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Rosenberg, Andrew Eric

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Rosenberg

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Andrew Eric

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Rosenberg, Andrew Eric
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    Whole-Slide Imaging Digital Pathology as a Platform for Teleconsultation: A Pilot Study Using Paired Subspecialist Correlations
    (College of American Pathologists, 2009) Lauwers, Gregory Y.; Wilbur, David; Madi, Kalil; Colvin, Robert; Duncan, Lyn; Faquin, William; Ferry, Judith; Frosch, Matthew; Houser, Stuart L.; Kradin, Richard; Louis, David; Mark, Eugene; Mino-Kenudson, Mari; Misdraji, Joseph; Nielsen, Gunnlauger P.; Pitman, Martha; Rosenberg, Andrew Eric; Smith, R. Neal; Sohani, Aliyah; Stone, James; Tambouret, Rosemary; Wu, Chin-Lee; Young, Robert; Zembowicz, Artur; Wlietmann, Wolfgang
    Context.—Whole-slide imaging technology offers promise for rapid, Internet-based telepathology consultations between institutions. Before implementation, technical issues, pathologist adaptability, and morphologic pitfalls must be well characterized. Objective.—To determine whether interpretation of whole-slide images differed from glass-slide interpretation in difficult surgical pathology cases. Design.—Diagnostically challenging pathology slides from a variety of anatomic sites from an outside laboratory were scanned into whole digital format. Digital and glass slides were independently diagnosed by 2 subspecialty pathologists. Reference, digital, and glass-slide interpretations were compared. Operator comments on technical issues were gathered. Results.—Fifty-three case pairs were analyzed. There was agreement among digital, glass, and reference diagnoses in 45 cases (85%) and between digital and glass diagnoses in 48 (91%) cases. There were 5 digital cases (9%) discordant with both reference and glass diagnoses. Further review of each of these cases indicated an incorrect digital whole-slide interpretation. Neoplastic cases showed better correlation (93%) than did cases of nonneoplastic disease (88%). Comments on discordant cases related to digital whole technology focused on issues such as fine resolution and navigating ability at high magnification. Conclusions.—Overall concordance between digital whole-slide and standard glass-slide interpretations was good at 91%. Adjustments in technology, case selection, and technology familiarization should improve performance, making digital whole-slide review feasible for broader telepathology subspecialty consultation applications.
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    Osteoblastoma-like Osteosarcoma of the Cuboid: A Case Report
    (BioMed Central, 2010) Kumar, Navin; Rosenberg, Andrew Eric; Raskin, Kevin
    Osteosarcoma most commonly arises in the long bones of the skeleton, and rarely develops in the bones of the foot. We describe a patient who presented with left foot pain, whose radiographic evaluation revealed a lytic destructive mass in the cuboid bone. A biopsy showed an osteoblastoma-like variant of osteosarcoma and the patient was treated with preoperative chemotherapy and amputation. Osteosarcoma of the foot is uncommon and the literature reveals that it is often associated with a delay in diagnosis.
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    Recurrent Chromosomal Copy Number Alterations in Sporadic Chordomas
    (Public Library of Science, 2011) Le, Long Phi; Nielsen, Gunnlaugur; Rosenberg, Andrew Eric; Thomas, Dafydd; Batten, Julie M.; Deshpande, Vikram; Schwab, Joseph; Duan, Zhenfeng; Xavier, Ramnik; Hornicek, Francis; Iafrate, Anthony
    The molecular events in chordoma pathogenesis have not been fully delineated, particularly with respect to copy number changes. Understanding copy number alterations in chordoma may reveal critical disease mechanisms that could be exploited for tumor classification and therapy. We report the copy number analysis of 21 sporadic chordomas using array comparative genomic hybridization (CGH). Recurrent copy changes were further evaluated with immunohistochemistry, methylation specific PCR, and quantitative real-time PCR. Similar to previous findings, large copy number losses, involving chromosomes 1p, 3, 4, 9, 10, 13, 14, and 18, were more common than copy number gains. Loss of CDKN2A with or without loss of CDKN2B on 9p21.3 was observed in 16/20 (80%) unique cases of which six (30%) showed homozygous deletions ranging from 76 kilobases to 4.7 megabases. One copy loss of the 10q23.31 region which encodes PTEN was found in 16/20 (80%) cases. Loss of CDKN2A and PTEN expression in the majority of cases was not attributed to promoter methylation. Our sporadic chordoma cases did not show hotspot point mutations in some common cancer gene targets. Moreover, most of these sporadic tumors are not associated with T (brachyury) duplication or amplification. Deficiency of CDKN2A and PTEN expression, although shared across many other different types of tumors, likely represents a key aspect of chordoma pathogenesis. Sporadic chordomas may rely on mechanisms other than copy number gain if they indeed exploit T/ brachyury for proliferation.