ORIGINAL STUDY
Atypical Spitzoid Neoplasms in Childhood:
A Molecular and Outcome Study
Christina Y. Lee, BA,* Lauren M. Sholl, MS,* Bin Zhang, MS,* Emily A. Merkel, BA,*
Sapna M. Amin, MD,* Joan Guitart, MD,*† and Pedram Gerami, MD*†
Abstract: The natural history of atypical Spitz neoplasms remains
poorly understood, resulting in significant patient and clinician
anxiety. We sought to better characterize outcomes that correlated
with molecular features by performing a prospective cohort study of
pediatric atypical spitzoid neoplasms in which fluorescence in situ
hybridization studies were obtained for diagnosis. Cases with
sufficient tissue underwent additional retrospective assessment for
translocations in ALK, NTRK1, BRAF, RET, and ROS1. Among 246
total patients assessed, 13% had a positive fluorescence in situ
hybridization result. Follow-up data was available in 85 patients.
Two patients had a recurrence of whom 1 had distant metastasis.
Both patients had homozygous deletions in 9p21. Homozygous de-
letions in 9p21 significantly correlated with recurrence of disease
(P = 0.027). Fifteen (36%) of 42 cases were found to have a kinase
fusion protein. However, the presence of kinase fusions was non-
prognostic of recurrence (P . 0.99). This study was limited by the
availability and length of follow-up data and the number of adverse
outcomes. The majority of atypical spitzoid neoplasms in childhood
have indolent behavior. Although the subgroup of patients with
homozygous deletions in 9p21 is at higher risk for aggressive clinical
behavior, their prognosis seems considerably better than similarly
staged conventional melanoma.
Key Words: spitzoid neoplasm, fluorescence in situ hybridization,
kinase fusion, pediatrics
(Am J Dermatopathol 2017;39:181–186)
INTRODUCTION
Despite being the subject of myriad studies in dermatol-
ogy and pathology, the natural history of childhood atypical
spitzoid neoplasms remains poorly understood. This is, in part,
a result of the case–control design used for most studies inves-
tigating atypical spitzoid neoplasms in childhood. These stud-
ies are highly valuable and have allowed investigators to better
characterize atypical spitzoid neoplasms with adverse behavior.
From the *Department of Dermatology, Feinberg School of Medicine, North-
western University, Chicago, IL; and †Robert H. Lurie Cancer Center,
Feinberg School of Medicine, Northwestern University, Chicago, IL.
Supported by the IDP Foundation.
P. Gerami has served as a consultant to Castle Biosciences, Inc, and
DermTech, Inc, and has received honoraria for this. The remaining
authors declare no conflicts of interest.
Reprints: Pedram Gerami, MD, Department of Dermatology, Northwestern
University, 676 N St. Clair St, Suite 1600, Chicago, IL 60611 (e-mail:
pgerami1@nm.org).
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
Am J Dermatopathol
Volume 39, Number 3, March 2017
Copyright Ó 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
For example, through a case-controlled study design, our group
previously identified homozygous deletions in 9p21 as a genetic
signature associated with aggressive behavior in atypical spit-
zoid neoplasms.1 However, case–control studies also have
many limitations and are unable to describe the natural history
of these lesions.
In this study, we report the findings in a prospective
cohort of pediatric atypical spitzoid neoplasms that have been
assessed by fluorescence in situ hybridization (FISH) for
diagnostic purposes. We sought to identify the frequency of
a positive FISH result among atypical spitzoid neoplasms in
which there was sufficient concern to request molecular
assessment and consultative opinion. Additionally, we sought
to determine the frequency of aggressive tumor behavior in the
entire cohort with follow-up information, and, in particular,
among cases with a positive FISH result. Finally, in light of the
recent discovery of a number of specific translocations
involving ROS1, ALK, NTRK1, BRAF, and RET as the primary
driver in Spitzoid neoplasms,2 we retrospectively analyzed our
cases for these translocations to determine if any are associated
with a positive FISH result or aggressive biological behavior.
MATERIALS AND METHODS
After obtaining approval from the Institutional Review
Board of the Northwestern University, we prospectively
followed all patients aged 18 years or younger with
a diagnosis of an atypical spitzoid neoplasm between 2006
and 2015. Only those with a diagnosis of atypical Spitz
nevus, atypical Spitz tumor, or spitzoid melanoma assessed
by FISH for risk assessment at the time of diagnosis were
included. FISH analysis and interpretation for a 4-probe assay
targeting 6p25, 11q13, 6p/CEP6, and 6q/CEP6 and/or for
a 2-probe assay targeting 9p21 and cep9 were used as
previously described.3,4 Clinical parameters were recorded,
which included age, sex, and anatomical location, along with
histological features, such as mitotic rate and ulceration.
Cases were retrospectively assessed for mitoses by a board
certified dermatopathologist (P.G.) if it was not reported at the
time of diagnosis. Eighteen patients in the current cohort were
previously reported in prior studies,5,6 which have included
both pediatric and adult patients. The remaining patients in
this study have not been included in any prior studies. When
follow-up was available, cases were classified into 4 groups
on the basis of their outcome: (1) those with no evidence of
disease after re-excision, (2) those with no evidence of disease
beyond the sentinel lymph node, (3) those with disease in the
www.amjdermatopathology.com | 181
Lee et al Am J Dermatopathol
Volume 39, Number 3, March 2017

complete lymphadenectomy but no further evidence of dis-

TABLE 1. Clinical, Pathologic, and Molecular Characteristics
ease, and (4) those with recurrence, which included patients
of Spitzoid Neoplasms
with a local recurrence, in transit metastasis, or distant
metastasis. Total (N = 246)
Spitz nevi 15.8% (39)
Immunohistochemistry Spitz tumors 72.0% (177)
For cases with available follow-up and sufficient addi- Spitzoid melanomas 12.2% (30)
tional tissue, immunohistochemical studies were conducted Average age (yr) 9.9
using unstained sections of formalin-fixed, paraffin-embedded Male:female 120:126
material. All immunohistochemistry was performed on the Location of lesion % (n)
Leica BOND-MAX (Leica Biosystems, Buffalo Grove, IL) Head/neck 34.6% (85)
using the Bond Polymer Refine Detection kit. The RET Trunk 22.4% (55)
antibody (1:250, EPR2871; Abcam, Cambridge, MA) used Upper extremities 17.9% (45)
a low pH retrieval. The BRAF (1:100, Clone pBR1; Spring Lower extremities 24.0% (59)
Biosciences, Atlanta, GA), NTRK1 (Anti-TrkA, 1:100, Clone Acral 0
EP 1058Y; Abcam), and ALK (clone M7195; DAKO, Unknown 0.8% (2)
Carpinteria, CA) immunostains used a high pH retrieval. The FISH positive 32 (13.0%)
BRAF immunostain used an additional rabbit anti-rat HRP 6p25 18
(DAKO) link step. The percentage of cells exhibiting staining 11q13 10
was assessed by our dermatopathologist (P.G.). Immunostain- 6p/CEP6 7
ing for ROS1 (1:250, Clone D4D6; Cell Signaling Technol- 9p21 19
ogy, Danvers, MA) was unsuccessful. FISH negative 214 (87.0%)

FISH Analysis for Kinase Fusion

To confirm the presence of a fusion, cases considered
positive by immunohistochemistry were tested with their
respective FISH break-apart probe. Cases with progression
beyond the sentinel node and available tissue were also assessed
for a fusion in ALK, NTRK1, BRAF, RET, and ROS1. The ALK,
BRAF, and NTRK1 break-apart probes (Empire Genomics,
Buffalo, NY) and the RET and ROS1 centromeric and telomer-
ic probes (Abbott Molecular, Des Plaines, IL) were prepared via
their respective manufacturer’s protocol. All slides were exam-
ined using a Zeiss Imager Z.2 microscope using Metafer soft-
ware (MetaSystems, Newton, MA) for nuclei detection and
image processing. Slides were considered positive for break
apart if signals were greater than 2 signals away from each
other, if the 50 colored probe was lost, or if there were uneven
gains between the 50 and 30 ends of the gene.
Statistical Analysis
Statistical analysis was performed using SPSS software
(IBM, Corp, Armonk, NY). Fisher exact test was used to
compare the frequency of recurrence between FISH-positive
and FISH-negative cases with follow-up data. Logistic
regression analysis was used to evaluate significance of
recurrence for variables such as age, sex, mitotic figures,
ulceration, FISH positivity, and fusion positivity.
RESULTS
Our cohort included 246 cases, 120 (48.7%) males and
126 (51.2%) females (Table 1). The median age was 9.9 years
(range, 1–18 years). Thirty-nine (15.8%) lesions were diag-
nosed as atypical Spitz nevi, 177 (72.0%) as atypical Spitz
tumors, and 30 (12.2%) as spitzoid melanomas. Overall, FISH
analysis using the conventional melanoma 4-probe and 2-probe
set was found to be positive in 32 (13.0%) of 246 cases.
Specifically, 18 were positive for 6p25 gains, 10 for 11q13
gains, 7 for 6p/CEP6, and 19 for 9p21 homozygous deletions.
Fifteen cases showed alterations in 2 or more of the tested loci.
Single chromosomal aberrations were detected in 17 cases:
6p25 in 4 cases, 6p/cep6 in 1 case, and 9p21 in 12 cases.
Thirty-two patients were found to have 6q23 deletions. How-
ever, we did not include 6q23 as a positive result if it was the
only positive FISH finding because we have previously found
this group of patients to have a uniformly indolent prognosis.7
Follow-up data were available for 85 patients, with
a median follow-up of 12 months (range, 3–89 months). Nine
(10.6%) of these 85 lesions were ulcerated. The median mitotic
rate was 2 square millimeter (range, 0–14/mm2). Seventeen
(20.0%) of these 85 cases had a positive FISH result (Table
1); of which, 9 tumors had homozygous deletions in 9p21.
None of the 68 cases with a negative FISH result and follow-
up data had a recurrence (median follow-up, 10 months).
Twenty-three (27.1%) of 85 patients underwent a sen-
tinel lymph node biopsy (SLNB). Ten patients with a negative
FISH result and 13 patients with a positive FISH result
underwent a SLNB. Twelve (52.2%) patients had a positive
SLNB result; of whom, 8 had a positive FISH result.
Overall, there were 4 patients with evidence of tumor
spread beyond the sentinel lymph node (Table 2). Three cases
had homozygous deletions in 9p21, whereas 1 case was pos-
itive for 6p/CEP6. Three patients, including 1 who had 3
instances of local recurrence despite wide excision (Fig. 1),
were disease free at the time of last follow-up (range, 3–43
months). One patient diagnosed with spitzoid melanoma
developed distant metastasis to the groin, axilla, brain, and
chest (follow-up 24 months). Both patients with either local
recurrent (Fig. 2) or metastatic disease had homozygous de-
letions in 9p21.
Using the Fisher exact test, FISH positivity significantly
correlated with recurrence (P = 0.0381). Furthermore, homo-
zygous deletions in 9p21 and recurrence remained significantly

182 | www.amjdermatopathology.com Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Copyright Ó 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol
Volume 39, Number 3, March 2017 Molecular and Outcome Study

TABLE 2. Spitzoid Neoplasms With Disease Progression Beyond the Sentinel Node
Age (yr), FISH FU Length,
Case Sex Location Diagnosis FISH Result Translocation mo Overall Outcome
48 6, male Abdomen Spitzoid melanoma 9p21 Negative 24 Positive SLNB; distant metastasis to groin,
axilla, brain, and chest
99 2, female Nose, tip Spitzoid melanoma 6p23, 11q13, Not tested 43 3 times local recurrence following wide
9p21 excision; positive SLNB; 1 positive node
on complete lymphadenectomy; no
evidence of disease
101 8, male Shin Spitzoid melanoma 9p21 NTRK1 39 Positive SLNB; 1 positive node on complete
lymphadenectomy 1 year of interferon
therapy; no evidence of disease
105 2, male Cheek Spitzoid melanoma 6p/CEP6 Negative 3 Positive SLNB; 2 positive nodes on complete
lymphadenectomy; no evidence of disease

correlated (P = 0.0271). Significant correlation was also
observed between FISH positivity and recurrence through
logistic regression analysis (P = 0.010). However, age, sex,
ulceration, mitotic figures, or fusion positivity did not signifi-
cantly correlate with recurrence.
Additional tissue was available for 42 of 85 cases with
follow-up to assess for the presence of a translocation in
ALK, NTRK1, BRAF, or RET. Six of 85 cases were tested for
ROS1 and were all negative. Kinase fusions involving 1 of
these 5 tyrosine kinases were found in 15 (35.7%) of 42
cases in mutually exclusive groups: ALK in 7 cases
(16.7%), NTRK1 in 4 cases (9.5%), and BRAF in 4 cases
(9.5%). No cases had a gene rearrangement in RET in our
series (Table 3). Of these 15 cases with a translocation, copy
number gains were also seen in 6 cases: 3 in ALK, 2 in
BRAF, and 1 in NTRK1. In the subset of cases (n = 4) with
disease progression beyond the sentinel lymph node, 1 case
could not be assessed, 2 cases were negative for the presence
of any translocation, and 1 case had a translocation in
NTRK1. This was the only case with a translocation detected
that also had homozygous deletions in 9p21. This patient
had 1 positive node in the completion lymph node dissection
but had no evidence of disease recurrence or progression at
the time of last follow-up (39 months).
DISCUSSION
There are still many unknowns regarding the natural
history of atypical spitzoid neoplasms in children. Most series
that have assessed this subject are of a case–control nature
often enriched with cases with adverse events to compare
morphologic or molecular features of aggressive and indolent
cases.5,8 There are few series of well-defined cohorts that
allow for estimates of the true frequency of aggressive

FIGURE 1. Spitzoid melanoma,

Breslow depth at least 6.5 mm, from
a 2-year-old female. A, Low-power
magnification showing a large
compound spitzoid melanocytic
proliferation with ulceration at the
surface and broad extension to the
base of the biopsy. B, Low-power
magnification showing expansile
nodular growth of nests near the
base of the lesion. C, Intermediate-
power magnification of deep ex-
pansile nests showing apoptotic and
mitotically active melanocytes. D,
High-power magnification showing
high-grade nuclear atypia with
coarse nuclear chromatin and
numerous deep mitotic figures.

Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. www.amjdermatopathology.com | 183

Copyright Ó 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Lee et al
FIGURE 2. Positive FISH result from
a spitzoid melanoma from a 2-year-
old girl. A, FISH with probe target-
ing 9p21 showing majority of cells
with homozygous deletions in
9p21. B, FISH with probe targeting
CEP9 showing normal to increased
copy numbers of the chromosome 9
centromere. C, FISH with probe
targeting 11q13 showing low level,
occasional gains. D, FISH with probe
targeting 6p25 showing the major-
ity of cells having copy number
gains.
behavior. Although atypical Spitz tumors have comparable
rates of sentinel lymph node positivity to conventional mela-
nomas, it is generally appreciated that the frequency of distant
metastasis or death in these cases is more rare than in con-
ventional melanomas.9–11 Still, clinicians and parents often
desire more concrete numbers to better understand the risk
level of the patient or their child.
In our study, we identified 2 (2.4%) of 85 patients who
had recurrence of their disease; of whom, 1 (1.2%) developed
distant metastasis. This percentage of distant metastasis is
similar to other cohort studies of atypical spitzoid neoplasms.
In separate studies, Ludgate et al9 and Sepehr et al12 each
identified 1 (1.5%) of 67 patients and 1 (0.007%) of 144
patients, respectively, who developed distant metastasis.
However, even these studies are subject to overestimate the
true rate of aggressive behavior for several reasons.
Our cohort is partially defined by patients in whom the
tumor was concerning enough to be sent to a tertiary referral
center for molecular assessment and consultative opinion.
Therefore, most of our cases have been assessed as morpho-
logically highly atypical by at least 1 pathologist. Further-
more, follow-up data are generally more attainable from
TABLE 3. Frequency of Kinase Fusions in Spitzoid Neoplasms
Spitz Nevus (n = 2) % Atypical Spitz Tumor (n = 34) %
Fusion (No. Cases) (No. Cases)
ALK 0 20.6% (7)
NTRK1 50% (1) 5.9% (2)
BRAF 0 11.8% (4)
RET 0 0
Total 50% (1) 30.9% (13)
184 | www.amjdermatopathology.com
Copyright Ó 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Am J Dermatopathol
Volume 39, Number 3, March 2017
patients with more aggressive disease who continue to have
follow-up visits to the hospital with documentation of their
health status. Alternatively, patients with low-grade lesions or
a negative FISH result are more likely lost to follow up,
presumably due to having a more benign clinical course.
Hence, we estimate that although 1 (1.2%) of 85 patients in
our cohort with follow-up had distant metastasis, the true rate,
even among the cases that are morphologically quite atypical,
is likely well below 1%. Among the 17 patients with follow-
up information and a positive FISH result, 4 had tumor spread
beyond the sentinel lymph node, which included 1 patient
who had a 3-time recurrence of the lesion and 1 patient who
developed distant metastasis. Nine of 17 FISH-positive
tumors had homozygous deletions in 9p21, including both
patients with local recurrence and distant metastasis. Based on
these figures, we estimate that less than 25% of children with
atypical spitzoid neoplasms with homozygous deletions in
9p21 will experience a recurrence after complete excision and
less than 12.5% will develop distant metastasis. For the same
reasons mentioned previously, these numbers are likely over-
estimates, as follow-up information is more consistently avail-
able for high-risk patients who return for subsequent visits.
Spitzoid Melanoma (n = 6) % Total (n = 42) %
(No. Cases) (No. Cases)
0 16.7% (7)
16.7% (1) 9.5% (4)
0 9.5% (4)
0 0
16.7% (1) 35.7% (15)
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
Am J Dermatopathol
Volume 39, Number 3, March 2017
Among the cases with follow-up in our study, sufficient
material was available to retrospectively perform immuno-
histochemistry and FISH studies for 42 cases to assess for the
presence of a translocation in ALK, NTRK1, BRAF, or RET.
Similar to previous reports,2,13 we found kinase fusions in
35.7% of tested cases (Table 3). The most common among
these were ALK fusions (n = 7), followed by NTRK1 (n = 4)
and BRAF (n = 4). None of these cases resulted in an adverse
event or metastasis. Similar to the study performed by Wies-
ner et al,2 we found fusions present in Spitz nevi (n = 1), Spitz
tumors (n = 13), and Spitzoid melanomas (n = 1). Only 1 case
in our study with a positive FISH result also had an NTRK1
fusion. This case was among the 4 cases with tumor deposits
found in the complete lymphadenectomy but had no evidence
of recurrence with 39 months of follow-up. Hence, in our
cohort, the presence of one of the aforementioned fusions
did not result in any increased incidence of aggressive dis-
ease. Importantly, among cases with fusions, 6 cases also had
copy number gains involving the chromosome locus of the
tyrosine kinase (Figs. 3, 4). This is further evidence that the
spectrum of copy number aberrations seen in atypical Spitz
tumors with indolent behavior is greater than previously sus-
pected. These results are similar to those from Lee et al,13 in
which only 1 of 23 spitzoid neoplasms with a fusion had an
adverse event. The fusions in these cases seem to be the
initiating driver events that can lead to either stable nevi or,
infrequently, malignancy through the acquisition of additional
mutations or aberrations. Lee et al13 also found that TERT
promoter mutations strongly correlated with adverse behavior
in spitzoid neoplasms. However, there is currently an insuf-
ficient amount of published data to determine if any of the
particular fusions carry a higher risk of progression or acqui-
sition of these additional genomic aberrations.
FIGURE 3. ALK-positive atypical
Spitz tumor from a 7-year-old boy. A
and B, Low-power magnification of
a large compound spitzoid melano-
cytic proliferation with plexiform
arrangement of superficial nests and
dumbbell-shaped base. C, Interme-
diate-power magnification of ex-
pansile nodular growth of the
dumbbell area near the base of the
biopsy specimen. D, High-power
magnification of an expansile nest of
intermediate-sized spitzoid melano-
cytic cells with moderate atypia and
occasional mitotic activity at the
base of the biopsy specimen.
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.
Copyright Ó 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Molecular and Outcome Study
Limitations of our study include the length of follow-up
and the number of patients who were lost to follow-up. We
suspect that patients lost to follow-up most likely consist of
a group of patients with uneventful outcomes and that the
incidence of adverse events is even lower than our current
estimation. Although the median follow-up time is limited, 22
patients were followed for at least 3 years after the initial
diagnosis. Although additional events are possible with
longer follow-up, even in the given time frame, we were
able to establish a statistically significant increase in risk of
recurrence of disease associated with homozygous deletions
in 9p21. Furthermore, considering the overall limited amount
of information and experience available in the current
literature regarding the behavior of atypical spitzoid neo-
plasms, we believe this study adds additional valuable
information.
Although the subgroup of tumors with homozygous
deletions in 9p21 constitutes a high-risk group, the majority
of these patients will likely do well with adequate surgical
therapy. Hence, the prognosis of pediatric atypical spitzoid
neoplasms, including those labeled as spitzoid melanoma,
will likely have a better prognosis than similarly staged
conventional melanoma.8,10,13 This further supports the sug-
gestion to designate spitzoid melanomas of childhood as
a separate entity from conventional melanomas. Although
different data series have shown that atypical spitzoid neo-
plasms in childhood with homozygous deletions in 9p21 are
at higher risk for aggressive tumor behavior than other spit-
zoid neoplasms of childhood,6 the precise incidence of
adverse events among these children still requires further
study. Hence, debate remains as to whether they should be
called “spitzoid melanoma” or “high-risk atypical Spitz tumor
of childhood with homozygous deletions in 9p21.” On a case-
www.amjdermatopathology.com | 185
Lee et al Am J Dermatopathol
Volume 39, Number 3, March 2017

FIGURE 4. Immunohistochemistry
and FISH break-apart probe con-
firming an ALK translocation in an
atypical Spitz tumor from a 7-year-
old boy. A, strong and diffuse
positive immunostaining for ALK
throughout the tumor. B, FISH using
ALK dual-colored break-apart re-
arrangement probe targeting the
kinase domain in yellow and the 50
end of the gene in green. Numerous
copy number increases of the kinase
domain are noted without associated
50 end of the gene, showing a break
apart with copy number gains.

by-case basis, assessment of the morphologic features in con-
junction with molecular findings should be considered in
making this decision.
REFERENCES
1. Gerami P, Scolyer RA, Xu X, et al. Risk assessment for atypical spitzoid
melanocytic neoplasms using FISH to identify chromosomal copy num-
ber aberrations. Am J Surg Pathol. 2013;37:676–684.
2. Wiesner T, He J, Yelensky R, et al. Kinase fusions are frequent in Spitz
tumours and spitzoid melanomas. Nat Commun. 2014;5:3116.
3. Gerami P, Wass A, Mafee M, et al. Fluorescence in situ hybridization for
distinguishing nevoid melanomas from mitotically active nevi. Am J Surg
Pathol. 2009;33:1783–1788.
4. Gerami P, Li G, Pouryazdanparast P, et al. A highly specific and dis-
criminatory FISH assay for distinguishing between benign and malignant
melanocytic neoplasms. Am J Surg Pathol. 2012;36:808–817.
5. Gerami P, Cooper C, Bajaj S, et al. Outcomes of atypical spitz tumors
with chromosomal copy number aberrations and conventional melano-
mas in children. Am J Surg Pathol. 2013;37:1387–1394.
6. Yazdan P, Cooper C, Sholl LM, et al. Comparative analysis of atypical
spitz tumors with heterozygous versus homozygous 9p21 deletions for
clinical outcomes, histomorphology, BRAF mutation, and p16 expres-
sion. Am J Surg Pathol. 2014;38:638–645.
7. Shen L, Cooper C, Bajaj S, et al. Atypical spitz tumors with 6q23
deletions: a clinical, histological, and molecular study. Am J Dermato-
pathol. 2013;35:804–812.
8. Raskin L, Ludgate M, Iyer RK, et al. Copy number variations and
clinical outcome in atypical spitz tumors. Am J Surg Pathol. 2011;35:
243–252.
9. Ludgate MW, Fullen DR, Lee J, et al. The atypical Spitz tumor of
uncertain biologic potential: a series of 67 patients from a single institu-
tion. Cancer. 2009;115:631–641.
10. Paradela S, Fonseca E, Pita-Fernandez S, et al. Spitzoid and non-spitzoid
melanoma in children: a prognostic comparative study. J Eur Acad Der-
matol Venereol. 2013;27:1214–1221.
11. Ghazi B, Carlson GW, Murray DR, et al. Utility of lymph node assess-
ment for atypical spitzoid melanocytic neoplasms. Ann Surg Oncol.
2010;17:2471–2475.
12. Sepehr A, Chao E, Trefrey B, et al. Long-term outcome of Spitz-type
melanocytic tumors. Arch Dermatol. 2011;147:1173–1179.
13. Lee S, Barnhill RL, Dummer R, et al. Tert promoter mutations are pre-
dictive of aggressive clinical behavior in patients with spitzoid melano-
cytic neoplasms. Sci Rep. 2015;5:11200.

186 | www.amjdermatopathology.com Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Copyright Ó 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.