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Abstracts Presented at the 49Th Annual Meeting of the American Society of Dermatopathology October 11–14, 2012 Chicago, Illinois USA

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Abstracts Presented at the 49Th Annual Meeting of the American Society of Dermatopathology October 11–14, 2012 Chicago, Illinois USA J Cutan Pathol 2013: 40: 70–201 © 2012 John Wiley & Sons A/S. doi: 10.1111/cup.12062 Published by Blackwell Publishing Ltd John Wiley & Sons. Printed in Singapore Journal of Cutaneous Pathology Abstracts presented at the 49th Annual Meeting of the American Society of Dermatopathology October 11–14, 2012 Chicago, Illinois USA Abstracts presented in the 13th Annual Duel in Dermatopathology Resident Competition, Oral Sessions 1, 2 and 3, the Fellows’ Case Presentations, and in Poster Sessions 1 and 2 are listed on the following pages in the order they were presented. 70 Abstracts ORAL ABSTRACT SESSION 1 pathology, and adjunct studies including immunohistochemical stains. Molecular diagnostic studies for T-cell receptor gene rearrangement by TCR-PCR were also performed. The 4 patients IMMUNOCYTOCHEMICAL P63 EXPRESSION carried diagnoses of: 1) pcALCL and MF, 2.) MF, LyP-type B, and IN PRIMARY CUTANEOUS B-CELL LYMPHOMA; pcALCL, 3.) LyP-type C, MF, and pcALCL, and 4.) LyP-type C FURTHER EVIDENCE FOR PATHOGENETIC HETEROGENEITY and MF with characteristic clinical presentation and histopathologic Zena Shukur MBBS BSc findings. The results of the TCR-PCR showed that all tumors Zena Shukur MBBS BSc1, Phillip Coates PhD2, John Goodlad expressed and retained a T-cell receptor clone(s) as follows: 1) MD FRCPath3, Alistair Robson FRCPath DipRCPath2 bilallelic clone, 2) single clone, 3) bilallelic clone and additional 1St John’s Institute of Dermatology, London, United Kingdom clone, and 4) single clone, respectively. The four patients in our (Great Britain) series demonstrated remarkably indolent clinical courses with good 2University of Dundee, Dundee, United Kingdom (Great Britain) response to treatment. We report a series of four cases of individuals 3 Western General Hospital, Edinburgh, United Kingdom (Great with coexisting diagnoses of some combination of MF, pcALCL, and Britain) LYP, with remarkably benign clinical courses, and whose tumors are analyzed by molecular analysis for T-cell receptor (TCR) gene The p63 gene is an important regulator of epithelial development, as rearrangement studies. it transcriptionally regulates the expression of genes involved in cell survival, proliferation, adhesion and differentiation. Over-expression EVALUATION OF FOLLICULAR T-HELPER CELLS IN of p63 has been demonstrated in various tumours, although it is PRIMARY CUTANEOUS CD4+ SMALL/MEDIUM not clear whether p63 serves to halt or enhance tumour growth. SIZED PLEOMORPHIC T-CELL LYMPHOMAS & A Through the use of alternate promoters certain isoforms (TAp63) SERIES OF INFLAMMATORY DERMATOSES transactivate p53 target genes and induce apoptosis, whereas other Alistair Robson FRCPath Dip RCPath isoforms (delta-Np63) appear to convey a dominant-negative effect Mina Ally MBBS BSc1, Manuel Rodriguez-Justo MD PhD2, on p53. p63 expression in nodal follicular lymphoma (FL) and Blanca Martin MD1, Natalie Attard MRCP PhD1, Ayoma, diffuse large B-cell lymphoma (DLBCL) has been observed and Attygalle MBBS PhD3, Roberto Verdolini FRCP4, Alistair correlated with proliferative index and mortality. The role of p63 Robson FRCPath Dip RCPath1 in cutaneous B-cell lymphoma has yet to be elucidated. This study 1St John’s Institute of Dermatology, London, United Kingdom assessed p63 expression in primary cutaneous follicle centre cell (Great Britain) lymphoma (pcFCCL) and diffuse large B-cell lymphoma, leg type 2University College Hospital, London, United Kingdom (Great (DLBCLL). Using an antibody that recognizes both p63 isoforms, 4 Britain) 3 of 8 of DLBCLL had diffuse strong expression. Of 8 pcFCCL, 6 were Royal Marsden Hospital, London, United Kingdom (Great completely negative, with weak expression in 2. Further labeling of Britain) 4 8 cases of DLBCLL and 5 pcFCCL using an antibody specific to the St Margarets Hospital, Epping, United Kingdom (Great delta-Np63 isoform of p63 failed to show expression, indicating the Britain) observed expression in the positive cases was of the TAp63 isoform. This pilot study further emphasizes the different biology of these There is evidence to support a follicular T-Helper phenotype in lymphomas, and might reflect one mechanism for their markedly primary cutaneous CD4+ small/medium sized pleomorphic T- differing clinical behavior. cell lymphoma (CSMTCL), with expression of PD-1, CXCL- and ICOS by the atypical cells. We describe fourteen cases of this entity COEXISTING PRIMARY CUTANEOUS and compare expression of these immunophenotypical markers LYMPHOPROLIFERATIVE DISORDERS WITH in these tumours with a series of forty inflammatory dermatoses. BENIGN CLINICAL COURSE AND RETAINED TUMOR All but one patient presented with solitary lesions on the head, CLONE: A SERIES OF 4 PATIENTS neck and upper trunk. Biopsies revealed a dense nodular non- Anne Stowman MD epidermotropic infiltrate of small to medium sized atypical T-cells. Anne Stowman MD1, Ling-Lun Hsia MS42, William Kanner Neoplastic cells had a CD3+/CD4+/CD8-/CD30- phenotype. MD1, James Patterson MD1, Mani Mahadevan MD1, Lawrence Silverman MD1, Grant Bullock MD, PhD1 Of 8 tumours analysed, TCR analysis was clonal in 5 and 1University of Virginia Health System, Charlottesville, VA, USA the Ki-67 fraction varied from 30–50%. Staging investigations 2University of Virginia Medical School, Charlottesville, VA, performed in 11cases were normal. All tumours regressed following USA treatment with topical steroids, excision or radiotherapy. All tumours widely expressed PD-1; and ICOS to a lesser extent. CXCL-13 stained fewer cells and was often less intense. Of the The majority of primary cutaneous lymphomas are cutaneous T-cell dermatoses, PD-1 and ICOS labelled lymphoid cells in all cases, lymphomas (CTCL), of which mycosis fungoides (MF) is the most albeit fewer than in the tumours, and CXCL-13 was negative common, followed by CD30+ lymphoproliferative disorders, which in 32; PD-1+ cells were particularly numerous in comparison include lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (pcALCL), and borderline cases between the to the other markers. A rosette pattern of PD-1 expression was two. Patients diagnosed with MF, LyP or pcALCL traditionally only identified in the CSMTCL cases. There remains uncertainty follow an indolent clinical course. However, in MF patients whose about the appropriate nosological status of CSMTCL, which tumors have undergone transformation or patients with multiple some authors consider to be a ‘‘pseudolymphoma’’. The presence lymphoproliferative diagnoses, there is a much more aggressive of atypical cells with a PD-1+ CXCL-13+ ICOS+ phenotype clinical course with poor prognosis. We identified four patients with helps differentiate CSMTCL from reactive infiltrates, and might coexisting combinations of MF, pcALCL, or LYP. We also reviewed account for the substantial B-cell fraction that characterises these the clinical information, treatment interventions, clinical course, tumours. 71 Abstracts A COLLABORATIVE STUDY USING FISH TO a total of 6 new or evolving melanocytic proliferations, with IDENTIFY HISTOLOGICALLY AMBIGUOUS one patient developing three unique sites of primary malignant MELANOCYTIC TUMORS WITH POTENTIAL FOR melanoma. Body distribution included face (n = 1), abdomen/back AGGRESSIVE CLINICAL BEHAVIOR (n = 1), upper extremities (n = 2) and lower extremities (n Pedram Gerami MD = 2). Patients had undergone therapy for an average of 143 1 Pedram Gerami MD days prior to biopsy of the clinically suspicious lesion. Lesions 1 Northwestern University, Department of Dermatology, pathologically demonstrated one case of compound melanocytic Chicago, IL, USA nevus with architectural disorder and severe cytologic atypia and five instances of new primary malignant melanoma arising at the site Previously we demonstrated a FISH assay could discriminate of a preexisting melanocytic nevus. Conclusions: We describe the melanomas from nevi with high accuracy. This includes the original histopathological findings of melanocytic proliferations, including melanoma FISH assay, targeting 6p25, 6q23, 11q13 and Cep6 as new primary malignant melanomas, following vemurafenib therapy. well as a second more recently described FISH assay with greater Additional investigation is necessary to elucidate the pathogenesis accuracy targeting 6p25, 9p21, 11q13 and 8q24. However, only of vemurafenib associated melanocytic proliferations; however, limited studies have addressed the ability of FISH to predict behavior frequent dermatological evaluations are warranted in patients in borderline melanocytic neoplasms. In this study, we investigated receiving BRAF inhibitors. the ability of FISH using the 2 aforementioned probe sets to identify those histologically ambiguous melanocytic tumors most likely to CUTANEOUS CLEAR CELL SARCOMA WITH result in clinically aggressive behavior. In a collaborative study JUNCTIONAL COMPONENT AND PAGETOID SPREAD involving 5 centers in the USA and 1 in Australia, we identified 89 MIMICKING MELANOMA histologically ambiguous melanocytic tumors. The diagnosis in all Alison Cheah MBBS cases was either atypical spitz tumor, possible nevoid melanoma or Alison Cheah MBBS1, Steven Billings MD1 deep penetrating nevus of uncertain malignant potential. In 13 cases 1Cleveland Clinic, Cleveland, OH, USA there was local regional metastasis beyond a sentinel node or death of disease (group1). In 76 cases, there was at least 5 years of follow up Cutaneous clear cell sarcoma can pose a diagnostic challenge to with no patients developing disease beyond the
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