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Dedifferentiation in Gastrointestinal Stromal Tumor to an Anaplastic KIT-negative Phenotype A Diagnostic Pitfall Morphologic and Molecular Characterization of 8 Cases Occurring Either De Novo or After Imatinib Therapy

Dedifferentiation in Gastrointestinal Stromal Tumor to an Anaplastic KIT-negative Phenotype A... ORIGINAL ARTICLE Dedifferentiation in Gastrointestinal Stromal Tumor to an Anaplastic KIT-negative Phenotype: A Diagnostic Pitfall Morphologic and Molecular Characterization of 8 Cases Occurring Either De Novo or After Imatinib Therapy Cristina R. Antonescu, MD,* Salvatore Romeo, MD,w Lei Zhang, MD,* Khedoudja Nafa, PhD,* Jason L. Hornick, MD, PhD,z Gunnlaugur Petur Nielsen, MD,y Mari Mino-Kenudson, MD,y Hsuan-Ying Huang, MD,8 Juan-Miguel Mosquera, MD,z Paolo A. Dei Tos, MD,w and Christopher D.M. Fletcher, MDz pression and de novo expression of either cytokeratin (4/8) or Abstract: Most gastrointestinal stromal tumors (GISTs) can be desmin (1/8). There was no difference in the KIT genotype be- recognized by their monotonous cytologic features and over- tween the 2 components. However, 2 imatinib-resistant tumors expression of KIT oncoprotein. Altered morphology and loss of showed coexistence of KIT exon 11 and exon 13 mutations. CD117 reactivity has been described previously after chronic Fluorescence in situ hybridization showed loss of 1 KIT gene in imatinib treatment; however, this phenomenon has not been 3 cases and low-level amplification of KIT in 2 other cases in the reported in imatinib-naive tumors. Eight patients with abrupt CD117-negative component, compared with the CD117-positive transition from a classic CD117-positive spindle cell GIST to an http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Surgical Pathology Wolters Kluwer Health

Dedifferentiation in Gastrointestinal Stromal Tumor to an Anaplastic KIT-negative Phenotype A Diagnostic Pitfall Morphologic and Molecular Characterization of 8 Cases Occurring Either De Novo or After Imatinib Therapy

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Copyright
Copyright © 2013 by Lippincott Williams & Wilkins
ISSN
0147-5185
eISSN
1532-0979
DOI
10.1097/PAS.0b013e31826c1761
pmid
23348204
Publisher site
See Article on Publisher Site

Abstract

ORIGINAL ARTICLE Dedifferentiation in Gastrointestinal Stromal Tumor to an Anaplastic KIT-negative Phenotype: A Diagnostic Pitfall Morphologic and Molecular Characterization of 8 Cases Occurring Either De Novo or After Imatinib Therapy Cristina R. Antonescu, MD,* Salvatore Romeo, MD,w Lei Zhang, MD,* Khedoudja Nafa, PhD,* Jason L. Hornick, MD, PhD,z Gunnlaugur Petur Nielsen, MD,y Mari Mino-Kenudson, MD,y Hsuan-Ying Huang, MD,8 Juan-Miguel Mosquera, MD,z Paolo A. Dei Tos, MD,w and Christopher D.M. Fletcher, MDz pression and de novo expression of either cytokeratin (4/8) or Abstract: Most gastrointestinal stromal tumors (GISTs) can be desmin (1/8). There was no difference in the KIT genotype be- recognized by their monotonous cytologic features and over- tween the 2 components. However, 2 imatinib-resistant tumors expression of KIT oncoprotein. Altered morphology and loss of showed coexistence of KIT exon 11 and exon 13 mutations. CD117 reactivity has been described previously after chronic Fluorescence in situ hybridization showed loss of 1 KIT gene in imatinib treatment; however, this phenomenon has not been 3 cases and low-level amplification of KIT in 2 other cases in the reported in imatinib-naive tumors. Eight patients with abrupt CD117-negative component, compared with the CD117-positive transition from a classic CD117-positive spindle cell GIST to an

Journal

American Journal of Surgical PathologyWolters Kluwer Health

Published: Mar 1, 2013

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