

Method: Immunohistochemistry

Medical Experts

Miller, Christine E., MS, LCGC, Genetic Counselor, Molecular Genetics at ARUP Laboratories; Faculty, Graduate Program in Genetic Counseling, University of Utah

Samowitz, Wade S., MD, Medical Director, Anatomic Pathology, at ARUP Laboratories; Professor of Anatomic Pathology, University of Utah

Wallander, Michelle L., PhD, R&D Investigator, ARUP Institute for Clinical and Experimental Pathology, Anatomic Pathology Group

References

Guidelines

Protocol for the Examination of Specimens from Patients with Melanoma of the Skin. Based on AJCC/UICC TNM, 7th ed. Protocol web posting date: Jan 2016. College of American Pathologists (CAP). Northfield, IL [Revised: Jan 2016; Accessed: Dec 2016]
NCCN Clinical Practice Guidelines in Oncology, Melanoma. National Comprehensive Cancer Network. Fort Washington, PA [Accessed: May 2017]
Hampel H, Bennett RL, Buchanan A, Pearlman R, Wiesner GL, Guideline Development Group, American College of Medical Genetics and Genomics Professional Practice and Guidelines Committee and National Society of Genetic Counselors Practice Guidelines Committee. A practice guideline from the American College of Medical Genetics and Genomics and the National Society of Genetic Counselors: referral indications for cancer predisposition assessment. Genet Med. 2015; 17(1): 70-87. PubMed
Choosing Wisely. An initiative of the ABIM Foundation. [Accessed: Aug 2019]
US Preventive Services Task Force, Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Ebell M, Epling JW, Garcia FA, Gillman MW, Kemper AR, Krist AH, Kurth AE, Landefeld S, Mangione CM, Phillips WR, Phipps MG, Pignone MP, Siu AL. Screening for Skin Cancer: US Preventive Services Task Force Recommendation Statement. JAMA. 2016; 316(4): 429-35. PubMed
Wong SL, Balch CM, Hurley P, Agarwala SS, Akhurst TJ, Cochran A, Cormier JN, Gorman M, Kim TY, McMasters KM, Noyes D, Schuchter LM, Valsecchi ME, Weaver DL, Lyman GH, American Society of Clinical Oncology, Society of Surgical Oncology. Sentinel lymph node biopsy for melanoma: American Society of Clinical Oncology and Society of Surgical Oncology joint clinical practice guideline. J Clin Oncol. 2012; 30(23): 2912-8. PubMed
Dummer R, Hauschild A, Lindenblatt N, Pentheroudakis G, Keilholz U, ESMO Guidelines Committee. Cutaneous melanoma: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol. 2015; 26 Suppl 5: v126-32. PubMed
Bichakjian CK, Halpern AC, Johnson TM, Hood AF, Grichnik JM, Swetter SM, Tsao H, Barbosa VH, Chuang T, Duvic M, Ho VC, Sober AJ, Beutner KR, Bhushan R, Begolka WS, American Academy of Dermatology. Guidelines of care for the management of primary cutaneous melanoma. American Academy of Dermatology. J Am Acad Dermatol. 2011; 65(5): 1032-47. PubMed
Garbe C, Peris K, Hauschild A, Saiag P, Middleton M, Bastholt L, Grob J, Malvehy J, Newton-Bishop J, Stratigos AJ, Pehamberger H, Eggermont AM, European Dermatology Forum (EDF), European Association of Dermato-Oncology (EADO), European Organisation for Research and Treatment of Cancer (EORTC). Diagnosis and treatment of melanoma. European consensus-based interdisciplinary guideline - Update 2016. Eur J Cancer. 2016; 63: 201-17. PubMed

General References

Grossmann AH, Grossmann KF, Wallander ML. Molecular testing in malignant melanoma. Diagn Cytopathol. 2012; 40(6): 503-10. PubMed

Igbokwe A, Lopez-Terrada DH. Molecular testing of solid tumors. Arch Pathol Lab Med. 2011; 135(1): 67-82. PubMed

Jiang X, Zhou J, Yuen NK, Corless CL, Heinrich MC, Fletcher JA, Demetri GD, Widlund HR, Fisher DE, Hodi S. Imatinib targeting of KIT-mutant oncoprotein in melanoma. Clin Cancer Res. 2008; 14(23): 7726-32. PubMed

Kashani-Sabet M. Molecular markers in melanoma. Br J Dermatol. 2014; 170(1): 31-5. PubMed

Khattak M, Fisher R, Turajlic S, Larkin J. Targeted therapy and immunotherapy in advanced melanoma: an evolving paradigm. Ther Adv Med Oncol. 2013; 5(2): 105-18. PubMed

Linos K, Slominski A, Ross JS, Carlson A. Melanoma update: diagnostic and prognostic factors that can effectively shape and personalize management. Biomark Med. 2011; 5(3): 333-60. PubMed

Long GV, Menzies AM, Nagrial AM, Haydu LE, Hamilton AL, Mann GJ, Hughes M, Thompson JF, Scolyer RA, Kefford RF. Prognostic and clinicopathologic associations of oncogenic BRAF in metastatic melanoma. J Clin Oncol. 2011; 29(10): 1239-46. PubMed

Mills O, Messina JL. Pediatric melanoma: a review. Cancer Control. 2009; 16(3): 225-33. PubMed

Nalejska E, Mączyńska E, Lewandowska MA. Prognostic and predictive biomarkers: tools in personalized oncology. Mol Diagn Ther. 2014; 18(3): 273-84. PubMed

Ohsie SJ, Sarantopoulos P, Cochran AJ, Binder SW. Immunohistochemical characteristics of melanoma. J Cutan Pathol. 2008; 35(5): 433-44. PubMed

Palmer SR, Erickson LA, Ichetovkin I, Knauer DJ, Markovic SN. Circulating serologic and molecular biomarkers in malignant melanoma. Mayo Clin Proc. 2011; 86(10): 981-90. PubMed

Paradela S, Fonseca E, Prieto VG. Melanoma in children. Arch Pathol Lab Med. 2011; 135(3): 307-16. PubMed

Postow MA, Carvajal RD. Therapeutic implications of KIT in melanoma. Cancer J. 2012; 18(2): 137-41. PubMed

Solus JF, Kraft S. Ras, Raf, and MAP kinase in melanoma. Adv Anat Pathol. 2013; 20(4): 217-26. PubMed

Strouse JJ, Fears TR, Tucker MA, Wayne AS. Pediatric melanoma: risk factor and survival analysis of the surveillance, epidemiology and end results database. J Clin Oncol. 2005; 23(21): 4735-41. PubMed

Resources from the ARUP Institute for Clinical and Experimental Pathology®

Chandler WM, Rowe LR, Florell SR, Jahromi MS, Schiffman JD, South ST. Differentiation of malignant melanoma from benign nevus using a novel genomic microarray with low specimen requirements. Arch Pathol Lab Med. 2012; 136(8): 947-55. PubMed

Grossmann AH, Grossmann KF, Wallander ML. Molecular testing in malignant melanoma. Diagn Cytopathol. 2012; 40(6): 503-10. PubMed

Grossmann AH, Yoo JH, Clancy J, Sorensen LK, Sedgwick A, Tong Z, Ostanin K, Rogers A, Grossmann KF, Tripp SR, Thomas KR, D'Souza-Schorey C, Odelberg SJ, Li DY. The small GTPase ARF6 stimulates β-catenin transcriptional activity during WNT5A-mediated melanoma invasion and metastasis. Sci Signal. 2013; 6(265): ra14. PubMed

Hall BJ, Schmidt RL, Sharma RR, Layfield LJ. Fine-needle aspiration cytology for the diagnosis of metastatic melanoma: systematic review and meta-analysis. Am J Clin Pathol. 2013; 140(5): 635-42. PubMed

Oakley GM, Curtin K, Layfield L, Jarboe E, Buchmann LO, Hunt JP. Increased melanoma risk in individuals with papillary thyroid carcinoma. JAMA Otolaryngol Head Neck Surg. 2014; 140(5): 423-7. PubMed

Szankasi P, Reading S, Vaughn CP, Prchal JT, Bahler DW, Kelley TW. A quantitative allele-specific PCR test for the BRAF V600E mutation using a single heterozygous control plasmid for quantitation: a model for qPCR testing without standard curves. J Mol Diagn. 2013; 15(2): 248-54. PubMed

Yang H, Kircher DA, Kim KH, Grossmann AH, VanBrocklin MW, Holmen SL, Robinson JP. Activated MEK cooperates with Cdkn2a and Pten loss to promote the development and maintenance of melanoma. Oncogene. 2017; 36(27): 3842-3851. PubMed

Educational Videos

Content Review:

May 2017

Last Update: October 2019

Melanoma

Key Points

Diagnosis

Indications for Testing

Histology

Imaging Studies

Genetic Testing

Prognosis

Differential Diagnosis

Screening

Monitoring

Background

Epidemiology

Inheritance

Classification

Risk Factors

Clinical Presentation

Pediatrics

Epidemiology

Risk Factors

Clinical Presentation

Histology

Differential Diagnosis

ARUP Lab Tests

Medical Experts

References

Guidelines

General References

Resources from the ARUP Institute for Clinical and Experimental Pathology®

ARUP Laboratories

ARUP Websites

ARUP Consult


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Melanoma

Key Points

Diagnosis

Indications for Testing

Histology

Imaging Studies

Genetic Testing

Prognosis

Differential Diagnosis

Screening

Monitoring

Background

Epidemiology

Inheritance

Classification

Risk Factors

Clinical Presentation

Pediatrics

Epidemiology

Risk Factors

Clinical Presentation

Histology

Differential Diagnosis

ARUP Lab Tests

Medical Experts

References

Guidelines

General References

Resources from the ARUP Institute for Clinical and Experimental Pathology®

ARUP Laboratories

ARUP Websites

ARUP Consult