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Quade, Bradley

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Quade

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Bradley

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Quade, Bradley
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    Intravenous Leiomyomatosis: An Unusual Intermediate between Benign and Malignant Uterine Smooth Muscle Tumors
    (2016) Ordulu, Zehra; Nucci, Marisa; Dal Cin, Paola; Hollowell, Monica; Otis, Christopher N.; Hornick, Jason; Park, Peter; Kim, Tae-Min; Quade, Bradley; Morton, Cynthia
    Intravenous leiomyomatosis is an unusual smooth muscle neoplasm with quasi-malignant intravascular growth but a histologically banal appearance. Herein, we report expression and molecular cytogenetic analyses of a series of 12 intravenous leiomyomatosis cases to understand better the pathogenesis of intravenous leiomyomatosis. All cases were analyzed for expression of HMGA2, MDM2 and CDK4 proteins by immunohistochemistry based on our previous finding of der(14)t(12;14)(q14.3;q24) in intravenous leiomyomatosis. Seven of 12 (58%) intravenous leiomyomatosis cases expressed HMGA2, and none expressed MDM2 or CDK4. Co-localization of hybridization signals for probes from the HMGA2 locus (12q14.3) and from 14q24 by interphase fluorescence in situ hybridization (FISH) was detected in a mean of 89.2% of nuclei in HMGA2-positive cases by immunohistochemistry, but in only 12.4% of nuclei in negative cases, indicating an association of HMGA2 expression and this chromosomal rearrangement (p=8.24×10−10). Four HMGA2-positive cases had greater than two HMGA2 hybridization signals per cell. No cases showed loss of a hybridization signal by interphase FISH for the frequently deleted region of 7q22 in uterine leiomyomata. One intravenous leiomyomatosis case analyzed by array comparative genomic hybridization revealed complex copy number variations. Finally, expression profiling was performed on three intravenous leiomyomatosis cases. Interestingly, hierarchical cluster analysis of the expression profiles revealed segregation of the intravenous leiomyomatosis cases with leiomyosarcoma rather than with myometrium, uterine leiomyoma of the usual histological type, or plexiform leiomyoma. These findings suggest that intravenous leiomyomatosis cases share some molecular cytogenetic characteristics with uterine leiomyoma, and expression profiles similar to that of leiomyosarcoma cases, further supporting their intermediate, quasi-malignant behavior.
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    Peritoneal Dissemination Complicating Morcellation of Uterine Mesenchymal Neoplasms
    (Public Library of Science, 2012) Seidman, Michael A.; Oduyebo, Titilope; Muto, Michael; Crum, Christopher; Nucci, Marisa; Quade, Bradley
    Background: Power morcellation has become a common technique for the minimally invasive resection of uterine leiomyomas. This technique is associated with dissemination of cellular material throughout the peritoneum. When morcellated uterine tumors are unexpectedly found to be leiomyosarcomas or tumors with atypical features (atypical leiomyoma, smooth muscle tumor of uncertain malignant potential), there may be significant clinical consequences. This study was undertaken to determine the frequency and clinical consequence of intraperitoneal dissemination of these neoplasms. Methodology/principal findings: From 2005–2010, 1091 instances of uterine morcellation were identified at BWH. Unexpected diagnoses of leiomyoma variants or atypical and malignant smooth muscle tumors occurred in 1.2% of cases using power morcellation for uterine masses clinically presumed to be “fibroids” over this period, including one endometrial stromal sarcoma (ESS), one cellular leiomyoma (CL), six atypical leiomyomas (AL), three smooth muscle tumor of uncertain malignant potential (STUMPs), and one leiomyosarcoma (LMS). The rate of unexpected sarcoma after the laparoscopic morcellation procedure was 0.09%, 9-fold higher than the rate currently quoted to patients during pre-procedure briefing, and this rate may increase over time as diagnostically challenging or under-sampled tumors manifest their biological potential. Furthermore, when examining follow-up laparoscopies, both from in-house and consultation cases, disseminated disease occurred in 64.3% of all tumors (zero of one ESS, one of one CL, zero of one AL, four of four STUMPs, and four of seven LMS). Only disseminated leiomyosarcoma, however, was associated with mortality. Procedures are proposed for pathologic evaluation of morcellation specimens and associated follow-up specimens. Conclusions/significance: While additional study is warranted, these data suggest uterine morcellation carries a risk of disseminating unexpected malignancy with apparent associated increase in mortality much higher than appreciated currently.
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    Hereditary leiomyomatosis and renal cell cancer: Cutaneous lesions & atypical fibroids
    (Elsevier, 2017) Bortoletto, Pietro; Lindsey, Jennifer L.; Yuan, Liping; Quade, Bradley; Gargiulo, Antonio; Morton, Cynthia; Stewart, Elizabeth A.; Anchan, Raymond
    Objective: To report a diagnosis of hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome following initial presentation with multiple cutaneous lesions. Design: Case report. Design classification N/A. Setting: Academic tertiary care center. Patient(s) 27-year-old nulligravid woman who presented with multiple red-brown lesions on her skin found to have cutaneous and uterine leiomyoma. Intervention(s) Biopsy of cutaneous lesions and fertility sparing robot-assisted laparoscopic myomectomy (RALM). Main outcome measures(s) Histological assessment of uterine leiomyoma. Results(s) Pathologic examination of uterine leiomyoma revealed diffuse atypia and fumarate hydratase loss phenotype concerning for genetic syndrome. Follow-up DNA sequencing via Sanger sequencing confirmed a pathogenetic R2333H mutation consistent with HLRCC. Conclusion(s) Consideration of HLRCC on differential diagnosis when patients present with cutaneous nodules and atypical or early onset uterine leiomyoma provides opportunity for early surveillance, family member testing, and more thoughtful surgical planning. Precis 27-year-old woman with multiple cutaneous lesions is found to have uterine leiomyomas and undergoes robotic myomectomy. Genetic testing of uterine leiomyomas reveals mutation in fumarate hydratase, etiologic in hereditary leiomyomatosis and renal cell cancer (HLRCC).