#dermpathJC June 2017 Summary:

#dermpathJC June 2017:

Thursday, June 29th, 9pm EST

Article discussed: “SOX10 immunohistochemistry in sweat ductal/glandular neoplasms.”

Authors: Cassarino D, Su A, Robbins B, Altree-Tacha D, Ra S.

Journal of Cutaneous Pathology, June 2017.

Free access at:  for 2 months.

Special thanks to Dr Annie Morrison (@AnnieMorrisonMDfor providing the summary below.

Journal Club Summary:

Background: Sox10 is a relatively new IHC stain that is used as a melanocytic and schwannian marker.

Prelim observation/previous study: Sox10 IHC positive in eccrine glands and negative in eccrine ducts, apocrine glands, and hair follicles

Hypothesis: Sweat gland tumors of suspected eccrine origin would show Sox10 expression while apocrine-derived sweat gland tumors would not.

Methods: 90 sweat gland tumors (all with classic histopathology) and 13 basal cell carcinomas evaluated:

Cylindroma 10

Spiradenoma 13

Syringocystademona papilliferum 10

Hidradenoma papilliferum 10

Poroma 12

Syringoma 10

Apocrine adenoma 10

Hidradenoma 15

Stain used: anti-Sox10 antibody (clone BC34: Biocare Medical,, Concord, California; dilution 1:20)

Stain evaluation: percentage of tumor cells (semiquantitative) and staining intensity (0, 1+, 2+, 3+) recorded.

Results Table:

Screen Shot 2017-07-03 at 1.28.27 AM.png

Discussion highlights: Strong diffuse positivity for Sox10 in cylindroma and spiradenoma and the complete absence of Sox10 staining in BCC may be helpful in the setting of a small, superficially sampled, and/or poorly oriented or fragmented specimen.

Sox10 staining in SCAP and HAP: diffuse myoepithelial cell staining, not unexpected

Myoepithelial cells: + Sox10 in normal salivary glands & ducts, salivary gland tumors, breast lobules, cutaneous myoepitheliomas, and cutaneous mixed tumors with predominate myoepithelial components.

SCAP, HAP, and apocrine adenomas: focal + Sox10 in apocrine epithelial cells, unexpected

New hypothesis: Sox10 expression may be upregulated in a portion of the lesional cells

Poroma & syringomas: Sox10 negative, expected

Both believed to be derived from sweat ducts

Hidradenoma: heterogenous Sox10 staining; somewhat expected

Hidradenomas are heterogenous tumors, two cell types (clear cells & dark/eosinophilic cells)

Weak/negative Sox10 staining appeared more common in lesions/areas with clear cell predominance.

Limitations of study:

Small sample size

Limited lesions evaluated (another study planned to look at follicular tumors and adnexal carcinomas)

Twitter Journal Club Discussion Summary:

A significant number of #dermpathJC participants use Sox10 with or without S100protein to distinguish melanocytic/neural lesions from other lesions, and/or in sentinal lymph nodes for melanoma.

Sox10 has been used by some participants to evaluate adenoid cystic carcinoma

Sox10 is negative in PEComas, fibrohistiocytic and histiocytic proliferations.

A known Sox10 pitfall is occasional staining in scars, particularly concerning when evaluating desmoplastic melanomas.

From this paper Sox10 does not appear to help distinguish between eccrine and apocrine differentiation in adnexal lesions. Histomorphology is still the “gold standard”.

Study confirms: Sox10 stains myoepithelial cells in cutaneous adnexal lesions.

The results of the pending study of Sox10 expression in follicular tumors and adnexal carcinomas is of interest to many participants.

More studies/references are needed to further characterize Sox10 expression in adnexal lesions.

Diagram of Sox10 role in neural crest cell migration:nrm2428-i1

Fun fact: SOX10 aka SRY-related HMG-box. SOX10 gene expression regulated by MITF in melanocytic lesions.

Interesting Link: Music from SOX10 protein sequence: https://www.youtube.com/watch?v=rA126rgymAo

See y’all next month!

#dermpathJC May 2017 Summary:

#dermpathJC May 2017:

Thursday, May 25th, 9pm EST

Article discussed: “Cutaneous Plasmacytosis: A Clinicopathologic Study of a Series of Cases and their Treatment Outcomes.”

Authors: Han X, Lee S, Tan S, Chong W, Ng S, Ooi M and Goh C.

American Journal of Dermatopathology, 2017.

Free access at:  from MAY21 to JUNE21!

Special thanks to Dr Adrienne Jordan @JordanDermPath for providing the summary below.

Journal Club Summary:

Review of the article:

1. Cutaneous plasmayctosis presents clinically as reddish brown nodules on the trunk of adults; most common in Asians; chronic course (lesions present for 2-10 years)
a. Axilla is almost always involved
b. Elevated serum immunoglobulins (IgG most common)
c. Elevated Kappa and lambda free light chains, but Kappa to lambda ratio is preserved
2. Histology:
a. Perivascular dermal infiltrate of mature polyclonal plasma cells; no atypia
b. Mast cells are increased (some are degranulating)
c. Increased basal melanin pigment
d. Vascular proliferation common
e. Psoriasiform epidermal hyperplasia
f. Lymphoid follicles may be present
g. HHV8 and EBV negative
3. Treatment:
a. Mask bath PUVA
b. Oral antibiotics
c. Topical and intralesional steroids
d. Topical tacrolimus
4. Poor prognostic factors:
a. IgG > 5000 mg/mL
b. High plasma cell count in bone marrow
5. Differential diagnosis
a. Secondary syphilis: Spirochetes seen on Warthin Starry stain or IHC
b. Rosai Dorfman: Infiltrate also has abundant histiocytes and emperipolesis
c. Plasmacytoma: monoclonality and plasma cell atypia
d. MZBCL: very difficult distinction; monoclonality (specifically performing heavy chain gene rearrangement studies) may be helpful

Review of Journal Club Discussion:
1. It was hypothesized that since IL-6 is increased in patients with CP and IL-6 receptors are localized on melanin this explains the increased basal melanin pigmentation
2. Castlemans disease and plasma cell granuloma were added to the list of differential diagnoses
3. Although not reported in this series, other articles have commented on perineural plasma cells being prominent in CP
4. Although other papers have described an increased IgG4, participants agreed that CP is not part of the IgG4 diseases as sclerosis is not generally a feature of CP as it is in the IgG4 diseases
a. If sclerosis is present, one should consider a plasma cell granuloma
5. Very nice chart provided to help differentiate plasma cell infiltrates in the skin:

Screen Shot 2017-05-30 at 6.53.44 PM

Next #dermpathJC is set for 5/25/17 at 9PM EST. We will be featuring the following article by Dr Han et al. PDF at https://tinyurl.com/kq8vzdb.

We are so thankful to the American Journal of Dermatopathology for their support!! FREE access from MAY21 to JUNE21! You can download the PDF at the link above.

Just remember, to follow the discussion all you need to do is search for the #dermpathJC hashtag on the allotted date and time (5/25/17 9PM EST). You can also tag our @dermpathJC twitter handle. If you want to contribute to the discussion and leave a comment, you will need to open a Twitter account.

We are excited for you to join us.



#dermpathJC April 2017 Summary:

#dermpathJC April 2017:

Thursday, April 27th, 9pm EST

Article discussed: “Acantholytic invasive squamous cell carcinoma: tumor diameter, invasion depth, grade of differentiation, surgical margins, perineural invasion, recurrence and death rate.”

Authors: J.H. Pyne, E. Myint, E. M. Barr, S. P. Clark, M. David, R. Na.

Journal of Cutaneous Pathology 2017: 44: 320-327.

Access at: http://onlinelibrary.wiley.com/doi/10.1111/cup.12869/full


Journal Club Summary:

Acantholysis (definition): loss of intercellular adhesion between keratinocytes (not intracellular).
Acantholytic SCC may be referred as adenoid SCC, adenoacanthoma, or pseudoglandular SCC. 1st described by Lever in 1947.
Even though it had “pseudoglandular appearance, the acantholytic phenomenon was entirely squamous in nature.
Acantholytic SCC has been more of a histological fascination and not a prognostic one.
Conflicting early papers with closing thoughts that acantholytic SCC could be prognostically bad. Those studies had low power.

Acantholytic SCC:
has been described as an intermediate risk SCC
more prevalent in male patients (male pattern baldness/increased risk of sun damage link perhaps?)
on chronically sun damaged skin such as the head & neck

Which histologic factors indicate higher-risk invasive SCC?
increased tumor diameter
increased tumor depth of invasion
shift towards poor differentiation
Perineural invasion – goes in the report if there

European guidelines for treatment of SCC – from 2015
low-risk SCC – treat with 5mm margin
high-risk SCC – treat with 10mm margin

US treatment guidelines for treatment of SCC of the skin:
Low-risk SCC use 4-6mm margin. If high risk, wider margins or Mohs.
NCCN 2017 guidelines talk about adenoid (acantholytic) SCC as a marker of an increased risk of recurrence or metastasis – Nappi et al. 1989
High risk marker for local recurrence or metastases

Pyne et al. Results:
total of 1656 invasive SCC identified for the study
4.9% cases (82 total) had acantholysis
confirmed independently by 2 pathologists
no significant difference in relation to sex and grade of differentiation bw acantholytic SCC and non-acantholytic SCC
median age (72 years) was similar for both patient groups (with and without acantholysis)
Site most favored for acantholytic SCC (head and cheek/chin)
Site most favored for non-acantholytic SCC (leg – particularly lower leg and forearm) – keratoacanthomatous morphology (from journal club)
Depth of non-acantholytic SCC was significantly deeper than acantholytic SCC: 1.5mm vs 1mm (p<0.001).
Shift from well to poor differentiation did not correlate with an increase in the acantholysis percentage.
Median follow up 25 months for 77 cases

single center study
SCC driving etiology was chronic sun exposure etc.

metastatic potential – SCC diameter of at least 15mm and depth of at least 2mm
poor differentiation and/or increased tumor depth may have confounded recurrence, rather than just the presence of acantholysis alone.
Nappi et al did nit find any PNI in any case of an acantholytic study (1989).

More appropriate measures of aggressive behavior for SCC: mortality, metastasis and perineural invasion
Low perineural invasion, low recurrence rates, no deaths on followup, may prompt us to think of acantholytic SCC as a low-risk tumor.

I want to extend a special Thank You to Dr. Shea and @JCutaneousPath for their support in making this article open-access for two moths for our first dermpath journal club!

Thank you all for participating,


Silvija P. Gottesman, MD

For our first #dermpathJC on 4/27/17 9PM EST we will be featuring the following article by Dr Pyne et al. PDF at .

We are so thankful to @JCutaneousPath for their support!! This article will be free access for the next two months!! You can download the PDF at the link above.

Just remember, to follow the discussion all you need to do is search for the  hashtag on the allotted date and time (4/27/17 9PM EST). You can also tag our @dermpathJC twitter handle. If you want to contribute to the discussion and leave a comment, you will need to open a Twitter account.

We are excited for you to join us. IMG_7444