Context.—Inflammatory myofibroblastic tumor is a predominantly benign, spindle cell, mesenchymal neoplasm with myxoid areas that occurs rarely in the female genital tract and may be confused with other spindle cell lesions, particularly leiomyosarcoma. Objective.—To investigate the utility of detecting anaplastic lymphoma kinase-1 protein expression and ALK gene rearrangements in the diagnosis of inflammatory myofibroblastic tumors in the female genital tract. Design.—Eight inflammatory myofibroblastic tumors arising in the female genital tract and seen in consultation (from 2004 to 2011) were reviewed. Immunohistochemistry for anaplastic lymphoma kinase-1 and fluorescence in-situ hybridization studies for ALK gene rearrangements were performed. Results.—The anatomic sites included myometrium (4 cases) and endometrium, fallopian tube, cervix, and a cervical polyp (1 each), with a patient age range from 25 to 52 years. Histologic features ranged from bland spindle cells to striking cytologic atypia, embedded in a prominent myxoid background. Anaplastic lymphoma kinase-1 immunohistochemistry was positive in 7 cases. Fluorescence in-situ hybridization studies detected ALK gene rearrangements in 5 cases. Five cases had both immunopositivity and fluorescence in-situ hybridization abnormalities, 2 cases had immunopositivity only, and 1 case was negative by both methods. Conclusions.—This is the first report, to our knowledge, of ALK gene rearrangements in inflammatory myofibroblastic tumors in the female genital tract. If a myxoid background is appreciated in a spindle cell lesion of the female genital tract, especially if inflammatory cells are present, anaplastic lymphoma kinase-1 staining along with fluorescence in situ hybridization studies, for ALK gene rearrangements, may aid in distinguishing inflammatory myofibroblastic tumors from their malignant mimics.
Context Atypical apocrine adenosis is a rare breast lesion in which the cellular population demonstrates cytologic alterations that may be confused with malignancy. The clinical significance and management of atypical apocrine adenosis are unclear because of the lack of long-term follow-up studies. Objective To determine the breast cancer risk in a retrospective series of patients with atypical apocrine adenosis diagnosed in otherwise benign, breast excisional biopsies. Design We identified 37 atypical apocrine adenosis cases in the Mayo Benign Breast Disease Cohort (9340 women) between 1967 and 1991 with a blinded pathology rereview. Breast cancer diagnoses subsequent to initial atypical apocrine adenosis biopsy were identified (average follow-up, 14 years). Results The mean age at diagnosis of atypical apocrine adenosis in the group was 59 years. Breast carcinoma subsequently developed in 3 women (8%) with atypical apocrine adenosis, diagnosed after follow-up intervals of 4, 12, and 18 years. The tumor from 1 of the 3 cases (33%) was ductal carcinoma in situ, contralateral to the original biopsy, and the other 2 cases (66%) were invasive carcinoma. Ages at the time of diagnosis of atypical apocrine adenosis were 55, 47, and 63 years for those that developed in situ or invasive carcinoma. Conclusions (1) Atypical apocrine adenosis was a rare lesion during the accrual era of our cohort (<1% of cases); (2) women found to have atypical apocrine adenosis were, on average, older than were other patients with benign breast disease, however, there does not seem to be an association with age and risk for developing carcinoma in patients diagnosed with atypical apocrine adenosis, as previously suggested; and (3) atypical apocrine adenosis does not appear to be an aggressive lesion and should not be regarded as a direct histologic precursor to breast carcinoma.
Follicular dendritic cell (FDC) proliferations and dysplastic FDCs can be seen in Hyaline-vascular Castleman disease (HVCD). The association between HVCD and FDC sarcoma is well-documented; dysplastic FDCs may be precursors to FDC sarcoma. Herein, we describe a case of HVCD with strikingly large and dysplastic FDCs, which raised the differential of Hodgkin lymphoma and other neoplasms. Scattered dysplastic FDCs were predominantly in germinal centers and mantle zones, and rarely in interfollicular areas. Although occasional germinal centers contained increased FDCs, no mass forming proliferations were present to suggest FDC sarcoma. Immunostaining demonstrated that the atypical FDCs expressed CD21, clusterin and CXCL13, but not CD23, S100, pankeratin or CD30; they aberrantly expressed epidermal growth factor receptor (EGFR). The present case demonstrates that dysplastic FDCs may be present as isolated cells that require immunophenotyping to distinguish them from malignant entities with similar morphologic features. A variety of FDC markers is required to confirm their origin as the expression of any single marker is not assured, as occurred in this case. Pathologists need be aware of FDC proliferations in HVCD because of their association with FDC sarcoma. Aberrant EGFR expression by dysplastic FDCs may indicate that they are pre-neoplastic and necessitate long-term patient follow-up.
A 48-year-old Hispanic man was evaluated for a suppurative plaque on the left side of the neck. The lesion began as an apparent insect bite several months before the time of consultation. Multiple oral courses of Bactrim and topical application of Neosporin had been advised without improvement. The patient denied constitutional symptoms, and his review of systems was otherwise negative. Social history was remarkable for prior homeless status, marijuana use, and limited alcohol consumption. On examination, he was afebrile and of thin build. Examination of the neck demonstrated a 3 3 2-cm, crusted, lichenified, and suppurative plaque on the left side of the neck, as pictured below (Fig. 1). There was also palpable lymphadenopathy in the left anterior cervical chain. Computed tomography scan demonstrated a focal area of dermal thickening and bilateral upper cervical lymphadenopathy. There were no other cutaneous, oral mucosal, or genital lesions present. The clinical differential diagnosis included scrofuloderma, deep fungal infection, other infectious processes, and malignancy. A shave biopsy showed irregular epidermal hyperplasia with overlying scale crust (Fig. 2) and a lichenoid infiltrate clouding the dermal-epidermal junction (Fig. 3). The infiltrate was composed mainly of plasma cells and histiocytes with scattered neutrophils, eosinophils, and lymphocytes (Fig. 4). The epidermis showed numerous necrotic keratinocytes and collections of neutrophils (Figs. 5, 6).What is your diagnosis?(Continued on page 99) FIGURE 1. Three by 2-cm, crusted, lichenified, and suppurative plaque on the left side of the neck.FIGURE 2. Scanning view showing irregular epidermal hyperplasia and a lichenoid infiltrate (H&E, 318). H&E, hematoxylin and eosin.FIGURE 3. Lichenoid infiltrate obscuring the dermal-epidermal junction (H&E, 384). H&E, hematoxylin and eosin.
A 37-year-old man presented with progressive gait ataxia for 2 weeks. He also complained of right neck tumefaction and general malaise for 1 month. His prior medical history included hypertension, depression, polysubstance abuse, and 1 year of mild short-term memory complaints. His Mini-Mental State Examination score was 26/30; he had mild left hemiparesis, and ataxia of the limbs, trunk, and gait. CSF examination showed protein 78 mg/dL, glucose 52 mg/dL, nucleated cell count 42 (87% lymphocytes, 13% monocytes); cytology, JC virus, and varicella zoster virus PCR were negative. Brain MRI, neck PET, and right cervical lymph node and frontal stereotactic brain biopsy (figures 1 and 2) were consistent with granulomatous angiitis of the CNS associated with Hodgkin lymphoma. 1,2 AUTHOR CONTRIBUTIONSDr. Fuehrer: drafting/revising the manuscript, contribution of vital reagents/tools/patients, acquisition of data. Dr. Hammack: drafting/ revising the manuscript, study supervision. Dr. Morris: drafting/ revising the manuscript, analysis or interpretation of data, acquisition of data, study supervision. Dr. Kaufmann: drafting/revising the manuscript, analysis or interpretation of data. Dr. Giannini: drafting/
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