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Your search keyword '"Carpentieri, David F."' showing total 26 results
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26 results on '"Carpentieri, David F."'

1. A comparative analysis of RAS variants in patients with disorders of somatic mosaicism

Author

Claire Hou, Ying-Chen, primary, Evenson, Michael J., additional, Corliss, Meagan M., additional, Mahapatra, Lily, additional, Aldawood, Ali, additional, Carpentieri, David F., additional, Chamlin, Sarah L., additional, Kulungowski, Ann M., additional, Madan-Khetarpal, Suneeta, additional, Sebastian, Jessica, additional, Pet, Mitchell A., additional, Coughlin, Carrie C., additional, Willing, Marcia C., additional, Pearson, Gregory D., additional, Setty, Bhuvana A., additional, El-Haffaf, Zaki, additional, Cottrell, Catherine E., additional, Parikh, Bijal A., additional, Krysiak, Kilannin, additional, Schroeder, Molly C., additional, Heusel, Jonathan W., additional, Neidich, Julie A., additional, and Cao, Yang, additional

Published
2023
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5. Protocol for the examination of specimens from pediatric and adult patients with ssseous and extraosseous Ewing Sarcoma family of tumors, including peripheral primitive neuroectodermal tumor and Ewing Sarcoma

Author

Carpentieri, David F., Qualman, Stephen J., Bowen, Jay, Krausz, Thomas, Marchevsky, Alberto, and Dickman, Paul S.

Subjects
Medical protocols -- Practice, Ewing's sarcoma -- Medical examination, Ewing's sarcoma -- Evaluation, Children -- Diseases, Children -- Diagnosis, Children -- Medical examination
Published
2005

12. Multilevel dysregulation of STAT3 activation in anaplastic lymphoma kinase-positive T/null-cell lymphoma

Author

Zhang, Qian, Raghunath, Puthryaveett N, Xue, Liquan, Majewski, Miroslaw, Carpentieri, David F, Odum, Niels, Morris, Stephan, Skorski, Tomasz, Wasik, Mariusz A, Zhang, Qian, Raghunath, Puthryaveett N, Xue, Liquan, Majewski, Miroslaw, Carpentieri, David F, Odum, Niels, Morris, Stephan, Skorski, Tomasz, and Wasik, Mariusz A

Abstract

Udgivelsesdato: 2002-Jan-1, Accumulating evidence indicates that expression of anaplastic lymphoma kinase (ALK), typically due to t(2;5) translocation, defines a distinct type of T/null-cell lymphoma (TCL). The resulting nucleophosmin (NPM) /ALK chimeric kinase is constitutively active and oncogenic. Downstream effector molecules triggered by NPM/ALK remain, however, largely unidentified. Here we report that NPM/ALK induces continuous activation of STAT3. STAT3 displayed tyrosine phosphorylation and DNA binding in all (four of four) ALK+ TCL cell lines tested. The activation of STAT3 was selective because none of the other known STATs was consistently tyrosine phosphorylated in these cell lines. In addition, malignant cells in tissue sections from all (10 of 10) ALK+ TCL patients expressed tyrosine-phosphorylated STAT3. Transfection of BaF3 cells with NPM/ALK resulted in tyrosine phosphorylation of STAT3. Furthermore, STAT3 was constitutively associated with NPM/ALK in the ALK+ TCL cell lines. Additional studies into the mechanisms of STAT3 activation revealed that the ALK+ TCL cells expressed a positive regulator of STAT3 activation, protein phosphatase 2A (PP2A), which was constitutively associated with STAT3. Treatment with the PP2A inhibitor calyculin A abrogated tyrosine phosphorylation of STAT3. Finally, ALK+ T cells failed to express a negative regulator of activated STAT3, protein inhibitor of activated STAT3. These data indicate that NPM/ALK activates STAT3 and that PP2A and lack of protein inhibitor of activated STAT3 may be important in maintaining STAT3 in the activated state in the ALK+ TCL cells. These results also suggest that activated STAT3, which is known to display oncogenic properties, as well as its regulatory molecules may represent attractive targets for novel therapies in ALK+ TCL.

Published
2002

20. A comparative analysis of RASvariants in patients with disorders of somatic mosaicism

Author

Claire Hou, Ying-Chen, Evenson, Michael J., Corliss, Meagan M., Mahapatra, Lily, Aldawood, Ali, Carpentieri, David F., Chamlin, Sarah L., Kulungowski, Ann M., Madan-Khetarpal, Suneeta, Sebastian, Jessica, Pet, Mitchell A., Coughlin, Carrie C., Willing, Marcia C., Pearson, Gregory D., Setty, Bhuvana A., El-Haffaf, Zaki, Cottrell, Catherine E., Parikh, Bijal A., Krysiak, Kilannin, Schroeder, Molly C., Heusel, Jonathan W., Neidich, Julie A., and Cao, Yang

Abstract

RASgenes (HRAS, KRAS, and NRAS) are commonly found to be mutated in cancers, and activating RASvariants are also found in disorders of somatic mosaicism (DoSM). A survey of the mutational spectrum of RASvariants in DoSM has not been performed.

Published
2023
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24. Ectomesenchymoma with Embryonal Rhabdomyosarcoma and Ganglioneuroma, Arising in Association with Benign Triton Tumor of the Tongue.

Author

VANDENHEUVE, KATHERINE A., CARPENTIERI, DAVID F., JIE CHEN, KAR-MING FUNG, and PARHAM, DAVID M.

Subjects
RHABDOMYOSARCOMA, CHARONIA, NERVE tissue, RETINAL ganglion cells, CANCER
Abstract

Soft-tissue tumors known as "triton" tumors are rare lesions containing neural tissue and skeletal muscle at varying levels of maturity and malignant potential. Benign triton tumors, also called "neuromuscular choristomas" or "neuromuscular hamartomas," consist of neural tissue containing mature skeletal muscle in intimate relationship with peripheral nerve. These tumors are rare in the head and neck in children. Ectomesenchymomas are similar tumors consisting of a malignant mesenchymal component, usually embryonal rhabdomyosarcoma, and a neuroectodermal component represented by mature ganglion cells or primitive neuroblastic/ neuroectodermal foci (primitive ectomesenchymoma). Benign triton tumors have been regarded as benign, whereas ectomesenchymomas have been operationally considered to be variants of rhabdomyosarcoma. We present here a unique case that combines features of these 2 entities in a recurrent lesion on the tongue of a 35- month-old girl. This lesion raises questions about the "benign" nature of benign triton tumor and its possible relationship to ectomesenchymoma. [ABSTRACT FROM AUTHOR]

Published
2014
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26. Coincident expression of the chemokine receptors CCR6 and CCR7 by pathologic Langerhans cells in Langerhans cell histiocytosis

Author

Fleming, Mark D., Pinkus, Jack L., Alexander, Sarah W., Tam, Carmen, Loda, Massimo, Sallan, Stephen E., Nichols, Kim E., Carpentieri, David F., Pinkus, Geraldine S., and Rollins, Barrett J.

Abstract

It has been suggested that a switch in chemokine receptor expression underlies Langerhans cell migration from skin to lymphoid tissue. Activated cells are thought to down-regulate CCR6, whose ligand macrophage inflammatory protein-3α (MIP-3α)/CCL20 is expressed in skin, and up-regulate CCR7, whose ligands are in lymphoid tissues. In Langerhans cell histiocytosis (LCH), pathologic Langerhans cells (LCs) accumulate in several tissues, including skin, bone, and lymphoid organs. We have examined 24 LCH cases and find that pathologic LCs expressed CCR6 and CCR7 coincidentally in all cases. Furthermore, MIP-3α/CCL20 is expressed by keratinocytes in involved skin and by macrophages and osteoblasts in involved bone. Expression of CCR6 by pathologic LCs may contribute to their accumulation in nonlymphoid organs such as skin and bone, whereas CCR7 expression may direct them to lymphoid tissue. Histiocytes in Rosai-Dorfman disease and hemophagocytic syndrome also coexpressed CCR6 and CCR7, suggesting that this may be a general attribute of abnormal histiocytes.

Published
2003
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